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Pediatric Sonography
FOURTH EDITION

Editor

Marilyn J. Siegel
Professor of Radiology and Pediatrics
The Edward Mallinckrodt Institute of Radiology
Washington University School of Medicine
St. Louis, Missouri
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Library of Congress Cataloging-in-Publication Data

Pediatric sonography / editor, Marilyn J. Siegel. 4th ed.

p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-60547-665-0 (alk. paper)
1. Diagnostic ultrasonic imaging. 2. Pediatric diagnostic imaging.
I. Siegel, Marilyn J.
[DNLM: 1. Ultrasonographymethods. 2. Child. 3. Infant. WN 240
P3726 2010]
RJ51.U45P43 2010
618.9200754dc22
2010022392

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10 9 8 7 6 5 4 3 2 1
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To my husband, Barry
my mentor, colleague, friend, and loving spouse. His unwavering support and
encouragement gave me the energy to make this project a reality.

To my parents, Harry and Bess

who taught me the value of learning and who were in large part responsible for my
achieving many of my academic goals and ultimately entering medicine.

To all the radiology residents and fellows with whom I have had the opportunity to work
at the Mallinckrodt Institute of Radiology. Their quest for knowledge acted as the stimulus
for me to write this book.
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Contributors

Ellen M. Chung, MD William D. Middleton, MD, FACR

Pediatric Radiologist Professor of Radiology
Department of Radiology and Radiologist Sciences The Edward Mallinckrodt Institute of Radiology
Uniformed Services University of the Health Sciences Washington University School of Medicine
Bethesda, Maryland Barnes Jewish Hospital
St. Louis, Missouri
Brian D. Coley, MD
Clinical Professor Marilyn J. Siegel, MD
Departments of Radiology and Pediatrics Professor of Radiology and Pediatrics
The Ohio State University College of Medicine and Public Health The Edward Mallinckrodt Institute of Radiology
Chief, Section of Ultrasound Washington University School of Medicine
Department of Radiology St. Louis, Missouri
Nationwide Childrens Hospital
Columbus, Ohio

Nirvikar Dahiya, MD
Assistant Professor
Department of Abdominal Imaging
The Edward Mallinckrodt Institute of Radiology
Washington University School of Medicine
Barnes and Jewish Hospital
St. Louis, Missouri

v
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ince the publication of the third edition of Pediatric Sonogra-
S phy in 2002, important technologic advances continue to be
made in ultrasonography. We have seen innovations in soft-
ware and technology, such as harmonic imaging, contrast agents,
and 3D imaging, which have contributed to an increased utiliza-
tion of ultrasonography as a diagnostic tool. These changes have
also impacted clinical practice by improving our understanding of
the role of ultrasonography in the evaluation of disease processes
in children. In addition, compared with computed tomography
and magnetic resonance imaging, ultrasonography is a more cost-
effective imaging test for investigating many pediatric problems.
Particularly important is the fact that ultrasonography is nonin-
vasive and does not use ionizing radiation, making a compelling
case for even more widespread use of this modality in the pedi-
atric population. Given these facts, there is a need for an updated
text for radiologists to use in practice or training.
The goal of the fourth edition of Pediatric Sonography is
again to provide a comprehensive text on the clinical applications
of sonography in a pediatric population. Virtually all chapters
have been extensively revised with new illustrations and images
added. To reflect the evolving clinical applications of sonography,
there is a new chapter on breast sonography. Top radiologists
who are recognized authorities in sonography again have been
recruited to share their expertise in special areas.
Preface
This book is intended primarily for practicing radiologists,
radiology residents and fellows, and sonographers. Other physi-
cians, such as pediatricians and surgeons, also can derive useful
information about the clinical indications and relative value of
sonography in the pediatric patient.
As in the first three editions, the first two chapters of this edi-
tion present a detailed review of ultrasound physics and the artifacts
and pitfalls that are encountered in practice. The remainder of the
book is divided into chapters covering thirteen anatomic areas:
head, neck, chest, breast, liver, biliary tract and gallbladder, spleen
and peritoneum, gastrointestinal tract, kidneys, retroperitoneum,
female and male pelvis, and musculoskeletal system. Each chapter
includes practical sonographic techniques, normal sonographic
anatomy, and abnormal sonographic findings specific for that organ
system. Instruction also is provided on how to avoid technical and
interpretative errors. Additionally, the use of sonography and alter-
native imaging studies for solving common clinical problems is dis-
cussed. The final chapter describes the role of sonography in guid-
ing aspiration, biopsy, and drainage procedures.
It is my sincere hope that readers will find this work to be a
cornerstone of pediatric imaging and one that they will use fre-
quently in their daily practices. I have strived to produce a text
that is readable and offers guidance for radiologists and sonog-
raphers on the appropriate use of sonography in children.
vii
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Acknowledgments
riting a book is a task that requires time and commitment
W from many people. As editor, it would not have been pos-
sible for me to complete this task without the contributions
of many other individuals, who I acknowledge below.
I offer sincere thanks to Dr. Brian Coley of Columbus Chil-
drens Hospital, Dr. Ellen M. Chung, Department of Radiologic
Pathology, Armed Forces Institute of Pathology, and Drs. William
Middleton and Nirvikar Dahiya of the Mallinckrodt Institute of
Radiology. They graciously shared their invaluable experience
and expertise to bring depth to important chapters.
A special note of gratitude goes to my secretary, Janine
Wuebbles, who spent many hours acquiring references and ulti-
mately checking their accuracy in the proofs. Without her sup-
port, this book could not have been finished in a timely fashion.
My thanks also goes to my sonographers, Deborah Reiter, Janet
Hurt, Angela Heffernan, Amy Devall, and Shelly Lopez, who
viii
remain dedicated to performing high-quality examinations on
children.
I would also like to express my appreciation to the publish-
ing team at Lippincott Williams & Wilkins for their effort and
professionalism in directing this project. Most particularly, I
would like to thank Ryan Shaw and Brian Brown, for their ded-
ication and advice. Of course, I need to thank Lisa McAllister
who cajoled me into taking up the editorial pen once again. With-
out her efforts, this book would not have happened. I also
express appreciation to Chris Miller, who transformed the pages
into print and prepared the illustrative material. Her dedication
is reflected in the high quality of the final product.
Finally, I wish to thank one more very important personmy
husband, Barry A. Siegel, M.D., for his support and patience dur-
ing the many hours that I spent writing and editing this book. His
unconditional support made the completion of this book a reality.
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Contents

Contributors v
Preface vii 10 Gastrointestinal Tract . . . . . . . . . . . . . . . 339
Acknowledgments viii Marilyn J. Siegel

1 Physical Principles and Instrumentation . . . 1 11 Urinary Tract . . . . . . . . . . . . . . . . . . . . . 384

Nirvikar Dahiya, William D. Middleton, and Marilyn J. Siegel Marilyn J. Siegel

2 Ultrasound Artifacts . . . . . . . . . . . . . . . . 21 12 Adrenal Glands, Pancreas, and Other

William D. Middleton, Marilyn J. Siegel, and Nirvikar Dahiya Retroperitoneal Structures . . . . . . . . . . . 461
Marilyn J. Siegel and Ellen M. Chung
3 Brain . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43
Marilyn J. Siegel
13 Female Pelvis . . . . . . . . . . . . . . . . . . . . 509
Marilyn J. Siegel
4 Head and Neck . . . . . . . . . . . . . . . . . . . 118
Marilyn J. Siegel
14 Male Genital Tract . . . . . . . . . . . . . . . . . 554
Brian D. Coley and Marilyn J. Siegel
5 Chest . . . . . . . . . . . . . . . . . . . . . . . . . . 164
Marilyn J. Siegel
15 Musculoskeletal System and
Vascular Imaging . . . . . . . . . . . . . . . . . . 602
6 Breast . . . . . . . . . . . . . . . . . . . . . . . . . 200 Marilyn J. Siegel
Ellen Chung and Marilyn J. Siegel

16 Spinal Ultrasonography . . . . . . . . . . . . . . 647

7 Liver . . . . . . . . . . . . . . . . . . . . . . . . . . 214 Brian D. Coley and Marilyn J. Siegel
Marilyn J. Siegel

17 Ultrasound-Guided
8 Gallbladder and Biliary Tract . . . . . . . . . . 275 Interventional Procedures . . . . . . . . . . . . 675
Marilyn J. Siegel Brian D. Coley

Appendix 701
9 Spleen and Peritoneal Cavity . . . . . . . . . 305
Marilyn J. Siegel Index 711

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Physical Principles and
Instrumentation
NIRVIKAR DAHIYA, WILLIAM D. MIDDLETON, AND MARILYN J. SIEGEL
Acoustics Real-Time Imaging
Wavelength and Frequency Mechanical Transducers
Propagation of Sound Multiple-element Array Transducers
Transducer Selection
Instrumentation
Transmitter Harmonic Imaging
Transducers
Extended-Field-of-View Imaging
Receiver
Image Display Real-Time Compounding
Image Storage Three-Dimentional Ultrasound Imaging
ltrasonography has been a valuable method for dis-
U playing normal and abnormal anatomy for many years.
There are many reasons why it is an especially attrac-
tive imaging technique in the pediatric age group. One of
the most important features of sonography is its lack of ion-
izing radiation. An important goal in imaging the pediatric
patient is to obtain diagnostic information with the least
amount of radiation exposure. Sonography can provide
clinically useful information without apparent biologic ef-
fects on the patient or the operator.
A second appealing aspect of sonography is the real-
time nature of the examination. This makes it easier to
examine patients who cannot suspend respiration, are
uncooperative, or are crying, all common problems among
pediatric patients. In addition, the real-time nature of the
examination allows evaluation of rapidly moving struc-
tures, such as the heart.
A third advantage of sonography is its multiplanar
imaging capability. Newer real-time equipment enables
great flexibility in the selection of imaging planes and the
ease of altering these planes. This capability is especially
helpful in determining the origin of pathologic masses
and in analyzing spatial relationships of various struc-
tures. These advantages have been expanded even fur-
ther with the advent of three-dimensional (3D) ultra-
sound.
Another advantage of sonography in the pediatric age
group is its excellent resolution, which is related to the
size of the patient and the smaller amounts of body fat.
The lack of significant body wall and intra-abdominal fat
in most small children is a great advantage in the exami-
nation of pediatric patients because fat generally
CHAPTER
1
Doppler Sonography
Continuous-wave Doppler
Pulsed Doppler
Color Doppler
Power Mode Doppler
Elastography
Contrast Agents
degrades the ultrasonographic image. For a given sono-
graphic unit and a given type of transducer, higher trans-
mitted frequencies provide better image resolution, but
poorer penetration. These conflicting characteristics of
transducer frequency force a compromise in adults, in
whom lower frequencies must be used to obtain adequate
depth of penetration at the expense of image resolution.
However, the need for greater depth of penetration is less
in children than it is in adults, reflecting the differences
in body habitus. Therefore, higher-frequency, higher-res-
olution transducers can be used routinely in pediatric
examinations.
The ability to perform the examination using portable
equipment is another advantage that sonography has over
other cross-sectional modalities, such as computed tomog-
raphy (CT) and magnetic resonance imaging (MRI). This
is obviously important in evaluating patients who cannot
be transported to the radiology department because of
their underlying condition or because of their dependence
on monitoring devices.
Finally, in the era of medical cost containment, the rel-
ative inexpensiveness of ultrasonography, compared with
CT or MRI, makes it an attractive imaging study for many
clinical problems. The issue of cost makes ultrasonography
especially appealing in situations in which multiple
sequential examinations are necessary or when screening
of large patient populations is desired.
All of these factors make ultrasonography an extremely
valuable tool in the investigation of pediatric disorders.
Therefore, any radiologist who performs diagnostic ultra-
sonography on pediatric patients must have an under-
standing of the physical principles of this technique and
1
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2 P E D I AT R I C S O N O G R A P H Y
the instrumentation available for detecting and displaying
the acoustic information. This information has been
described in detail in several comprehensive textbooks,
chapters, and review articles (16). This chapter will be
limited to the basic physical principles and the instrumen-
tation that are most relevant to the practice of diagnostic
ultrasound.
ACOUSTICS
Wavelength and Frequency
Sound is the result of mechanical energy traveling
through matter in the form of a wave with alternating
compression and rarefaction of the conducting medium.
Human hearing encompasses a range from 20 to 20,000
Hz. Ultrasound differs from audible sound only in its
higher frequency. The term ultrasound refers to sound
above the audible range (i.e., 20 kHz). Diagnostic
sonography generally operates at frequencies of 1 to
20 MHz.
Propagation of Sound
Most diagnostic ultrasound examinations use brief bursts
of energy that are transmitted into the body, where they
travel through tissue. In tissue and fluid, sound is propa-
gated along the direction of the particles being displaced.
The resistance of the tissues being compressed largely
determines the speed at which the sound wave travels. The
velocity of propagation is constant for a given tissue and is
not affected by the frequency or wavelength of the sound
wave. In soft tissues, the assumed average propagation
velocity is 1540 meters/sec. Fluid and fat have slightly
slower propagation velocities.
After the sound pulse is generated and transmitted
into the body, it can be reflected, refracted, scattered, or
absorbed (7). Reflection or backscatter occurs whenever
the sound pulse encounters an interface between tissues
that have different acoustic impedances. Acoustic
impedance is equal to the tissue density times the speed
of sound propagation in that tissue. The amount of
sound that is reflected at an interface varies with the dif-
ference in acoustic impedance between the tissues and
the angle of incidence of the sound beam. The greater
the acoustic impedance mismatch is, the greater the
backscatter or sound reflection. Reflection does not
occur in a homogeneous medium that has no interfaces
to reflect sound and, consequently, the medium appears
anechoic or cystic.
Refraction refers to a change in the direction of the
sound as it passes from one tissue into another. Refraction
occurs when sound encounters an interface between two
tissues that transmit sound at different speeds. Because the
sound frequency remains constant, the sound wavelength
must change to accommodate the difference in the speed of
sound in the two tissues. The result of this change in wave-
length is a redirection of the sound pulse as it passes
through the interface. Refraction is important because it is
one of the causes of misregistration of a structure on an
ultrasound image. Refraction and its resultant artifacts are
discussed in more detail in Chapter 2.
Scattering refers to the redirection of sound in many
different directions. This phenomenon occurs when the
sound pulse encounters an acoustic interface that is not
smooth. Scattering can also occur in solid tissues and
organs as a result of the heterogeneity (i.e., multiple small
interfaces) of biologic tissues.
Absorption refers to the loss of sound energy secondary
to its conversion to thermal energy. Absorption is greater
in soft tissues than in fluid, and it is greater in bone than
in soft tissues. Sound absorption is the major cause of
acoustic shadowing.
The combined effects of reflection, scattering, and
absorption are a decrease in the intensity of the sound
pulse as it travels through matter. This decrease in inten-
sity is termed attenuation. As a result of attenuation, an
acoustic interface in the deeper tissues produces a
weaker reflection than an identical interface in the super-
ficial tissues. To compensate for this degradation in
sound intensity, echoes returning from the deeper por-
tions of the image are electronically amplified. This is
referred to as distance gain compensation or time gain
compensation.
INSTRUMENTATION
The essential components of all scanners are a transmitter
to energize the transducer; the transducer, which is the
source of the sound pulses; a receiver to detect the reflected
signals; a display that presents the data for viewing; and,
finally, a storage module.
Transmitter
The transmitter activates the transducer, which causes it to
vibrate and create a pulse of sound that can be transmitted
into the body. This is done by the application of short,
high-amplitude voltage pulses. The maximum voltage that
may be applied to the transducer and, hence, the acoustic
output of diagnostic scanners is limited by federal regula-
tions.
Transducers
The transducer converts electric energy generated by the
transmitter into acoustic pulses, which are transmitted into
the patient. It also receives the reflected echoes, converting
pressure changes back into electric signals. Because the
crystal element converts electric energy into pressure waves
and vice versa, it is referred to as a piezoelectric crystal
(i.e., pressure electric).
The sound pulses used for diagnostic sonography are
generated by ceramic crystal elements housed within the
ultrasonic transducer. These ceramic crystals deform
when the transducer is electrically stimulated, resulting
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Chapter 1 P H Y S I C A L P R I N C I P L E S A N D I N S T R U M E N TAT I O N
in a band of frequencies. The range of frequencies pro-
duced by a given transducer is referred to as the band-
width. The preferential frequency produced by a trans-
ducer is equal to the resonant frequency of the crystal
element, which in turn is dependent on the thickness of
the crystal.
The ultrasound pulses produced by the transducer
must travel through tissue to generate diagnostic infor-
mation. The transfer of energy from the transducer to
tissue requires the use of a coupling gel. After entering
the body, the ultrasound pulses may be propagated,
reflected, refracted, scattered, or absorbed as discussed
previously. The small pressure changes from reflections
that return to the transducer distort the crystal element
and stimulate the transducer. This distortion once again
generates an electric pulse that can then be processed
into an image.
Receiver
The returning echoes hit the transducer face, producing
voltage differences across the piezoelectric crystal. The
receiver detects, amplifies, and processes the voltage
changes that return to it. The time gain compensation con-
trol amplifies the weaker signals from deeper structures,
thus compensating for tissue attenuation. The receiver also
compresses and remaps the backscattered signals. This
changes the brightness of different echo levels in the image,
which in turn affects image contrast.
Image Display
A- AND B-MODE IMAGING
Ultrasound images have been displayed in A-mode and B-
mode formats. The A (amplitude)-mode format was the
earliest format for displaying sound signals returning to
the transducer. With this format, the reflections arising
from tissue interfaces were displayed in graphic form with
time on the horizontal axis and echo amplitude on the ver-
tical axis.
The B (brightness) mode displays the returning
sound signal two-dimensional (2D) image with higher-
amplitude echoes appearing brighter than lower-amplitude
echoes. In both A- and B-mode sonography, the distance
of the reflector from the transducer is obtained by con-
verting the time taken for the echo to return to the trans-
ducer to a distance. This is based on the speed of sound
in soft tissues, which is equal to 1540 meters/sec. In gen-
eral, the range of brightness should be as wide as possi-
ble in order to differentiate small differences in echo
intensity.
In the early two-dimensional units, the B-mode trans-
ducer was attached to an articulated arm that was capa-
ble of determining the exact location and orientation of
the transducer in space. This allowed the origin of the
returning echoes to be localized in two dimensions. Then,
by sweeping the transducer across the patients body, a
series of B-mode lines of information could be added
3
together to produce a two-dimensional image. With static
B-mode imaging it was possible to view large organs, such
as the liver, in one cross-sectional image. The major dis-
advantage of static B-mode imaging was its lack of real-
time capabilities. Because of this limitation, static articulated-
arm B-mode devices have now been replaced by real-time
units.
Image Storage
Permanent storage of images for analysis and archiving
was originally done in the form of transparencies printed
on hard-copy radiographic film. However, computers
and digital storage are now used for reviewing images and
archiving the sonographic data. Digital Imaging and
Communications in Medicine (DICOM) standards are in
place to sustain image compatibility between different
ultrasound systems and transfer and storage of these
images.
REAL-TIME IMAGING
Real-time imaging permits investigation of both anatomy
and motion. The effect of motion is achieved when images
are displayed at rates of several frames per second. Thus,
the information is regarded as being viewed in real time.
Several transducers are available for real-time imaging.
Mechanical Transducers
The earliest and simplest transducer design was the
mechanical sector transducer, which used a single large
piezoelectric element to generate and receive the ultra-
sound pulses. Beam steering was accomplished by an oscil-
lating or rotating motion of the crystal element itself or by
reflection of the sound pulse off an oscillating acoustic mir-
ror. Beam focusing was done by using different-shaped
crystal elements or by attaching an acoustic lens to the
transducer. The disadvantage of the mechanical sector
transducer was the absence of variable focusing. The only
way to vary the focus distance was to switch to a com-
pletely different transducer. Because of their lack of flexi-
bility, mechanical sector transducers have been almost
entirely replaced by multiple-element electronic transduc-
ers, commonly called arrays.
Multiple-element Array Transducers
The array transducers contain groups of small crystal ele-
ments that can steer and focus the ultrasound beam elec-
tronically (8). The basic types of arrays are the phased
array and the linear array.
PHASED ARRAY SECTOR TRANSDUCER
With the phased array transducer, each sound pulse is cre-
ated by the composite of multiple pulses generated by each
element in the array. By varying the time and sequence in
which the individual elements are fired, the composite
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4 P E D I AT R I C S O N O G R A P H Y
A C
D ter of the probe. Therefore, the apex of the sector comes to a point.
sound beam can be steered in different directions (Fig. 1.1)
and can be focused at different depths (Fig. 1.2). Because
the sound beams are generated at varying angles from one
side of the transducer to the other, a sector image format is
produced (Fig. 1.3). The focal zone can be adjusted by the
operator, depending on the location of the structure of
interest. Another capability of phased array sector trans-
ducers is the ability to focus at multiple levels simultane-
ously, although this is accomplished at the expense of a
decreased frame rate. Compared with the other electronic
array transducers (discussed later), the phased array type is
smaller and has a larger deep field of view. However,
phased arrays have a small superficial field of view and
A B
Phased array viewed from the side. In this illustration, there
Fig. 1.1
are 16 elements in the array. All of the elements are acti-
vated to generate each individual composite sound pulse. A: By firing
the elements on the right side of the array first, a composite pulse is
created that is steered to the left. B: By firing all of the elements simul-
taneously, the composite pulse is steered straight down. C: By firing
the left elements first, the pulse is steered to the right. D: The resulting
image has a sector format. Because all the elements are used for each
sound pulse, the center axis of the beam always arises from the cen-
poor near-field focusing capabilities. The focusing capabil-
ities in the periphery of the image are also limited, because
the center axis of the beam arises from the center of the
transducer (Fig. 1.4).
LINEAR ARRAY OR LINEAR SEQUENCED ARRAY TRANSDUCERS
Unlike phased arrays, in which all individual crystal ele-
ments are used to generate the sound pulse, linear arrays
activate a group of adjacent elements to generate each
pulse. The individual elements of this transducer are
arranged in a linear fashion. By firing groups of transducer
elements in succession, a series of sound pulses is produced
along the face of the transducer and thus has the same effect
Focusing of array transducers. Sixteen-element phased
Fig. 1.2
array viewed from the side. A: By slightly delaying the firing
of the center elements, the composite pulse is focused in the far field.
B: By increasing the delay in firing of the central elements, the com-
posite pulse is focused in the near field.
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Chapter 1 P H Y S I C A L P R I N C I P L E S A N D I N S T R U M E N TAT I O N 5

Longitudinal view of the right kidney (RK) and liver (L) obtained with a 3-MHz electronic phased array transducer. The multiple focal zone
Fig. 1.3
indicators to the right of the image reflect the ability of phased array transducers to focus at variable and multiple depths.

Focusing capabilities of phased array transducers. View of an ultrasound phantom shows a number of identical metal pins that are
Fig. 1.4
imaged in cross section. Note that the pins at the edge of the image (open arrows) are displayed as larger reflectors than the pins in the
center of the image (solid arrow). This is secondary to the poorer focusing capabilities of phased array transducers in the periphery of the image.
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6 P E D I AT R I C S O N O G R A P H Y

A B C D E

B
Linear array transducer viewed from the side. In this illustra-
Fig. 1.5
tion there are 40 individual elements. A: Each composite
pulse is created by the activation of three adjacent elements. The first
pulse is created by activation of elements one through three, the second
pulse by elements two through four, the third pulse by elements three
through five, and so on. B: The resulting image format is rectangular.
F
Trapezoidal array viewed from the side. In this eight-
Fig. 1.7
element array the beam is sequentially steered and moved
from the left to the right (AE) by varying the timing of activation of four
adjacent elements. This mechanism borrows the steering action of a
phased array, but like a linear array, only uses a limited number of ele-
ments to form each sound pulse. F: The image format is a sector.
Because each pulse arises from a different segment of the transducer,
the apex is flat instead of pointed.

A B
Transverse view of the scrotum using a 10-MHz linear array transducer. A: Using the standard rectangular format, the two testes are par-
Fig. 1.6
tially imaged. The limited field of view excludes the lateral aspect of both testes. B: Using the trapezoidal format, the field of view is larger
and both testes are seen in their entirety. As with the phased array transducer, the linear array can focus at multiple and variable depths. It also
provides excellent resolution in the superficial field of view.
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Chapter 1 P H Y S I C A L P R I N C I P L E S A N D I N S T R U M E N TAT I O N 7

Fig. 1.8 Longitudinal view of the right kidney (RK) and liver (L) obtained with a trapezoidal array. The format is a sector with a flat apex.

as scanning with a single-element transducer (Fig. 1.5). With TWO-DIMENSIONAL ARRAYS

early linear arrays, each sound pulse traveled in the same The array transducers described previously allow for vari-
direction (parallel) and was oriented perpendicular to the able depth and electronically controlled focusing of the
transducer surface, resulting in a rectangular image (Fig. sound beam in the plane of the image but not in the direc-
1.6A). Currently, beam steering is available with most lin- tion perpendicular to the plane of imaging. The net effect of
ear array transducers so that a trapezoidal format is also
available (Fig. 1.6B). The major advantages of linear array
transducers are high resolution in the near field and a large
superficial field of view. Focusing is more uniform in the
center and periphery of the image because there is little or
no beam steering. The major disadvantages of linear arrays A
are their limited deep field of view and their large size,
which limits their use in areas where access is limited, such
as in intercostal scanning.
The disadvantages of the linear array transducers can
be minimized by steering the sound pulses so that they
diverge from each other. The two types of probes that
diverge sound pulses are the vector and curved linear
arrays. Both transducers produce images with sector dis-
play formats and large superficial fields of view. The vector
or trapezoidal array transducers can be thought of as small
linear arrays that operate only in the trapezoidal format
(Fig. 1.7). They produce a sector-like image format with a
flat apex (Fig. 1.8) in contradistinction to the pointed apex B
of the sector transducer. The curved linear array trans- Curved array viewed from the side. A: Operation is similar
ducer (also known as the curved array, convex array, and Fig. 1.9
to the linear array shown in Figure 1.7. B: The image format
curvilinear array) (Fig. 1.9) produces an image with a con- is a sector. Due to the curved surface of the transducer, the apex of the
vex instead of a flat apex (Fig. 1.10). sector is curved.
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8 P E D I AT R I C S O N O G R A P H Y
Fig. 1.10 Longitudinal view of the right kidney (RK) and the liver (L) obtained with a curved array transducer.
conventional in-plane focusing is on lateral resolution in
the plane of imaging. Focusing the beam in the out-of-plane
direction (also called the elevation plane) affects the out-of-
plane resolution, which is identical to the slice thickness.
With the conventional array transducers, the slice thickness
is fixed and cannot be varied by the operator (Fig. 1.11).
A solution to variable focusing in the elevation plane is
the matrix or two-dimensional array (Fig. 1.12). These
probes have crystal elements that are stacked in columns as
well as rows. They allow for variable slice thickness that is
A B
controlled electronically, allowing for integration of color
Doppler techniques and other time-consuming techniques.
THREE-DIMENSIONAL VOLUME PROBES
As the name suggests, three-dimensional volume probes
are dedicated 3D ultrasound transducers that are capable
of volume acquisition. They are bulky in size and house a
2D array transducer in a casing. The 2D array transducer
is surrounded by a coupling gel and is driven by a motor
as it sweeps through a preselected volume angle. Added to
Focusing of standard array transducers. A: Illustration of
Fig. 1.11
one individual composite sound pulse generated by firing
three adjacent elements of a linear array transducer. B: The slice
thickness is least in the middle of the pulse due to the curvature of the
elements. This is fixed and cannot be controlled by the operator. The
in-plane focusing is least in the middle of the pulse due to the elec-
tronic focusing. This is variable.
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B
Comparison of conventional array and two-dimensional array. A: Conventional dual scans of the radial artery (cursors) in transverse
Fig. 1.12
and longitudinal plane obtained with an operating frequency of 9 MHz. Notice that the artery appears relatively anechoic on the trans-
verse image because in this plane, volume-averaging effects are not an issue. However, in the longitudinal plane, the slice thickness is greater than
the lumen of the vessel and volume-averaging effects with the adjacent soft tissues produce significant echoes within the lumen. B: Two-dimensional
array scans obtained with an operating frequency of 9 MHz. Because the slice thickness can be better controlled and reduced with this type of
transducer, the luminal diameter no longer exceeds the thickness of the slice and this eliminates the volume averaging in the longitudinal plane.
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10 P E D I AT R I C S O N O G R A P H Y

the motor is a magnetic sensing device that coordinates the

slices of acquisition with their relative position to each
other. This allows an acquisition of volume by maintaining
the geometric relationships. Maintaining geometric accu-
Coupling racy is important for spatial orientation and measurements
fluid when the information is viewed in multiplanar format or
as a volume (Fig. 1.13).
2D Array Transducer Selection
The selection of a transducer for a given application is
dependent on the distance of the object of interest from the
transducer. In general, the highest-frequency transducer
Gear for that permits penetration of sound to the target organ
moving
Case array should be used. Frequencies of 5.0 or occasionally 3.5
MHz are usually required for evaluation of deeper struc-
tures in the abdomen or pelvis. In obese children and ado-
lescents, frequencies as low as 2.0 MHz may be necessary.
For evaluation of superficial structures, 7.5- to 13.0-MHz
transducers are usually used.

Position
INTRACAVITARY PROBES
Motor sensing Recently, transducers have been designed that can be
device placed within various body lumens. These transducers
can be positioned close to the organ of interest, and thus,
higher frequencies can be used and higher-resolution
images can be obtained. The ability to image organs
without having to transmit the sound beam through the
abdominal wall and intra-abdominal tissues helps to
minimize the image-degrading properties of adipose
Cable tissue. The overall result is that the images are of much
higher quality than those obtained with a standard trans-
abdominal approach. The two most common intralumi-
Three-dimensional transducer. Illustration shows the nal probes are the transrectal and transvaginal transduc-
Fig. 1.13
basic design of a volume transducer. Inside the outer cas-
ers (Fig. 1.14). These are currently used in adults to
ing is a two-dimensional transducer that sweeps through a predefined
angle to acquire a volume. The magnetic sensor is incorporated inside
the probes outer case.

A B
Hemorrhagic ovarian cyst demonstrated with a 3.5-MHz transducer from a transabdominal approach (A) and a 7.5-MHz transvaginal
Fig. 1.14
approach (B). A nonspecific ovarian cyst is seen on the transabdominal scan. The improved resolution on the transvaginal scan demon-
strates lacy fibrinous intraluminal membranes typical of hemorrhagic cysts.
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image the prostate and female pelvic organs, respectively.
The endovaginal transducer has some applications in
adolescent girls (see Chapter 13). The rectal transducer
has no widespread use in children.
ENDOSCOPIC PROBES
Very small transducers have been added to flexible endo-
scopes to evaluate pathology in both the upper and lower gas-
trointestinal tract in adults. In the upper gastrointestinal tract,
these transducers can aid in evaluating esophageal and
periesophageal abnormalities, gastric wall lesions, and peri-
gastric organs. In the lower gastrointestinal tract, these endo-
scopic probes have been used to evaluate colonic carcinomas
and other mucosal and submucosal lesions. These transduc-
ers have not had widespread applications in children.
INTRA-ARTERIAL PROBES
Intra-arterial probes are the most recent addition to the
armamentarium of intraluminal sonographic devices. They
have been used in adults to evaluate a variety of abnor-
malities of the arterial wall.
HARMONIC IMAGING
Tissue harmonic sonography is based on the principle of non-
linear distortion of the fundamental sound signal as it travels
through body tissues. Harmonic wave frequencies are higher-
integer multiples of the fundamental or transmitted sound fre-
quency. They are produced by propagation of the sound wave
within tissues and progressively increase in intensity before
eventually decreasing because of attenuation. By comparison,
conventional sound waves are generated at the surface of the
transducer and progressively decrease in intensity as they
travel through the body. The same frequency that is transmit-
ted into the patient is subsequently received to create the
sonographic image. Although many harmonic frequencies are
generated with propagation of the initial wave, the current
technology uses only the second harmonic, which is twice the
transmitted frequency, for harmonic imaging. A filter is used
to remove the original transmitted frequency so that only the
returning high-frequency harmonic signal is processed to pro-
duce an image (915).
Experimental studies have shown that harmonic beams
are narrower than the transmitted beam and have fewer
side-lobe artifacts. Side-lobe artifacts are artifactual echoes
that are especially noticeable in fluid-filled structures. The
reduced width of the beam improves lateral resolution and
the reduction in artifacts improves the signal-to-noise
ratio. The increased lateral resolution improves the resolu-
tion of small objects. The higher signal-to-noise ratio
results in images where the tissues appear brighter and cav-
ities appear darker (Fig. 1.15) (9,12,14). Furthermore,
because harmonic signals are produced after the beam
enters the tissues of the body, the defocusing effects of body
wall fat are minimized. Results of clinical series have shown
that harmonic imaging can improve resolution of lesions
containing calcification (i.e., ureteral stones), fat, and air (9,
12). Harmonic imaging is particularly valuable in improv-
ing lesion visibility in obese patients.
Harmonic imaging also appears to have several theoret-
ical advantages over conventional contrast-enhanced
Doppler sonography in the evaluation of tissue blood flow.

A B
Harmonic ultrasound. A: Conventional scan of the liver obtained at a fundamental frequency of 3.4 MHz. A lesion is seen (cursors), but
Fig. 1.15
diffuse internal echoes make it impossible to diagnose a cyst with confidence. B: Harmonic scan of the same lesion obtained with a
transmit frequency of 1.9 MHz and a harmonic signal of 3.8 MHz. The lesion now appears anechoic and the diagnosis of a simple cyst can be made
with confidence.
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12 P E D I AT R I C S O N O G R A P H Y
By receiving the second harmonic frequency, backscatter
from contrast agents is much greater than that from tissue.
In addition, flash artifacts are eliminated, shadowing arti-
facts are minimized, and both spatial and temporal resolu-
tions are improved (1620). Experimental studies have sug-
gested that contrast-enhanced harmonic imaging may help
in detection of early acute urinary obstruction and focal
renal perfusion defects, such as those associated with
pyelonephritis or infarction (20,21).
EXTENDED FIELD-OF-VIEW IMAGING
Compared to other imaging techniques such as CT and
MRI, sonography has the advantages of being less
expensive, having real-time capabilities, and being non-
invasive. On the other hand, anatomic spatial relation-
ships and lesion size are readily appreciated using tech-
niques with large fields of view such as CT or MRI. One
disadvantage of ultrasound is its limited field of view.
This is especially true with the high-resolution linear
array transducer, which has a limited field of view due to
the small footprint of the transducer. Thus, anatomic
B
Extended field-of-view scans. A: Conventional longitudinal scan of the right lower quadrant shows a complex fluid collection (FC).
Fig. 1.16
B: Extended field-of-view scan shows the relationship of the fluid collection (FC) and the right kidney (K).
spatial relationships and sizes in ultrasound must often
be synthesized in the mind of the sonologist from multi-
ple real-time images that display only portions of the rel-
evant anatomy. It is often difficult to illustrate pertinent
findings and relevant anatomy to clinicians when using
high-frequency probes.
Image registrationbased position-sensing techniques
can now extend the sonographic field of view. The
extended field-of-view (EFOV) technology generates
panoramic images with no loss in resolution and without
an external position sensor (Fig. 1.16). The technology
uses an echo-trackingbased technique for estimating
probe motion that is applicable to all conventional real-
time transducers (22,23). Geometric measurement accu-
racy up to a 60-cm scan distance has been verified in phan-
toms (24). Small-scale tissue motion and off-plane probe
motion do not compromise accuracy.
REAL-TIME COMPOUNDING
With conventional linear array imaging, the sound beams
are steered straight down. With real-time compounding,
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B
Real-time compounding. A: Conventional scan of the rotator cuff. B: Scan obtained with real-time compounding produces a smoother
Fig. 1.17
image with better display of tissue interfaces and superior display of the fibrillar architecture of the cuff (arrow).

the sound is steered at multiple angles, as well as straight
down, and the resulting frames are averaged together.
Weak reflectors such as fluid will produce a minimal signal
from all directions. Intermediate reflectors may produce a
small signal from some angles but a larger signal from
other angles. Strong reflectors will produce a large signal
from many angles. When the signals resulting from the dif-
ferent sound angles are averaged together, the result is to
accentuate high-level reflectors and de-emphasize weak
reflectors. The net result is an improvement in image qual-
ity (Fig. 1.17). In addition, since noise varies randomly
from frame to frame, the frame averaging reduces image
noise. It is important to realize that as frame averaging
increases, it takes longer to generate an individual frame,
so structures that move rapidly, such as the heart, may be
blurred.
THREE-DIMENSIONAL ULTRASOUND IMAGING
Most recently, 3D sonography has been developed (22,
2528). The potential of this application is a virtually
unlimited viewing perspective, which should allow more
accurate evaluation of anatomic structures and disease
entities and more accurate volumetric measurements than
can be obtained from conventional 2D sonography. Data
for 3D sonography are acquired as a stack of parallel
cross sections with the use of a 2D sector scanner or as a
volume with the use of a mechanical or an electronic array
probe. The resultant 3D images can be displayed with a
variety of formats, including multiplanar reformatting
and surface rendering (Fig. 1.18). Virtual endoscopy (fly-
through) using perspective volume rendering also is possi-
ble (29). Attention has been most focused on gray scale,
but 3D imaging is also possible in the color and power
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14 P E D I AT R I C S O N O G R A P H Y

B
Multiplanar display of information in a three-dimensional scan. A: Three orthogonal views of a gallbladder with calculi (arrows). Bot-
Fig. 1.18
tom right image shows an additional surface-rendered view of the gallbladder calculus. B: Like computed tomography multiple axial
images are displayed of a lesion in the liver and its relationship to the diaphragm, inferior vena cava, and hepatic vein. The top left image is a ref-
erence image in sagittal plane.
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Power Doppler three-dimensional view of renal parenchy-

Fig. 1.19
mal vessels as an indication of good perfusion in a trans-
plant kidney in the right lower quadrant. The adjacent iliac vessels are
labeled.

Doppler mode (Fig. 1.19). Clinical applications so far have

been primarily in adults and have concentrated on evalua-
tion of fetal anatomy, although the gynecologic structures,
prostate, kidneys, urinary bladder, heart, and carotid arter-
ies have also been investigated. Three-dimensional ultra-
sound can provide a different perspective to a pathology
and, especially in pediatrics, the small size of the abdomen
can allow for large multiplanar reconstructions that show
spatial relationships better than 2D imaging alone (Fig.
1.20). Although 3D imaging is gaining popularity as a clin-
ical tool, further technical developments, particularly faster
data acquisition and reconstruction, will be needed before
this technology becomes practical for widespread use.
DOPPLER SONOGRAPHY
The ultrasound signals reflected back to the transducer
contain amplitude, frequency, and phase information.
Real-time two-dimensional images use only the amplitude
of the returning echoes to generate gray-scale information.
An analysis of the frequency of the returning echo can also
yield important information. Sound that reflects off a mov-
ing target undergoes a change in frequency as it returns to
the transducer. This is the Doppler effect. Objects moving
toward the transducer reflect sound at a higher frequency
than that of the incident beam. Objects moving away
reflect sound at a lower frequency. The difference between
the transmitted and received frequency is called the
Doppler frequency shift. The magnitude of the Doppler
frequency shift is determined by the equation: Fd  2  Ft 
(V/c)  cos , where Fd  the Doppler frequency shift, Ft 
the transmitted frequency, V  the speed of the moving
B
Three-dimensional scan of renal mass. A: Two-dimen-
Fig. 1.20
sional scan shows a large renal mass (nephroblastoma).
B: Three-dimensional coronal plane rendering shows the spatial rela-
tionship of the mass with the liver and invasion of the renal vein and
inferior vena cava (arrows). The curved white line at the top of the liver
represents the diaphragm in coronal plane.
target (blood flow velocity), c  the speed of sound in soft
tissue, and   the angle between the direction of blood
flow and sound beam. The faster the object is moving, the
greater the Doppler shift (30,31).
An accurate estimate of target velocity requires precise
measurement of both the Doppler frequency shift and the
angle of insonation relative to the vessel of interest. At an
angle of insonation of 90 degrees, there is no flow toward
or away from the transducer and, hence, no detectable
Doppler frequency shift. At an angle of 60 degrees, the fre-
quency shift is approximately 50% of that detected at an
angle of 0 degrees. The use of Doppler angles less than
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16 P E D I AT R I C S O N O G R A P H Y
60 degrees is recommended for making velocity measure-
ments (4).
Continuous-wave Doppler
A number of transducer designs have evolved to take
advantage of the Doppler principle. The earliest and sim-
plest Doppler instrumentation transmits a continuous
wave rather than a pulsed wave. This device consists of
one crystal, which continuously transmits sound, and a
second crystal, which continuously receives the returning
echoes. Continuous-wave Doppler ultrasonography is able
to determine the direction of blood flow. Its major disad-
vantage is that it cannot determine the exact source of the
Doppler signal because motion coming from any depth
along the sound beam produces a signal.
Pulsed Doppler
Pulsed Doppler ultrasonography has largely replaced con-
tinuous-wave Doppler sonography. The pulsed Doppler
device transmits short pulses of sound and then listens for
the returning echo. Because the speed of the sound is con-
stant, the delay in the time between the transmission and
reception is proportional to the distance. By varying the
delay time between the transmission and reception of the
sound wave, it is possible to determine the source (i.e.,
depth) from which the Doppler signal arises. The standard
gray-scale image is used to visualize the vessels of interest
and to position the Doppler sample volume at selected
points within the vessel. This combination of gray-scale
sonography with pulsed Doppler sonography is called
duplex Doppler sonography (Fig. 1.21). By convention,
the Doppler shift from objects moving toward the trans-
Duplex Doppler scan of the right kidney showing the sample volume in the renal sinus and a corresponding renal venous waveform
Fig. 1.21
beneath the image. Venous flow is away from the transducer and is therefore recorded below the baseline.
ducer is displayed above a reference line; the Doppler shift
from objects moving away from the transducer is depicted
below the line.
The major disadvantage of pulsed Doppler sonography
is that only a single point in the vessel can be sampled at
one time. The evaluation of an entire vessel can be time
consuming and require a great deal of perseverance. In
addition, pulsed Doppler relies on the gray-scale image to
identify a vessel for interrogation. Therefore, analysis of
vessels in small organs, such as the testes, can be extremely
difficult because the vessels are too small to be resolved
with gray-scale imaging.
Color Doppler
Color Doppler ultrasonography represents an improvement
over duplex Doppler sonography because it is sensitive to
Doppler signals throughout the field of view. It provides
both a real-time gray-scale image of tissue morphology and
an image displaying blood flow in color. Color Doppler
ultrasonography analyzes the phase information, fre-
quency, and amplitude of the returning echoes. Signals
from moving red blood cells are assigned a color based on
the direction of the phase shift (i.e., the direction of blood
flow toward or away from the transducer) and a shade. By
convention, movement toward the transducer is recorded
in red and movement away from the transducer in blue
(Fig. 1.22A). The shade or degree of saturation of the color
is displayed as a function of the relative velocity of the mov-
ing red cells. Rapid movement, which produces a high-
frequency shift, is assigned a lighter color, approaching
white. Slower flow produces a lower-frequency shift and is
assigned a darker color. Stationary objects produce no
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A B
Color and power Doppler imaging of the common carotid and jugular vein. The Doppler pulse is steered from the left to the right (thick
Fig. 1.22
white arrow). A: Color Doppler view. Flow in the common carotid is directed from the right to the left (thin white arrow), which is toward
the Doppler pulse. This produces a positive frequency shift and is therefore displayed as red. Flow in the jugular vein (thin black arrow) is in the
opposite direction producing a negative frequency shift and a blue color display. B: Power Doppler view shows flow in the vessels but does not dif-
ferentiate the direction of flow.

phase shift and, therefore, are assigned a gray-scale value,
as in conventional gray-scale imaging.
The major advantage of color Doppler sonography over
pulsed Doppler sonography is that the entire vessel or large
parts of the vessel can be displayed. This display format is
ideal for showing small areas of turbulence or stenosis that
may not be seen by duplex Doppler imaging. Color flow
Doppler also allows visualization of vessels in small organs
that may not be detectable on conventional gray-scale images.
The limitations of color flow Doppler imaging include angle
dependence, aliasing, and insensitivity to low-flow signal.
Power Mode Doppler
An alternative to frequency-based color flow Doppler imag-
ing is power Doppler imaging, which estimates the inte-
grated power or strength of the Doppler signal rather than
estimating the mean frequency shift, which is the parameter
typically encoded in color in standard color Doppler imag-
ing (3235). The power of the Doppler signal is related to
the number of red blood cells producing the Doppler fre-
quency shift. The Doppler detection sequence used in power
Doppler sonography is identical to that employed in fre-
quency-based color Doppler imaging. However, once the
Doppler shift has been detected, the frequency components
are removed through integration. Because all the frequency
data are removed, power Doppler sonography provides no
information about velocity. In power Doppler imaging, the
hue and brightness of the color signal represent the total
energy of the Doppler signal (Fig. 1.22B).
Power Doppler imaging has several theoretical advan-
tages over color Doppler imaging (3235). One advantage
of this technique is that it is less dependent on the angle of
incidence. As the angle of incidence changes, the total
energy is not affected in power Doppler imaging, and hence,
flow can be seen in vessels that travel at right angles to the
ultrasound beam. Conventional color flow Doppler is
dependent on the vessel beam angle and as the Doppler shift
frequency nears zero, flow becomes less apparent.
Power Doppler sonography is also slightly more sensi-
tive to low-flow signal. In the power Doppler display, low-
level noise is assigned to a homogeneous background even
when the gain is increased greatly. This results in an
increase in the usable dynamic range of the scanner, which
allows for the use of higher gain settings. The result is a
minimal increase in the sensitivity to blood flow. In con-
ventional color flow Doppler, noise appears over the entire
Doppler frequency shift, which means that gain settings
must be limited in order to reduce excessive noise. If the
gain is too high, flow signal is obscured by a background
of random noise.
Power Doppler sonography has significant limita-
tions. Perhaps the most significant limitation is that
power Doppler gives no information about direction of
blood flow. Another important limitation is that it is
more susceptible to flash artifact, which are zones of
intense color that result from motion of soft tissues, such
as that resulting from respiration, and motion of the
transducer. An important artifact present on color
Doppler images is called aliasing (see Chapter 2). This
artifact is very useful in localizing areas of high-flow
velocity and is not demonstrated on power Doppler. Addi-
tionally, power Doppler sonography does not measure the
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18 P E D I AT R I C S O N O G R A P H Y

speed of blood flow (i.e., tissue perfusion), but rather
depicts an estimate of fractional moving blood volume.
True perfusion is time dependent and requires an estimate
of how rapidly a volume of blood moves through tissue
(i.e., frequency) (34). Finally, flow that is too slow to pro-
duce a Doppler shift (i.e., capillary flow) is not detectable
by power Doppler imaging, nor is it detectable by the
standard color imaging techniques. However, it is possible
that with contrast agents, such extremely slow flow may
be detectable by power Doppler imaging (21).
Because of these limitations and only marginal and
often imperceptible increases in flow sensitivity, power
Doppler has remained an ancillary mode, with color
Doppler being the primary flow imaging technique. Never-
theless, power Doppler sonography has proven useful in
clinical practice. It has been shown to be effective in
depicting normal vasculature in the kidney, brain, and
testes and in detecting abnormalities that alter perfusion,
such as ischemia, inflammation, and tumor (3643).
ELASTOGRAPHY
Different ultrasound methods have been used over the years
to document relationships in terms of tissue elasticity
between normal organs and pathologic lesions (4446).
Elastography is a method of estimating the difference
between the stiffness, or elasticity, of normal and abnormal
tissues using ultrasound. Compressibility parameters of tis-
sues are evaluated by subjecting them to external pressure
using an ultrasound transducer. These changes of tissue dis-
placement or degree of distortion secondary to external
pressure are recorded using a high-frequency transducer and
differentiated according to static compression, dynamic
oscillation, and pulsed oscillation excitation. Ultrasound
extricates the data related to elasticity from the reflected
waves. Essentially, the longitudinal (axial and lateral) strains
are estimated from the ultrasound signals (47,48).
Malignant lesions are often regarded as causing changes
in mechanical properties of a tissue, and thus, a large com-
ponent of ultrasound elastography effort has been devoted to
trying to differentiate between benign and malignant lesions
(4951). Generally speaking, lesions that are malignant are
stiffer than benign lesions in their elastography characteris-
tics. The elastography data obtained can be superimposed on
the gray-scale image and a real-time simultaneous visualiza-
tion of the 2D image and the elastography image is obtained.
Alternatively, the elastography image can be color coded
with different colors representing different levels of stiffness
(Fig. 1.23). By convention, red color represents hard or stiff
areas, while green or purple represents the less stiff or softer
areas of the lesion. Early studies have looked at breast and
thyroid lesions with varying success. The initial clinical
results suggest that this is a theoretically promising new
method for differentiation of benign and malignant lesions.
CONTRAST AGENTS
The concept of using an ultrasound contrast agent to
enhance blood pool signals was first described by Gramiak
and Shah in 1968 (52). These investigators injected saline
into the left atrium during cardiac catheterization. The
saline produced visible echoes on echocardiographic
recordings in the normally anechoic lumen of the aorta
and the chambers of the heart. Further investigation
showed that backscattered echoes were the result of free
air bubbles that came out of solution during the injection

A B
Elastography scan of a thyroid nodule. A: Representative gray-scale image of a hypoechoic indeterminate nodule. B: Color depiction of
Fig. 1.23
the strain results. Correlation with the color scale on the right of the image shows the periphery of the nodule (arrows), which has a red
hue and constitutes the stiffer or harder (nonelastic) component of the nodule. The central portion of the nodule, which has a green hue, constitutes
the softer central component. Overall, this nodule is stiffer than the rest of the thyroid gland, which theoretically increases the risk of malignancy.
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Chapter 1 P H Y S I C A L P R I N C I P L E S A N D I N S T R U M E N TAT I O N
itself. The limitation of free bubbles is that they are large,
so they are filtered by the lungs, and they are unstable,
going back into solution within several seconds. Hence,
free bubbles, while suitable for imaging the right cardiac
chambers, are not effective for imaging left-sided chambers
or abdominal vessels or organs (53).
Subsequent investigations have attempted to create
more stable blood pool particles by encapsulating the air
bubbles in a shell (54). Several such agents have been com-
bined with albumin and with galactose (5557). Experi-
mental and clinical studies have shown that these agents
are able to traverse the pulmonary bed in large enough
concentrations to enhance the color Doppler signal in
small and large intra-abdominal arteries (5860). How-
ever, they have no effect on parenchymal enhancement.
Additional research has led to the production of several
agents that selectively increase the reflectivity of tissues in
solid organs (59,61,62). These selective agents include
colloidal suspensions, emulsions, and aqueous solutions.
Of these, the colloidal suspensions appear to be the most
promising for use as parenchymal contrast agents. Perfluo-
roctylbromide (PFOB), developed primarily as a plasma
volume expander, is a colloidal suspension that has been
used as a contrast agent to enhance the liver and spleen.
After intravenous administration, PFOB is phagocytized
by normal cells in the liver and spleen (63). With PFOB, it
has been possible to demonstrate an echogenic rim around
hepatic tumors (64).
The major effect of an ultrasound contrast agent is to
enhance the echo strength of flowing blood, especially in
the arterial system (59,62,65). The ability to detect blood
flow in smaller vessels, which currently are below the res-
olution of ultrasound, has promise for identifying tumor
vascularity (55); detecting areas of infarction or ischemia
in the brain, kidney, and testis (21,6668); and visualizing
stenotic areas in the renal arteries (6971).
In conclusion, ultrasonography is a versatile means of
imaging pediatric patients. Both morphologic and physio-
logic information can be obtained in a relatively easy, non-
invasive manner without radiation exposure and with rel-
atively little expense. The following chapters address the
specific applications for pediatric sonography and the
sonographic appearances of a variety of pediatric diseases.
REFERENCES
1. Hangiandreous NJ. B-mode US: basic concepts and new tech-
nology. Radiographics 2003;23:10191033.
2. Kremkau FW, Eckenhoff JE, Vandam LD. Diagnostic ultra-
sound: physical principles and instruments. 7th ed. Philadelphia,
PA: Elsevier Science, 2005.
3. Lawrence JP. Physics and instrumentation of ultrasound. Crit
Care Med 2007;35:S314S322.
4. Merritt CB. Physics of ultrasound. In: Rumack CM, Wilson ST,
Charboneau JW, eds. Diagnostic ultrasound. 3rd ed. St. Louis,
MO: Elsevier Mosby, 2005:334.
5. Wells PNT. Advances in ultrasound techniques and instrumen-
tation. New York: Churchill-Livingstone, 1993.
19
6. Wells PNT. Ultrasound imaging. Phys Med Biol 2006;51:
R83R98.
7. Ziskin MC. Fundamental physics of ultrasound and its propa-
gation in tissue. Radiographics 1993;13:705709.
8. Kremkau FW. Multiple-element transducers. Radiographics
1993;13:11631176.
9. Choudhry S, Gorman B, Charboneau JW, et al. Comparison of
tissue harmonic imaging with conventional US in abdominal
disease. Radiographics 2000;20:11271135.
10. Desser TS, Jeffrey BR. Tissue harmonic imaging techniques:
physical principles and clinical applications. Semin Ultrasound
CT MR 2001;22:110.
11. Muir TG, Carstensen EL. Prediction of nonlinear acoustic
effects at biomedical frequencies and intensities. Ultrasound
Med Biol 1997;6:345357.
12. Shapiro RS, Wagreich J, Parsons RB, et al. Tissue harmonic
imaging sonography: evaluation of image quality compared
with conventional sonography. AJR Am J Roentgenol 1998;
171:12031206.
13. Staritt HC, Duck FA, Hawkins AJ, et al. The development of
harmonic distortion in pulsed finite-amplitude ultrasound pass-
ing through the liver. Phys Med Biol 1986;31:14011409.
14. Ward B, Baker AC, Humphrey VF. Nonlinear propagation
applied to the improvement of resolution in diagnostic medical
ultrasound. J Acoust Soc Am 1997;101:143154.
15. Whittingham TA. Tissue harmonic imaging. Eur Radiol 1999;9:
S323 S326.
16. Burns PN. Harmonic imaging with ultrasound contrast agents.
Clin Radiol 1996;51(suppl 1):5055.
17. Claudon M, Barnewolt CE, Taylor GA, et al. Renal blood flow
in pigs: changes depicted with contrast-enhanced harmonic US
imaging during acute urinary obstruction. Radiology 1999;
2112:725731.
18. Leen E. Ultrasound contrast harmonic imaging of abdominal
organs. Semin Ultrasound CT MR 2001;22:1124.
19. Lencioni R, Cionic D, Bartolozzi C. Tissue harmonic and con-
trast-specific imaging: back to gray scale in ultrasound. Eur
Radiol 2002;12:151165.
20. Taylor GA, Barnewolt CE, Claudon M, et al. Depiction of renal
perfusion defects with contrast-enhanced harmonic sonography
in a porcine model. AJR Am J Roentgenol 1999;173:757760.
21. Taylor GA, Barnewolt CE, Adler BH, et al. Renal cortical
ischemia in rabbits revealed by contrast-enhanced power
Doppler sonography. AJR Am J Roentgenol 1998;170:417422.
22. Weng L, Tirumalai AP, Lowery CM, et al. US extended-field-of-
view imaging technology. Radiology 1997;203:877.
23. Yerli H, Eksioglu SY. Extended field-of-view sonography: evalua-
tion of the superficial lesions. Can Assoc Radiol J 2009;60:3539.
24. Fornage BD, Atkinson EN, Nock LF, et al. US with extended
field-of-view: phantom tested accuracy of distance measure-
ments. Radiology 2000;214:579584.
25. Coll DM, Herts BR, Davros WJ, et al. Preoperative use of 3D
volume rendering to demonstrate renal tumors and renal
anatomy. Radiographics 2000;20:431438.
26. Downey DB, Fenster A, Williams JC. Clinical utility of three-
dimensional US. Radiographics 2000;20:559571.
27. Downey DB, Fenster A. Vascular imaging with a three-dimen-
sional power Doppler system. AJR Am J Roentgenol 1995;165:
665668.
28. Nelson TR, Pretorius DH. Three-dimensional ultrasound imag-
ing. Ultrasound Med Biol 1998;24:12431270.
29. Yuh El, Jeffrey RB, Birdwell RL, et al. Virtual endoscopy using
perspective volume-rendered three dimensional sonographic
data: technique and clinical applications. AJR Am J Roentgenol
1999;172:11931197.
30. Boote EJ. Doppler US techniques: concepts of blood flow detec-
tion and flow dynamics. Radiographics 2003;23:13151327.
31. Taylor KJW, Holland S. Doppler US. Part I: basic principles,
instrumentation, and pitfalls. Radiology 1990;174:297307.
LWBK505-C01_p1-20.qxd 7/7/10 1:21 PM Page 20 Aptara Inc
20 P E D I AT R I C S O N O G R A P H Y
32. Bude RO, Rubin JM. Power Doppler sonography. Radiology
1996;200:2123.
33. Hamper UM, DeJong MR, Caskey CI, et al. Power Doppler
imaging: clinical experience and correlation with color Doppler
US and other imaging modalities. Radiographics 1997;17:499
513.
34. Rubin JM, Alder RS, Fowlkes JB, et al. Fractional moving blood
volume: estimation with power Doppler US. Radiology 1995;
197:183190.
35. Rubin JM, Bude RO, Carson PL, et al. Power Doppler US: a
potential useful alternative to mean frequency-based color
Doppler US. Radiology 1994;190:853856.
36. Babcock DS, Patriquin H, LaFortune M, et al. Power Doppler
sonography: basic principles and clinical applications in chil-
dren. Pediatr Radiol 1996;26:109115.
37. Bude RO, Rubin JM, Adler RS. Power versus conventional color
Doppler sonography: comparison in the depiction of normal
intrarenal vasculature. Radiology 1994;192:777780.
38. Choi BY, Kim TK, Han JK, et al. Power versus conventional
color Doppler sonography: comparison in the depiction of vas-
culature in liver tumors. Radiology 1996;200:5558.
39. Durick JE, Winter TC III, Schmiedl UP, et al. Renal perfusion:
pharmacologic changes depicted with power Doppler US in an
animal model. Radiology 1995;197:615617.
40. Luker GD, Siegel MJ. Testicular sonography in children: com-
parison of power vs. color US. Radiology 1996;198:381385.
41. Newman JS, Adler RS, Bude RO, et al. Detection of soft-tissue
hyperemia: value of power Doppler sonography. AJR Am J
Roentgenol 1994;163:385389.
42. Newman JS, Adler RS, Rubin JM. Muscle perfusion with exer-
cise: evaluation with power Doppler sonography. Radiology
1994;193(P):337.
43. Turetschek K, Nasel C, Wunderbaldinger P, et al. Power
Doppler versus color Doppler imaging in renal allograft evalua-
tion. J Ultrasound Med 1996;15:517522.
44. Bercoff J, Chaffai S, Tanter M, et al. In vivo breast tumor detec-
tion using transient elastography. Ultrasound Med Biol 2003;
10:13871396.
45. Konofagou EE. Quo vadis elasticity imaging? Ultrasonics 2004;
42:331336.
46. Parker KJ, Lerner RM. Sonoelasticity of organs: shear waves
ring a bell. J Acoust Soc Am 1999;105:29412950.
47. Hall TJ. Beyond the basics: elasticity imaging with US. Radi-
ographics 2003;23:16571671.
48. Ophir J, Cespedes I, Ponnekanti H, et al. Elastography, a quan-
titative method for imaging the elasticity of biological tissues.
Ultrason Imaging 1991;13:111134.
49. Garra BS, Cespedes EI, Ophir J, et al. Elastography of breast
lesions: initial clinical results. Radiology 1997;202:7986.
50. Cochlin DL, Ganatra RH, Griffiths DF. Elastography in the
detection of prostatic cancer. Clin Radiol 2003;57:10141020.
51. Lyshchik A, Higashi T, Asato R, et al. Thyroid gland tumor
diagnosis at US elastography. Radiology 2005;237:202211.
52. Gramiak R, Shah PM. Echocardiography of the aortic root.
Invest Radiol 1968;3:356366.
53. Sahn DJ, Valdex-Cruz LM. Ultrasonic contrast studies for the
detection of cardiac shunts. J Am Coll Cardiol 1983;3:978985.
54. Carroll BA, Turner RJ, Tickner EG, et al. Gelatin-encapsulated
nitrogen microbubbles as ultrasonic contrast agents. Invest Radiol
1980;15:260266.
55. Blomley MJK, Albrecht T, Cosgrove DO, et al. Improved imag-
ing of liver metastases with stimulated acoustic emission in the
late phase of enhancement with the US contrast agent SHU
508A; early experience. Radiology 1999;210:409416.
56. Fujimoto M, Moriyasu F, Nishikawa K, et al. Color Doppler
sonography of hepatic tumors with a galactose-based contrast
agent: correlation with angiographic findings. AJR Am J
Roentgenol 1994;163:10991104.
57. Schlief R. Echo enhancement: agents and techniquesbasic
principles. Adv Echo Contrast 1994;4:519.
58. Fritzsch T, Schartl M, Siegert J. Preclinical and clinical results
with an ultrasonic contrast agent. Invest Radiol 1998;23:5.
59. Goldberg BB, Liu J-B, Forsberg F. Ultrasound contrast agents: a
review. Ultrasound Med Biol 1994;20:319333.
60. Keller MW, Glasheen W, Kaul S. Albunex: a safe and effective
commercially produced agent for myocardial contrast echocar-
diography. J Am Soc Echocardiogr 1989;2:3852.
61. Albrecht T, Cosgrove DO, Correas JM, et al. Renal, hepatic, and
cardiac enhancement on Doppler and gray-scale sonograms
obtained with EchoGen. Academ Radiol 1996;3:S198S200.
62. Burns PN. Microbubble contrast for ultrasound imaging: where,
how, and why? In: Rumack CM, Wilson ST, Charboneau JW,
eds. Diagnostic ultrasound. 3rd ed. St. Louis, MO: Elsevier
Mosby, 2005:5576.
63. Mattrey RF, Scheible FW, Gosink BB, et al. Perfluoroctylbro-
mide: a liver/spleen-specific and tumor-imaging ultrasound con-
trast material. Radiology 1982;145:759762.
64. Mattrey RF, Leopold GR, vanSonnenberg E, et al. Perfluoro-
chemicals as liver- and spleen-seeking ultrasound contrast
agents. J Ultrasound Med 1983;2:173176.
65. Grant EG. Sonographic contrast agents in vascular imaging.
Semin Ultrasound CT MR 2001;22:2541.
66. Bauer A, Becker G, Krone A, et al. Transcranial duplex sonog-
raphy using ultrasound contrast enhancers. Clin Radiol 1996;
51:1923.
67. Ries F, Honisch C, Lambertz M, et al. A transpulmonary con-
trast medium enhances the transcranial Doppler signal in
humans. Stroke 1993;24:19031909.
68. Taylor GA, Ecklund K, Dunning P. Renal cortical perfusion in
rabbits: visualization with color amplitude imaging and an
experimental microbubble-based US contrast agent. Radiology
1996;201:125129.
69. Balen FG, Allen CM, Lees WR. Ultrasound contrast agents. Clin
Radiol 1994;49:7782.
70. Missouris CG, Allen CM, Balen FG, et al. Non-invasive screen-
ing for renal artery stenosis with ultrasound contrast enhance-
ment. J Hyperten 1996;14:519524.
71. Taylor GA. Potential pediatric applications for US contrast
agents: lessons from the laboratory. Pediatr Radiol 2000;30:
101109.
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Ultrasound Artifacts
WILLIAM D. MIDDLETON, MARILYN J. SIEGEL, AND NIRVIKAR DAHIYA
Gray-Scale Artifacts Slice-thickness Artifacts
Mirror-image Artifacts Anisotropy
Refraction Artifacts
Doppler Artifacts
Reverberation Artifacts
Technically Related Doppler Artifacts
Ring-down Artifacts
Anatomically Related Doppler Artifacts
Side-lobe Artifacts
Tissue Vibration Artifacts
Shadowing
Twinkle Artifact
Increased Through-transmission
he basis of all diagnostic sonograms is the detection
T and display of acoustic energy reflected from interfaces
within the body. The scanning technique and a number
of physical principles determine the quality of the resultant
images. The most basic principle is that sound travels in a
straight line and at a constant speed. Therefore, the origin
of a returning echo can be determined by converting the
time taken for the echo to return to the transducer into a
distance based on the speed of sound in soft tissues.
Another principle is that individual reflectors generate only
a single echo. Finally, as with any cross-sectional imaging
method, thickness of the slice is assumed to be infinitely
thin. In the majority of instances, these principles hold true
and the sonogram is an accurate reproduction of the struc-
tures that are imaged. This chapter will describe those cir-
cumstances in which violations of these principles result in
an inaccurate reproduction of an internal structure or
object. Echoes that do not correspond in location or inten-
sity to actual structures are termed imaging artifacts.
Because artifacts follow the same basic physical principles
of image production discussed in Chapter 1, it may be dif-
ficult to avoid them. Therefore, it is important to recog-
nize them so that they are not mistaken for pathologic
conditions (14).
GRAY-SCALE ARTIFACTS
Mirror-image Artifacts
Acoustic mirrors can be compared to optical mirrors.
Optical mirrors have smooth surfaces that reflect a large
amount of light, which causes a visual duplication of struc-
tures on the other side of the mirror. Flat surfaces will pro-
duce a mirror image that is identical in size and shape to
the original object, whereas curved surfaces (like mirrors
at the carnival) will produce a distorted mirror image (1).
Because gas reflects almost 100% of the sound that hits
it, gas is the best acoustic mirror in the body. This phe-
nomenon is particularly common in areas where there are
CHAPTER
2
Three-dimensional Ultrasound Artifacts
Ultrasound Contrast Agents: Artifacts
Blooming artifact
Systolic Peak Velocity Increase
High-intensity Transient Signals
large, smooth gassoft tissue interfaces, such as the lung.
Therefore, mirror-image artifacts are especially common
on sonograms of the right upper quadrant that include an
interface between the lung and adjacent soft tissues. The
mechanism of production of mirror-image artifacts is
shown in Figure 2.1.
There are three well-recognized mirror-image artifacts
on sonograms of the right upper quadrant where the lung
serves as a mirror. One of these artifacts is duplication of
the liver, which produces supradiaphragmatic echogenicity
similar to hepatic parenchyma. A second mirror image is
duplication of the diaphragm (Fig. 2.2). A third mirror
image is duplication of focal hepatic lesions that have an
echogenicity different from that of the normal hepatic
parenchyma (Fig. 2.3). Because the diaphragm is curved,
the mirror image may not be an exact reproduction of the
actual lesion. In addition, the mirror image may arise from
lesions that are outside of the plane of the image. If the
sound pulse travels out of the imaging plane after reflect-
ing off of the lung, an apparently isolated supradiaphrag-
matic lesion may be displayed.
The trachea is another structure with a large, smooth
gas interface. It is therefore capable of acting as a mirror
on sonograms of the neck (Fig. 2.4). Mirror images also
may be created in the abdomen or pelvis adjacent to a
highly reflective interface, such as gas-filled bowel (Fig.
2.5). The mirror-image artifact may simulate thickened gut
(5). Pseudothickened gut occurs when there is a large con-
tiguous pocket of gas without discrete bubbles. Successive
reflections from the one large bubble reach the transducer
at progressively later times and are therefore artifactually
duplicated distal to their true locations (5). Changing the
angle of insonation may eliminate the artifact.
Refraction Artifacts
Sound beam refraction occurs when sound passes obliquely
through an interface between two tissues that transmit the
sound at different speeds (Fig. 2.6). The result is that the
21
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22 P E D I AT R I C S O N O G R A P H Y

Mirror-image artifact generation. Sound reflects at the

Fig. 2.1
interface between the base of the lung and the diaphragm
and re-enters the liver. This reflected sound pulse interacts with struc-
tures in the liver and is subsequently reflected back to the
lungdiaphragm interface and then back to the transducer. Since the
sound is assumed to have traveled in a straight line, the structure in
the liver is duplicated above the diaphragm.

Mirror image of the diaphragm.

Fig. 2.2
Longitudinal view of the liver
shows the interface between the liver and
diaphragm (first line), the interface
between the diaphragm and lung (second
line), and the muscular tissue of the
diaphragm (d). The third line represents a
mirror image of the interface between the
liver and diaphragm. Also notice the simi-
lar echogenicity above and below the
diaphragm due to a mirror image of the
liver itself.

Mirror image of a hepatic hemangioma.

Fig. 2.3
Longitudinal view of the liver shows an
echogenic hemangioma (h) in the hepatic
parenchyma. This lesion has been duplicated in the
suprahepatic region (h). The solid arrows indicate the
path of the true sound beam. The dashed arrows indi-
cate the path of the assumed sound beam.
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Mirror image caused by the trachea. Longitudinal view of

Fig. 2.4
the neck demonstrates duplication of multiple structures.
The gas in the trachea produces a reflecting surface (arrows) that acts
as a mirror to duplicate a nodule in the thyroid (N) and tracheal carti-
laginous rings (arrowheads).

A B
Mirror image of fluid-filled uterus. A: Transverse view of an obstructed left horn (L) of a duplicated uterus shows fluid in the endometrial
Fig. 2.5
cavity. Open arrows, nonobstructed right horn. B: Longitudinal view shows a mirror-image artifact of the uterus. In this case, gas in the
rectum (arrowheads) served as the mirror.

Sound beam refraction. When the ultrasonic wavefront

Fig. 2.6
passes obliquely from soft tissue into fat or fluid, refraction
occurs, causing the beam to be redirected.

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24 P E D I AT R I C S O N O G R A P H Y

Rectus muscle refraction artifact. Due to its shape and the

Fig. 2.7
fact that it is surrounded by fat, the rectus muscle acts as a
strong refractor of sound. Since sound is assumed to travel in a straight
line, echoes arising from the refracted sound will be incorrectly dis-
played along the straight scan path. The end result is a phantom-image
artifact, such as duplication of abdominal and pelvic structures. Solid
line, true path of sound; hatched line, assumed path of sound.

sound is bent relative to the incident beam. This phenom-
enon is analogous to redirection of light by an optical lens.
The magnitude of the refraction is proportional to the
difference in the speed of sound between the two tissues.
In the human body, the speed of sound in soft tissues is
approximately 1540 meters/sec. The speed of sound in
fluid is approximately 1480 meters/sec, and through fat
it is approximately 1450 meters/sec. Therefore, refrac-
tion artifacts are most frequent between soft tissue and
fat and to a lesser extent between soft tissue and fluid
interfaces.
There are two major types of refraction artifacts: a
duplication artifact and a shadowing artifact (1). The most
common type of refractive artifact involves duplication of a
deep structure by sound beam refraction from a superficial
structure. Duplication artifacts commonly occur at the junc-
tion of the rectus abdominus muscle and adjacent abdomi-
nal wall fat, when the transducer is positioned in a trans-
verse plane of section over the midline (6,7) (Fig. 2.7). The
result is a duplication of deep abdominal and pelvic struc-
tures. In the upper abdomen, this midline type of artifact
causes vessels, such as the superior mesenteric artery or vein
and azygos vein, to be duplicated (Fig. 2.8). In the pelvis, the
artifact can cause the uterus, gestational sacs, or intrauter-
ine devices to appear duplicated. Duplication-type refrac-
tion artifacts can also arise when the kidneys are scanned
because of the refraction of sound at the interface between
the spleen and liver and adjacent fat (Fig. 2.9) (8). In this

A B
Rectus muscle refraction artifact. A: Transverse view of the upper abdomen with the transducer positioned lateral to the midline shows
Fig. 2.8
the left lobe of the liver (L), aorta (A), vena cava (C), and a single azygous vein (arrow). B: With the transducer positioned in the midline,
rectus muscle refraction has resulted in duplication of the azygous vein (arrows).
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Chapter 2 U LT R A S O U N D A R T I F A C T S 25

A B
Renal duplication artifact. A: Longitudinal view of the liver (L) and the right kidney (K) shows a normal sonographic appearance and a
Fig. 2.9
measured renal length of 105 mm. B: With the transducer positioned more inferiorly, the inferior edge of the liver and perihepatic fat (F)
cause a refractive duplication of the upper pole cortex (arrows) and the superior central sinus fat (f). This duplication of upper pole structures has
also caused the renal length to be artifactually exaggerated to 114 mm.

case, the refraction error results in apparent duplication of
the superior aspect of the kidney. Less often, the refraction
artifact simulates a suprarenal mass. Renal duplication arti-
fact occurs more frequently in the left kidney than in the
right kidney.
Although refractive duplication artifacts are most
prominent at soft tissuefat interfaces, as mentioned previ-
ously, they can also occur between soft tissuefluid inter-
faces (9,10). Duplication of the diaphragm is not uncom-
mon on sonograms of the right upper quadrant in patients
with hepatic cysts (9) or ascites (Fig. 2.10).
The second type of refractive artifact typically occurs at
the edge of a fluid collection and has the appearance of a
refractive shadow (1). The refractive shadowing is caused
by defocusing and loss of beam energy or intensity at the
edge of the fluid or cystic structure (Fig. 2.11) (1).
Reverberation Artifacts
Reverberation artifacts result when there is repetitive reflec-
tion of the returning sound signal (i.e., the sound bounces
back and forth between two interfaces) (14). Most com-
monly, sound reflects off of highly reflective acoustic inter-
faces in the near field and then returns to the transducer,
where it is reflected back into the patient. That pulse inter-
acts with the same near-field interfaces and is reflected back
to the transducer a second time (Fig. 2.12) or multiple times
(Fig. 2.13). This produces an additional echo or several sets
of echoes that are interpreted as arising from a structure

Diaphragmatic duplication artifact. Transverse view of the liver (L) shows perihepatic ascites (A). In this case, refraction between the
Fig. 2.10
liver and ascitic fluid has caused a refractive duplication of the diaphragm (arrows).
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26 P E D I AT R I C S O N O G R A P H Y
that is deeper within the body than is the original reflective
interface. All of the reverberations are equally spaced and
the increased distance is multiplied with successive rever-
beration artifacts (1).
Reverberation artifacts occur most often in cystic struc-
tures and appear as echoes in the anechoic background of
the fluid (Fig. 2.14A). Artifactual echoes appear as bright
bands or as diffuse low-level echoes in the near aspect of
the cystic spaces. Real echoes from sludge or debris occur
in the dependent portion of fluid collections and, unlike
reverberation artifacts, are affected by gravity. Reverbera-
tion artifacts can be eliminated by decreasing power out-
put and gain or by changing the position of the transducer
Reverberation artifact. Longitudinal view of the gallbladder shows a bright reflection from a large stone (arrow) and a weak artifact
Fig. 2.12
(open arrow ). Note that the distance between the stone and the transducer (D) is equal to the distance between the stone and the
reverberation artifact (D1).
Refractive shadow. Longitudinal view of the testis shows
Fig. 2.11
a cyst. Note the shadowing (arrows) that arises at the
edge of the cyst secondary to the effects of refraction.
or the scanning angle so that the cystic structure is no
longer in the near field (Fig. 2.14B).
Occasionally, reverberation artifacts are seen in soft tis-
sues, although they are more difficult to recognize because
they are surrounded by other echoes. In particular, the adi-
pose tissue in the deep surface of the abdominal wall can
act as a strong acoustic interface. If a reverberation artifact
is suspected, the original acoustic interface can usually be
identified halfway between the transducer and the rever-
beration artifact (Fig. 2.15). Changing the plane of imag-
ing can help to resolve this issue.
Reverberation artifacts may also occur in the pelvis and
simulate a retrovesical fluid collection (Fig. 2.16). This
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Chapter 2 U LT R A S O U N D A R T I F A C T S 27

Reverberation artifact. Longitudinal view of the testis (T)

Fig. 2.13
following a gunshot wound shows a bright reflection in
the superior aspect of the scrotum (closed arrow ) due to gas. Multiple
reverberation artifacts (open arrows) are present deep to the gas
interface. Note that the distance between each of the multiple rever-
beration artifacts (D1, D2, D3) is equal to the distance between the
transducer and the gas (D).

artifact occurs when sound reverberates between a bright
reflector behind the fluid-filled bladder, such as air-filled
rectum or other bowel loops, and the anterior bladder wall
or the transducer. In this respect, it is similar to a mirror-
image artifact. Because the returning echoes travel back
and forth through the bladder, they create the appearance
of a fluid collection deep to the bladder. The near wall
of the pseudomass results from the primary reflection from
the bladder wallfluid interface and the far wall from
the reverberated echoes (4).
Ring-down Artifacts
The ring-down artifact is secondary to resonance and
occurs most frequently when the ultrasound beam encoun-
ters gas. Multiple bubbles of gas are required to produce
this artifact. The sound pulse excites the fluid that is

A B
Reverberation artifact. A: View of a hepatic cyst shows multiple reverberation echoes filling much of the lumen of the cyst. B: By reposi-
Fig. 2.14
tioning the transducer so that the cyst is deeper in the image, the reverberation artifacts are eliminated and the cyst is entirely anechoic.
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28 P E D I AT R I C S O N O G R A P H Y

Reverberation artifact simulating subcapsular renal hematoma. Longitudinal view of kidney shows a reverberation artifact (open arrow)
Fig. 2.15
that mimics an interface between a subcapsular hematoma and renal cortex. Because the reverberation artifact is displayed in the
hypoechoic background of the renal cortex, it is more conspicuous than the original interface (arrow) at the deep surface of the abdominal wall.

entrapped between the gas bubbles, causing it to resonate
and send a continuous sound wave back to the transducer.
Because the sound wave returns to the transducer later
than the original echo, it is perceived as having originated
from reflectors deep to the original gas reflector and is
displayed as a series of bright echoes with straight margins
distal to the gas bubbles (Fig. 2.17) (11). If the resonating
structure rings for a long time, then the artifact continues
down to the bottom of the image. If the ringing is short in
duration, then the artifact is short in length.
Very short ring-down artifacts are sometimes called
comet-tail artifacts. The comet-tail artifact is often due to
crystals and is frequently seen in the gallbladder due to
cholesterol crystals (Fig. 2.18) (5,12). Metallic objects such
as surgical clips can also cause ring-down and comet-tail
artifacts.
Side-lobe Artifacts
Side-lobe artifacts arise from sound beams that are periph-
eral to the main sound beam. The majority of the energy

Pseudopelvic fluid collection. Longitudinal view of the left

Fig. 2.16
pelvis shows an apparent fluid collection (FC) deep to the
bladder. This actually represented a reverberation artifact between
gas-filled bowel (arrow) and the anterior bladder wall (open arrow).
Ring-down artifact. Transverse view of the upper abdomen
Fig. 2.17
shows a gas-filled loop of bowel with a posterior ring-
down artifact (arrows).
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Chapter 2 U LT R A S O U N D A R T I F A C T S 29

Comet-tail artifact. Longitudinal view of the gallbladder

Fig. 2.18
shows three comet-tail artifacts (arrows) arising from
cholesterol crystals deposited in the superficial wall of the gallbladder.
Comet tails are generally weak, but they can be well seen in the ane-
choic background of cystic structures such as the gallbladder. They
are rarely seen behind the deep wall of the gallbladder because the
surrounding soft tissues obscure them.

transmitted by the ultrasound transducer is concentrated in
the center of the sound beam. Only a small amount of energy
(approximately 1%) arises from the side lobes that radiate
outward from the center beam (Fig. 2.19). Because these side
lobes are weak, they are not a common cause of imaging
artifacts. Artifacts may occur if a side lobe interacts with a
highly reflective surface. The resultant echoes are displayed
as if they had arisen from the center sound beam (3,13).
Side-lobe artifacts are usually not recognizable when
they occur in soft tissue, but they become visible when they
are displayed on the anechoic background of fluid-filled
cystic structures (Fig. 2.20). They cause low-level echoes
within the fluid, mimicking sludge, debris, or pus. Pseu-
dosludge in the gallbladder is one of the more common
types of side-lobe artifact (Fig. 2.21). Repositioning the
patient so that the gallbladder falls away from the adjacent
gas-filled bowel loops, changing transducer angulation, and
reducing gain and power can diminish or eliminate side-
lobe artifacts. Unlike true sludge, artifactual echoes will not
layer with changes in patient position. Additionally, the

Ultrasound side lobes. Diagram showing the strong center

Fig. 2.19
portion of the ultrasound beam that contains 99% or more
of the sound energy. Weak side lobes surround the center beam in a
cone-shaped fashion and account for 1% or less of the beam energy.
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30 P E D I AT R I C S O N O G R A P H Y
anterior surface of the artifactual sludge may be curved,
whereas true sludge has a flat surface (13).
Shadowing
Acoustic shadowing is so common in diagnostic sonogra-
phy that it is often not even considered to be an artifact.
Generation of side-lobe artifacts. This diagram simulates
Fig. 2.20
imaging of the gallbladder and a strong reflector located
outside of the gallbladder. A: When the center portion of the beam of
the linear array transducer passes through the strong reflector outside
of the gallbladder, the resulting echo from this reflector is appropri-
ately positioned as indicated in the lower image. B: When the center
beam is directed toward the gallbladder, the weak side lobe can inter-
act with the strong reflector outside of the gallbladder, producing
weak echoes that are assumed to have arisen from the center beam.
The echoes are displayed within the interior of the gallbladder, as
shown in the lower image.
Moreover, it often can be helpful in characterizing the
nature of the shadowing source, such as a renal stone or
gallstone. Acoustic shadowing refers to attenuation of the
sound pulse by reflection and/or absorption, such that the
sound wave does not reach the deeper tissues to produce
an echo. It most commonly occurs behind gas, stones, and
Side-lobe artifact. Longitudinal view of the gallbladder
Fig. 2.21
demonstrates intraluminal echoes (white arrow) second-
ary to the side-lobe artifact. In this case, an adjacent loop of bowel,
containing gas (black arrow), is a strong enough reflector to produce
the side-lobe artifacts seen within the gallbladder lumen.
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Acoustic shadowing. Transverse view of the right upper quadrant demonstrates a gallstone (GS) and gas (G) in a loop of bowel adja-
Fig. 2.22
cent to the gallbladder. There is a clean shadow (CS), which is devoid of secondary reflections, behind the gallstone. A dirty shadow
(DS) with multiple secondary reflections is seen behind the gas.
calcified structures (Fig. 2.22). Shadowing that occurs dis-
tal to gas is due to sound reflection at airtissue interfaces.
After the sound pulse reflects off of the gas, it interacts
with the interfaces in front of the gas and produces multi-
ple secondary reflections that travel back to the gas surface
and then reflect from this surface back to the transducer.
These secondary reflections produce low-level echoes deep
to the gas, referred to as dirty shadows (Fig. 2.22) (14).
The shadowing that occurs distal to calculi and bone is
primarily due to sound attenuation by these structures.
Since most of the incident sound is absorbed within the
matrix of these structures, there is less energy available for
the generation of secondary reflections. The shadowing in
this case tends to be more anechoic and clean appearing
(Fig. 2.22) (4,14). Unfortunately, there are exceptions to
the rule that gas produces dirty shadowing and stones pro-
duce clean shadowing. Air at times can generate a rela-
tively clean appearance and stones can produce a dirty
appearance with multiple reverberations. The production
of a clean or dirty shadow is most dependent on the sur-
face characteristics of the shadowing object (i.e., the
roughness and the radius of curvature of the reflecting sur-
face). Flat, smooth surfaces reflect a large amount of the
incident sound and the result is dirty shadowing. Curved,
rough surfaces scatter sound in many different directions
so that it is defocused and diminished in intensity and the
result is clean shadowing (15). The matrix of the shadowing
structure has little effect, if any, on the type of shadowing.
Partial shadowing can occur behind highly attenuating
soft tissues. This occurs most often when structures con-
tain large amounts of fatty tissue (Fig. 2.23). Partial shad-
owing or lack of shadowing can also occur behind calcifi-
cation and stones if the cross section of the sound beam (at
Chapter 2 U LT R A S O U N D A R T I F A C T S 31
the depth of the stone) is greater than the diameter of the
stone. To increase the likelihood of demonstrating shad-
owing associated with stones or calcifications, the focal
zone of the transducer should be directed at the level of the
stone or calcification (Fig. 2.24). Higher-frequency probes
are preferred over lower-frequency probes, since they can
be more tightly focused and are less penetrating. However,
it may not be possible, even in the focal zone of the trans-
ducer, to demonstrate sharply marginated shadows distal
to very small calculi. When the calculus is smaller than the
beam, some of the sound is reflected back to the transducer
but some goes around the stone, resulting in echoes return-
ing from deeper structures (14,15).
Increased Through-transmission
Increased through-transmission refers to an increase in the
intensity of the echoes deep to an internal structure.
Enhanced transmission is more common in fluid than in
soft tissues because fluid-filled structures attenuate the
sound beam much less than solid structures do. As a result,
the interfaces deep to fluid-filled structures will appear
brighter than identical interfaces deep to solid tissues. The
presence of increased through-transmission is helpful in
distinguishing cystic from solid lesions, particularly when
their gray-scale appearance is nonspecific (Fig. 2.25).
However, it is important to realize that solid masses that
attenuate the sound less than adjacent soft tissues can also
be associated with increased through-transmission, mim-
icking a fluid-filled mass (Fig. 2.26).
Slice-thickness Artifacts
Slice-thickness artifact, also referred to as beam-width
artifact, is a partial volume effect. The thickness of the
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32 P E D I AT R I C S O N O G R A P H Y

Partial acoustic shadowing. Longitudinal view of

Fig. 2.23
the right kidney demonstrates an echogenic fat-
containing angiomyolipoma (A). Due to sound beam attenua-
tion by the fatty tumor, there is a partial shadowing (PS) seen
posterior to the tumor.

ultrasound beam can be separated into two components:
one in the plane of imaging and the other (elevational) out
of the plane of imaging. Although the thickness of each of
these components can be minimized by a combination of
electronic and mechanical focusing, the beam does have a
finite thickness. The slice-thickness artifact results when the
beam is not narrow enough, such that a part of the ultra-
sound beam interacts with a fluid-filled structure and a part
of it interacts with solid tissue, producing artifactual
low-level echoes within the fluid-filled structure (see Fig.
1.12) (16).
Pseudosludge is a common slice-thickness artifact. Pseu-
dosludge secondary to slice-thickness artifact is created by
the averaging of echoes from the liver adjacent to the gall-
bladder with the normally anechoic bile. Slice-thickness
artifacts can also arise at gassoft tissue interfaces.
Pseudopneumatosis is an example of a misregistration
artifact due to elevation averaging. This artifact is produced

A B

Effect of focal zone placement on acoustic shadowing. A: Longitudinal view of the testis with the focal zone (arrowhead) positioned in
Fig. 2.24
the near field demonstrates a very distinct shadow (arrows) posterior to a calcification. B: When the focal zone is positioned in the far
field (arrowhead), the shadow is no longer present.
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Increased through-transmission. Longitudinal view of the
Fig. 2.25
liver demonstrates a nonspecific complex lesion (arrows).
The increased through-transmission seen posterior to this lesion sug-
gests that it is fluid filled rather than a solid lesion. Percutaneous aspi-
ration confirmed that the lesion was a hepatic abscess.
when intraluminal gas bubbles are outside the scanning
plane but within the elevation thickness of the ultrasound
beam.
Anisotropy
Certain tissues composed almost entirely of strong specular
reflectors generate variable echogenicity depending on the
angle of insonation. This phenomenon is called anisotropy.
Anisotropy is particularly prominent in the sonographic
imaging of tendons (Fig. 2.27). Tendons are composed of
longitudinally oriented collagen bundles with little cellular
A B
Anisotropy. A: Dual longitudinal views of the flexor pollicis longus tendon. The hyperechoic fibrillar architecture is shown well when the
Fig. 2.27
tendon is oriented perpendicular to the sound beam (left image) but is shown poorly when the tendon is not perpendicular (right image).
B: Similar results are noted in the transverse plane.
Chapter 2 U LT R A S O U N D A R T I F A C T S 33
Solid mass with increased through-transmission. View of
Fig. 2.26
the liver shows a hypoechoic mass with increased
through-transmission. This was a solid liver metastasis identified dur-
ing intraoperative sonography.
stroma. This histology produces a fibrillar pattern that is
displayed as parallel, linear, hyperechoic reflections when
the sound is oriented perpendicular to the long axis of the
tendon. If the angle of insonation of sound is not perpendi-
cular, the fibrillar pattern is poorly displayed and the ten-
don appears hypoechoic. This occurs because the sound
waves that get reflected do not return to the active elements
of the transducer. It can be corrected by changing the align-
ment of the transducer or steering the sound such that the
sound beam hits the tendons at 90 degrees. Failure to rec-
ognize this artifact can result in inaccurate interpretations
of tendon tears or tendinosis. This artifact is often seen at
insertion of the rotator cuff tendons where there is a natu-
rally curved course of the tendons (1722).
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34 P E D I AT R I C S O N O G R A P H Y

DOPPLER ARTIFACTS Doppler gain setting by increasing it to the point at which

Artifacts in spectral and Doppler imaging can be grouped
into two basic categories: technically related and anatomi-
cally related artifacts (2325).
Technically Related Doppler Artifacts
ABSENT DOPPLER SIGNAL (INAPPROPRIATELY LOW DOPPLER SETTINGS)
The factors important in displaying flow in vessels, espe-
cially those with relatively slow flow, are gain, velocity
scale (pulse repetition frequency), transmit frequency, fil-
tration setting, and transmit focal distance. Spectral and
color flow Doppler shifts may not be displayed if the gain
setting (Fig. 2.28) or transducer frequency is too low or the
wall filter (Fig. 2.29) or velocity scale is too high. The
resultant effect is that patent vessels appear thrombosed.
The spectral Doppler gain setting should be adjusted so
that the velocity envelope is thin and distinct and flow man-
ifests in a uniform direction. It is appropriate to set the color
noise starts to appear on the image and then decreasing it
until the noise just clears from the image or is barely notice-
able (Fig. 2.28). The velocity scale should be set as low as
possible until aliasing, noise, or tissue motion becomes a
problem. A lower scale setting displays more flow; a higher
setting displays less flow. The wall filter controls the ability
to distinguish moving blood from moving tissue by sup-
pressing low-frequency shifts. A low setting increases the
likelihood of low-velocity flow detection. A high filter sup-
presses low-frequency shifts arising from slowly flowing
blood (Fig. 2.29). Finally, transducers operating at different
frequencies should be used. High-frequency transducers are
more sensitive for detecting flow, provided the sound pulse
can penetrate the depth of the vessels.
DOPPLER NOISE
Inappropriately high Doppler settings produce spectral or
color noise and aliasing. Noise is often related to errors in

A B

C
Effect of gain setting on color Doppler flow detection. A: Gain setting at 58 dB. Color Doppler image of the portal vein at a high gain set-
Fig. 2.28
ting demonstrates excessive color noise. B: Gain setting at 20 dB. An image with a low color gain setting shows minimal detectable flow
in the portal vein. C: Gain setting at 50 dB. The appropriate gain setting shows normal flow in the portal vein and adjacent hepatic artery and elimi-
nates the color noise.
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Chapter 2 U LT R A S O U N D A R T I F A C T S 35

A B

C
Effect of wall filter on flow detection in the right kidney. A: High filter setting indicated by the large gap in color assignment at the low-
Fig. 2.29
frequency portion of the color scale (arrow). Color Doppler image of the kidney shows minimal detectable flow. B: Low filter. An image
with a low filter setting shows excessive color noise within the renal and hepatic parenchyma. C: Medium filter. With medium filtration, flow is now
correctly displayed and noise has been eliminated.

Doppler gain, whereas aliasing is related to velocity scale
errors. A spectral gain setting that is too high degrades the
velocity envelope, causing it to appear thickened. This
appearance mimics spectral broadening and can create the
erroneous impression of poststenotic turbulence. When the
color gain setting is too high, color signal appears in a ran-
dom distribution throughout the image.
Any structure that moves can also cause a random
Doppler shift. Rapid movement of the transducer is
another cause of a Doppler shift and artifactual color sig-
nal. Power Doppler is particularly sensitive to artifactual
motion, such as movement of the transducer. Color noise
is usually easy to recognize because it appears as a random
admixture of red and blue (i.e., color speckles) rather than
having homogeneous color, which is typical of flow within
a vessel.
ALIASING
Aliasing occurs when the Doppler sampling rate (pulse-rep-
etition frequency) is not high enough to display the Doppler
frequency shift. When this occurs, the spectral tracing will
show wraparound with the higher-velocity systolic peaks
projecting below the baseline (Fig. 2.30). Color imaging
shows an abrupt change in color from the high end of the
red scale to the high end of the blue scale (Fig. 2.31). With
true flow reversal, the color change occurs from the low
end of the red and blue Doppler scales. Increasing the
pulse-repetition frequency can usually eliminate aliasing. If
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36 P E D I AT R I C S O N O G R A P H Y

C
Pulsed Doppler tracing of aliasing. A: Pulse repetition frequency (RPF) of 6944 (Doppler scale  80). A pulsed Doppler waveform of the
Fig. 2.30
internal carotid artery shows normal systolic peaks. B: PRF of 3125 (Doppler scale  40). With the sampling rate set too low, aliasing
occurs, and the higher systolic peaks wrap around and project below the spectral baseline. C: PRF of 1500 (Doppler scale  20). A further decrease
in the sampling rate produces wraparound of the lower as well as the higher systolic peaks.

aliasing is still present after the pulse-repetition frequency
has been maximized, switching to a lower-frequency trans-
ducer or imaging at a lower Doppler angle will decrease the
Doppler frequency shift and may help eliminate the alias-
ing artifacts (24,25). In actuality, color aliasing is a valu-
able artifact because it dramatically displays the location
of the highest Doppler frequency shifts, thus highlighting
sites of potentially abnormal flow.
FLOW DIRECTIONAL ABNORMALITIES
Flow direction can be inappropriately displayed if the
interrogating ultrasound beam intersects the vessel at a 90-
degree angle. If a sector or curvilinear array transducer is
used for vascular interrogation, flow perpendicular to the
insonating beam results in a small colorless segment in the
lumen of the vessel (Fig. 2.32).
LWBK505-C02_p21-42.qxd 7/7/10 1:22 PM Page 37 Aptara Inc
Color Doppler aliasing. A longitudinal view of a stenotic
Fig. 2.31
internal carotid artery shows localized aliasing as a
region of turquoise color assignment at the origin of the internal
carotid artery (arrows). The dark blue area (arrowhead) at the origin of
the internal carotid represents true reversal of flow relative to the
interrogating beam. Note the difference in transition between red and
blue in the area of aliasing and the area of flow reversal.
Anatomically Related Doppler Artifacts
MIRROR-IMAGE ARTIFACTS
Mirror-image artifacts can occur on pulsed and color
Doppler sonograms, as well as on gray-scale sonograms
(4,26). Similar to gray-scale imaging, mirror images on
Doppler sonograms occur most often around the air-filled
lung, which is a very strong acoustic interface (Fig. 2.33).
The back wall of the common carotid artery can also
function as a mirror and produce artifactual Doppler sig-
nal deep to the vessel (27). The artifactual arterial signal
from the carotid artery is referred to as the carotid ghost,
and it can be detected both on pulsed and color Doppler
images (Fig. 2.34). Occasionally, weaker acoustic inter-
faces will act as mirrors for color Doppler imaging. For
example, bone can reflect enough sound to produce color
Doppler mirror images.
Because the artifactual signal is generated by blood
flow in a real vessel but is simply inappropriately local-
ized, it should have the same size and shape as the signal
from the true vessel, which should be nearby on the same
image (Figs. 2.33 and 2.34). The intensity of the wave-
forms, however, may differ. The Doppler signal from the
true vessel arises from the original sound pulse, thereby
having a relatively strong signal. The artifactual signal
arises from the sound reflected off the mirror. If virtually
all of the sound is reflected, as with a gas interface, then
the mirror-image signal will be almost as strong as the
original signal (Fig. 2.33). If some of the sound is trans-
mitted through the mirror and only a portion of it is
reflected, then the mirror-image signal will be much
Chapter 2 U LT R A S O U N D A R T I F A C T S 37
Effect of insonating angle on color Doppler imaging.
Fig. 2.32
Curvilinear color Doppler image of the common carotid
artery with direction of flow from right to left. The narrow area of
absent color signal (arrow) in the lumen of the vessel represents
absence of Doppler shift. At this point, the flow is perpendicular to the
insonating angle. In this case, the color Doppler scale has been
inverted so that the flow to the right of the image is toward the trans-
ducer (blue), whereas the flow at the left of the image is away from the
transducer (red).
weaker than the original signal (Fig. 2.34). Scanning from
an angle that excludes the source vessel or decreasing the
power output and Doppler gain setting should eliminate
or reduce the mirror image.
PULSATILITY AND COLOR NOISE ARTIFACTS
Anatomic structures, like technical factors, can cause
spectral and color noise that mimics flow. Transmitted
pulsations from the right heart are a cause of artifactual
spectral and color noise on scans of the liver, especially
the left lobe (Fig. 2.35). Transmitted cardiac or vascular
pulsations can also cause color to appear in cystic struc-
tures, such as hepatic cysts or ascites, where there should
be no flow.
Tissue Vibration Artifacts
Turbulent blood flow causes pressure fluctuations in the
lumen of the vessel and vibration of the vessel wall. This is
a phenomenon familiar to anyone who has felt a kink in a
garden hose. If the vessel wall vibration is strong enough, it
will transmit into the perivascular tissues. Tissue vibration
causes the bruit heard on auscultation and the thrill felt on
palpation (2831). Because the vibrating tissue interfaces
are moving, they generate a detectable Doppler signal. The
back-and-forth vibratory motion is displayed as focal ran-
dom red and blue color assignments in the perivascular
space at the site of the abnormal vessel. The artifact is most
prominent during systole, when the velocities are greatest,
and less prominent during diastole. Waveforms from
vibrating tissues are typically strong, low-frequency signals
that are symmetric above and below the baseline. Perivas-
cular tissue vibration artifact can be seen in any situation
where there is sufficiently turbulent blood flow. The com-
monly encountered lesions include arteriovenous fistulas,
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38 P E D I AT R I C S O N O G R A P H Y

A B

Internal mammary artery, mirror image. A: Longitudinal

Fig. 2.33
color Doppler view in the parasternal region shows the
interface between the pleura and lung as a bright line (arrows). This
interface acts as a mirror to duplicate the internal mammary artery (A).
B, C: The pulsed Doppler waveforms from the internal mammary artery
and the mirror-image artifact, respectively, are similar in size and shape.
Because minimal sound energy is lost after reflecting off of the gas in
the lung, the strength of the signal from the mirror image is almost the
C same as the signal from the actual artery.

A B

Carotid artery mirror-image artifact (or ghost). A: Longi-

Fig. 2.34
tudinal view of the common carotid artery (A) shows a
color mirror image (M) deep to the true vessel. B, C: Pulsed Doppler
waveforms from the common carotid artery and the mirror-image
artifact, respectively, are similar in size and shape. The signal from
C the source vessel is stronger than that of the mirror-image artifact.
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Chapter 2 U LT R A S O U N D A R T I F A C T S 39

A B
Color Doppler pulsation artifact. A: Sagittal scan of the left lobe of the liver shows extensive color artifact due to transmitted tissue motion
Fig. 2.35
from cardiac pulsations. This makes it difficult to visualize flow in the left hepatic vein. B: With an increase in the pulse repetition rate
and the filter settings, transmitted tissue pulsation produces less of an artifact, and flow in the left hepatic vein is much easier to identify.

stenotic arteries, aneurysms, and vascular anastomotic sites
(Fig. 2.36).
Twinkle Artifact
Twinkle artifact, also known as color Doppler comet-tail
artifact, occurs behind very strong, granular, and irregular
reflecting interfaces such as crystals, calculi, or calcifica-
tions (32,33) (Fig. 2.37). When a transmitted sonographic
beam contacts such an interface, a phase shift causes a
faint variation of the transmitted sonographic beam at the
interface and an increase of pulse duration results in multiple
reflections in the medium (34). This is visualized as a ran-
dom mixture of red and blue pixels in the high-frequency
shift spectrum located deep to the interface. Associated
waveforms show a high-intensity, nonphysiologic signal
with aliased components on both sides of the baseline. The
artifact is typically accentuated at low transmit frequencies
and high Doppler scale settings (35).
This artifact has been exploited most commonly in the
detection of urinary stones. Because urinary stones become
larger particles by aggregation of primary crystal forms, they
are predominantly composed of a highly reflecting crystalline
aggregate of varying chemical composition with a mucopro-
tein organic matrix (36). The twinkling artifact from urinary
stones is likely generated by a random strong reflection and
multiple inner reflections of the incident pulse at the rough
interface formed by the crystalline aggregate. Although the
twinkle artifact is most often used to aid in detection of small
renal calculi, it is also helpful in the setting of ureteral and
bile duct stones, pancreatic calcifications, and foreign bodies
(35). This artifact may be easier to detect than acoustic shad-
owing and may aid in stone identification (37,38).

Perivascular tissue vibration. Longitudinal color Doppler

Fig. 2.36
view of a renal transplant (K) with a stenotic arterial anas-
tomosis. Vibrating tissues adjacent to the anastomotic site are dis-
played as a random mixture of red and blue color assignment (arrows).
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40 P E D I AT R I C S O N O G R A P H Y
A B
Twinkle artifact. A: Transverse color Doppler view of the kidney shows a strong twinkle artifact (arrow) associated with a stone.
Fig. 2.37
B: Pulsed Doppler waveform from the artifact shows a high-intensity, highly aliased, nonphysiologic signal on both sides of the baseline.
THREE-DIMENSIONAL ULTRASOUND ARTIFACTS
Three-dimensional (3D) ultrasound artifacts are related to
those that originated on the two-dimensional (2D) image
or those that are unique to the 3D technique. Either way,
they can distort the final image and create a diagnostic
dilemma.
An important point to remember is that 3D ultrasound
cannot circumvent the artifacts related to 2D imaging.
Therefore, artifacts such as shadowing, through-transmis-
sion, and others described previously are as relevant in 3D
as they are in 2D ultrasound. Since the final 3D image is
dependent upon the size and angle of the volume sample
box, many 2D artifacts may get represented on 3D image
without the presence of the causative structure. For exam-
ple, the rendering of shadow from an overlying structure
such as bone or calculus may be seen as a hollow void on
3D without the representation of the bone or calculus
itself. Therefore, it is important to interpret 3D images in
combination with 2D imaging.
Three-dimensional ultrasound artifacts can also be
related to the technique of acquisition. Manual acquisition
of volume by sliding the transducer can result in artifacts
related to the varying speed of transducer movement and
breathing by patient. Slice misregistration can skew the
final 3D images geometric proportions. Automatic volume
acquisition by newer ultrasound probes has overcome this
issue to a large extent.
Finally, many artifacts in 3D ultrasound imaging are
also related to the postacquisition processing software
application. There are multiple options available for use
on the acquired volume that can change the way diagnos-
tic information is viewed. The most important option is
the threshold value, which is used to define the level of
gray voxels that need to be visualized. A threshold param-
eter, once set, can limit the number of voxels with gray val-
ues below the threshold value (Fig. 2.38). This can help
minimize or eliminate noise and improve image quality.
Very high threshold values can exclude important infor-
mation (Fig. 2.38).
ULTRASOUND CONTRAST AGENTS: ARTIFACTS
Most artifacts related to use of contrast agents are bloom-
ing artifacts, increased systolic peak velocity, and transient
high-intensity signals (39).
Blooming Artifact
Blooming artifact, also known as color bleed, can be
seen on conventional color Doppler images and with the
use of ultrasound contrast agents. It occurs soon after the
administration of contrast agent at the time of peak
enhancement. The unwanted result is that information
within a vessel, such as a nonocclusive thrombus, can be
obscured. On conventional color ultrasound, blooming
artifacts can be limited by reducing the color gain or by
increasing the color Doppler wall filter and the pulse repe-
tition frequency, which decreases sensitivity of the color
Doppler system. If contrast agent is given, a slow injection
limits blooming artifacts because it decreases peak signal
intensity.
Systolic Peak Velocity Increase
An artifactual increase in systolic peak velocity of up to
50% can occur at the time of peak enhancement, reflecting
the limited dynamic range of the system. This artifact can
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A B
Threshold artifact. A: Section of the gallbladder lumen with a calculus. The lumen is dark and the luminal surface is not appreciated
Fig. 2.38
due to low threshold settings. B: Section of the gallbladder with better rendering of the luminal surface with appropriate threshold
settings.
be minimized by reducing the Doppler gain and using a
slow injection. Potentially, the increased systolic velocity
can result in overestimation of the degree of stenotic
lesions if contrast images are interpreted without conven-
tional color images. The presence of flow disturbances on
color Doppler images should help in grading stenotic
lesions.
High-intensity Transient Signals
High-intensity transient artifacts can be seen with pulsed
Doppler at the time of peak enhancement or during late
enhancement. They can also be detected with color and
power Doppler ultrasound as higher-intensity color pixels
within the more uniform background of the vessel.
REFERENCES
1. Chooi WK, Mugli V, Cooperberg PL. Artifacts. In: McGaha JP,
Goldberg BB, eds. Diagnostic ultrasound. 2nd ed. New York, NY:
Taylor & Francis, Inc., 2008:1937.
2. Keogh MB, Cooperberg PL. Is it real or is it an artifact? Ultra-
sound Q 2001;17:201210.
3. Lee RK. Grayscale ultrasound artifacts. In: Dogra V, Rubens DJ,
eds. Ultrasound secrets. Philadelphia, PA: Hanley & Belfus,
2004:813.
4. Feldman MK, Katyal S, Blackwood MS. US artifacts. Radi-
ographics 2009;29:11791189.
5. Wilson SR, Burns PN, Wilkinson LM, et al. Gas at abdominal
US: appearance, relevance and analysis of artifacts. Radiology
1999;210:113123.
Chapter 2 U LT R A S O U N D A R T I F A C T S 41
6. Muller N, Cooperberg PL, Rowley VA, et al. Ultrasonic refrac-
tion by the rectus abdominus muscles: the double image artifact.
J Ultrasound Med 1984;3:515519.
7. Sauerbrei EE. The split image artifact in pelvic ultrasonography:
the anatomy and physics. J Ultrasound Med 1985;4:2934.
8. Middleton WD, Melson GL. Renal duplication artifact in US
imaging. Radiology 1989;173:427429.
9. Mayo J, Cooperberg PL. Displacement of the diaphragmatic
echo by hepatic cysts: a new explanation with computer simula-
tion. J Ultrasound Med 1984;3:337340.
10. Middleton WD, Melson GL. Diaphragmatic discontinuity asso-
ciated with perihepatic ascites: a sonographic refractive artifact.
AJR Am J Roentgenol 1988;151:709711.
11. Avruch L, Cooperberg PL. The ring-down artifact. J Ultrasound
Med 1985;4:2128.
12. Shapiro RS, Winsberg F. Comet-tail artifact from cholesterol
crystals: observations in the postlithotripsy gallbladder and an
in vitro model. Radiology 1990;177:153156.
13. Laing FC, Kurtz AB. The importance of ultrasonic side-lobe
artifacts. Radiology 1982;145:763768.
14. Sommer FG, Taylor KJW. Differentiation of acoustic shadowing
due to calculi and gas collections. Radiology 1980;135:399403.
15. Rubin JM, Adler RS, Bude RO, et al. Clean and dirty shadow-
ing at US: a reappraisal. Radiology 1991;181:231236.
16. Fiske CE, Filly RA. Pseudo-sludge. A spurious ultrasound appear-
ance within the gallbladder. Radiology 1982;144:631632.
17. Connolly DJA, Berman L, McNally EG. The use of beam angu-
lation to overcome anisotropy when viewing human tendon
with high frequency linear array ultrasound. Br J Radiol
2001;74:183185.
18. Crass JR, van de Vegte GL, Harkavy LA. Tendon echogenicity:
ex vivo study. Radiology 1988;167:499501.
19. Dussik KT, Fritch DJ, Kyriazidou M, et al. Measurements of artic-
ular tissues with ultrasound. Am J Phys Med 1958;37:160165.
LWBK505-C02_p21-42.qxd 7/7/10 1:22 PM Page 42 Aptara Inc
42 P E D I AT R I C S O N O G R A P H Y
20. Erickson SJ. High-resolution imaging of the musculoskeletal
system. Radiology 1997;205:593618.
21. Fornage BD. The hypoechoic normal tendon: a pitfall. J Ultra-
sound Med 1987;6:1922.
22. Middleton WD, Reinus WR, Melson GL, et al. Pitfalls of rota-
tor cuff sonography. AJR Am J Roentgenol 1986;146:555560.
23. Nilsson A. Artifacts in sonography and Doppler. Eur Radiol
2001;11:13081315.
24. Pozniak MA, Zagzebski JA, Scanlan KA. Spectral and color
Doppler artifacts. Radiographics 1992;12:3544.
25. Rubens DJ, Bhatt S, Nedelka S, et al. Doppler artifacts and pit-
falls. Radiol Clin North Am 2006;44:805835.
26. Reading CC, Charboneau JW, Allison JW, et al. Color and spec-
tral Doppler mirror image artifact of the subclavian artery.
Radiology 1990;174:4142.
27. Middleton WD, Melson GL. The carotid ghost. A color
Doppler ultrasound duplication artifact. J Ultrasound Med
1990;9:487493.
28. Aaslid R, Nornes H. Musical murmurs in human cerebral arter-
ies after subarachnoid hemorrhage. J Neurosurg 1984;60:3236.
29. Middleton WD, Erickson S, Melson GL. Perivascular color arti-
fact: pathologic significance and appearance on color Doppler
US images. Radiology 1989;171:647652.
30. Mitchell DG. Color Doppler imaging: principles, limitations
and artifacts. Radiology 1990;177:110.
31. Zwiebel WJ, Pellerito J. Basic concepts of Doppler frequency
spectrum analysis and ultrasound blood flow imaging. In:
Zwiebel WJ, Pellerito J, eds. Introduction to vascular ultra-
sonography. 5th ed. Philadelphia, PA: Saunders, 2004:6190.
32. Lee JY, Kim SH, Cho JY, et al. Color and power Doppler twin-
kling artifacts from urinary stones: clinical observations and
phantom studies. AJR Am J Roentgenol 2001;176:14411445.
33. Camplbell SC, Cullinan JA, Rubens DJ. Slow flow or no flow?
Color and power Doppler US pitfalls in the abdomen and pelvis.
Radiographics 2004;24:497506.
34. Rahmouni A, Bargoin R, Herment A, et al. Color Doppler
twinkling artifact in hyperechoic regions. Radiology 1996;
199:269271.
35. Tchelepi H, Ralls PW. Color comet-tail artifact: clinical appli-
cations. AJR Am J Roentgenol 2009;192:1118.
36. Rutchik SD, Spirnak JP, Resnick MI, et al. Calculous disease of
the urinary tract. In: Pollack HM, McClennan BL, eds. Clinical
urography. 2nd ed. Philadelphia, PA: W.B. Saunders, 2000:
21372146.
37. Shabana W, Bude RO, Rubin JM. Comparison between color
Doppler twinkling artifact and acoustic shadowing for renal
calculus detection: an in vitro study. Ultrasound Med Biol
2009;35:339350.
38. Turrin A, Minola P, Costa F, et al. Diagnostic value of colour
Doppler twinkling artifact in sites negative for stones on B mode
renal sonography. Urol Res 2007;35:313317.
39. Correas J-M, Bridal L, Lesavre A, et al. Ultrasound contrast
agents: properties, principles of action, tolerance and artifacts.
Eur Radiol 2001;11:13161328.
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CHAPTER

Brain
MARILYN J. SIEGEL
3
Technique and Equipment Ischemic Lesions of the Term Neonate Meningitis
Gray-scale Imaging Techniques Ischemic Lesions of the Older Infant
Hydrocephalus
Equipment
Vascular Occlusive Disease Normal Cerebrospinal Fluid
Cross-sectional Sonographic Anatomy Neonatal Arterial Occlusive Disease Production
Coronal Sections (Neonatal Stroke) Disturbances in Cerebrospinal Fluid
Sagittal Sections Extracorporeal Membrane Production and Circulation
Normal Anatomy in Other Imaging Planes Oxygenation Gray-scale Sonographic Findings
Normal Variants and Scanning Artifacts Sickle Cell Disease Doppler Interrogation
Venous Thrombosis Benign External Hydrocephalus
Spectral and Color Doppler Imaging
Technique: Imaging Approaches Congenital Malformations Intracranial Cysts and Neoplasms
Normal Arterial Blood Flow Patterns Disorders of Histogenesis Arachnoid Cysts
Normal Venous Blood Flow Patterns Disorders of Neural Tube Closure Other Cystic Lesions
Disorders of Diverticulation Brain Neoplasms
Intracranial Hemorrhage
Disorders of Migration, Sulcation, and
Premature Infants Suture Evaluation
Proliferation
Term Infants
Destructive Brain Lesions Calvarial Masses
Hypoxic-ischemic Injury
Congenital Infections
Ischemic Lesions of the Premature Neonate

igh-resolution, real-time sonography has proven to be rickets, osteogenesis imperfecta, cleidocranial dysostosis).

H an extremely valuable tool in identifying normal and

pathologic intracranial anatomy (14). Because it is
portable and can be quickly performed, particularly in
unstable premature infants, it is nearly always the initial
examination of choice for identifying hydrocephalus;
periventricular, intraventricular, and intracerebral hemor-
rhages; ischemic lesions; and congenital anomalies. This
chapter reviews the scanning techniques for performing
cranial sonography, the indications for this examination,
the normal sonographic anatomy of the brain, and the
sonographic spectrum of intracranial abnormalities. The
role of sonography in evaluating cranial vault abnormali-
ties, such as craniosynostosis, and soft tissue masses of the
scalp is also described.
TECHNIQUE AND EQUIPMENT
Gray-scale Imaging Techniques
Sonography of the neonatal brain is performed through
the anterior fontanelle, which is available as an acoustic
window through the first year of life. Anterior fontanelle
closure begins at about 9 months and is usually complete
at about 15 months of age. The fontanelle may remain
open after this time period in premature infants and in
some patients with increased intracranial pressure,
hypothyroidism, chromosomal abnormalities (trisomies
13, 18, and 21), and bone disorders (hypophosphatasia,
Although the fontanelle can remain open after age 1 year,
scanning is best performed early in life. With increasing
age, the anterior fontanelle becomes smaller, limiting
image quality.
Images are obtained in coronal and sagittal planes
through the anterior fontanelle. Coronal images are
obtained by placing the transducer transversely across
the anterior fontanelle and angling the ultrasound beam
from anterior to posterior. Sagittal images are obtained
by placing the transducer longitudinally on the anterior
fontanelle and angling it medially to laterally (Fig. 3.1).
It is also common practice to obtain axial views
through the posterior and mastoid fontanelles (Fig. 3.2)
(510). The midline posterior fontanelle, located slightly
above the external occipital protrusion, closes at about
3 months of age. Sonography through the posterior
fontanelle is performed with the neonatal head turned to
one side. Sagittal views are acquired through the midline of
each occipital horn, and coronal scans are acquired
through the occipital horns posterior to the choroid
plexus. The posterior fontanelle view can improve visuali-
zation of the occipital horns and the posterior periventric-
ular halo (5,7,8).
The mastoid (posterolateral) fontanelle is located at
the junction of the squamosal, lambdoidal, and occipi-
tal sutures (810). It can remain open until 2 years of
age (6). Scans are obtained by placing the transducer

43
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44 P E D I AT R I C S O N O G R A P H Y

CC CS
BV

FH
3 OH
TH
3

CB
4

A B
Schematic representations of standard scanning planes. Coronal (A) and sagittal (B) planes. BV, body of ventricle; CB, cerebellum; CC,
Fig. 3.1
corpus callosum; CS, cavum septum pellucidum; FH, frontal horns; OH, occipital horn; TH, temporal horn; 3, third ventricle; 4, fourth ven-
tricle. (Modified from Rumack CM, Johnson ML, eds. Perinatal and infant brain imaging. Chicago: Year Book Medical Publishers, Inc.; 1984:337.)

just behind the pinna of the ear and just about above the
tragus. Angling the transducer slightly cephalad can
optimize display of anatomy. Mastoid fontanelle images
are usually obtained at least at two levels: the brainstem
and posterior fossa. The mastoid view is useful for eval-
uating the brainstem, posterior fossa, and cerebral cir-
culation (6,810).
AF
PF
The coronal and squamosal sutures, foramen magnum,
and temporal bone also can serve as acoustic windows.
Scanning through the coronal and squamosal sutures is use-
ful for visualizing the convexities of the brain when evaluat-
ing extracerebral fluid collections. Scanning through the
foramen magnum may be useful in evaluating the upper
cervical spinal canal, particularly in patients with Chiari
malformation.
Transtemporal scanning can show the major
branches of the circle of Willis. Axial images are
acquired with the transducer parallel and approximately
1 cm superior and anterior to the tragus of the ear.
Because of the relative thinness of the squamosal portion
of the temporal bone, the transtemporal approach can
be used to evaluate the circle of Willis in children and
adults as well as neonates. Sonographic examinations of
the brain also can be performed through surgically
created bone windows, such as Burr holes or craniotomy
defects.

MF
Diagram of posterior fontanelle and mastoid views. Dia-
Fig. 3.2
gram of the lateral skull illustrating the anterior fontanelle
(AF), posterior fontanelle (PF), and mastoid fontanelle (MF). Transduc-
ers are positioned over the three fontanelles. (Adapted from Correa F,
Enriquez G, Rossello J, et al. Posterior fontanelle sonography: an
acoustics window into the neonatal brain. AJNR Am J Neuroradiol
2004;25:12741282.)
Equipment
The transducer frequency should be selected to maximize
resolution and depth of penetration. A 7.5-MHz phased
array or vector transducer is usually adequate for the
evaluation of the premature infant. A 5-MHz may be
needed in term or older, larger infants with closing
fontanelles. High-frequency, linear array transducers (7.5
to 12 MHz) are helpful to image superficial structures in
the near field, such as the extracerebral spaces, brain cor-
tex, and superior sagittal sinus (11). Pulsed and color
flow Doppler sonography are valuable to evaluate vascu-
lar anatomy, cerebral blood flow, and congenital vascular
anomalies.
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CROSS-SECTIONAL SONOGRAPHIC ANATOMY
Coronal Sections
The ventricular system and cerebrospinal fluid (CSF)
spaces serve as references for identifying intracranial
anatomy and selecting scan planes. The six standard coro-
nal scans are (a) frontal horns anterior to the foramen of
Monro, (b) foramen of Monro, (c) posterior aspect of the
third ventricle through the thalami, (d) quadrigeminal cis-
tern, (e) trigones of the lateral ventricles, and (f) parietal
and occipital cortex.
The most anterior coronal scan is through the frontal
horns of the lateral ventricles (Fig. 3.3). The frontal
horns are anechoic, paramedian, fluid-filled spaces with
triangular or crescentic configurations. The hypoechoic
corpus callosum forms the roof of the frontal horns; the
anechoic cavum septi pellucidi forms the medial walls;
and the echogenic heads of the caudate nucleus form the
lateral walls. The echogenic pericallosal sulcus separates
the hypoechoic corpus callosum from the hypoechoic
cingulate gyrus. Immediately lateral and inferior to the
caudate nucleus are the putamen and globus pallidus,
which are slightly hypoechoic to isoechoic to surround-
ing parenchyma. Lateral to the putamen and globus pal-
lidus are the sylvian fissures, which appear as Y-shaped
structures. The sylvian fissures separate the frontal and
Coronal scan through the frontal horn. At this level, the
Fig. 3.3
frontal horns appear as crescentic fluid-filled spaces
(arrowheads) separated by the cavum septi pellucidi (C). The heads of
the caudate nuclei (N) lie adjacent to the walls of the lateral ventricles.
The hypoechoic corpus callosum (cc) forms the roof of the cavum and
the lateral ventricles. Paralleling the corpus callosum is the cingulate
gyrus (CG) subadjacent to the echogenic callosal sulcus. Also note the
echogenic sylvian fissure (open arrows) between the frontal (F) and
temporal (T) lobes. BC  basilar cistern.
Chapter 3 B R A I N 45
Coronal scan through foramen of Monro. The lateral ven-
Fig. 3.4
tricles (arrowheads) are identified as fluid-filled structures,
with the bodies of the caudate nuclei (N) lying adjacent to the lateral
ventricles. The third ventricle (3) is usually slit-like or not visualized on
coronal views when normal because its transverse diameter is so
small. Between the lateral ventricles and superior to the third ventricle
is the triangular cavum septi pellucidi (C). The corpus callosum (cc) is
again noted superior to the cavum and lateral ventricles. Again, note
the echogenic sylvian fissure (open arrows) between the frontal (F)
and temporal (T) lobes. P  pons; M  medulla oblongata.
temporal lobes. Pulsations from the anterior and middle
cerebral arteries may be observed in the interhemispheric
and sylvian fissures, respectively, during real-time scan-
ning.
The next scan is acquired through the foramen of
Monro (Fig. 3.4). At this level, the frontal horns of the
lateral ventricles point superiorly and laterally. The ane-
choic cavum septi pellucidi is again seen between the
lateral ventricles. The lateral ventricles are bordered by
the bodies of the caudate nuclei, which have an
echogenicity similar to or slightly less than that of adja-
cent parenchyma. The normal-size third ventricle is usu-
ally not visualized, because its transverse diameter is
quite small. When dilated, it can be recognized as a mid-
line anechoic structure beneath the bodies of the lateral
ventricles. The echogenic brainstem (i.e., the pons and
medulla) is visualized on this image. Again, the sylvian
fissures can be seen. Pulsations from the anterior cerebral
artery in the interhemispheric fissure and middle cerebral
artery in the sylvian fissure can be seen on real-time
imaging.
The third scan is obtained posterior to the third ven-
tricle just behind the foramina of Monro (Fig. 3.5). At this
level, the bodies of the lateral ventricles lie on either side
of the cavum septi pellucidi. They are bordered by the
caudate nuclei laterally and thalami inferiorly. The thal-
ami are separated from each other by the third ventricle.
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46 P E D I AT R I C S O N O G R A P H Y
Coronal scan through posterior aspect of third ventricle.
Fig. 3.5
At this level, the bodies of the lateral ventricles, the cau-
date nuclei (N) lateral to the ventricles, and the thalami (T) inferior to
the ventricles are imaged. The three central echogenic areas
(three-dot sign) represent the choroid plexus in the floor of the lat-
eral ventricles (arrows) and in the roof of the third ventricle (arrow-
head). The cerebral peduncles (CP) and the echogenic tentorium
(open arrows) are also included in this plane. cc  corpus callosum;
CG  cingulate gyrus.
Again, the third ventricle usually is not imaged unless
dilated. The body of the corpus callosum forms the roof
of the bodies of the lateral ventricles. Echogenic choroid
plexus is seen in the floor of the lateral ventricles and in
the roof of the third ventricle, producing three echogenic
foci (the three-dot sign). The hypoechoic cerebral
peduncles are inferior to the thalami. These are separated
from the hypoechoic cerebellar hemispheres by the
echogenic tentorium.
On a slightly more posterior scan, the echogenic, star-
shaped, quadrigeminal cistern is visualized, lying superior
to the echogenic cerebellar tentorium (Fig. 3.6). The cister-
nal hyperechogenicity is thought to be secondary to the
presence of arachnoid septations, which create multiple
interfaces, or to pulsations of large vessels within the cis-
tern. The bodies of the lateral ventricles, bordered by the
caudate nuclei and thalami, and the temporal horns are
seen on this scan. The posterior continuation of the septum
pellucidum, termed the cavum vergae, may be seen at
this level. In the posterior fossa, the cerebellar vermis
appears as an echogenic midline structure surrounded by
the relatively hypoechoic cerebellar hemispheres. Posterior
and inferior to the vermis is the cisterna magna. Pulsations
from the middle cerebral artery in the sylvian fissure and
pericallosal artery in the pericallosal sulcus may also be
observed.
Coronal scan through quadrigeminal cistern. The quadrigem-
Fig. 3.6
inal cistern (Q) appears as an echogenic, star-shaped struc-
ture inferior to the thalami (T). The bodies of the lateral ventricles (arrow-
heads), cerebellum (CB), and tentorium (open arrows) also are imaged on
this section. C  cavum septi pellucidi.
The next most posterior coronal scan is through the
trigones of the ventricles (Fig. 3.7). The ventricular
trigones diverge laterally and are separated by the sple-
nium of the corpus callosum. Within the trigones are the
highly echogenic glomi of the choroid plexus. Parallel and
lateral to both trigones are linear areas of increased
echogenicity, termed the periventricular halo or blush.
The echogenicity of the periventricular halo should be less
than that of the choroid plexus. Below the ventricles and
superior to the cerebellum is the echogenic V-shaped ten-
torium cerebelli.
The final coronal scan, cephalad to the trigones and
cerebellum, shows the cortex of the occipital and parietal
lobes and the posterior interhemispheric fissure (Fig. 3.8).
The number of visualized gyri and sulci vary inversely with
gestational age (see below).
Sagittal Sections
Sagittal images are obtained by turning the transducer
90 degrees on the fontanelle perpendicular to the coro-
nal plane, placing the transducer longitudinally across
the anterior fontanelle, and scanning each side from a
midline-to-lateral direction. Planes are obtained through
(a) the midline, (b) the caudothalamic groove, (c) the
body of each lateral ventricle, and (d) each cerebral cor-
tex. On the midline images, the cavum septi pellucidi
appears as a comma-shaped, fluid-filled structure lying
between the frontal horns of the lateral ventricles
(Fig. 3.9). The cavum vergae, which is the posterior
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Coronal scan through trigones of lateral ventricles. At this
Fig. 3.7
level, the lateral ventricles containing the echogenic
choroid plexus (Ch) diverge laterally. The splenium (S) of the corpus
callosum is seen as a horizontally oriented echogenic line between the
ventricles. Note the normal periventricular echoes (arrows) and the
top of the echogenic cerebellum (CB).
Coronal scan posterior to occipital horns. The normally
Fig. 3.8
echogenic white matter (arrows) is seen on either side of
the midline. Also seen are echogenic cortical sulci (arrowheads)
extending medially from the lateral margins of the brain.
Chapter 3 B R A I N 47
Normal midline sagittal plane. The cavum septi pellucidi
Fig. 3.9
(CS) and vergae (CV) are identified as a comma-shaped
fluid-filled structure. Superior to the cavum is the hypoechoic corpus
callosum (arrowheads) and cephalad and adjacent to the corpus cal-
losum is the cingulate gyrus (CG). The echogenic line between the cor-
pus callosum and cingulate gyrus is the pericallosal sulcus. The third
ventricle (3) with the echogenic massa intermedia (MI) and the choroid
plexus (open arrow) forming its roof lies below the cavum. The
echogenic cerebellar vermis (V) is posterior to the fourth ventricle. The
pons (P) and medulla (M) are seen as moderately echogenic struc-
tures anterior to the fourth ventricle (4). Beneath the vermis is the fluid-
filled cisterna magna (CM).
extension of the cavum septi pellucidi, lies between the
bodies of the lateral ventricles. The size of these midline
structures varies from slit-like spaces to large cystic
structures.
Cephalad to the cavi septi pellucidi and vergae is the
thin, crescentic, hypoechoic corpus callosum. It is bor-
dered inferiorly by the echogenic sulcus of the corpus cal-
losum (i.e., pericallosal sulcus), which contains the perical-
losal arteries. Cephalad and paralleling the pericallosal
sulcus is the cingulate gyrus, which appears as a broad,
curvilinear hypoechoic band. The cingulate gyrus is sepa-
rated from more superficial gyri by the cingulate sulcus,
which appears as a thin hyperechoic line. The more super-
ficial gyri are separated by short, thin hyperechoic sulci
paralleling the cingulate gyrus and sulcus. The normal gyri
and sulci never extend to the ventricles. Within the cere-
bral sulci are branches of the anterior cerebral artery.
Pulsations from these vessels can be noted on real-time
examination.
The normal third and fourth ventricles can be visual-
ized on midline sagittal scans, appearing as anechoic,
fluid-filled structures. The echogenic choroid plexus is
seen in the roof of the third ventricle. The echogenic massa
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48 P E D I AT R I C S O N O G R A P H Y

intermedia lies more caudally within the third ventricle.

Posterior to the third ventricle is the quadrigeminal plate
cistern, appearing as an echogenic band. Inferior to the cis-
tern is the echogenic cerebellar vermis, which is bordered
anteriorly by the triangular fourth ventricle. The brain-
stem, which lies anterior to the fourth ventricle and poste-
rior to the clivus, is of medium echogenicity in contrast to
the higher-level echoes of the adjacent clivus. Pulsations
within the basilar artery anterior to the brainstem can be
seen on real-time sonography. Inferior to the vermis is the
anechoic cisterna magna.
Slight lateral and oblique angulation of the trans-
ducer, with the anterior part of the probe directed more
medially than the posterior portion, produces a sagittal
image of the frontal horn and bodies of the lateral ven-
tricles (Fig. 3.10). The important anatomic landmark on
this image is the caudothalamic groove, a thin echogenic
band that lies at the junction of the caudate nuclei ante-
riorly and thalami posteriorly. This landmark is the
most common site of hemorrhage in the premature
Parasagittal scan through body of lateral ventricles. At
neonate. The caudate nucleus is slightly more echogenic Fig. 3.11
this level, the frontal horn (F), body (B), and occipital horn
than the thalamus. The caudothalamic groove is con- (O) of the lateral ventricles can be defined. The highly echogenic
tiguous with the choroid plexus lying in the roof of the choroid plexus (Ch) is noted within the trigone of the lateral ventricle.
third ventricle. Superior to the lateral ventricle is the Below the lateral ventricle is the caudate nucleus (N) and thalamus
cerebral cortex. (T). Posterior to the trigones of the lateral ventricles is the normal
Further lateral and oblique angulation of the trans- periventricular halo (arrows). Although this area is echogenic, it is less
ducer, with the anterior part angled medially and the echogenic than the adjacent choroid plexus.
posterior part laterally, produces the third sagittal sec-
tion, which shows the entire lateral ventricle in a single
image (Fig. 3.11). The highly echogenic glomi of the
choroid plexus are seen within the trigones of the lateral
ventricles. The choroid plexus has a comma-shaped con-
figuration as it extends from the roof of the third ventri-
cle through the foramen of Monro into the trigones. It is
most prominent in the trigones (or atria) of the lateral
ventricles, tapering anteriorly as it courses toward the
third ventricle and tapering posteriorly as it courses
toward the temporal horns. The amount of intraventric-
ular CSF is variable, ranging from a tiny anechoic col-
lection above the choroid plexus to a larger crescentic or
C-shaped collection filling the ventricles. The lateral ven-
tricles are surrounded by the cerebral hemispheres (i.e.,
frontal, parietal, occipital, and temporal lobes). Inferior
to the ventricles are the caudate nucleus and thalamus.
Posterior to the ventricular trigones is the normal hyper-
echoic halo or blush.
The fourth most lateral sagittal image shows the
peripheral brain parenchyma, peritrigonal hypere-
chogenicity or blush, sylvian fissure, and a variable num-
ber of cerebral convolutions, which increase with gesta-
tional age (Fig. 3.12). In this view, there are no major
vascular or ventricular structures.
Parasagittal plane through head of caudate nucleus. The
Fig. 3.10
head of the caudate nucleus (N) anteriorly and thalamus Normal Anatomy in Other Imaging Planes
(T) posteriorly lie inferior to the body of the lateral ventricle (arrow-
heads). Between these structures is the caudothalamic groove con- POSTERIOR FONTANELLE SCANS
taining the anterior extent of the choroid plexus (arrow). CB, cerebel- Axial scans through the posterior fontanelle show the
lar hemisphere. trigones of the lateral ventricles. The echogenic choroid
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Parasagittal scan lateral to ventricle. The moderately
Fig. 3.12
echogenic brain parenchyma and sylvian fissure (arrows)
are imaged on this section.
plexus lies in the anterior part of the trigone and extends
into both the body and temporal horns of the lateral ven-
tricle. The posterior part of the occipital horn is anechoic
(Fig. 3.13). The posterior axial view is useful to show
dependently layering blood in the posterior occipital horn
(5,7,8).
A B
Posterior fossa anatomy. A: A standard coronal image obtained through the anterior fontanelle demonstrates the body of the right lat-
Fig. 3.13
eral ventricle (V) as well as the occipital horn (arrow) and choroid glomus (G). B: Image obtained through the posterior fontanelle also
demonstrates the body of the right lateral ventricle (V), occipital horn (arrow), and choroid glomus (G), but the occipital horn is better seen on this
image than on the anterior fontanelle image.
Chapter 3 B R A I N 49
MASTOID FONTANELLE SCANS
Axial images through the mastoid fontanelle show the
brainstem and posterior fossa (6,810) (Fig. 3.14). Ante-
rior axial images at the level of the brainstem show the
third ventricle, cerebral peduncles, thalamus, and basilar
cisterns. The thalami and cerebral peduncles are paired
hypoechoic structures. The third ventricle is anechoic and
slit-like and lies between the thalami. The basilar cisterns
are thin, echogenic curvilinear structures adjacent to the
midbrain (8).
More posterior images show the fourth ventricle, pos-
terior vermis and folia of the cerebellar hemispheres, ten-
torium, and cisterna magna. The fourth ventricle appears
as an anechoic space between the cerebellar hemispheres.
The vermis and cerebellar hemispheres lie just below the
echogenic tentorium and posterior and lateral to the fourth
ventricle. The vermis is more echogenic than the cerebellar
hemispheres. The cisterna magna is a hypoechoic, triangu-
lar structure below the vermis and cerebellar hemispheres.
The cerebellar vallecula, a thin anechoic midline cleft, may
be noted between the inferior surfaces of the cerebellar
hemispheres (see below discussion).
Normal Variants and Scanning Artifacts
BRAIN PARENCHYMA
In premature infants, the brain appears featureless because
the gyri and sulci are underdeveloped. Sulcal development
begins during the fifth month of gestation. By the seventh
month, the primary sulci are present. During the eighth
and ninth months of gestation, the sulci bend and branch
and ultimately anastomose, resulting in the formation of
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50 P E D I AT R I C S O N O G R A P H Y

A B

Mastoid fontanelle scans. A: Anterior image of the brainstem and posterior fossa shows the cerebral peduncles (CP) and cerebellar
Fig. 3.14
hemispheres (CB). B: More posterior image shows the tentorium (open arrows), fourth ventricle (4), vermis (V), cerebellar hemispheres
(CB), and cisterna magna (CM). T  trigones.

secondary and tertiary sulci in the periphery of the brain
(1215). Not unexpectedly, therefore, the number of sulci
seen on sonography increases as the infant reaches term.
The sulci also become more serpiginous in their configura-
tion (Fig. 3.15).
The first sulcus that forms is the sylvian fissure. Early
in gestation it is wide and relatively rectangular in shape.
Close to term, it becomes a narrow, echogenic Y-shaped
structure. The sylvian fissure contains branches of the mid-
dle cerebral artery.

A B
Premature versus term infant. A: Immature brain. Lateral ventricle (LV), choroid plexus (Ch), and normal periventricular echogenicity
Fig. 3.15
(open arrows) are identified. Note that the gyri and sulci are not well developed. B: Mature brain. The number of convolutions increases
with gestational age. More gyri and sulci (arrowheads) are seen in the term infant than in the preterm infant. The anterior part of the lateral ventri-
cle (arrows) is slit-like, a normal variant.
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Chapter 3 B R A I N 51

Cortical pseudolesion. An anterior coronal scan shows a

Fig. 3.16 Asymmetric ventricle size. The left ventricle (arrow) is
broad hyperechoic area (arrows) in the left cerebral Fig. 3.17
larger than the right ventricle, which is closed.
hemisphere adjacent to the frontal horn. This is an artifact occurring
when a normal sulcus is imaged tangentially as it courses around a
gyrus.

eral ventricles are not an indicator of cerebral edema.

Closed or slit-like ventricles also occur in infants with
When a sulcus or the edge of a gyrus is imaged in its cerebral edema, but in this clinical setting, there are
long axis, it can appear relatively hyperechoic to adja- other findings, such as increased parenchymal echogenic-
cent parenchyma, mimicking a focal mass lesion. This ity, poor definition of sulci and gyri, and decreased vas-
pseudolesion is most often seen on coronal images, cular pulsations, that should suggest the diagnosis of
when a normal sulcus is imaged tangentially as it edema (22).
courses around a gyrus (Fig. 3.16). Rotation of the
transducer to an orthogonal plane can confirm that the
brain parenchyma is normal. Other features that can
differentiate a pseudolesion from a true mass are its
contiguity with normal sulci and gyri and lack of mass
effect (16).

LATERAL VENTRICLES
Asymmetry of the lateral ventricles has been reported in
up to 90% of normal neonates (17). More often, the left
ventricle is larger than the right and the occipital horns
are larger than the frontal horns (17) (Fig. 3.17). Refer-
ence standards for normal ventricular size have been
published, but these generally are not needed for diag-
nosis (18,19).
Ventricle size changes with brain maturity. The size
of the lateral ventricles progressively decreases with
increasing fetal age. Thus, the ventricles of the prema-
ture infant appear relatively larger than those of the term
infant and are easier to recognize. In approximately
80% of term infants and 30% of premature infants, the
lateral ventricles, especially the frontal horns, are closed
or slit-like (2 to 3 mm in diameter) (Fig. 3.18) (20,21). Normal slit-like ventricles. Term infant, coronal view. Both
The estimated median time to partially open ventricles is Fig. 3.18
lateral ventricles (arrows) are partially closed (i.e., slit-
1.5 to 3 days after birth, with an estimated mean time of like). The ventricles in term infants are usually smaller than those of
2.5 days (21). As a solitary finding, closed or slit-like lat- premature infants.
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52 P E D I AT R I C S O N O G R A P H Y
A B
Coarctation. A: Coronal view. B: Right parasagittal view. There is focal approximation of the ventricular walls near the external angle of
Fig. 3.19
the right frontal horn (F), producing the appearance of a cyst (arrow). This should not be mistaken for a pathologic germinal matrix cyst,
which occurs below the lateral ventricles at the level of the caudothalamic groove.
Ventricular size also can change with changes in patient
positioning. When the infant is scanned in a decubitus
position, the ventricle on the dependent side may be
smaller than the ventricle on the up side (23).
Coarctation of the lateral ventricles is another com-
mon anatomic variant. Coarctation refers to a focal
approximation of the ventricular walls in close proximity
to the external angle, giving the appearance of a cyst
(17,24). Coarctation should not be mistaken for a patho-
logic germinal matrix cyst. The latter occurs below the lat-
eral ventricles and medial to the external angle. The
pseudocyst in ventricular coarctation occurs at the exter-
nal angle (Fig. 3.19).
CAVI SEPTI PELLUCIDI AND CAVUM VERGAE
The cavum septi pellucidi lies between the anterior horns
of the lateral ventricles and anterior to the foramen of
Monro. The cavum vergae lies between the bodies of the
lateral ventricles and posterior to the foramen of Monro
(Fig. 3.20). The cavum septi pellucidi and the cavum ver-
gae communicate with each other and obliterate from pos-
terior to anterior. During the sixth month of gestation, the
cavum vergae begins to close. Just before term, the cavum
septi pellucidi begins to close. A cavum vergae without a
cavum septi pellucidi would thus be unexpected. Patho-
logic studies have shown that the cavum vergae is closed in
nearly all infants (97%) at birth, while the cavum septi pel-
lucidi is often open, usually closing 2 to 6 months after
birth (25).
Sonographically, the cavum septi pellucidi and vergae
appear as fluid-filled spaces between the lateral ventricles
(see Fig. 3.9) (26). They communicate with each other but
not with the ventricular or subarachnoid spaces. They usu-
ally range between 2 and 10 mm in width. Linear echoes,
representing septal veins, may be seen in the cavum septum
pellucidum.
In very premature infants, the cavum vergae may
extend posteriorly beyond the bodies of the lateral ventri-
cles. Sonographically, this extension, known as the cavum
veli interpositi, appears as a fluid-filled anechoic space
extending from the cavum vergae and projecting behind
the quadrigeminal cistern (Fig. 3.20) (26). It may be sepa-
rated from the cavum vergae by a thin septation. The inter-
nal cerebral veins run inferiorly to it.
GERMINAL MATRIX
The germinal matrix is a highly vascular structure found
early in gestation. It is rarely seen in term infants. The ger-
minal matrix is located inferolateral to the ependymal lin-
ing in the floor of the lateral ventricle and superior to the
head and body of the caudate nucleus. It is also present in
the roof of the third and fourth ventricles. In the third
month of gestation, the germinal matrix begins to involute,
and by 36 weeks gestation, this involution is usually com-
plete. Although the germinal matrix is not seen at sonog-
raphy, it has clinical significance because it is the site of
hemorrhage in premature neonates (see below section on
Intracranial Hemorrhage).
CHOROID PLEXUS
The choroid plexus is responsible for the production of
CSF in the ventricles. The largest part of the choroid
plexus, known as the glomus, partially or totally fills the
trigones of the lateral ventricles. The glomus tapers poste-
riorly as it courses from the trigones into the temporal
horns of each lateral ventricle. It also tapers anteriorly as
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Chapter 3 B R A I N 53

CSP
CV
CVI

CSP
CV

CVI

A B
Cavum veli interpositi. A: Diagram shows the midline cavities and their positions in the sagittal plane (top) and coronal plane (bottom).
Fig. 3.20
The shaded areas represent the fluid-filled spaces, which include the cavum septi pellucidi (CSP), cavum vergae (CV), and cavum veli
interpositi (CVI). B: Magnified midline sagittal ultrasound scan obtained with a linear array transducer shows the cavum veli interpositi (arrows).
(Parts A & B reprinted from Epelman M Daneman A, Blaser SI, et al. Differential diagnosis of intracranial cystic lesions at head US: correlation with
CT and MR imaging. Radiographics 2006;26:173196, with permission.)

it courses along the floor of the lateral ventricle into the

foramen of Monro, where it joins the choroid plexus from
the opposite side and continues along the roof of the third
ventricle to the suprapineal recess (see Figs. 3.11 and
3.13A). Whereas the glomus can appear bulbous and have
irregular margins, the choroid plexus within the body and
temporal horn of each lateral ventricle usually is thin with
smooth borders. Of note, the choroid plexus never
extends into the frontal or occipital horns (such extension
indicates hemorrhage). Choroid plexus is also present in
the roof of the fourth ventricle, although it is not usually
seen on sonography.
The glomus of the choroid plexus can have a central
cleft. This finding, termed a split choroid sign, can mimic
a choroid or intraventricular hemorrhage (Fig. 3.21). Color
Doppler imaging will differentiate this vascular anatomic
variant from an avascular echogenic bleed (17).
Small cysts are common in the choroid plexus, espe-
cially in the glomus, with a prevalence of approximately
3% (27) (Fig. 3.22). The cysts are 1 cm or less in diame-
ter, usually unilateral and clinically insignificant. They are
not associated with other central nervous system (CNS)
or chromosomal abnormalities. Large cysts, greater than Cleft sign, right parasagittal view. The glomus of the
1 cm in diameter, or bilateral choroid plexus cysts are Fig. 3.21
choroid plexus has a central cleft (split choroid sign;
more likely to be associated with chromosomal disorders. arrow).
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54 P E D I AT R I C S O N O G R A P H Y
Choroid plexus cyst. Right parasagittal scans show a
Fig. 3.22
small, not clinically significant cyst (arrow) in the choroid
plexus of the trigone.
PERITRIGONAL ECHOGENICITY
The echogenic peritrigonal halo or blush is a normal finding
in neonates, caused by an anisotropic effect of scanning (17).
It has been suggested that the echogenicity represents white
matter fibers and vascular plexus that course radially from
the cortex to the subependymal layer of the ventricle (28).
On sonographic studies through the anterior fontanelle, the
beam strikes these nerve fibers and vessels perpendicularly,
creating multiple interfaces, which appear as a cluster of
A B
Periventricular halo versus periventricular bleed, parasagittal scans in two patients. A: Normal halo. The echogenicity of the normal
Fig. 3.23
halo (arrows) is less than that of the choroid plexus (Ch). The halo has a feathery, homogeneous appearance. B: Grade 4 periventricu-
lar hemorrhage. The echogenicity of hemorrhage (arrows) is equal to that of the choroid plexus (Ch).
echoes posterior to the trigone. On studies through the pos-
terior fontanelle, the nerve fibers and vessels parallel the
ultrasound beam, and the hyperechogenicity is less evident.
The echogenicity is less than normal choroid plexus and it
has a homogeneous, brush-like or flame-shaped appearance
with poorly defined borders (see Fig. 3.11). The periventric-
ular blush is more prominent in premature than in term
neonates.
The normal periventricular halo needs to be differen-
tiated from cerebral hemorrhage and periventricular
leukomalacia. Either of the latter conditions should be
suspected if the periventricular echogenicity is asymmet-
ric, heterogeneous, isoechoic or hyperechoic to normal
choroid plexus, or in areas other than the external
angles (28) (Fig. 3.23). Hemorrhage and periventricular
leukomalacia will also persist on scans acquired through
the posterior fontanelle.
CISTERNA MAGNA
The cisterna magna is an arachnoid-lined, anechoic
structure that lies inferior to the vermis and communi-
cates with the fourth ventricle (see Fig. 3.9). In the mid-
sagittal plane, the height of the cisterna magna varies
from 3 to 8 mm, with a mean of 4.5 mm  1.29 mm
(29). Measurements decrease in the Arnold-Chiari mal-
formation and are greater than normal in the Dandy-
Walker syndrome.
EXTRA-AXIAL FLUID SPACES
The midline extra-axial fluid spaces are more easily seen
by sonography than those located over the anterior,
posterior, or lateral surfaces of the cerebral hemispheres.
Measurements in the coronal plane at the level of the
foramen of Monro have been reported for (a) the
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A B
Thalamic pseudolesion. A: A scan through the posterior fontanelle shows an area of increased echogenicity (arrow) in the posterior
Fig. 3.24
aspect of the thalamus. B: The thalamus appears normal on images obtained via the anterior fontanelle.
interhemispheric subarachnoid space, which is the widest
horizontal distance between the hemispheres; (b) the
sinocortical space, which is the shortest distance between
the lateral wall of the triangular superior sagittal sinus
and the surface of the adjacent cerebral cortex; and (c)
the craniocortical space, which is the shortest vertical dis-
tance between the calvarium and the surface of the cortex
(30,31). The upper limits of normal, based on the 95th
percentiles, are 3 mm for the sinocortical width, 4 mm for
the craniocortical width, and 6 mm for the interhemi-
spheric width (32).
VARIANTS AND ARTIFACTS ON OTHER IMAGING PLANES
Thalamic Pseudolesion
The thalamus contains multiple parallel fibers. On poste-
rior fontanelle views, the ultrasound beam strikes these
fibers perpendicularly, occasionally producing a rounded
hyperechoic focus, termed a thalamic pseudolesion (17)
(Fig. 3.24). Similar echogenic foci are not seen on sono-
grams obtained through the anterior fontanelle (33). This
anisotropic scanning artifact can mimic a thalamic bleed
or infarct. However, a pseudolesion will disappear on
scans acquired through the anterior fontanelle, whereas a
pathologic lesion will persist.
Calcar Avis
On posterior fontanelle views, the calcar avis, a normal
gyrus, can protrude into the lateral ventricle at the junction
of the trigone with the occipital horn (17), mimicking
intraventricular hemorrhage. This scanning artifact results
when the occipital horn is imaged slightly off center,
so that adjacent brain is averaged with the ventricle
(Fig. 3.25). The calcar avis can be differentiated from hem-
orrhage by its continuity with the adjacent brain and its
central echogenic fissure (sulcus).
Chapter 3 B R A I N 55
Posterior Fossa Vallecula
On axial scans through the mastoid fontanelle, a narrow
communication, termed the vallecula, may be visualized
between the fourth ventricle and cistern magna (Fig. 3.26).
Recognition of the vallecula is important so that it is not
mistaken for a Dandy-Walker malformation. The presence
of a normal-size inferior vermis and cerebellum on other
images will differentiate the normal vallecula from a
Dandy-Walker malformation.
SPECTRAL AND COLOR DOPPLER IMAGING
Doppler imaging is not routinely used in the evaluation of the
asymptomatic neonate, but it is useful as an ancillary tool in
selected clinical scenarios. Pulsed or spectral Doppler imag-
ing makes identification of flow direction, flow velocity, and
vascular resistance possible and is essential for evaluation of
intracranial hemodynamics (34,35). Color Doppler imaging
identifies the orientation of flow relative to the transducer
(antegrade or retrograde) and the origin of the Doppler sig-
nal (artery or vein) (36,37). Power mode Doppler (amplitude
mode color or color flow Doppler energy) improves detection
of low-velocity and low-amplitude flow (38). Power mode
Doppler is particularly useful when the detection of flow is
more important than information about flow direction.
Technique: Imaging Approaches
ANTERIOR FONTANELLE APPROACH
Intracranial vessels are easily interrogated from the ante-
rior fontanelle approach (34,3841). A 5- to 7.5-MHz sec-
tor or vector transducer is used to evaluate abnormalities
of cerebral blood flow in the major intracranial arteries,
including the anterior, middle cerebral, and internal
carotid arteries, and central veins, including the vein of
Galen and straight sinus. A high-resolution linear array
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56 P E D I AT R I C S O N O G R A P H Y

A B

Calcar avis simulating intraventricular bleed. A: Scan obtained through the posterior fontanelle shows the calcar avis (arrow) super-
Fig. 3.25
imposed on the occipital horn mimicking an intraventricular clot and normal echogenic choroid plexus (Ch). B: Another scan with
slightly different angulation shows the calcar avis (arrow) in continuity with the adjacent cerebral cortex. Ch  choroid plexus.

transducer is used to insonate the superficially located
arteries, veins, and dural sinuses.
The midline sagittal scan shows the vertebral, basilar,
internal carotid, anterior cerebral, and pericallosal arteries
as well as the vein of Galen and the straight and superior
sagittal sinuses (Fig. 3.27). The course of the inferior sagit-
tal sinus parallels that of the posterior part of the perical-
losal artery; therefore, it may not be resolved as a separate
vessel. The smaller thalamostriate arteries may be seen on
laterally angled sagittal images (Fig. 3.28).
Coronal images through the anterior and midbrain
show the internal carotid arteries, middle cerebral arteries,
thalamostriate arteries, anterior cerebral arteries, and ter-
minal cerebral veins (Fig. 3.29). Coronal scans through the

A B
Vallecula. A: Axial sonogram through the mastoid fontanelle shows a narrow communication, termed the vallecula (arrow), between
Fig. 3.26
the fourth ventricle (4) and cistern magna (CM). B: A more cephalad, angulated axial view shows normal vermis (V) and cerebellar hemi-
spheres (CB), which helps differentiate the vallecula from a Dandy-Walker malformation.
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Chapter 3 B R A I N 57

A B

Normal cerebral arteries and veins, anterior fontanelle scanning. A: Sagittal midline scan shows the basilar artery (straight white
Fig. 3.27
arrow), anterior cerebral artery (orange arrows), callosal margin (red arrows), and pericallosal artery (green arrows). Flow is also noted
in the vein of Galen (curved white arrow) and straight sinus (open arrow). B: High-resolution scan demonstrates flow in the pericallosal artery
(arrowhead), small vessels in the cerebral cortex, and the sagittal sinus (arrow).

Normal cerebral arteries and veins, anterior fontanelle

Fig. 3.29
scanning. Anterior coronal scan shows the basilar artery
Thalamostriate vessels, anterior fontanelle scanning. (straight white arrow), callosal marginal (red arrow), pericallosal artery
Fig. 3.28 (green arrow), right middle cerebral arteries (pink arrows), and thalam-
Angled sagittal scan shows thalamostriate vessels in the
basal ganglia. ostriate arteries (blue arrows).
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58 P E D I AT R I C S O N O G R A P H Y

Mean Arterial Velocities and Mean Resistance Indices in

Table 3.1 Intracranial Arteries*

Resistive
Vessel Mean Systolic End Diastolic Index

Internal carotid 48 (14) 11 (5) 0.77 (0.08)

Basilar 41 (12) 10 (5) 0.76 (0.07)
Anterior cerebral 38 (13) 9 (5) 0.76 (0.09)
Middle cerebral 45 (14) 11 (5) 0.75 (0.08)
Posterior cerebral 39 (12) 10 (5) 0.74 (0.08)

*Velocity in cm/s. Standard deviation shown in parenthesis. Modified from: d0rey C,

Mateus M, Guimaraes H, et al. Neonatal cerebral Doppler: arterial and venous flow
velocity measurements using color and pulsed Doppler system. J Perinat Med 1999;
27:352361.

EDV/PSV), are the commonly used spectral Doppler mea-

Transtemporal Doppler scanning, normal circle of Willis.
Fig. 3.30
Axial scan obtained through the left temporal bone shows
the left middle cerebral artery (arrow), A1 segment of the left anterior
cerebral artery (open arrow), posterior communicating artery (arrow-
head), and posterior cerebral artery (curved arrow).
trigones of the lateral ventricles show the straight and
transverse sinuses.
sures for assessing cerebral blood flow (CBF). Systolic and
diastolic blood flow velocities increase and resistive indices
decrease with increasing gestational age (4548), related to
changes in cerebrovascular resistance. The range for RIs
and normal mean systolic and end-diastolic flow velocities
in major cerebral arteries is shown in Table 3.1. Although
the range of normal values is relatively wide, the variabil-
ity for an individual neonate is limited. In healthy
neonates, changes in flow velocity should not exceed 50%
above the baseline.
In full-term infants, antegrade flow is present through-
out systole and diastole (Fig. 3.31). In premature infants

TEMPORAL BONE APPROACH

Doppler interrogation can also be performed through the
thinnest part of the temporal bone. The transtemporal
approach using axial scans interrogates the middle cerebral
artery, A1 segment of the anterior cerebral artery, posterior
communicating artery, and posterior cerebral artery
(4244) (Fig. 3.30). The transtemporal approach is supe-
rior to the anterior fontanelle approach for evaluating the
middle cerebral artery because of a more favorable Doppler
angle. With use of the anterior fontanelle approach, the
angle of insonation between the middle cerebral artery and
transducer is almost 90 degrees, and the resultant fre-
quency shifts from flowing red blood cells approach zero.
With transtemporal sonography, the angle of insonation
approaches zero since the direction of blood flow is
towards the transducer.

POSTERIOR FONTANELLE APPROACH

The posterior fontanelle approach using axial scans can be
used to assess the interpeduncular, quadrigeminal, and dis-
tal segments of the posterior cerebral arteries and distal-
most parts of the vein of Galen and the straight sinus.
Normal Arterial Blood Flow Patterns
Flow velocity and the resistive index (RI), which is the
peak or maximum systolic velocity (PSV) minus the end-
diastolic or minimum velocity (EDV) divided by PSV (PSV
Spectral Doppler, normal arterial flow pattern. The cursor
Fig. 3.31
is on the anterior cerebral artery (arrow). Doppler interro-
gation shows rapid systolic acceleration, a sharp systolic peak, grad-
ual diastolic decline, and antegrade flow throughout diastole, typical
of the cerebral arterial circulation. The resistive index is 0.7.
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Chapter 3 B R A I N 59

A B
Transducer pressure, effect on arterial flow. Neonate with mild hydrocephalus. A: Pulsed wave Doppler tracing of the anterior cerebral
Fig. 3.32
artery with transducer held lightly over anterior fontanelle shows a resistive index (RI) of 0.69. B: On a repeat tracing obtained a few
seconds later with firm compression of the fontanelle, the RI had increased to 0.87.

under 30 weeks gestation, diastolic flow may be absent. Normal Venous Blood Flow Patterns
This pattern has been attributed to a diastolic steal related There are two common venous flow patterns: sinusoidal
to a patent ductus arteriosus. In patients with a patent (low-amplitude pulsations) and monophasic (continuous)
ductus arteriosus, resistance to flow in the cerebral vascu- (37). Sinusoidal pulsations are typical of larger, central
lature bed is higher than that in the pulmonary vessels, veins, such as the sagittal sinus and vein of Galen. These
resulting in shunting of blood from the brain during dias- pulsations are thought to represent referred atrial pressure
tole.
Several factors can affect the RI. Intracranial processes,
such as hemorrhage, brain edema, subdural effusions,
periventricular leukomalacia, and hydrocephalus, increase
vascular resistance, which in turn preferentially reduces
flow during diastole and increases the RI (49). In addition,
transducer pressure on the anterior fontanelle by the trans-
ducer may transiently increase intracranial pressure,
thereby increasing the RI. In normal infants, firm scanning
produces a small increase in mean RI (average increase,
5.2%). In infants with cerebral edema, ventricular dilata-
tion, or extra-axial fluid collections, firm transducer pres-
sure results in an even higher elevation of the RI (average
increase, 17.4%) (Fig. 3.32) (50). Extracranial factors that
reduce diastolic flow velocities, such as patent ductus arte-
riosus, also will increase the RI.
Although elevated RIs are not specific, they have been
used to follow patients with increased intracranial pres-
sures to assess the effectiveness of ventricular tapping,
shunting, or indomethacin administration (48,49).
A low resistive index (60) has been reported in
neonates with severe or prolonged asphyxia and in those
with growth retardation (48,51) (Fig. 3.33). In this popu-
lation, it has been suggested that the production of intra- Perinatal asphyxia. Doppler insonation of the anterior
Fig. 3.33
cellular nitric oxide increases, leading to vasodilatation cerebral artery shows elevated diastolic flow. Resistive
and elevated diastolic flow velocity (52). index is less than 0.5. Cursors mark peak systolic and diastolic flow.
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60 P E D I AT R I C S O N O G R A P H Y

A B
Normal venous waveform patterns, term neonate. A: Sinusoidal pulsations, from referred atrial contractions, are typical of larger, cen-
Fig. 3.34
tral veins, such as the sagittal sinus. B: Continuous flow or a monophasic pattern is typical of the smaller intracerebral veins, such as
the subependymal and terminal veins.

waves. The monophasic pattern is typical of the smaller
intracerebral veins, such as the terminal veins (Fig. 3.34).
Mean blood flow velocities in several intracranial veins
and sinuses in normal neonates are shown in Table 3.2
(37). Flow velocity is relatively higher in larger veins than
in smaller veins (34,37).
High-flow velocities and high-amplitude waveforms
(saw-tooth pattern) are abnormal and have been
described in neonates with elevated right heart pressures or
tricuspid regurgitation (40). Changes in cerebral venous
Table 3.2 Venous Blood Flow Velocities in Term Newborns
Vessel Mean Velocity (cm/sec)a
flow velocity are uncommon during normal quiet respira-
tion, but wide fluctuations can occur during forceful cry-
ing as a result of rapid changes in intrathoracic pressure
and with motion of the infants head (34).
INTRACRANIAL HEMORRHAGE
Premature Infants
Intracranial hemorrhage and periventricular leukomalacia
are the most common central nervous system complications
of prematurity. The most important risk factors for hemor-
rhage are gestational age of less than 30 weeks and birth
weight of less than 1500 g (53). The incidence of intracra-
nial hemorrhage in premature infants weighting less than
1500 g is approximately 20% to 25% (53). Approximately
67% of premature infants less than 32 weeks have intracra-
nial hemorrhage, versus 5% of term infants.

Terminal veins 3.0  0.3 SITE OF ORIGIN OF INTRACRANIAL HEMORRHAGE

Internal cerebral veins 3.3  0.3 The classic anatomic site of origin of hemorrhage in the
Vein of Galen 4.3  0.7 premature infant is the subependymal germinal matrix in
Straight sinus 5.9  1.0 the lateral ventricle (5356). The germinal matrix is a
Superior sagittal sinus 9.2  1.1 highly cellular, very vascular region that gives rise to neu-
Inferior sagittal sinus 3.5  0.3 roblasts that migrate peripherally to form the neurons of
a
Standard error of the mean. the cerebral cortex and basal ganglia. The thin-walled
Adapted from Taylor GA. Intracranial venous system in the newborn: evaluation of normal vessels in this matrix are extremely friable and a ready
anatomy and flow characteristics with color Doppler US. Radiology 1992;183:449452, source of bleeding (53). Early in gestation, the germinal
with permission. matrix lines the entire ventricular system, reaching its
LWBK505-C03_p43-117.qxd 7/7/10 1:23 PM Page 61 Aptara Inc
greatest size at 23 to 24 weeks gestation (53). Toward
the end of the second trimester, it regresses, with the invo-
lution occurring first around the third ventricle and then
around the temporal and occipital horns. By 28 to 32
weeks gestation, only a small amount of germinal matrix
remains in the caudothalamic groove at the level of the
caudate nucleus, at or slightly posterior to the foramen of
Monro. By 36 weeks gestation, the involution is essen-
tially complete.
The site of origin of germinal matrix hemorrhage
appears to be at the capillary-venule or small venule
level (5356). In approximately 80% of patients with
germinal matrix hemorrhage, blood enters the lateral
ventricles (53).
PATHOGENESIS OF INTRACRANIAL HEMORRHAGE
The important factors in the pathogenesis of intracranial
hemorrhage in the premature infant are the pressure-pas-
sive state of the cerebral circulation and the abrupt
increases in systemic blood pressure. In the term neonate,
blood vessels in the brain dilate when blood pressure
decreases and constrict when it increases, a phenomenon
termed autoregulation. Premature neonates have
impaired cerebrovascular autoregulation and as a result
have pressure-passive cerebral circulation (53,5759). Ele-
vations in arterial and/or venous pressure in combination
with the pressure-passive circulation lead to increase in
cerebral blood flow and rupture of fragile vessels in the
germinal matrix. Clinical events associated with elevations
in arterial blood pressure include rapid volume expansion
(rapid colloid infusion or exchange transfusion), hyper-
carbia (increased carbon dioxide in the blood), and
decreased hemoglobin. Events related to elevations in
cerebral venous pressure include asphyxia, tension pneu-
mothorax, congestive heart failure, and therapeutic events
(mechanical ventilation, tracheal suctioning, and rapid
volume expansion) (53,60,61).
Decreases in cerebral perfusion (i.e., ischemia) also
play a role in the pathogenesis of germinal matrix hemor-
rhage. The major consequence of decreased cerebral blood
flow is rupture of germinal matrix vessels on reperfusion
(i.e., reperfusion injury). Causes of decreased perfusion
include hypoxia (decreased oxygen content in the blood),
systemic hypotension, and reduced hemoglobin concentra-
tion (53,60,61).
CLINICAL FINDINGS
Clinical signs of intracranial hemorrhage include dimin-
ished consciousness levels, hypotonia, abnormal posturing,
seizures, apnea, coma, and low hematocrit. However, 25%
to 50% of intracranial hemorrhage is clinically silent and
detected only by imaging (53).
Intracranial hemorrhage usually occurs in the first 3
days of life, with approximately 50% occurring on day 1,
25% on day 2, and 15% on day 3 to day 4 (53,62,63). By
Chapter 3 B R A I N 61
72 to 96 hours, 80% to 90% of intracranial hemorrhage
has occurred.
In symptomatic neonates with changes in neurologic
status, unexplained hematocrit drop, or unexplained
apnea or bradycardic episodes, cranial sonograms are
performed on demand. In asymptomatic premature
neonates of less than 1000 g birth weight, screening
sonography is recommended on days 3 to 5, days 10 to
14, and day 28. In neonates of 1000 to 1250 g birth
weight, sonography is recommended at days 3 to 5 and at
day 28. Neonates with birth weights of 1251 to 1500 g
can be scanned at days 3 to 5 and again before discharge
(62,64).
GRADING SYSTEM
The classification of Papile and colleagues is the most
widely used system to grade the severity of intracranial
hemorrhage in the premature infant (65). In this system,
there are four grades of intraventricular hemorrhage
(IVH): grade 1, germinal matrix hemorrhage only; grade 2,
germinal matrix and intraventricular hemorrhage without
hydrocephalus; grade 3, germinal matrix and intraventric-
ular hemorrhage with ventricular enlargement; and grade
4, germinal matrix hemorrhage, intraventricular hemor-
rhage with or without ventricular enlargement, and intra-
parenchymal blood.
Grade 1 bleeds occur in approximately 40% of very
premature infants, grade 2 in 25%, grade 3 in 20%, and
grade 4 in 15% (53,66).
Grade 4 hemorrhage is the result of hemorrhagic
cerebral infarction rather than direct extension of blood
from the germinal matrix (53). The periventricular white
matter normally drains via the medullary veins into the
terminal and internal cerebral veins. It has been shown
that germinal matrix hemorrhage obstructs the drainage
of these small terminal veins causing venous hypertension
and ultimately hemorrhagic infarction.
SONOGRAPHIC FINDINGS OF GERMINAL
MATRIXINTRAVENTRICULAR HEMORRHAGE
Grade 1 Hemorrhage
On coronal images, grade 1 (subependymal) hemorrhage
appears as a region of increased echogenicity inferolateral
to the floor of the frontal horns and medial to the head of
the caudate nucleus (67,68). Sagittal sections show an area
of increased echogenicity immediately anterior to or within
the caudothalamic groove (Fig. 3.35). The echogenicity is
attributed to the formation of fibrin mesh within the
organized clot. Large germinal matrix hemorrhages may
elevate the floor of the lateral ventricle, compressing or
obliterating the frontal horn or body. Doppler sonography
can help in differentiating hemorrhage from the echogenic
choroid plexus. Hemorrhage has no flow signal, whereas
normal choroid plexus is a highly vascular structure
(Fig. 3.36).
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62 P E D I AT R I C S O N O G R A P H Y

A B
Acute subependymal hemorrhage. A: Coronal sonogram shows a focus of increased echogenicity (arrow) in the left subependymal
Fig. 3.35
area. B: Left parasagittal image shows increased echogenicity in the caudothalamic groove (arrow).

Over a period of days to weeks, the germinal matrix Grade 2 Hemorrhage

clot regresses in size. As the clot retracts, it undergoes cen-
tral liquefaction, either completely resolving or forming a
subependymal cyst. Posthemorrhagic subependymal cysts
usually measure between 3 and 5 mm in diameter (Fig.
3.37). They appear to be of little clinical significance, and
most disappear within a year. Subependymal cysts are not
specific for hemorrhage. They can be seen with intrauter-
ine viral infections, Zellweger syndrome (cerebrohepa-
torenal syndrome), and trisomy 13, and in some patients
they are an isolated finding without an obvious cause
(6971). The ventricles usually remain normal in size in
patients with uncomplicated subependymal hemorrhage.
Grade 2 hemorrhage results when the germinal matrix rup-
tures through the ependymal wall, entering the lateral ven-
tricles. Grade 2 IVH appears as echogenic material that fills
part or all of a nondilated ventricular system (67,68) (Fig.
3.38). Intraventricular hemorrhage without ventricular
dilatation can be difficult to diagnose by sonography. The
findings of an area of increased echogenicity or a
CSFblood fluid level in the dependent part of the ventricle
(i.e., the occipital horn or ventricular trigone) are clues to
the diagnosis of intraventricular blood. Posterior fontanelle
scanning facilitates the detection of IVH in normal-sized
ventricles (Fig. 3.39).

A B
Grade 1 hemorrhage, color flow Doppler scan. A: Subependymal hemorrhage. The hematoma (arrow) inferolateral to the frontal horn
Fig. 3.36
is avascular. Note normal color signal in the caudothalamic groove posterior to the germinal matrix hemorrhage. B: Normal germinal
matrix for comparison. Parasagittal image shows flow in the caudothalamic groove (arrow) adjacent to the ventricular floor.
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Chapter 3 B R A I N 63

Resolving subependymal hemorrhage (same patient as in

Fig. 3.37 Grade 2 hemorrhage. Right parasagittal scan demon-
Figure 3.35). Left parasagittal scan show a thick-walled
Fig. 3.38
cyst (arrow) in the subependymal area, representing a resolving strates a small clot (arrow) in the occipital horn of a
hematoma. nondilated lateral ventricle. Ch, choroid plexus.

In some cases, the echogenic clot may adhere to the
choroid plexus and be indistinguishable from it. Asym-
metric enlargement and irregularity of the choroid plexus
and extension of the trigonal choroid plexus into the
occipital horns are findings that favor intraventricular
blood and clot adherent to the choroid plexus. Color
Doppler flow imaging also can be used to differentiate
between clot and the choroid plexus. Clot is avascular,
whereas normal choroid plexus is vascular (see Fig. 3.36).
The intraventricular clot decreases in size and echogenic-
ity over a period of several weeks. The subependymal lining
of the ventricle typically becomes thicker and more echogenic
secondary to a chemical ventriculitis, which occurs in response
to blood in the cerebrospinal fluid (72). The subependymal
echogenicity usually disappears within 6 to 8 weeks.
Grade 2 hemorrhage is usually self-limiting and resolves
without sequelae. Mild to moderate ventricular dilatation,
as a result of intraventricular obstruction by clot, septations,

A B
Grade 2 hemorrhage, posterior fontanelle scan approach. A: Right parasagittal view shows faintly increased echogenicity in the occip-
Fig. 3.39
ital horn (arrow), which could represent blood versus volume averaging of adjacent parenchyma. B: View through the posterior
fontanelle confirms clot (arrow) in the occipital horn. Ch  choroid plexus.
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64 P E D I AT R I C S O N O G R A P H Y

A B
Grade 3 hemorrhage. A: Coronal scan demonstrates dilated, echogenic blood-filled frontal horns (arrows). B: Left parasagittal scan
Fig. 3.40
shows blood filling nearly the entire left lateral ventricle (arrows).

or debris or because of obliterative arachnoiditis with
obstruction of CSF flow over the convexities, is an occa-
sional complication. Marked hydrocephalus is a rare
sequela.
Grade 3 Hemorrhage
Grade 3 hemorrhage expands one or both lateral ventric-
ular cavities (67,68). Because the ventricles are dilated, it
is easier to diagnose grade 3 IVH on sonography than it
is to diagnose grade 2 IVH. With severe IVH, the blood
may completely fill the ventricular cavity, forming a cast
of the ventricle (Fig. 3.40). A bloodcerebrospinal fluid
level may be seen in the occipital horn. Blood also may fill
the third and fourth ventricles and the cavum septi pellu-
cidi.
Grade 3 IVH usually become smaller and disappears
over 5 to 6 weeks. As the clot retracts, it can produce a
ventricle within a ventricle appearance (Fig. 3.41), diffuse

A B
Evolution of grade 3 hemorrhage (same patient as in Figure 3.40). Coronal (A) and right parasagittal (B) scans 2 weeks after the initial
Fig. 3.41
bleed show persistent ventricular dilatation and retraction of the intraventricular clot (arrows). The hematoma has decreased in
echogenicity and has well-defined margins, creating a ventricle within ventricle appearance. The ependymal lining of the ventricle (arrowheads)
has increased in echogenicity, reflecting reactive ventriculitis.
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Grade 3 hemorrhage. Left parasagittal scans show
Fig. 3.42
low-level echoes filling the ventricle and a blood
cerebrospinal fluid level (arrow) in the occipital horn.
low-level echoes, or a bloodcerebrospinal fluid level (Fig.
3.42). Low-level echoes that are a sequela of intraventricu-
lar hemorrhage are nearly always a benign finding. How-
ever, if there is an increase in the extent of echogenicity or
the sudden appearance of echogenicity in a previously ane-
choic ventricle, the possibility of new bleeding or infection
needs be considered.
Over time, the echogenic clot becomes hypoechoic and
may resolve completely or persist as linear septations or
bands. The acute hydrocephalus, resulting from ventricular
blockage by hemorrhagic particulate matter, arrests or
A B
Grade 4 hemorrhage. A: Coronal image demonstrates intraventricular blood in the left lateral ventricle and an area of increased
Fig. 3.43
echogenicity with ill-defined margins in the occipital parenchyma (arrows). B: Parasagittal image adjacent to the ventricle confirms
intraparenchymal blood (arrows).
Chapter 3 B R A I N 65
resolves spontaneously in most patients (65% to 75%).
Mild to moderate hydrocephalus develops in the remaining
patients. A diversionary shunt placement is required in only
a small percentage of infants (73).
Grade 4 Hemorrhage
Grade 4 hemorrhage is a hemorrhagic infarction of the
periventricular parenchyma (53,56,74,75). The intra-
parenchymal hemorrhage (IPH) appears as an intensely
echogenic focus with irregular margins in the parenchyma
adjacent to one or both lateral ventricles (67,68)
(Fig. 3.43). The interface between the ventricular wall
and hemorrhage is often effaced. Mass effect with shift of
the midline structures to the unaffected contralateral side
may be present with larger hemorrhages. Occlusion of
the small, terminal veins by the germinal matrix hemor-
rhage may be shown on color flow Doppler imaging (see
Fig. 3.36A).
Intraparenchymal hemorrhage is most common in the
frontal and parietal lobes. It is usually unilateral and tends
to be located on the same side as the germinal matrix-
intraventricular hemorrhage. If there is bilateral IPH, it is
usually asymmetric, with the larger IPH occurring on the
side of the larger IVH.
Similar to the other types of hemorrhages, the parenchy-
mal clot liquefies and retracts over 2 to 4 weeks. As this
occurs, the edges of the hematoma become echogenic rela-
tive to the center, which is hypoechoic. By 2 to 4 weeks fol-
lowing the injury, the clot retracts from the surrounding
brain parenchyma, and by 2 to 3 months, a cystic area
(encephalomalacia) develops (Fig. 3.44). The encephaloma-
lacic area can communicate with the ipsilateral ventricle,
which often is dilated. The hydrocephalus may resolve,
arrest, or progress.
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A B

C D

E F
Evolution of intraparenchymal hemorrhage. Coronal (A) and left parasagittal (B) views in a 2-day-old girl demonstrate intraparenchy-
Fig. 3.44
mal blood (arrows) in the left frontoparietal region. Coronal (C) and left parasagittal (D) scans 2 weeks later show lysis of the clot
(arrows) and ventriculomegaly. Coronal (E) and left parasagittal (F) scans 2 months later show an area of encephalomalacia (E), which communi-
cates with the ventricle, and increasing hydrocephalus.
LWBK505-C03_p43-117.qxd 7/7/10 1:23 PM Page 67 Aptara Inc
Trapped fourth ventricle. A markedly dilated fourth (4)
Fig. 3.45
ventricle is noted on this sagittal midline scan. The other
ventricles were of normal size.
Hydrocephalus
Ventricular dilatation following IVH occurs as a result of
an obliterative arachnoiditis obstructing the basilar cis-
terns or fourth ventricular outflow tract or because of
intraventricular obstruction by clot, septations, or debris.
With moderate to severe hemorrhage, ventricular dilata-
tion may be present at the time of the initial bleed. Ven-
tricular dilatation is diagnosed in most patients by day 28
and in virtually all patients by 3 months. The clinical signs
of hydrocephalus (i.e., increasing head size, suture diasta-
sis, and findings of increased intracranial pressure, such as
apnea, bradycardia, stupor, vomiting, and ocular changes)
may not appear for days to weeks after the onset of ven-
tricular dilatation.
The trigones and occipital horns dilate before the
frontal horns. These may be the only areas of ventricular
enlargement in infants with small ventricular hemorrhages,
whereas the entire ventricle may enlarge in infants with
larger hemorrhages. The lateral ventricles usually dilate
more than the third or fourth ventricles.
Marked enlargement of the fourth ventricle can occur
when the ventricle is isolated or trapped (Fig. 3.45).
This occurs when there is combined obstruction of the
aqueduct of Sylvius and the foramina of Luschka and
Magendie. The dilated fourth ventricle can compress and
displace the brainstem and cerebellum and a markedly
enlarged ventricle can herniate transtentorially into the
middle cranial fossa (76,77). The fourth ventricle is com-
pressed where it herniates through the tentorial incisures
(76,77).
In premature neonates weighing between 750 and
1500 g, hydrocephalus occurs in approximately 4% of
Chapter 3 B R A I N 67
grade 1 bleeds, 14% of grade 2 bleeds, 75% of grade 3
bleeds, and 66% of grade 4 bleeds (53). The ventricular
dilatation arrests or resolves in 50% to 75% of infants
with posthemorrhagic hydrocephalus. Resolution usually
commences within 4 weeks of the development of ven-
triculomegaly. The probability that ventricular dilatation
will resolve spontaneously varies directly with the sever-
ity of intracranial hemorrhage. Hydrocephalus after
grades 1 or 2 hemorrhage rarely requires ventricular
drainage, whereas hydrocephalus after grade 3 or 4 IVH
is more likely to require ventricular drainage. In general,
less than 15% of neonates with posthemorrhagic hydro-
cephalus will require ventriculoperitoneal shunting (53).
Serial sonography is recommended in neonates with pos-
themorrhagic hydrocephalus until ventricular size stabi-
lizes.
Prognosis
The morbidity and mortality associated with periventricu-
lar hemorrhage (PVH)/IVH relates to the severity of the
hemorrhage (53). The short-term mortality rates for grades
1, 2, 3, and 4 hemorrhage are approximately 0% to 12%,
2% to 24%, 8% to 32%, and 22% to 45%, respectively.
The incidence of long-term neurologic sequelae, namely,
motor and intellectual deficits, for grades 1, 2, 3, and 4
hemorrhage is approximately 15%, 25%, 50%, and 75%,
respectively (53).
CEREBELLAR HEMORRHAGE
Intracerebellar hemorrhage is more frequent in the pre-
mature than in the full-term infant, and has been found at
autopsy in 10% to 25% of infants under 32 weeks gesta-
tion (78). Reports based on sonographic imaging, includ-
ing scanning through the mastoid window, have shown an
incidence of 2% to 3% in infants weighing less than 1500
g (79,80). The incidence varies with birth weight, with
infants weighing less than 750 g having a higher incidence
(8.7% to 17%) of cerebellar hemorrhage than those
weighing between 750 and 1499 g (incidence 2.7%) (79).
The causes for cerebellar hemorrhage in the preterm
infant include primary intracerebellar hemorrhage,
venous infarction, and extension of intraventricular or
subarachnoid hemorrhage into the cerebellum (78). Cere-
bellar hemorrhage tends to be localized, with 70% occur-
ring in one cerebellar hemisphere and 20% in the vermis
(79).
Small cerebellar hemorrhages may be asymptomatic.
Large hemorrhages cause signs of brainstem compression
(apnea or respiratory abnormalities) and increased
intracranial pressure. The sonographic findings of cerebel-
lar hemorrhage include asymmetric echogenicity or an
echogenic mass in the cerebellar hemispheres (Fig. 3.46),
loss of definition of the interfaces between the fourth ven-
tricle and cerebellum, and lateral and third ventricular
dilatation. Hemorrhage is more readily detectable on mas-
toid fontanelle images than on scans acquired through the
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68 P E D I AT R I C S O N O G R A P H Y
A B
Intracerebellar hemorrhage. A: Coronal image shows a poorly defined area of increased echogenicity (open arrow) within the right
Fig. 3.46
cerebellar hemisphere and bilateral intraventricular blood (arrows). B: Axial mastoid view shows increased echogenicity in the right
cerebellar hemisphere (R) compared with the left cerebellar hemisphere (L) and intraventricular blood (arrows). Mastoid fontanelle scanning opti-
mizes delineation of posterior fossa bleeds.
anterior fontanelle. Cerebellar hemorrhage can resolve
completely or produce an area of encephalomalacia.
SUBARACHNOID HEMORRHAGE
Subarachnoid hemorrhage in the premature neonate is
usually secondary to extension of intraventricular hemor-
rhage. The sonographic diagnosis can be difficult because
the subarachnoid spaces are normally enlarged in this
population (Fig. 3.47). Large subarachnoid hemorrhages
Normal subarachnoid spaces, premature infant. Coronal
Fig. 3.47
view shows large interhemispheric and sylvian fissures.
Differentiation from subarachnoid hemorrhage is difficult unless there
is asymmetric fissural widening.
may be identified if they cause asymmetric widening of
the sylvian fissure, subarachnoid cisterns, or spaces over-
lying the cerebral cortex (specificity 93%, sensitivity
69%) (81).
Term Infants
Sites of hemorrhage in term infants include the extra-axial
spaces, subpial cortex, basal ganglia, choroid plexus,
germinal matrix, and cerebellum.
SUBARACHNOID HEMORRHAGE
Subarachnoid hemorrhage can be primary or secondary
(subsequent to extension from subdural, intraventricular,
or intracerebellar hemorrhage) (78). Primary hemorrhage
is the result of traumatic or hypoxic events, and the source
of the blood is thought to be either the anastomoses
between the leptomeningeal arteries or the bridging
meningeal veins. Most infants with minor degrees of sub-
arachnoid hemorrhage exhibit minimal or no neurologic
signs. Infants with large hemorrhages can present with
seizures. Infants with subarachnoid hemorrhage usually
have a good outcome with minimal or no neurologic
signs.
Sonography is relatively insensitive for detection of
small amounts of subarachnoid hemorrhage because the
echogenicity of the blood and brain surface is similar.
Large subarachnoid hemorrhages can be diagnosed on
sonography and present as unilateral or bilateral fluid col-
lections in the interhemispheric fissure, sylvian fissure, or
subarachnoid cisterns or over the cerebral convexities.
Communicating hydrocephalus is an occasional complica-
tion (78).
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Chapter 3 B R A I N 69

A B

C D
Infratentorial subdural hematoma. Coronal (A) and left parasagittal (B) sonograms in an infant on extracorporeal membrane oxygena-
Fig. 3.48
tion show an echogenic hematoma under the left leaf of the tentorium (arrows). Coronal (C) and parasagittal (D) sonograms 2 weeks
later show a hypoechoic fluid collection (arrowheads) indicating evolution of the blood products.

SUBDURAL HEMORRHAGE signs referable to the brainstem (respiratory and oculomotor

Subdural hemorrhage is more frequent in the full-term
infant than in the premature infant and is most commonly
the result of birth trauma, such as breech or forceps delivery
or vacuum extraction (78). Other causes are coagulopathy
and hypernatremic dehydration (82). There are four sources
of subdural hemorrhage: (a) tentorial laceration with rup-
ture of the straight sinus, transverse sinus, or vein of Galen;
(b) occipital osteodiastasis with rupture of the occipital
sinus; (c) falx laceration with rupture of the inferior sagittal
sinus; and (d) rupture of bridging, superficial cerebral veins
(78). The hemorrhage is infratentorial in the first two
injuries and supratentorial in the other two injuries.
Infratentorial hematomas are associated with neurologic
abnormalities). Supratentorial hematomas are associated
with signs referable to the cerebrum (hemiparesis, seizure).
Infants with large tentorial lacerations and occipital diasta-
sis have a poor prognosis and such infants often die. Most
infants with smaller posterior fossa and convexity subdural
hematomas have a relatively good prognosis and are either
normal or exhibit minor neurologic deficits (78).
Infratentorial subdural hemorrhage presents as a fluid
collection between the tentorium and the cerebellar hemi-
sphere on gray-scale imaging. The fluid may cause mass
effect, resulting in compression of the cerebellum, brain-
stem, and fourth ventricle, and it may silhouette the con-
tours of these structures (Fig. 3.48). Hydrocephalus results
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A B
Supratentorial subdural hemorrhage. Anterior coronal (A) and sagittal (B) views show an echogenic extra-axial fluid collection (arrows)
Fig. 3.49
in the interhemispheric space (arrow) and over the right convexity displacing the cortical surface caudally. The echogenicity indicates
an acute bleed.

Supratentorial subdural hemorrhage. Anterior (A) and pos-

Fig. 3.50
terior coronal (B) sonograms through the anterior
fontanelle show a large echogenic frontal extra-axial fluid collection
with midline shift to the left and bilateral ventricular dilatation. C: T1-
wieghted coronal magnetic resonance image shows high-signal extra-
B axial fluid collection.
LWBK505-C03_p43-117.qxd 7/7/10 1:23 PM Page 71 Aptara Inc
if the hematoma compresses the fourth ventricle or aque-
duct (83). Use of the posterior fontanelle as an acoustic
window can increase the detection of small collections.
Gray-scale sonographic findings of supratentorial hem-
orrhage include a fluid collection in the interhemispheric
fissure or over the cerebral convexity (Fig. 3.49) and mass
effect with flattening of gyri, compression of the ventricles,
and shift of midline structures (Fig. 3.50). While moderate
to large supratentorial hematomas can easily be identified,
small hematomas can be difficult to recognize because of
the inability to angle the transducer sufficiently to image
the curved surface of the brain. Imaging with a high-
frequency linear transducer can facilitate identification of
fluid collections in the supratentorial spaces. Acute extra-
axial collections, both the supratentorial and infratentorial
types, are echogenic. As they evolve, they become hypo-
echoic (see Fig. 3.48).
SUBARACHNOID VERSUS SUBDURAL HEMORRHAGE: COLOR DOPPLER IMAGING
Color flow Doppler ultrasonography with high-frequency
linear transducers is useful to separate subarachnoid and
subdural fluid based on displacement of vessels. Normally,
the superficial cortical blood vessels lie on the cortical sur-
face of the brain within the pia-arachnoid (84). Subarach-
noid fluid displaces cortical vessels away from the brain sur-
face toward the cranial vault. Color Doppler shows the
cortical veins crossing the wide subarachnoid space to reach
the superior sagittal sinus, the so-called cortical vein sign
(Fig. 3.51) (84). Subdural fluid pushes the superficial
Subarachnoid fluid. Color Doppler imaging shows vessels
Fig. 3.51
(arrow) extending from the surface of the frontal cortex
(FL) into the extra-axial fluid (F) collection (arrows).
Chapter 3 B R A I N 71
cortical vessels against the brain surface. Color Doppler
sonography shows the color-coded cortical veins embedded
within the echogenic pia-arachnoid that surrounds the
brain. The subdural space itself is devoid of flow (84)
(Fig. 3.52).
EPIDURAL HEMORRHAGE
Epidural hemorrhage is rare and usually the result of trau-
matic delivery. It can be supratentorial or infratentorial
and arterial or venous in origin. Sonographic findings of
an acute hematoma are an echogenic fluid collection
between the brain and the skull and mass effect with dis-
placement of adjacent parenchyma and the ipsilateral ven-
tricle. As the hematoma ages, it becomes hypoechoic. Dif-
ferentiation of subdural and epidural hematomas is
difficult by sonography and is accomplished best by com-
puted tomography (CT) or magnetic resonance imaging
(MRI).
PARENCHYMAL HEMORRHAGE
Parenchymal hemorrhage in term infants can be the result
of ischemia, hypotension, birth trauma, coagulation
defects, vein of Galen malformation, hypertension, emboli,
polycythemia, and extracorporeal membrane oxygenation
(ECMO) (78,85,86). Neonates on ECMO are predisposed
to intracranial hemorrhage because of continuous heparinizat-
ion and hypoxia (87).
The acute parenchymal hemorrhage appears as a focal
echogenic mass in the cerebral cortex (Fig. 3.53) or basal
Subdural fluid. Color Doppler imaging shows flow in corti-
Fig. 3.52
cal veins lying in the pia-arachnoid (arrows). The subdural
fluid (F) itself is devoid of flow.
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72 P E D I AT R I C S O N O G R A P H Y
A B
Parenchymal hemorrhage in a term infant with a congenital diaphragmatic hernia on extracorporeal membrane oxygenation. Coronal
Fig. 3.53
(A) and right parasagittal (B) images show a right parietal lobe intraparenchymal hemorrhage (arrows) containing fluid-fluid levels,
reflecting the presence of clotted and unclotted blood. There is associated mass effect with obliteration of the right lateral ventricle and midline
shift (open arrow) to the left.
ganglia. Multiple, complex, intraparenchymal hematomas
are not uncommon in infants on ECMO. These may be
hypoechoic rather than hyperechoic relative to normal
parenchyma, because heparinization, required for ECMO,
prevents normal clotting of blood. Parenchymal hemor-
rhage can resolve completely or undergo central liquefac-
tion resulting in an area of encephalomalacia.
CHOROID PLEXUS
Choroid plexus hemorrhage is more common in term
infants than in premature infants. Sonographic findings
include an enlarged choroid plexus with irregular, lobulated
margins and loss of normal anterior tapering of the choroid
plexus. The diagnosis of choroid plexus hemorrhage can be
difficult because the normal choroid plexus, particularly in
the trigones, is echogenic and bulbous. Concomitant intra-
ventricular hemorrhage or decreasing size of the choroid
plexus on serial sonograms supports the diagnosis of hem-
orrhage. Extension of choroid plexus into the occipital
horn also should raise the suspicion of clot within or adher-
ent to the choroid plexus. Choroid plexus hemorrhage can
resolve completely, undergo central liquefaction resulting in
a well-defined cyst, or rupture into the ipsilateral ventricle.
SUBEPENDYMAL HEMORRHAGE
Subependymal germinal matrix hemorrhage is primarily a
problem of premature infants. It rarely occurs in term new-
borns. Such hemorrhages have been reported in less than
5% of term infants. Affected infants are often small for
gestational age.
CEREBELLAR HEMORRHAGE
In term infants, the cause of cerebellar bleeding is thought to
be traumatic delivery leading to cerebellar laceration or rup-
ture of cerebellar veins, posterior fossa veins, or occipital
sinuses. Other causes include the use of facemask ventilation,
which increases venous pressure, and coagulation disorders.
By comparison with the hemispheric predominance in pre-
mature neonates, the cerebellar vermis is the predominant
site of bleeding in term infants (78). The sonographic find-
ings are similar to those described in premature infants.
PRENATAL HEMORRHAGE
In utero intracranial hemorrhage is an uncommon event. It
usually is associated with an underlying coagulopathy or a
twin-to-twin transfusion. Subependymal cysts may be seen
on postnatal sonograms obtained on the first day of life.
HYPOXIC-ISCHEMIC INJURY
Hypoxic-ischemic brain injury is a significant cause of
perinatal and neonatal morbidity and mortality (8890).
Hypoxia refers to decreased oxygenation of blood as a
result of respiratory depression. Ischemia is defined as a
decrease in cerebral blood flow. The most important factor
in neonatal hypoxic-ischemic brain injury is asphyxia,
which may occur intrapartum, peripartum, or postpartum.
Postpartum factors predisposing to ischemic injury include
congenital heart disease, polycythemia, trauma, meningi-
tis, and ECMO.
Chorioamnionitis, or intrauterine infection, has been
implicated as a potential intrapartum cause of hypoxic-
ischemic encephalopathy (HIE) (91,92). The hypothesized
mechanisms by which chorioamnionitis lead to HIE and
cerebral palsy include (a) elevated levels of inflammatory
cytokines in the fetus causing direct injury to the fetal
brain, (b) inflammation of the placenta leading to inter-
ruption of placental gas exchange and blood flow, and
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(c) maternal fever, which increases the core temperature of
the fetus, resulting in damage to the developing brain (92).
In the premature infant, ischemia tends to affect the deep
white matter in the immediate periventricular region.
Periventricular leukomalacia (PVL) is the most common
pathologic finding. In the term infant, the watershed area is
the subcortical gray and white matter (i.e., at the junction of
the major cerebral arteries) (89). The deep structures of the
brain (thalami, basal ganglia, posterior limbs of the internal
capsule, brainstem) may also be damaged in premature and
term infants who have profound ischemia (85,88,89).
Ischemic Lesions of the Premature Neonate
The risk factors for ischemic injury in the premature brain
include (a) absence of cerebral blood flow autoregulation,
which allows changes in systemic blood pressure (e.g.,
hypotension) to be directly transmitted to the cerebral vascula-
ture bed; (b) immaturity of the cardiovascular system, which
can result in sudden hypotensive episodes; and (c) vulnerability
of the white matter oligodendroglia to ischemia. The latter cells
are extremely sensitive to injury by free radicals, which are pro-
duced in the ischemia-reperfusion sequence (90). Clinical signs
include hypotonia, seizures, and apnea or bradycardia.
The ischemic lesion in the premature neonate most
commonly affects the deep white matter at the level of the
optic radiations adjacent to the trigones of the lateral ven-
tricles and the frontal horns near the foramen of Monro.
The cerebral cortex in premature infants is largely unaf-
fected by ischemic injury because of its collateral blood
supply from meningeal intra-arterial anastomoses, which
are present throughout gestation and involute at term (93).
Histologic changes of ischemic injury in the premature
infant are coagulation necrosis of periventricular white
A B
Periventricular leukomalacia. Coronal image posterior to the ventricles (A) and right parasagittal image (B) show symmetrically
Fig. 3.54
increased echogenicity in the white matter bilaterally (arrows). Within the periventricular echogenicity are more punctate hyperechoic
areas, consistent with hemorrhagic foci.
Chapter 3 B R A I N 73
matter, followed by proliferation of astrocytes and
macrophages. Phagocytosis of necrotic tissue begins within
5 to 7 days and cavitation usually within 2 weeks of the ini-
tial insult. The cystic cavities can communicate with the lat-
eral ventricles if there is concomitant destruction of the
ependyma. About 25% of the ischemic lesions contain
areas of petechial hemorrhage (89,94). The presence of cav-
itation is termed periventricular leukomalacia (85,89).
SONOGRAPHY OF PERIVENTRICULAR LEUKOMALACIA
The sonographic examination immediately after the
ischemic event is often normal. Within the first 2 weeks of
injury, the echogenicity of the periventricular white matter
increases (88,9496). The echogenicity is greater than that
of the adjacent choroid plexus and it is usually bilateral
and symmetric (Fig. 3.54), although it may be unilateral or
asymmetric. Smaller foci of relatively increased reflectivity
may be noted in the area of diffuse hyperechogenicity, rep-
resenting hemorrhage or hemorrhagic infarction (Fig.
3.54). Doppler interrogation in acute severe injury can
show increased diastolic flow, decreased arterial pulsatility
and a low resistive index (60). In very profound ischemic
injury, the basal ganglia and thalami appear focally or dif-
fusely hyperechoic. Echogenic linear striations, termed
lenticulostriate vasculopathy, also may be seen (97,98).
The periventricular echogenicity may resolve completely
or undergo cavitation and cyst formation (88,89, 99). Cystic
changes in areas of increased echogenicity develop 2 to 6
weeks after the ischemic insult and are the definitive finding
of PVL (85) (Fig. 3.55). The larger the area of periventricular
echogenicity, the greater is the likelihood of cystic necrosis.
The cysts can be single or multiple, and they may be localized
to the anterior or posterior areas of the lateral ventricles or
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74 P E D I AT R I C S O N O G R A P H Y

A B

C D
Periventricular leukomalacia. A: Posterior coronal image shows symmetrically increased echogenicity (arrows) in both periventricular
Fig. 3.55
areas. The echogenicity of the periventricular disease is similar to that of the choroid plexus (CH). B: A right parasagittal image shows
increased echogenicity at the angles of the lateral ventricle (arrows). Follow-up coronal (C) and right parasagittal (D) sonograms 3 weeks later
reveal small cystic areas adjacent to the frontal and occipital areas of the ventricle. Also note a widened interhemispheric fissure (open arrow)
related to brain atrophy.

may extend along the entire length of the ventricles. They
measure between 1 mm and several centimeters in diameter
(100).
Late findings of ischemic injury include thinning of the
deep white matter, enlarged ventricles, and prominent inter-
hemispheric fissures and cerebral sulci, related to cerebral
atrophy. PVL may also involve the corpus callosum, leading to
cystic changes and volume loss (Fig. 3.56) (101). The clinical
manifestations of ischemia in the premature infant include
hypotonia, seizures, and apneic or bradycardiac episodes.
Results of autopsy and magnetic resonance studies sug-
gest that the incidence of PVL is as high 50% (85,102,103).
The sensitivity of sonography for detection of white matter
injury is 5% to 10%. The low sensitivity likely reflects the
insensitivity of sonography in detection of noncavitary
white matter damage.
DIFFERENTIAL DIAGNOSTIC CONSIDERATIONS
The increased echogenicity accompanying ischemic injury
must be differentiated from the normal periventricular
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Periventricular leukomalacia of the corpus callosum, 32-
Fig. 3.56
week preterm male infant. Midline sagittal image shows
cystic changes within the corpus callosum (curved arrow). (Reprinted
from Coley BD, Hogan MJ. Cystic periventricular leukomalacia of the
corpus callosum. Pediatr Radiol 1997;27:583585 with permission.)
halo/blush and from parenchymal blood in grade 4 IVH.
The normal periventricular halo has ill-defined borders
and an echogenicity less than that of the choroid plexus.
PVL has better-defined borders and an echogenicity equal
or greater than that of the choroid plexus. Posterior
fontanelle scanning can help in differentiating the two con-
ditions. The echogenicity of the periventricular halo will
decrease, whereas the echogenicity of PVL will persist
using the posterior fontanelle approach.
The characteristic distribution of PVL should distin-
guish it from grade 4 hemorrhagic venous infarction.
Grade 4 hemorrhage is unilateral or asymmetric and asso-
ciated with IVH, whereas PVL is usually symmetric and
may or may not be associated with IVH. The sequela of
venous infarction is a large parenchymal cyst (i.e., area of
encephalomalacia), whereas the result of PVL is multiple
small cysts.
PROGNOSIS
The sequelae of PVL are intellectual, motor, and visual
deficits, occurring in approximately 72%, 24%, and 36%,
respectively, of extremely premature infants (25 weeks
gestation) (85,89,90,104). Spastic diplegia involving both
lower extremities is the classic neurologic sequela of PVL.
This abnormality occurs because the lower extremity
axons lie closer (i.e., more medial) to the lateral ventricles
than do the upper extremity axons. The arms can be
affected in cases of severe PVL, resulting in spastic quadri-
plegia. Visual deficits are common in infants with ischemic
lesions in the peritrigonal region, due to the fact that the
optic radiations and visual association pathways course
Chapter 3 B R A I N 75
adjacent to the posterior periventricular white matter
(85,89).
There appears to be an association between the extent
of periventricular echogenicity on sonography and the
development of neurologic deficits (105108). Infants with
small, unilateral lesions may have a normal outcome or
exhibit only mild neurologic deficits, while infants with
extensive unilateral or bilateral periventricular echogenicity
frequently exhibit motor and cognitive deficits (80%)
(104,106108). Small lesions are commonly limited to the
frontal area. Large lesions tend to involve the frontoparietal
or fronto-parieto-occipital areas. The presence of cystic
changes has an especially poor prognosis, with a greater
than 75% incidence of cerebral palsy, and the risk is greater
in patients who have posterior (parietal/occipital) lesions
(104,106).
CEREBELLAR ISCHEMIA OF PREMATURITY
Cerebellar ischemic injury is not as common as periventric-
ular ischemic injury, with an incidence between 2% and 8%
(80,109). Sonographic findings of cerebellar ischemic/
infarction include increased parenchymal echogenicity, lack
of Doppler signal or flow, and decreased gyral-sulcal defini-
tion. Similar to cerebral cortical injury, late changes include
parenchymal atrophy and cystic encephalomalacia. Distin-
guishing between cerebellar hemorrhage and ischemia
requires CT or MRI.
Ischemic Lesions of the Term Neonate
Asphyxia in the term infant results in a different pattern of
brain damage than that seen in preterm infants
(85,88,110). The area of injury is in the end fields between
the major vascular territories. Beginning about 36 weeks
gestation, the watershed area moves from the periventric-
ular area to the periphery of the brain. By 40 weeks, the
border zone between the major arterial territories
(the anterior, middle, and posterior cerebral arteries) is in
the cortical gray matter and subcortical white matter in a
parasagittal distribution, rather than deep in the white
matter. Risk factors for intrapartum and peripartum
ischemic injury include traumatic delivery, prolapse of the
umbilical cord, abruptio placentae, and chorioamnionitis.
Postnatal factors include severe respiratory distress, sepsis,
and shock.
Pathologically, ischemic injury in the term infant pro-
duces cerebral edema, neuronal necrosis, and white matter
gliosis (89). Affected patients present with lethargy, irri-
tability, jitteriness, hypotonia, and/or seizures.
SONOGRAPHY OF ISCHEMIC INJURY IN THE TERM INFANT
The ischemic lesions in term infants are commonly located
in the frontal and parieto-occipital regions (85,88,110). In
mild ischemic encephalopathy (i.e., mild cerebral edema),
the initial sonogram may be normal. With moderate or
severe edema, the cortex becomes hyperechoic to normal
brain, usually in the first 24 hrs of insult (Fig. 3.57).
This finding decreases within one to two weeks. Other
findings include poorly defined gyral-sulcal interfaces
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76 P E D I AT R I C S O N O G R A P H Y

A B
Diffuse hypoxic-ischemic injury in a full-term infant. Anterior coronal (A) and right parasagittal (B) images show generalized increased
Fig. 3.57
echogenicity in the cortical gray matter along the course of the anterior cerebral artery (arrowheads) and middle cerebral arteries
(arrows), associated with obliteration of the gyral-sulcal interfaces. The ventricles are slit-like.

and slit-like ventricles. Slit-like ventricles are not specific
for ischemia, and they are commonly seen as a normal
finding in full-term infants (22). With mild degrees of
asphyxia and accompanying edema, cerebral hemodynam-
ics may be normal. With severe or prolonged asphyxia,
Doppler interrogation can show increased diastolic flow,
decreased arterial pulsatility, and a low resistive index
(60) (111113).
The thalamus and basal ganglia are vulnerable to severe
hypoxia. Sonographically, the affected basal ganglia and thal-
amus appear echogenic (Fig. 3.58). Focal hyperechogenicity
can be globular or linear, paralleling the vessels, a pattern
termed lenticulostriate vasculopathy (114116). Increased
basal ganglia echogenicity, particularly a linear pattern, is not
specific for neonatal asphyxia and it can also be seen in
intrauterine viral infections, nonimmune hydrops, fetal
alcohol syndrome, and trisomies 13 and 21 (115). Cerebellar
and brainstem infarction are not as common as cerebral and
basal ganglia infarction. Hypoxic-ischemic lesions of the pos-
terior fossa structures can be difficult to appreciate at sonog-
raphy because normal and ischemic tissues have similar
echogenicity.

A B
Ischemic injury of the term infant. Coronal (A) and right parasagittal (B) scans of a 1-day-old girl with severe perinatal asphyxia reveal
Fig. 3.58
increased echogenicity in the parasagittal areas (arrowheads), thalami (arrows), and caudate nucleus (open arrow).
LWBK505-C03_p43-117.qxd 7/7/10 1:23 PM Page 77 Aptara Inc
Hypoxic-ischemic encephalopathy, late changes. Coronal
Fig. 3.59
image of a 4-week-old term neonate boy with perinatal
ischemia shows cystic areas (arrows), consistent with encephaloma-
lacia, and hydrocephalus related to brain atrophy.
Late findings, 2 to 6 weeks after the insult, are similar to
those seen in PVL and include ventriculomegaly, widened
interhemispheric and sylvian fissures, and cystic encephalo-
malacia (Fig. 3.59). The cystic changes involve both gray
and white matter and are most commonly found in the
frontal and occipital lobes. Ventriculomegaly and enlarged
extra-axial fluid spaces are the result of atrophic changes.
PROGNOSIS
There is an association between increased parenchymal
echogenicity and the development of motor and intellec-
tual deficits. Neurologic sequelae occur in approximately
90% of patients with abnormally echogenic parenchyma.
By comparison, only about 10% of patients with normal
parenchyma have neurologic impairment (22).
A low resistive index has been associated with a poor
neurologic outcome. Approximately 80% of infants with
initially low RIs develop severe neurodevelopmental deficits
(115,116). As diffuse cerebral edema develops, cerebrovascu-
lar resistance increases and there is an increase in the RI with
loss of forward diastolic flow. In some cases, there may be
reversal of diastolic flow. As the edema increases, systolic
blood flow decreases and it may even be absent during part of
the cardiac cycle. Complete absence of intracranial blood flow
is a sign of absent cortical function and brain death (117). The
presence of flow, however, does not ensure viable brain tissue.
Ischemic Lesions of the Older Infant
After the neonatal period, ischemic brain injury is com-
monly the result of motor vehicle accidents, nonaccidental
injuries, or near drowning. The early sonographic findings
include diffusely increased cerebral echogenicity, loss of
gyral-sulcal interfaces, effacement of the ventricles and cis-
terns, and increased echogenicity of the basal ganglia. Late
Chapter 3 B R A I N 77
findings include widened cortical sulci and ventricular
dilatation secondary to cortical atrophy.
VASCULAR OCCLUSIVE DISEASE
Neonatal Arterial Occlusive Disease (Neonatal Stroke)
Arterial occlusion leading to neonatal stroke is more com-
mon in term than in premature infants (118). Most neona-
tal strokes are ischemic rather than hemorrhagic and are
the result of thrombosis rather than embolization. The
most common site of occlusion is the middle cerebral
artery. Involvement of the anterior and posterior circula-
tion is relatively uncommon.
Neonatal stroke can occur in utero, at delivery, or post-
natally. In utero stroke is due to placental emboli. Emboli
originate from thrombosed placental veins, enter the umbil-
ical vein, flow to the right side of the heart, and pass
through a patent foramen ovale into the left side of the
heart and then to the brain (119). At delivery, vascular
occlusion can occur secondary to a stretching injury of the
cervical carotid artery, a hyperextension injury, or excessive
torsion of the head or neck, leading to vasospasm and/or
arterial thrombosis. Postnatal causes are emboli from con-
genital heart disease associated with a left-to-right shunt or
indwelling arterial lines and vasospasm due to meningitis,
sepsis, or dehydration (119). Maternal use of cocaine has
also been associated with small vessel occlusion and neona-
tal stroke (120,121). Clinical findings of neonatal stroke
include hypotonia, lethargy, poor feeding, and seizures.
The gray-scale findings of acute arterial occlusion are
echogenic gyri and sulci in the distribution of an arterial
territory, mass effect from edema with ventricular com-
pression or midline shift (Fig. 3.60), and absent arterial
Arterial occlusive disease with cortical infarct. Coronal
Fig. 3.60
image shows an area of increased echogenicity (arrows),
representing the infarct, in the distribution of the left middle cerebral artery.
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78 P E D I AT R I C S O N O G R A P H Y

pulsations. Color and power Doppler studies may show
increased flow in the tissues around the infarcted tissue
and in vessels supplying and draining the infarcted area,
representing hyperemia or luxury perfusion (122124).
Pulsed Doppler sonography can show increased mean
blood flow velocity (higher-frequency shifts) in tissues
around the infarcted artery. Late changes of vaso-occlusive
disease are cystic encephalomalacia and ipsilateral ventric-
ular dilatation secondary to brain atrophy.
Extracorporeal Membrane Oxygenation
Extracorporeal membrane oxygenation is a technique of
cardiopulmonary bypass used to treat infants with acute,
usually reversible respiratory failure who are unresponsive
to conventional ventilatory therapy. Deoxygenated blood
from the right atrium is shunted to an external membrane
for oxygenation and then the oxygenated blood is returned
to the aorta via the arterial cannula. In the early use of
ECMO, cannulas were placed in the right common carotid
artery and the internal jugular vein, referred to as venoar-
terial cannulation. The cranial openings of the vessels were
ligated, resulting in alterations in cerebral hemodynamics
(125129). In recent years, venoarterial cannulation has
been replaced by direct cannulation of the superior vena
cava or right atrium and the aortic arch, thereby eliminat-
ing changes in cerebral hemodynamics.
VASCULAR ALTERATIONS IN VENOARTERIAL CANNULATION
Although no longer widely used in clinical practice, the vas-
cular complications associated with carotid artery and
jugular vein cannulation are described for interest. Doppler
studies of intracranial blood flow at the time of jugular and
carotid cannulation have shown that collateral flow
through the circle of Willis is quickly established and cere-
bral perfusion is maintained. Retrograde flow to the right
cerebral hemisphere occurs via the left anterior communi-
cating artery and the left posterior communicating artery in
the circle of Willis. Antegrade flow to the right carotid
artery occurs from periorbital or external carotid artery
collateral vessels (Fig. 3.61) (125128).
Immediately following carotid cannulation and liga-
tion, there is a transient decrease in systolic flow velocity
in the right middle cerebral artery. Systolic flow returns to
nearly normal levels within 5 minutes. The diastolic flow
velocity in the middle cerebral territory increases concur-
rently with the increase in systolic flow velocity (127,128).
Cerebral artery pulsatility often decreases and in some
patients may disappear completely. Retrograde flow may

ACA
MCA

Distal ICA

oph
ICA

CCA
ECA

RT LT X

A B

Periorbital flow

X X
ECA flow

C D

Extracorporeal membrane oxygenation patterns. A: Normal flow patterns. Solid lines indicate antegrade flow; open area indicates
Fig. 3.61
retrograde flow. ACA  anterior cerebral artery; ECA  external carotid artery; ICA  internal carotid artery; MCA  middle cerebral
artery; oph  ophthalmic artery. B: Retrograde flow is present throughout the ACA and ICA. X  site. C: Flow is retrograde in the ACA and in the
proximal ICA, but antegrade in the distal ICA. X  site. D: Flow is retrograde in the ACA and antegrade throughout the ICA. ICA flow is supplied by
periorbital or ECA flow. X  site of common carotid artery ligation. (Adapted from Mitchell DG, Merton DA, Graziani JL, et al. Right carotid artery lig-
ation in neonates: classification of collateral flow with color Doppler imaging. Radiology 1990;175:117123, with permission.)
LWBK505-C03_p43-117.qxd 7/7/10 1:23 PM Page 79 Aptara Inc
be noted in the right vertebral artery, consistent with a
vertebral steal.
Doppler studies of the intracranial venous circulation
following internal jugular ligation show decreased flow in
the sagittal sinus (127,129). Other findings associated with
obstructed cerebral venous drainage include hemorrhagic
infarction, extra-axial fluid collections, and ventricular
dilatation. Following vascular reconstruction, flow in the
carotid artery and jugular vein usually returns to normal.
CEREBRAL ABNORMALITIES
Hemorrhagic and ischemic lesions of the brain are com-
mon in infants on ECMO (87). Continuous heparinization
during ECMO increases the risk of intracranial hemor-
rhage. Approximately 65% of intracranial hemorrhages
are intraparenchymal and about 25% are ventricular or
subependymal. The most common site of parenchymal
hemorrhage is the cerebellum. Extra-axial hemorrhage
occurs in less than 10% of infants. Due to heparinization,
which prevents normal clotting of blood, the cerebral hem-
orrhages in infants on ECMO may be hypoechoic rather
than hyperechoic relative to normal parenchyma. Non-
hemorrhagic abnormalities include periventricular leuko-
malacia, cortical infarction, ventriculomegaly, and widen-
ing of the interhemispheric fissures.
Sickle Cell Disease
Sickle cell disease, vasculitis, and moyamoya disease are
common causes of acute cerebral infarction in older
infants and children. Small vessel diseases, such as moy-
amoya and vasculitis, cannot be seen by sonography and
require MRI or conventional angiography for diagnosis.
Large vessel occlusion associated with sickle cell anemia
can be seen with transcranial sonography.
Cerebral infarction or stroke is the most common and
debilitating neurologic event in patients with sickle cell dis-
ease, with an estimated incidence of 11% in patients under
A B
Transcranial Doppler, sickle cell anemia. A: Normal. Transcranial Doppler interrogation of the right middle cerebral artery shows a time
Fig. 3.62
average mean of the maximum flow velocity of 87 cm/sec and a normal arterial waveform. B: Doppler interrogation of the left middle
cerebral artery shows an abnormal flow velocity of 220 cm/sec and reversed flow below the baseline, indicating turbulence.
Chapter 3 B R A I N 79
20 years of age with homozygous sickle cell disease
(130,131). The major risk factor associated with stroke in
children with sickle cell disease is a previous stroke. The
strokes can be overt (acute onset of focal neurologic
deficit) or silent (decreased cognitive function) (132134).
Silent infarcts can have significant neuropsychological
sequelae. Identification of children with cerebral infarction
is important because prophylactic transfusion treatment
may reduce the risk of recurrent stroke and also may
decrease the extent of neurologic damage in acute cerebral
infarction. Recurrent stroke is high without transfusion
therapy (regular red cell transfusions adequate to maintain
hemoglobin S to 30% of total hemoglobin) (135).
Ischemic infarction accounts for approximately 70% to
75% of cerebrovascular episodes. Approximately 75% of
ischemic strokes are the result of occlusion of the large
arteries at the base of the brain. The distal intracranial por-
tion of the internal carotid artery and the proximal por-
tions of the middle cerebral artery are most susceptible to
stenosis/occlusion. Involvement of the vertebral-basilar cir-
culation and the posterior cerebral arteries is relatively
infrequent. The remaining 25% of ischemic strokes are
secondary to occlusion of the small cortical branches in the
deep white matter. Hemorrhagic strokes account for about
25% of strokes in children with sickle cell disease.
Transcranial Doppler sonography is used to screen for
overt and silent infarctions and monitor response to transfu-
sion therapy (136143). High cerebral blood flow velocity
has been shown to be an effective predictor of stroke. Based
on a multicenter Stroke Prevention Trial in Sickle Cell Ane-
mia (STOP), risk stratification of stroke by transcranial
Doppler is based on the time-averaged mean of the maxi-
mum velocity (TAMMX) of the middle cerebral or distal
internal carotid artery (144). TAMMX is classified as fol-
lows: normal, velocities less than 170 cm/sec; conditional, at
least one mean velocity of 170 to 199 cm/sec; and abnormal,
at least one velocity greater than 200 cm/sec (144) (Fig. 3.62).
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80 P E D I AT R I C S O N O G R A P H Y

It is recommended that transcranial Doppler be performed Venous Thrombosis

every 6 to 12 months in early childhood, the time when risk
of stroke is highest (135).
Transcranial Doppler is performed with a 2- to 3-MHz
transducer placed over the temporal window and color
flow Doppler is used to identify the arteries in the circle of
Willis. After the middle cerebral artery is identified, a 4- to
6-mm Doppler sample volume is used to image the artery
at 2-mm intervals from its most superficial part to the mid-
dle cerebral/anterior cerebral artery bifurcation. Flow
direction is forward. At the bifurcation, there is bidirec-
tional flow. Flow in the anterior cerebral artery will be
away from the transducer. Angling the transducer caudally
will locate the distal internal carotid artery if insonation of
this vessel is of interest.
The sensitivity of transcranial Doppler sonography for
diagnosing stenosis/occlusion based on TAMMX is 86%
to 94%, with a specificity of 51% to 91% (137,143,144).
Sources of error in the detection of cerebrovascular disease
are low-grade stenosis, which does not alter flow dynam-
ics, and distal branch disease, which is too small to be
detected. The gray or white matter findings of cerebral
infarction are best evaluated by CT or MRI.
Cerebral venous thrombosis is a rare disorder in the pedi-
atric population, with an incidence of 0.67 cases per
100,000 children per year (145). Causes of neonatal
venous thrombosis include birth trauma with injury to
the superficial cortical veins or dural sinuses, sepsis, dehy-
dration with hypotension, and hypercoagulable condi-
tions, such as polycythemia, hereditary protein C defi-
ciency, and disseminated intravascular coagulation.
Venous thrombosis in infants and children is usually due
to either head and neck infection (meningitis, cerebral
abscess, sinusitis, mastoiditis) or dehydration, and is
less often due to trauma or hematologic disorders (coag-
ulation or hemolytic abnormalities, polycythemia).
Clinical findings include decreased level of consciousness,
headache, lethargy, seizures, focal neurologic deficit such
as hemiparesis, and cranial nerve palsies. The complica-
tion of venous thrombosis is parenchymal infarction.
Sonography, especially color flow Doppler imaging, can
demonstrate thrombus in the sagittal sinus and larger deep
veins and an associated parenchymal infarction (Fig. 3.63)
(39). Thrombosis of small cortical veins is difficult to

A B

Sinus thrombosis. A: Superior sagittal sinus in a 6-week-old

Fig. 3.63
boy with seizures. Coronal gray-scale image shows diffusely
increased parenchymal echogenicity with loss of sulcal-gyral interfaces
and obliteration of the ventricle indicating edema. B: Midline sagittal
Doppler image shows absent flow in the expected area of the superior
sagittal sinus (arrowheads). Flow is noted in some cortical vessels
(arrows). C: Color Doppler image in another infant with seizures shows non-
visualization of the vein of Galen (arrows, expected location) and straight
C sinus. Thrombosis was confirmed by magnetic resonance imaging.
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diagnose with sonography. Acute parenchymal infarction
appears as a focal area of increased echogenicity.
CONGENITAL MALFORMATIONS
Congenital malformations of the brain can be classified
based on the time of arrested brain development. Brain
development has three stages: cytogenesis (development of
molecules into cells), histogenesis (development of cells
into tissues), and organogenesis (development of tissues
into organs) (146). Organogenesis can be further divided
into at least five stages: (a) neural tube closure (3 to 4
weeks gestational age); (b) diverticulation of the fore-
brain creating two lateral ventricles, cerebral hemispheres,
thalami, caudate nuclei, olfactory bulbs, and optic tracts
(5 to 10 weeks); (c) neuronal proliferation (2 to 6
months); (d) sulcation and migration (2 to 5 months); and
(e) myelination (7 months in utero to 2 years postnatal)
(146). Alterations of brain development due to errors in
cytogenesis are microscopic and not identifiable by sonog-
raphy, whereas alterations in histogenesis and organogen-
esis are macroscopic and can produce anatomic changes
recognizable by sonography. Injuries can also occur at
later stages of gestation after structures initially have
developed normally. These usually cause destructive
changes rather than malformations.
Disorders of Histogenesis
The disorders of histogenesis include the vein of Galen
malformation, tuberous sclerosis, Sturge-Weber syndrome,
and neurofibromatosis.
VEIN OF GALEN MALFORMATION
The vein of Galen malformation is an arteriovenous malfor-
mation resulting from failure of the median prosencephalic
vein of Markowski to be replaced by the internal cerebral
veins. The result is a fistulous connection between the cere-
bral arteries and this primitive midline vein. Although the
draining vein is the primitive prosencephalic vein rather than
the actual vein of Galen, the term vein of Galen malforma-
tion is still used to refer to this malformation (147149).
The prosencephalic vein drains into a falcine sinus located in
the cerebral falx, which in turn drains into the sagittal sinus.
The sagittal sinus empties into the transverse/sigmoid sinuses
and internal jugular veins (147149).
Two major anatomic types of galenic malformations
have been described: choroidal and mural (148). In the
more common choroidal malformation (90% of vein of
Galen malformations), numerous arteries in the midbrain
(usually thalamoperforator, choroidal, pericallosal, anterior
cerebral, and superior cerebellar arteries) connect with the
aneurysmally dilated prosencephalic vein. This form has a
large amount of arteriovenous shunting and presents in the
neonate. The clinical manifestations are high-output con-
gestive heart failure and an intracranial bruit. In the less
common mural type, one or only a few arterial feeders,
usually from posterior choroidal arteries, drain directly into
the midline prosencephalic vein. This type usually presents
Chapter 3 B R A I N 81
later in infancy with clinical manifestations of hydro-
cephalus, resulting from compression of the cerebral aque-
duct and posterior third ventricle by the aneurysmally
dilated midline vein, or with seizures, but not with conges-
tive heart failure. In older children, headache and hemor-
rhage are the presenting neurologic signs.
The galenic malformation appears as a well-circum-
scribed cystic mass in the midline between the lateral ventri-
cles and posterior to the third ventricle (Fig. 3.64). On sagit-
tal views, the vein may be followed posteriorly into a dilated
straight sinus and enlarged torcular herophili. The sagittal
and transverse/sigmoid sinuses and internal jugular veins are
usually dilated and there may be hydrocephalus (147149).
Other findings include dilated feeding arteries, parenchymal
calcifications, and brain atrophy as a result of ischemia sec-
ondary to shunting of blood away from the cerebral cortex
(vascular steal phenomenon). Calcifications may develop
within the malformation if it contains thrombus (150).
Pulsed and color Doppler studies can best demonstrate
the vascular nature of the mass and flow within the dilated
arterial feeders and draining veins (Fig. 3.64C,D). Spectral
tracings show elevated flow velocities with dampened pul-
satility in the arterial feeders and arterialization in the
draining veins (151). Color Doppler imaging demonstrates
turbulent flow within the malformation. Insonation of the
peripheral cerebral cortex may show diminished or absent
flow secondary to diversion of blood away from the normal
cerebral circulation to the low-resistance malformation.
Treatment includes medical therapy to control the
congestive heart failure and embolization of the galenic
malformation. Although sonography can detect the
galenic malformation, MRI or conventional angiogra-
phy is required to precisely identify the feeding arteries
and draining vein, especially if embolization is planned.
Pulsed and color flow Doppler imaging can be used to
follow and quantify the hemodynamic effects of emboliza-
tion therapy (151,152). Hemodynamic changes after
embolization include (a) increase in blood flow velocity in
normal vessels in the uninvolved areas of the brain indicating
rerouting of blood as a result of the elimination of an arterial
steal, (b) increase in caliber and flow of feeding vessels that
were not occluded during embolization, and (c) decrease in
the caliber and flow velocity of embolized feeding vessels
(Fig. 3.65) (152). Persistent color signal in embolized feeding
arteries or draining veins suggests incomplete embolization.
OTHER VASCULAR MALFORMATIONS
Vascular malformations can be classified into four cate-
gories: arteriovenous malformation (including both
galenic and nongalenic malformations), venous malfor-
mations, cavernous malformations, and capillary malfor-
mations. They may be asymptomatic and discovered inci-
dentally or they may present with seizures or neurologic
findings secondary to intracranial hemorrhage (153).
Arteriovenous Malformation
An arteriovenous malformation (AVM) is a low-resis-
tance, high-flow lesion characterized by a vascular nidus
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A B

C D

Galenic venous malformation, choroidal form. A: Coronal

Fig. 3.64
scan shows a dilated vein of Galen (VG) between the lateral
ventricles (V). B: Midline sagittal scan shows the dilated prosencephalic
vein, referred to as the vein of Galen (VG), located superior to the cere-
bellar vermis (CV) and posterior to the third ventricle (3). C: Coronal pulsed
Doppler view shows markedly elevated systolic and diastolic flow veloc-
ities with dampened pulsatility and arterialization of venous flow below
the baseline. D: Sagittal color Doppler image shows turbulent flow within
the galenic malformation, dilated feeding arteries (white arrows), and a
dilated anterior cerebral artery (open arrows). E: Sagittal T1-weighted
magnetic resonance image shows the dilated vein of Galen (VG) draining
E into the transverse/sigmoid sinus.
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A B
C flow in the feeding arteries and vein of Galen malformation.
of abnormal thin-walled vessels connecting enlarged arte-
rial feeders to draining veins without an intervening cap-
illary network. The absence of capillaries produces a low-
resistance shunt, which results in arteriovenous shunting
within the malformation. The vein of Galen malforma-
tion is a particular type of arteriovenous malformation
specific to neonates and infants (see above discussion).
Nongalenic malformations commonly involve the dura.
Nongalenic arteriovenous malformations usually
become symptomatic in adults, although dural fistulas can
present in the neonate (153). The clinical findings are sim-
ilar to those of the vein of Galen malformation, including
heart failure, macrocephaly, increased intracranial pres-
sure, and hemorrhage. Nongalenic fistulas commonly
involve the dura at the site of the torcular herophili. Sonog-
raphy shows a markedly enlarged torcular herophili with
Chapter 3 B R A I N 83
Vein of Galen aneurysm, postembolization. A: Midline
Fig. 3.65
sagittal color flow Doppler image at time of diagnosis
shows turbulent flow in the aneurysmally dilated vein of Galen
(arrows) and in pericallosal (open arrow) and internal carotid feeding
vessels. B: Postembolization sagittal image shows increased
echogenicity (arrows) with indistinct posterior shadowing, consistent
with embolization material, in the vein of Galen malformation. C: Sagit-
tal color Doppler image following embolization shows decrease in
turbulent blood flow (154) (Fig. 3.66). Dilatation of the
sigmoid sinuses and jugular veins is frequent. The lesions
are usually supplied by bilateral middle meningeal artery
feeders. Additional feeders may come from the occipital,
anterior inferior, and posterior cerebellar arteries. The
cerebral cortical vessels are of normal size or only mildly
dilated. Arteriovenous fistulas of the cavernous sinus are
less common. Treatment is endovascular embolization.
Malformations without Arteriovenous Shunting
Venous malformations are characterized by a collection of
small dilated veins that drain into a single, dilated vein.
There is no abnormal arterial component and thus, no
arteriovenous shunting (Fig. 3.67). Cavernous malforma-
tions are collections of endothelium-lined vascular spaces
with normal feeding arteries and draining veins and no
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84 P E D I AT R I C S O N O G R A P H Y
A B
C posteriorly (open arrow). The cortical vessels are normal in size.
arteriovenous shunting. Capillary telangiectasia is a focal
collection of dilated capillaries. The latter two malforma-
tions are best seen on MRI or CT.
PHAKOMATOSES
The phakomatoses are congenital malformations character-
ized by abnormalities of ectodermal origin (e.g., the skin,
central nervous system, retina, and viscera) (155157). These
include Von Recklinghausen neurofibromatosis, tuberous
sclerosis (Bourneville disease), retinocerebellar angiomatosis
(Von Hippel-Lindau disease), and encephalotrigeminal
angiomatosis (Sturge-Weber syndrome). Intracranial compli-
Dural arteriovenous fistula of the torcular herophili. Poste-
Fig. 3.66
rior coronal (A) midline sagittal (B) sonograms show a
large posterior fossa hypoechoic mass (arrows), representing a dilated
torcular herophili. C: Midline sagittal color Doppler scan shows flow in
the dilated torcula herophili (arrows), which is partially thrombosed
cations of tuberous sclerosis may occur in neonates and
infants and therefore may be diagnosed with sonography.
The intracranial complications of neurofibromatosis, Sturge-
Weber syndrome, and Von Hippel-Lindau disease are usually
seen later in life after fontanelle closure and are best diag-
nosed by CT or MRI.
Tuberous sclerosis is a heredofamilial neurocutaneous
condition transmitted as an autosomal dominant trait with
variable penetrance. Two genes have been identified in
patients with tuberous sclerosis. The TSC1 gene is located
on chromosome 9q34, which codes for a protein named
hamartin, and the TSC2 gene is on chromosome 16p13.3,
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Venous malformation. Coronal spectral Doppler image
Fig. 3.67
demonstrates a dilated vein of Galen superior to the ver-
mis with venous waveforms. The diagnosis of venous malformation,
which was an incidental finding in this 2-month-old boy, was con-
firmed by magnetic resonance imaging.
which codes for a protein named tuberin (155,156). These
genes may be associated with the regulation of cell prolif-
eration and differentiation.
Classically, tuberous sclerosis is characterized by the
clinical triad of adenoma sebaceum, mental retardation, and
seizures, although only about one third of patients exhibit
this triad (155157). At least 90% exhibit some cutaneous
lesions (156). About 90% have seizures and 50% have men-
tal retardation (156). Subependymal nodules and cortical
tubers are the most common nervous system lesions, occur-
ring in about 95% of patients with tuberous sclerosis (156).
Histologically, these are hamartomatous lesions containing
glial tissue, giant cells, and heterotopic neurons.
Subependymal and cortical hamartomas can be seen
at sonography. Subependymal nodules appear as well-
circumscribed, echogenic nodules protruding from the
walls into the lumen of the lateral ventricles (Fig. 3.68).
They can be difficult to differentiate from gray matter het-
erotopia by sonography. The ventricles may enlarge as a
result of obstruction of the foramen. Cortical tubers are
more common in the frontal regions than in the occipital
regions and are infrequent in the occipital lobes and cere-
bellum. They appear as foci of hyperechogenicity. Occa-
sionally, cyst-like lesions can be seen in the cerebral white
matter (155). Lesions can also occur in the heart, kidneys,
liver, lung, and spleen.
Chapter 3 B R A I N 85
Tuberous sclerosis. Left sagittal scan shows nonshadow-
Fig. 3.68
ing, echogenic subependymal nodules (arrows). Also note
multiple echogenic cortical masses or tubers (open arrows).
Disorders of Neural Tube Closure
Dysraphic disorders include anencephaly, encephalocele,
meningocele, and myelomeningocele.
ANENCEPHALY
Anencephaly is the result of failure of brain development
except for the base of the skull. There is complete absence
of the brain and calvarium above the brainstem. The diag-
nosis is usually made in utero. Imaging studies are rarely
needed postnatally.
ENCEPHALOCELE
Encephalocele refers to herniation of intracranial struc-
tures through a defect in the skull. Meningoceles are her-
niation of meninges and CSF only. Meningoencephalocele
refers to herniation of brain tissue, meninges, and CSF
(158). Occipital encephaloceles account for approximately
70% of encephaloceles. The remaining encephaloceles usu-
ally arise in frontoethmoidal or sphenoidal locations.
Along with meninges and brain tissue, which is usually
dysplastic, encephaloceles may contain a venous sinus or
one of the ventricles. Congenital anomalies associated with
encephaloceles include Dandy-Walker and Meckel-Gruber
syndromes, callosal agenesis, holoprosencephaly, Chiari II
malformations, and migrational defects.
The sonographic diagnosis of encephalocele is based on
demonstration of a scalp mass containing CSF and/or
brain parenchyma protruding through a bony calvarial
defect (Fig. 3.69).
CHIARI MALFORMATION
The Chiari malformation is a complex brain anomaly that
is associated with cerebellar dysplasia, spinal dysraphism,
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86 P E D I AT R I C S O N O G R A P H Y

A B

Occipital encephaloceles. A: Longitudinal image shows an

Fig. 3.69
anechoic scalp mass (M) communicating with the cerebral
hemisphere via a defect in the calvarium (open arrow). B: Longitudinal
scan in another patient showing an encephalocele (arrows) containing
a herniated occipital lobe (O) and ventricle. Open arrow shows a defect
in the calvarium. C: Color Doppler image shows vessels crossing the
C defect. (Case courtesy of Brian Coley, MD.)

and an encephalocele or myelomeningocele (159,160).
There are three classic types of Chiari malformations. The
type I malformation is characterized by elongation and cau-
dal displacement of the cerebellar tonsils below the foramen
magnum without displacement of the medulla or fourth
ventricle. This type usually is diagnosed in adulthood. The
type III Chiari malformation is characterized by displace-
ment of the medulla and fourth ventricle and a dysplastic
cerebellum into a high cervical or occipital encephalocele.
The type II malformation is the most common Chiari
anomaly in childhood. It is seen in neonates and infants
and is nearly always associated with a clinically obvious
myelomeningocele. The pathologic findings of the Chiari
II malformation are an abnormally small posterior fossa,
low tentorial attachment, and caudal displacement of the
cerebellum, cerebellar vermis, pons, medulla, and fourth
ventricle into the upper spinal canal. Hydrocephalus is
common, although it may not develop until after repair
of the myelomeningocele alters the flow of CSF.
Sonographic Findings
Supratentorial abnormalities in the Chiari II malformation
include an enlarged massa intermedia partially or totally
filling the third ventricle, ventriculomegaly, and anterior
and inferior angulation of the frontal horns, referred to as
a bat-wing appearance. The occipital horns of the lateral
ventricles are often larger than the frontal horns, resulting
in a configuration termed colpocephaly. Partial or total
absence of the corpus callosum is a common associated
anomaly. Infratentorial findings include displacement of the
cerebellum and herniation of the vermis into the cervical
spinal canal, loss of visualization of the cisterna magna, a
small or absent fourth ventricle, a low-lying tentorium, and
a small posterior fossa (Fig. 3.70) (159,161).
Using the suboccipital area as an acoustic window with
the transducer just below the arch of C-1 may improve
visualization of the cerebellar tonsils and vermis. To avoid
errors in diagnosis, it needs to be recognized that the cere-
bellar tonsils normally can be positioned at or below the
foramen magnum in the pediatric population (162). In
children under 15 years of age, the cerebellar tonsils can be
located up to 6 mm below the foramen magnum on
parasagittal sections. Tonsillar ectopia greater than 6 mm
is abnormal and may produce symptoms.
Lckenschdel (lacunar skull), which is thought to be
due to a mesenchymal dysplasia, is common in patients
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Chapter 3 B R A I N 87

A B

Chiari II malformation. A: Anterior coronal scan shows

Fig. 3.70
inferior pointing (batwing appearance) of the frontal
horns (F). B: Posterior coronal scan shows dilated occipital horns (O).
C: Midline sagittal scan shows the low-lying cerebellar vermis (arrow)
C and nonvisualization of the fourth ventricle and cisterna magna.

with the Chiari II malformation. The sonographic finding
is an irregular or wavy inner table of the skull (Fig. 3.71)
(163). The parietal and occipital bones are most affected.
This appearance disappears within the first year of life,
even without ventriculoperitoneal shunting, likely related
to remodeling in response to normal expansion of brain
tissue or the development of hydrocephalus (163).
DANDY-WALKER COMPLEX
Posterior fossa cystic malformations represent a spectrum
of disorders that includes the Dandy-Walker complex and
mega-cisterna magna. The Dandy-Walker complex con-
sists of the Dandy-Walker malformation and the Dandy-
Walker variant (also known as vermian-cerebellar
hypoplasia) (164166). This group of malformations is
thought to be the result of an insult to the developing cere-
bellar hemispheres and/or the developing fourth ventricle
(164). If the insult involves the cerebellum and fourth ven-
tricle, the result is the Dandy-Walker malformation. If the
insult is primarily to the developing cerebellum, the result
is the Dandy-Walker variant. If the fourth ventricle is more
involved, the result is the mega-cisterna magna.
Neuropathologic findings of Dandy-Walker malforma-
tion are an enlarged posterior fossa, dilated fourth ventri-
cle (i.e., the Dandy-Walker cyst), inferior vermian agenesis
or hypoplasia, and hypoplastic cerebellar hemispheres.
Hydrocephalus occurs in up to 80% of cases. Pathologi-
cally, the Dandy-Walker variant is characterized by a nor-
mal size or mildly enlarged posterior fossa, a mildly to
moderately dilated fourth ventricle, relatively normal
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88 P E D I AT R I C S O N O G R A P H Y
Lacunar skull. Coronal image in a patient with Arnold
Fig. 3.71
Chiari II malformation shows irregularity of the inner cal-
varium (arrows). (Reprinted from Coley BD. Ultrasound diagnosis of
luckenschadel (lacunar skull). Pediatr Radiol 2000;30:8284, with per-
mission.)
cerebellar hemispheres, and a hypoplastic cerebellar ver-
mis. Hydrocephalus can occur, but is less common than in
Dandy-Walker malformation.
Patients with Dandy-Walker malformation and variant
may present with macrocrania due to hydrocephalus or an
enlarged posterior fossa, neurologic signs due to hydro-
cephalus, and/or developmental delay (165). Other CNS
anomalies are present in up to 70% of cases and include
complete or partial callosal absence, gray matter hetero-
topia, polymicrogyria, agyria, schizencephaly, lipoma,
A B
Dandy-Walker syndrome. A: Midline sagittal scan demonstrates a large retrocerebellar fluid-filled cyst (C), which is the dilated fourth
Fig. 3.72
(4) ventricle; an elevated tentorium (arrows); rudimentary cerebellar hemispheres (CB); and an absent vermis. B: Posterior coronal scan
shows the large cyst (C) filling the posterior fossa and absence of the vermis.
encephalocele, and holoprosencephaly (165,166). Chro-
mosomal abnormalities, including trisomy 13, 18, and
21, and syndromes such as Goldston (Dandy-Walker
complex and cystic renal disease), Joubert (Dandy-Walker
complex, malformed brainstem, ataxia, abnormal eye
movements, hyperpnea, and mental retardation), and
Walker-Warburg (cerebellar malformations, lissencephaly,
hydrocephalus, and hypotonia) have been reported in up
to 50% of patients (165). The Dandy-Walker complex
also is associated with cardiac anomalies, polydactyly, and
syndactyly.
SONOGRAPHIC FINDINGS
The sonographic features of the Dandy-Walker malforma-
tion include a fluid-filled posterior fossa cyst, which repre-
sents the dilated fourth ventricle; a small or absent cerebellar
vermis; small cerebellar hemispheres, which are superiorly
displaced; a high position of the tentorium cerebelli and tor-
cular herophili; and hydrocephalus (Figs. 3.72 and 3.73)
(161).
The sonographic findings of the Dandy-Walker variant
(vermian-cerebellar hypoplasia) are a normal-size or mildly
enlarged posterior fossa; mild to moderate dilatation of
the fourth ventricle; normal or slightly small cerebellar
hemispheres; a small cerebellar vermis; and hydrocephalus.
The cerebellar hemispheres may almost appose each other
in the midline, creating the false appearance of an intact
vermis on the midline sagittal scan. Coronal images
through the posterior fossa scanning will show the mildly
dilated fourth ventricle and the small intervening vermis
(161) (Fig. 3.74).
The mega-cisterna magna is characterized by an
enlarged cisterna magna, which freely communicates with
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A B
Dandy-Walker syndrome and renal cystic disease (Goldston syndrome). A: Midline coronal scan shows a large posterior fossa cyst (C)
Fig. 3.73
and small cerebellar hemispheres (CB). B: Transverse scan of the right kidney demonstrates multiple cysts.

A B

Dandy-Walker variant. A: Coronal sonogram shows the

Fig. 3.74
small posterior fossa cyst (C). B: Midline sagittal scan
demonstrates a small posterior fossa cyst (C), mildly dilated fourth
ventricle (4), and small vermis inferiorly. Also notice absence of the
corpus callosum. C: Axial transmastoid sonogram shows nearly nor-
mal cerebellar hemispheres (CB) and the vallecula (arrow) connect-
ing the anterior part of the fourth ventricle (4) with the cystic poste-
C rior part of the ventricle.
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90 P E D I AT R I C S O N O G R A P H Y

A B

Arachnoid cyst. Coronal (A) and midline sagittal (B) views

Fig. 3.75
show a supracerebellar cyst (C) arising in the cerebel-
lomedullary angle cistern. The cyst displaces the vermis (V) inferiorly,
but it does not communicate with the normal-size fourth ventricle (4).
C: Sagittal color Doppler view confirms absence of flow within the
C lesion, confirming its cystic (C) nature.

subarachnoid spaces, and a normal-size or mildly enlarged
posterior fossa (165). The fourth ventricle, cerebellar
hemispheres, and cerebellar vermis are normal. There is no
mass effect.
The Dandy-Walker complex needs to be differentiated
from a posterior fossa arachnoid cyst. The arachnoid cyst
is a fluid-filled lesion that has no communication with the
fourth ventricle or subarachnoid spaces. The fourth ventri-
cle, cerebellar hemispheres, and cerebellar vermis are of
normal size, although they may be displaced or com-
pressed by the arachnoid cyst (Fig. 3.75).
ANOMALIES OF THE CORPUS CALLOSUM
The corpus callosum is a midline interhemispheric com-
missure that bridges the two cerebral hemispheres, allow-
ing for shared learning and memory. It forms during the
third and fourth months of fetal life, developing from the
rostral end of the neural tube. The corpus callosum is com-
posed of four sections: rostrum, genu, body, and splenium.
The genu and body of the corpus callosum form first and
then the splenium develops posteriorly and rostrum anteri-
orly (158).
The corpus callosum may be completely absent (age-
nesis) or partially absent (hypoplasia), leaving thick bun-
dles of fibers (Probst bundles) coursing along the superior
medial aspect of each ventricle. Complete absence occurs
early in gestation, usually before the 12th week, and
is due to primary embryonic agenesis. Partial absence
occurs later in development and can affect the anterior
or posterior portion of the corpus callosum. The pres-
ence of anterior parts of the corpus without the posterior
body and splenium suggests a developmental error. The
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A B
C burst pattern.
presence of posterior portions of the corpus callosum
without anterior elements suggests partial destruction of
a previously developed corpus callosum, secondary to an
inflammatory or ischemic process. The exception to this
rule is holoprosencephaly, in which only the posterior
part (splenium) of the corpus callosum may develop.
Callosal dysgenesis may be isolated or it can occur with
other midline anomalies, including Dandy-Walker spectrum,
Chiari II malformation, holoprosencephaly, septo-optic dys-
plasia, anomalies of migration and organization, lipomas,
median cleft face syndrome, and Aicardia syndrome. Aicar-
dia syndrome is an X-linked dominant disorder characterized
Chapter 3 B R A I N 91
Agenesis of the corpus callosum. A: Coronal sonogram
Fig. 3.76
shows absence of the corpus callosum and widely sep-
arated frontal horns (arrows). B: A more posterior coronal image
reveals parallelism of the occipital horns (O). C: On a midline sagittal
sonogram, the medial gyri and sulci (arrowheads) radiate to the roof
of the elevated third (3) ventricle, creating a characteristic sun-
by callosal agenesis or hypoplasia, chorioretinopathy, mental
retardation, and infantile spasms. It affects only females.
Patients with isolated callosal agenesis are usually asympto-
matic. When present, symptoms are due to the associated
anomalies and include seizures and mental retardation.
On coronal images, the sonographic findings of com-
plete callosal agenesis are absence of the corpus callosum,
widely separated lateral ventricles, dorsal extension of the
third ventricle between the lateral ventricles and into the
interhemispheric fissure, and parallel orientation of the bod-
ies and occipital horns of the lateral ventricles (colpocephaly)
(Figs. 3.76 and 3.77) (161). The elevated third ventricle may
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92 P E D I AT R I C S O N O G R A P H Y

A B
Agenesis of the corpus callosum with a dilated third ventricle. A: Coronal sonogram demonstrates absence of the corpus callosum and
Fig. 3.77
widely separated frontal horns (F) with sharply angulated, concave medial borders (arrows). The dilated third (3) ventricle is displaced
superiorly between the bodies of the lateral ventricles. B: Midline sagittal view demonstrates the elevated and dilated third (3) ventricle and a nor-
mal fourth (4) ventricle. Note again the radially arranged sulci (arrows). The large third ventricle and small fourth ventricle are consistent with the
associated diagnosis of aqueductal stenosis.

be dilated, forming a dorsal midline cyst (Fig. 3.77). The
frontal horns are sharply angled laterally and indented
medially by the thickened bundles of Probst, which can
bulge into the lateral ventricles. On the sagittal midline
image, the medial cerebral gyri and sulci are radially
arranged, extending perpendicular to the roof of the third
ventricle, causing a sunburst appearance. The pericallosal
sulcus and cingulate sulcus are absent and the third ventri-
cle may be elevated. In partial agenesis, there is absence of
the hypoechoic fibers in the anterior or posterior aspects of
the corpus callosum.
Lipoma of the corpus callosum is a congenital malfor-
mation that is found in about half of the cases of callosal
dysgenesis. It is associated with both callosal agenesis and
hypoplasia (158,167). Typically, lipomas arise in the ante-
rior portion of the dysplastic corpus callosum and extend
superiorly into the interhemispheric fissure or laterally into
the sulci (Fig. 3.78) (168,169). Sonographically, the lipoma
appears as a highly echogenic midline lesion, which may
contain areas of acoustic shadowing representing calcifica-
tion (161,169). Other locations for intracranial lipomas
include the quadrigeminal plate/supracerebellar cisterns, the
cerebellopontine angle cisterns, and the sylvian cisterns
(158).
Disorders of Diverticulation
HOLOPROSENCEPHALY
Holoprosencephaly results when there is total or partial
failure of cleavage of the prosencephalon into the telen-
cephalon and diencephalon, which normally occurs
between the fourth and eighth weeks of fetal life. The
telencephalon forms the paired cerebral hemispheres, ven-
tricles, and caudate nuclei. The diencephalon develops
into the third ventricle, thalami, and hypothalamus (170).
Holoprosencephaly is characterized by varying degrees of
fusion of the paired cerebral hemispheres, lateral ventri-
cles, olfactory tracts, and optic tracts. Associated chromo-
somal abnormalities include trisomy 13, 18, and 13q syn-
drome, short-arm deletion of 18, and Meckel-Gruber
syndrome (central nervous system anomalies, renal cysts,
hepatic ductal dysplasia and cysts, and polydactyly)
(170,171). Since the fetal face develops at the same time
as the brain, facial anomalies, ranging from cyclopia to
cleft lip and palate, are commonly seen with this brain
anomaly.
The three forms of holoprosencephaly are alobar, semi-
lobar, and lobar types. The brain is small in alobar and
semilobar holoprosencephaly and is almost always normal
in size in lobar holoprosencephaly.
Alobar
Alobar holoprosencephaly, the most severe form of this con-
dition, is characterized by complete absence of diverticula-
tion. There is no separation into frontal, temporal, and
occipital horns. Affected patients are stillborn or die soon
after birth. Midline facial anomalies are common and severe
and include cyclopia (one orbit and globe with a proboscis
but no nose); a single, double, or rudimentary proboscis;
hypotelorism; cleft palate and cleft face; and micrognathia
(172). Sonographic abnormalities include a single, horse-
shoe- or crescent-shaped midline ventricle (monoventricle);
fused echogenic thalami; and a thin, pancake-like mantle of
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Chapter 3 B R A I N 93

A B

Agenesis of corpus callosum with lipoma. Coronal

Fig. 3.78
(A) and sagittal (B) scans demonstrate a highly
echogenic mass (arrows) in the expected region of the corpus callo-
sum. C: T1-weighted sagittal magnetic resonance image shows the
high-signal-intensity lipoma (arrows) as well as the radially oriented
C gyri and sulci.

undifferentiated cerebral parenchyma in the rostral part of
the calvarium. The monoventricle commonly dilates and
herniates superiorly, forming a large dorsal sac or cyst (Fig.
3.79). The third ventricle, falx cerebri, corpus callosum, and
interhemispheric and sylvian fissures are absent. The supe-
rior sagittal and straight sinuses and internal cerebral veins
are also absent. The cerebellum and brainstem are relatively
normal.
Semilobar
Semilobar holoprosencephaly is an intermediate form of
holoprosencephaly in which there is partial separation of
the two cerebral hemispheres posteriorly. The anterior
(frontal) areas of the brain are fused and underdeveloped.
Facial anomalies are absent or mild and include cleft lip
and palate and hypotelorism. Sonographic features of
semilobar holoprosencephaly include a single frontal
horn and ventricular body, fused thalami and caudate
nuclei, separate rudimentary occipital and temporal
horns, and partial development of the posterior falx
cerebri and interhemispheric fissure. The frontal lobes are
poorly developed and the septum pellucidum is absent.
The anterior and middle portions of the corpus callosum
are absent or underdeveloped; the splenium may develop
(173). The third ventricle is small or absent (Fig. 3.80).
The fourth ventricle, brainstem, and cerebellum are usu-
ally normal.
Lobar
Lobar holoprosencephaly is the least severe form of holo-
prosencephaly. Facial anomalies are absent or mild and
similar to those in the semilobar form. The two cerebral
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94 P E D I AT R I C S O N O G R A P H Y

A B

Alobar holoprosencephaly. A: An anterior coronal scan

Fig. 3.79
shows a single midline ventricle (V), fused thalami (T), and
a thinned cerebral mantle (arrows) with no separation into cerebral
hemispheres. The interhemispheric fissure is absent. B: More poste-
rior coronal image reveals a dilated single ventricle, termed a dorsal
sac (DS). C: On a midline sagittal sonogram, the dilated monoventricle
(V) balloons posteriorly, producing a large dorsal sac (DS). Coronal
(D) and sagittal magnetic resonance T2-weighted (E) images show a
single ventricle (V), fused thalami (T), absence of the interhemispheric
E fissure, and the dorsal sac (DS).
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A
B

C D

Semilobar holoprosencephaly. A: Anterior coronal scan

Fig. 3.80
demonstrates a monoventricle (V) draped over fused thalami
(T). B, C: More posterior coronal sonograms demonstrate separate occip-
ital horns (O) and a partially developed posterior interhemispheric fissure
(arrowheads). D: Midline sagittal sonogram shows a small third (3) ventri-
cle inferior to the monoventricle and absence of the corpus callosum.
E: Left parasagittal image shows an anterior monoventricle (V) and dilated
occipital horn (O). The gyri and sulci radiate to the roof of the monoventri-
E cle, related to the associated callosal agenesis.
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96 P E D I AT R I C S O N O G R A P H Y

A B

C D
Lobar holoprosencephaly. A: Coronal sonogram demonstrates fused frontal horns (F) with squared flat roofs and absence of the sep-
Fig. 3.81
tum pellucidum. Posterior coronal (B) and right parasagittal (C) scans show normal bodies and occipital horns of the lateral ventricles.
D: Midline sagittal view. The corpus callosum (arrows), third (3) ventricle, and posterior fossa structures are normal. 4  fourth ventricle;
V  vermis.

hemispheres are separated posteriorly, but there is failure Septo-optic Dysplasia

of cleavage of the frontal lobes. Sonography shows
squared, fused frontal horns with flat roofs and angular
corners; absence of the septum pellucidum; and two nor-
mal thalami. The bodies and occipital and temporal
horns of the lateral ventricles are separated, although the
lateral ventricular bodies may be closely apposed. The
corpus callosum is present, but the anterior body and
genu may be small or absent (173). The anterior inter-
hemispheric fissure is present but commonly shallow. The
third ventricle, posterior interhemispheric fissure and
falx, and posterior fossa structures are normal (Fig.
3.81).
Septo-optic dysplasia (de Morsier syndrome) is a develop-
mental anomaly characterized by partial or complete
absence of the septum pellucidum, optic nerve hypoplasia,
and pituitary deficiencies. The condition is more common
in girls, but it does occur in boys. Affected patients have
hypopituitarism, usually related to deficiencies of growth
hormone and thyroid-stimulating hormones; hypotelorism;
and blindness or near blindness (170). Sonography shows
complete or partial absence of the septum pellucidum,
squared and flattened roofs of the frontal horns of the
lateral ventricles producing a box-like configuration, and
an enlarged anterior recess of the third ventricle. The falx
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Absent septum pellucidum. Coronal scan shows fused
Fig. 3.82
frontal horns with absence of the septum pellucidum. The
roof of the frontal horns (arrows) is concave rather than squared, as
noted in lobar holoprosencephaly.
and interhemispheric fissures are normal. The diagnosis of
septo-optic dysplasia is usually made by ophthalmoscopic
examination in combination with CT or MRI. Schizen-
cephaly and heterotopia are the most common associated
abnormalities (174).
Absence of the Septum Pellucidum
Partial or complete absence of the septum pellucidum may
be an isolated anomaly, or it can be seen with other abnor-
malities including septo-optic dysplasia, holoprosen-
cephaly, Chiari II malformation, schizencephaly, and
hydranencephaly (175). Differentiation among isolated
septal absence, lobar holoprosencephaly, and septo-optic
dysplasia can be difficult. The presence of an anterior
interhemispheric fissure, normally developed frontal lobes,
and normal optic tracts should suggest benign absence
of the septum pellucidum, rather than other anomalies
(Fig. 3.82).
Disorders of Migration, Sulcation, and Proliferation
NORMAL DEVELOPMENT OF THE CEREBRAL CORTEX
Neurons that form the cerebral cortex arise in the
subependymal layer of the walls of the lateral and third ven-
tricles. During the second week of gestation, these neurons,
known as the germinal matrix, proliferate. Between the
third and sixth month of brain development, the neurons
migrate from the germinal matrix to the developing cerebral
cortex. After their arrival in the cortex, they undergo a tan-
gential migration and further organization and differentia-
tion to form the mature brain. Insults, such as infections,
ischemia, drugs, alcohol, and chromosomal disorders, can
Chapter 3 B R A I N 97
impair neuronal proliferation, migration, or organization
and result in malformations of the cerebral cortex. The
resultant malformations include hemimegalencephaly,
lissencephaly (agyria-pachygyria complex), schizencephaly,
gray matter heterotopia, and polymicrogyria (multiple small
gyri).
HEMIMEGALENCEPHALY
Unilateral megalencephaly is characterized by hamartoma-
tous overgrowth of part or all of a cerebral hemisphere
with migrational defects in the affected hemisphere (176).
Microscopically, the cortical neurons are enlarged with
increased nuclear and nucleolar volumes. Polymicrogyria,
pachygyria, heterotopic gray matter, and lissencephaly are
associated findings (see discussion below). Hemimegalen-
cephaly may be an isolated anomaly or it can occur with
other disorders, including hemihypertrophy, neurofibro-
matosis type I, tuberous sclerosis, Klippel-Trenaunay-
Weber syndrome (characterized by a triad of port wine
stain, varicose veins, and bony and soft tissue hypertrophy
in an extremity), and linear sebaceous nevus syndrome.
Affected patients present with macrocephaly, intractable
seizures, hemiplegia, and developmental delay.
The sonographic findings of hemimegalencephaly
include an enlarged cerebral hemisphere, ipsilateral lateral
ventricular dilatation with contralateral shift of midline
structures, and absent or diminished gyri and ulci
(177179) (Fig. 3.83). The gyri that develop are commonly
broad and flat (pachygyria) (178).
LISSENCEPHALY
Lissencephaly, also known as the agyria-pachygyria complex,
means smooth brain. Agyria (complete lissencephaly) indi-
cates the complete absence of gyri and sulci, whereas pachy-
gyria (partial lissencephaly) refers to the presence of a reduced
number of gyri, which are broad and flat. This abnormality
of development results in a smooth four-layer cortex, instead
of the normal six-layer cortex (158,180). Complete agyria is
rare and most lissencephalic brains contain areas of both
agyria and pachygyria.
Patients with the agyria-pachygyria complex can be clas-
sified into three major groups: type 1 lissencephalypatients
are microcephalic and have characteristic dysmorphic facies;
type 2 lissencephalypatients have hydrocephalus and mus-
cular dystrophy without characteristic dysmorphic facies;
and type 3 lissencephalypatients have microcephaly with-
out dysmorphic facies. Type 1 lissencephaly is associated
with the Miller-Dieker, Norman-Roberts, and Neu-Laxova
syndromes. Type 2 lissencephaly may be associated with the
Walker-Warburg syndrome (lissencephaly, hydrocephalus,
vermian hypoplasia, hypotonia, and retinal dysplasia) and
the cerebro-ocular muscle dystrophy syndrome.
Sonographic findings of lissencephaly include a smooth
cortical surface due to the absence of sulcation and gyral
development, nonobstructive ventricular dilatation with a
colpocephalic configuration, and widened sylvian fissures
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98 P E D I AT R I C S O N O G R A P H Y

A B

C
Hemimegalencephaly. A: Coronal sonogram shows enlargement of the left cerebral hemisphere, left lateral ventricle (LV), and sylvian
Fig. 3.83
fissure (arrow) with midline shift to the right. There are fewer sulci in the left hemisphere compared with the right hemisphere. B: Left
sagittal view shows a paucity of gyri in the left hemisphere. C: Coronal magnetic resonance imaging shows findings identical to those on sonogra-
phyenlarged left hemisphere with few gyri, dilated ventricle, and midline shift.

(181183) (Fig. 3.84). The sylvian fissures appear as wide
linear grooves with an oblique orientation, rather than hav-
ing the normal Y-shaped configuration with a horizontal ori-
entation. The few gyri that develop are usually broad and
shallow (pachygyria).
SCHIZENCEPHALY
Schizencephaly is a migrational anomaly characterized by
gray matterlined clefts that extend through the entire
hemisphere from the subependymal layer of the lateral
ventricles to the cortical surface of the brain (158). The
clefts may be unilateral or bilateral and symmetric or
asymmetric and the lips of the clefts may be open (gaping
lips) or closed (opposed lips). In open-lip schizencephaly,
the walls of the clefts are separated by CSF. In closed-lip
schizencephaly, the walls are apposed. Patients with open-
lip schizencephaly generally have macrocephaly, retarda-
tion, seizures, and developmental delay. Patients with
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Chapter 3 B R A I N 99

A B

Lissencephaly. Coronal (A) and right parasagittal (B) sono-

Fig. 3.84
grams and T2-weighted magnetic resonance image (C) in a
1-day-old term girl show smooth cerebral cortex without gyri or sulci,
C dilated lateral ventricles (V), and wide sylvian fissures (arrows).

closed-lip schizencephaly may be asymptomatic or have
seizure disorders and hemiparesis.
Sonographic findings of open-lip schizencephaly are
fluid-filled clefts that communicate with a dilated lateral
ventricle; absent septum pellucidum; and a small corpus
callosum (Fig. 3.85). The margins of the clefts may be
echogenic, reflecting the gray matter lining. The sulci in the
cortex adjacent to the clefts may radiate into the clefts.
Closed-lip schizencephaly is not well demonstrated on
sonography and will require MRI for diagnosis.
HETEROTOPIC GRAY MATTER
Gray matter heterotopia is a developmental anomaly result-
ing from an arrest in the axial migration of primitive neu-
rons. The heterotopic tissue is usually located in the
subependymal layer of the lateral ventricles. Because it has
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100 P E D I AT R I C S O N O G R A P H Y
A B
C septum pellucidum.
the same echogenicity as normal gray matter, it is only
apparent on sonography when it protrudes into the ventric-
ular cavity, producing nodular masses on the lateral margins
(Fig. 3.86). Associated anomalies include agenesis of the
corpus callosum, lissencephaly, schizencephaly, and polymi-
crogyria.
POLYMICROGYRIA
Polymicrogyria is an abnormality of neuronal migration
and cortical organization characterized by formation of
multiple small gyri and serrated or thickened cortex. His-
tologically, there is a four-layer cortex. The diagnosis
requires MRI or tissue sampling, because the abnormal
gyri are not easily demonstrated by sonography.
Unilateral open-lip schizencephaly. Coronal (A) and
Fig. 3.85
sagittal (B) scans and T2-weighted coronal magnetic
resonance image (C) show a large fluid-filled cleft (arrows) extend-
ing from the left convexity to a dilated lateral ventricle with an absent
Destructive Brain Lesions
Destructive lesions can occur at any time during brain
development (85). Three major patterns are recognized:
hydranencephaly, porencephaly, and encephalomalacia.
HYDRANENCEPHALY
Hydranencephaly is a condition in which the cerebral hemi-
spheres are replaced by a thin-walled sac containing CSF. It
usually is a sporadic disorder, although a rare form appears
to have an autosomal recessive inheritance. The outer layer
of the CSF-filled sac contains leptomeningeal tissue and
dura. The inner layer contains remnants of cortex and white
matter (184). The thalami, basal ganglia, inferomedial
aspects of the temporal lobes, brainstem, and cerebellum,
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Chapter 3 B R A I N 101

A B
Gray matter heterotopia. A, B: Two coronal images show nodular masses (arrows) on the lateral walls of the right lateral ventricle. Also
Fig. 3.86
note absence of the corpus callosum (i.e., elevation of the third ventricle and widely separated frontal horns) and Dandy-Walker
malformation (i.e., posterior fossa cyst, C). (Case courtesy of Brian Coley, MD.)

which are supplied by the vertebrobasilar arterial circula-
tion, are normal. The cranial vault, falx, and meninges are
also normal. Hydranencephaly is thought to be the result of
cerebral infarction secondary to bilateral occlusion of the
supraclinoid segments of the internal carotid arteries during
fetal development. Ischemia and intrauterine infection have
been suggested as causes for the arterial occlusion.
Sonography demonstrates complete absence of a corti-
cal mantle and replacement of the cerebral hemispheres by
a sac of hypoechoic cerebrospinal fluid. The basal ganglia
and posterior fossa are usually normal (Fig. 3.87). The
supratentorial fluid sac may be echogenic if it contains pro-
teinaceous contents. Color flow is absent in the supracli-
noid portion of the internal carotid arteries, although flow
may be seen in the basilar artery, posterior cerebral artery,
and proximal portion of the internal carotid artery (185).
Hydranencephaly needs to be differentiated from severe
hydrocephalus. This is important because some infants
with severe hydrocephalus may have normal or nearly
normal motor and intellectual skills after CSF shunting,

A B
Hydranencephaly. Coronal (A) and right parasagittal (B) images show replacement of the cerebrum by a large fluid-filled sac. The
Fig. 3.87
thalami (T), cerebellar vermis (V), and falx cerebri (arrows) are normal.
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102 P E D I AT R I C S O N O G R A P H Y

whereas those with hydranencephaly will not improve after
CSF diversion (85). The presence of a thin rim of brain
parenchyma and color flow in the branches of the internal
carotid artery establishes the diagnosis of hydrocephalus
rather than hydranencephaly. The presence of the falx helps
to distinguish hydranencephaly from alobar holoprosen-
cephaly, in which there is no falx formation.
PORENCEPHALY (PORENCEPHALIC CYST)
Porencephaly refers to brain destruction during the first
half of gestation, which is the time before the brain can
incite a glial response. Porencephalic cysts also have been
called encephaloclastic porencephaly. They result from
focal tissue destruction due to ischemic, hemorrhagic, or
infectious causes, prior to the 26th gestational week (85).
Sonographic findings are a smooth- or irregular-walled,
unilocular fluid-filled cavity. Porencephalic cysts can com-
municate with the ventricles, but they usually do not
extend to the cortical surface.
CYSTIC ENCEPHALOMALACIA
Cystic encephalomalacia is an area of brain destruction
late in gestation or after birth. Pathologically, it has irreg-
ular walls, is lined by gliotic white matter and reactive
astrocytes, and often contains septations. Causes include
infarction, hemorrhage, and infectious etiologies. Sonogra-
phy shows an irregular hypoechoic cavity (see Fig. 3.44).
Septations may be seen in the cystic cavity. The lesion usu-
ally does not communicate with the ventricular system.
CONGENITAL INFECTIONS
The causes of meningoencephalitis in the fetus include Tox-
oplasma gondii, rubella virus, cytomegalovirus, and herpes
simplex type 2 virus, collectively referred to as the TORCH
complex (186,187). The O refers to other diseases,
such as syphilis and human immunodeficiency virus (HIV)
infection. Most congenital infections are transmitted by
transplacental passage of microorganisms. Herpes simplex

A B

Congenital infection, spectrum of sonographic findings.

Fig. 3.88
A, B: Cytomegalovirus infection. Coronal (A) and left
parasagittal (B) scans show highly echogenic nonshadowing thalamo-
striate vessels (arrows) and subependymal cysts (arrowhead).
C: Toxoplasmosis. Left parasagittal view shows nonshadowing
echogenic foci, representing parenchymal calcifications (arrows), in
C the cortical gray matter.
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virus infection is an exception with cases transmitted at the
time of birth, either as an ascending infection or as the baby
passes through an infected vaginal canal. HIV can be trans-
mitted in utero or during delivery (186,187).
The CNS manifestations of these infections depend on
the age of the fetus at the time of infection. Infections early
in utero, before 20 to 24 weeks, affect organogenesis. These
result in cerebral malformations, including lissencephaly,
schizencephaly, hydranencephaly, and disturbances in neu-
ronal proliferation. Later infections cause destructive
changes in the white matter and cortex and parenchymal
calcifications.
Of the TORCH infections, cytomegalovirus infection is
the most common, followed by toxoplasmosis (186,187).
Neonatal herpes infection is caused by the herpes simplex
type 2 virus. The type 1 virus is generally associated with
orofacial herpes infection and causes herpes simplex
encephalitis in patients 6 months of age or older. CNS find-
ings associated with congenital viral infections are micro-
cephaly, microphthalmia, chorioretinitis, cataracts, and
seizures. Other findings include hepatosplenomegaly, hepa-
titis, jaundice, pneumonitis, petechiae, thrombocytopenia,
and anemia due to disseminated intravascular coagulation.
SONOGRAPHIC FINDINGS
The most common sonographic findings in congenital infec-
tion are dystrophic calcifications, increased parenchymal
echogenicity, a mineralizing vasculopathy, and subependy-
mal cysts (Figs. 3.88 and 3.89) (186194). Cytomegalovirus
infection commonly causes periventricular calcifications,
while infection by toxoplasmosis classically results in corti-
cal and basal ganglia calcifications. In herpes virus infection,
calcifications occur in the cortex, basal ganglia, and periven-
tricular white matter. Calcifications appear as brightly
echogenic foci with or without acoustic shadowing. The
sonographic findings are not specific for a particular infec-
tion, and a final diagnosis is based on laboratory data.
Lenticulostriate or mineralizing vasculopathy is charac-
terized by linear or curvilinear, nonshadowing areas of
Lenticulostriate vasculopathy. Left parasagittal view
Fig. 3.89
shows linear, echogenic structures (arrows) within the
basal ganglia, representing mineralized vessels. Cultures were posi-
tive for cytomegalovirus.
Chapter 3 B R A I N 103
echogenicity in the thalami and basal ganglia (Figs. 3.88
and 3.89). The echogenic foci follow the distribution of the
lenticulostriate arteries. Spectral insonation of the lenticu-
lostriate arteries shows a Doppler signal typical for
medium-sized arteries (slow systolic rise and descent) (188).
It should be noted that normal lenticulostriate arteries are
not visible on gray-scale sonography, although they are
identifiable on spectral and color Doppler sonography.
Mineralizing vasculopathy is not specific for the TORCH
infections, and it can also be seen in neonates with
ischemia, trisomy 21, trisomy 13, twintwin transfusion,
intrauterine cocaine exposure, neonatal asphyxia, fetal
alcohol syndrome, neonatal lupus, neonatal hypoglycemia,
and encephalitis (189,195,196).
Other findings of congenital infection include ventricu-
lar dilatation from obstruction of CSF flow by inflamma-
tory exudate or from brain atrophy, porencephaly, cystic
encephalomalacia, and cortical malformations, such as
lissencephaly, schizencephaly, and polymicrogyria. The lat-
ter are more common in cytomegalovirus infection than in
the other infections. Subdural effusions are uncommon in
congenital infections.
MENINGITIS
Escherichia coli and group B Streptococcus account for
65% to 70% of CNS infections in the newborn (186,197).
Gram-negative bacilli, such as Enterococcus, Klebsiella,
Proteus mirabilis, Citrobacter, and Listeria monocyto-
genes, are less common, but they are more likely to cause
extensive brain destruction. In the newborn, bacterial
meningitis can occur as a result of an ascending infection
following rupture of amniotic membranes or from
hematogenous spread. In infants older than 1 month of
age, Streptococcus pneumoniae is the commonly isolated
organism. In this age group, meningeal inoculation occurs
by hematogenous spread, penetrating trauma or surgery,
or contiguous spread of an adjacent infection, usually
otitis media or sinusitis (186).
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104 P E D I AT R I C S O N O G R A P H Y

Fungal infections of the CNS occur less frequently

than bacterial infections (187). The common organism is
Candida albicans. This organism is part of the normal
flora of the gastrointestinal tract and oral cavity, but it
can invade beyond these portals. Risk factors for infec-
tion include prematurity, immunosuppression, parenteral
nutrition, indwelling catheters, and antibiotic therapy.
Meningeal infection initially seeds the choroid plexus
and then spreads to the CSF, causing inflammation of the
ventricles (ventriculitis). From the ventricles, it can extend
to the meninges and subarachnoid and subdural spaces.
Meningeal inflammation can spread to the walls of bridg-
ing and cortical veins, resulting in thrombophlebitis, and
to the arterial walls, producing vasculitis. Vascular inflam-
mation, in turn, can lead to vessel occlusion, cortical
infarction, and edema (186,197).
The diagnosis of bacterial or fungal meningitis is based
on clinical findings and laboratory analysis of CSF. Imag-
ing studies are not needed in most uncomplicated cases of
meningitis. They, however, are useful to evaluate for com-
plications when the patient is not responding to antibiotic
treatment. As with the congenital infections, imaging can
identify complications of meningitis, but the findings are
not specific for a particular organism.

Sonographic Findings Fig. 3.90

Subdural effusion due to enterococcus meningitis. Ante-
rior high-resolution coronal scan with a linear array trans-
Ultrasonography is usually normal in uncomplicated ducer reveals a hypoechoic fluid collection in the interhemispheric fis-
meningitis. Sonographic findings in severe disease include sure (IH) and over the brain convexity. The surface of the brain
extra-axial fluid collections, ventriculitis, cerebral edema (arrows) is easily visualized, due to displacement of the gyri and sulci
(cerebritis), venous thrombosis and infarction, abscess from the calvarium. V  lateral ventricles.
formation, and hydrocephalus (190,197). Late findings
include hydrocephalus, multicystic encephalomalacia,
and cerebral cortical and white matter atrophy. ation is important because surgical evacuation is the treat-
ment of choice for subdural empyema.
EXTRA-AXIAL FLUID Subarachnoid fluid collections are occasional findings in
Extra-axial fluid collections include subdural effusion and meningitis, but usually have no clinical importance (197).
empyema. Subdural effusions are reactive and sterile and Color Doppler sonography can be useful in distinguishing
usually have no prognostic significance (186,197). They
are thought to be the result of inflammation of subdural
veins with efflux of intravascular fluid and protein into the
subdural space. Less than 5% of subdural effusions
become infected and develop into an empyema. Effusions
and empyemas can be unilateral or bilateral, and both are
most common over the frontal and parietal convexities
and in the interhemispheric fissure.
Sonographic findings include a crescentic or elliptical
extra-axial collection, flattening of the subadjacent cortex,
visualization of the cortical gyri over the cerebral convex-
ity, widening of the interhemispheric fissure, and mass
effect with displacement and effacement of the ventricles
and shift of midline structures (Figs. 3.90 and 3.91). Ster-
ile collections are usually anechoic, whereas empyemas are
often echogenic or complex secondary to the presence of
an increased protein content, internal debris, and fibrinous
strands (198). Although the presence of echogenic debris
favors empyema, it is not specific. Differentiation between Subdural empyema. Anterior high-resolution sagittal scan
a sterile and infected effusion is usually a clinical diagnosis Fig. 3.91
shows an echogenic subdural fluid collection (arrows)
and requires aspiration and analysis of the CSF. Differenti- containing debris over the brain convexity.
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Chapter 3 B R A I N 105

A B
Ventriculitis. Coronal (A) and longitudinal (B) sonograms show hydrocephalus, ventricular debris and septations, and a thickened
Fig. 3.92
ependymal lining (arrows).

between subarachnoid and subdural effusions. Cortical ves- ventricles and complicate shunt placement and administra-
sels cross the subarachnoid fluid space, whereas they are com- tion of intraventricular antibiotics. Ultrasonography is
pressed along the surface of the brain in subdural effusion. superior to CT for identification of these septations.

VENTRICULITIS CEREBRAL EDEMA

Ventriculitis refers to the presence of inflammatory exu-
date in the ventricles. Organisms probably gain access to
the ventricles through the choroid plexus. Sonographic
findings include ventricular dilatation, a thickened and
irregular ependymal lining, intraventricular septations and
debris, and increased echogenicity of the choroid plexus
(Fig. 3.92) (190,197). The identification of intraventricular
septations is important as they can compartmentalize the
The sonographic findings of cerebral edema, also termed
cerebritis, are echogenic sulci and parenchyma. In severe
edema, the sulcal-gyral interfaces, ventricles, and cisterns
can be compressed or obliterated. Doppler interrogation
may demonstrate increased or decreased flow velocities in
the major arteries depending on the severity of the edema.
Severe edema can increase intracranial pressure, resulting
in an elevated resistive index (Fig. 3.93).

A B
Bacterial meningitis, cerebral edema. A: Coronal sonogram in a 7-day-old term girl shows diffusely echogenic parenchyma with loss of
Fig. 3.93
gyral-sulcal interfaces and effaced ventricles. B: Doppler interrogation demonstrates decreased diastolic flow with an elevated resis-
tive index (RI  0.82), indicating increased intracranial pressure.
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106 P E D I AT R I C S O N O G R A P H Y
Bacterial meningitis, cortical infarct. Anterior coronal
Fig. 3.94
view demonstrates focally increased echogenicity
(arrows) in the left hemisphere with obliteration of the lateral ventricle.
The echogenicity follows the distribution of cortical gyri. Diagnosis
was confirmed by magnetic resonance imaging (not shown).
VENOUS THROMBOSIS AND INFARCTION
The common sites of thrombosis are the cortical veins and
dural sinuses. An acute thrombosis appears as an area of
increased intravascular echogenicity on gray-scale sonog-
raphy. Color flow Doppler imaging shows absence of flow
in the affected vessels. The sonographic finding of infarc-
tion is focally increased cortical echogenicity (Fig. 3.94).
The sulcal-gyral interface is often preserved, in contrast to
edema, which obliterates the interfaces (199). Doppler
A B
Brain abscess due to Citrobacter meningitis. Posterior coronal (A) and left parasagittal (B) scans show a well-defined mass (arrows)
Fig. 3.95
with echogenic debris in the left occipital area. Ch  choroid plexus.
imaging of cerebral infarction shows absent signal or color
flow, although increased flow secondary to luxury perfu-
sion may be seen in the periphery of the ischemic tissue.
BRAIN ABSCESS
Brain abscess is a rare complication of meningitis and
results when an area of infected parenchyma infarcts, liq-
uefies, and then is surrounded by a capsule of granulation
tissue. Proteus mirabilis, Citrobacter diversus, Enterobac-
ter species, and Serratia marcescens appear to have an
unusual propensity for causing tissue necrosis, liquefac-
tion, cavitation, and brain abscess (197,200,201). The
sonographic findings of a mature cerebral abscess are a
well-circumscribed, thick-walled, hypoechoic lesion with
debris or a fluid-debris level and peripheral hyperemia.
Mass effect causing midline shift and ipsilateral ventricular
compression also may be noted (Fig. 3.95).
HYDROCEPHALUS
Hydrocephalus can occur in the acute or chronic phase of
infection. The level of obstruction can be within the ven-
tricle, usually at the aqueduct and outlet of the fourth ven-
tricle; over the cerebral convexity; or in the basilar cisterns.
In aqueductal occlusion, the lateral and third ventricles are
dilated out of proportion to the fourth ventricle, and the
aqueduct is thickened and echogenic. When the exit
foramina of the fourth ventricle are occluded, there is pan-
ventricular enlargement.
HYDROCEPHALUS
Normal Cerebrospinal Fluid Production
Approximately 80% to 90% of CSF production is pro-
duced by the choroid plexus of the lateral, third, and
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fourth ventricles, and the remainder is from the ventricular
ependyma and the arachnoid lining of the brain and spinal
cord (202). CSF normally flows from the lateral ventricles
through the foramen of Monro into the third ventricle,
through the Sylvian aqueduct into the fourth ventricle, and
through the foramina of Magendie and Luschka into the
cisterna magna and the basal subarachnoid cisterns,
respectively. From this point, the CSF flows cephalad and
anteriorly into the chiasmatic cisterns and the pericallosal
cisterna and posteriorly into the quadrigeminal and poste-
rior callosal cisterns to reach the cerebral hemispheres,
where it is eventually resorbed by the arachnoid granula-
tions and recirculated into the subarachnoid space.
Disturbances in Cerebrospinal Fluid Production
and Circulation
Hydrocephalus refers to dilatation of the ventricular system
associated with increased intraventricular pressure. Ventricu-
lomegaly is a less specific term and may imply ventricular
dilatation either secondary to hydrocephalus or brain atro-
phy or a combination of the two conditions. The mechanisms
for the development of hydrocephalus are obstruction of ven-
tricular outflow of CSF and impaired absorption by the
arachnoid villi. CSF overproduction from a choroid plexus
papilloma is a rare cause of hydrocephalus (202204).
Hydrocephalus resulting from intraventricular obstruc-
tion of CSF flow is also termed noncommunicating hydro-
cephalus, while hydrocephalus resulting from extraven-
tricular obstruction of CSF flow in the subarachnoid spaces
and cisterns or secondary to impaired absorption at the
level of the arachnoid villi is termed communicating
hydrocephalus. Intraventricular or noncommunicating
obstruction may be a result of congenital or acquired
causes. The common congenital causes of obstruction are
aqueduct stenosis, which often is an X-linked recessive
A B
Congenital aqueductal stenosis. Coronal (A) and midline sagittal (B) images show dilated lateral (LV) and third (3) ventricles. The fourth
Fig. 3.96
ventricle (4) is normal in size.
Chapter 3 B R A I N 107
trait; Chiari II malformation (Fig. 3.70); Dandy-Walker
cyst (Figs. 3.72 and 3.73); encephalocele; and galenic mal-
formation. The common acquired causes of intraventricu-
lar obstruction are hemorrhage, infection, and tumor.
Causes of extraventricular obstruction are hemorrhage and
infection, which incite an adhesive arachnoiditis.
Gray-scale Sonographic Findings
Patients with hydrocephalus present with a large or an
increasing head circumference or signs of increasing
intracranial pressure. Ultrasonography is performed in this
clinical setting to document the diagnosis of hydrocephalus
and its severity.
The early finding of ventricular dilatation is ballooning of
the superolateral angles of the frontal horns and dilatation of
the occipital horns. Because these areas are larger and require
less pressure for distention, they dilate before the trigones
and body of the ventricles. To avoid an error in diagnosis, it
needs to be recognized that the ventricles are normally larger
in premature infants than they are in term infants and that
ventricular asymmetry is a normal variant (see Fig. 3.17).
The level of obstruction is identified as the point of
transition from a dilated to a small ventricle. Dilatation of
the lateral and third ventricles indicates obstruction of the
aqueduct of Sylvius (Fig. 3.96). Isolated dilatation of the
fourth ventricle (termed trapped fourth ventricle) indi-
cates obstruction of the aqueduct and fourth ventricular
outlet (see Fig. 3.45). Panventricular enlargement indicates
either an extraventricular obstruction or a nonobstructive
hydrocephalus secondary to CSF overproduction.
Other findings in severe hydrocephalus include cortical
thinning, herniation of part of a ventricle forming a diver-
ticulum, and rupture of the septum pellucidum. The com-
mon areas for ventricular herniation are the trigones of the
lateral ventricles and the suprapineal, anterior, and posterior
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108 P E D I AT R I C S O N O G R A P H Y
Hydrocephalus, ventricular herniation. Posterior coronal
Fig. 3.97
scan at the level of the trigones shows dilated lateral ven-
tricles and a fluid-filled diverticulum (arrow) communicating with the
left lateral ventricle. Ch  choroid plexus.
recesses of the third ventricle. The anatomic basis for herni-
ation is focal dehiscence of the atrial wall through which pia
and CSF protrude. The sonographic finding of herniation is
a CSF-filled diverticulum-like structure protruding through
the ventricular wall (Fig. 3.97) (205). Rupture or fenestra-
tion of the septum pellucidum has sonographic findings that
are similar to those of primary agenesis of the septum pellu-
cidum (206).
Measurements of normal ventricular size have been pub-
lished (18,19), but they are rarely needed for the diagnosis
A B
Ventricular shunt. Coronal (A) and right parasagittal (B) images show the echogenic tip (arrow) of the intracranial shunt in the right lat-
Fig. 3.98
eral ventricle. Acoustic shadowing can be noted on the sagittal view.
of hydrocephalus. However, they can be used to monitor the
progression of hydrocephalus and its response to treatment.
It needs to be recognized that if serial studies are performed
to follow ventricular size, the scan depth needs to be con-
stant. Changes in depth scale can result in misdiagnosis of
progressive ventricular enlargement or decompression.
Following placement of ventriculoperitoneal shunts or
reservoirs, sonography can be used to monitor changes in
ventricular size and detect complications, including recur-
rent obstruction, trapped fourth ventricle, intraventricular
hemorrhage, and subdural hematomas. On sonography,
intracranial shunts are highly echogenic tubular foci with
acoustic shadowing (Fig. 3.98).
Doppler Interrogation
With moderate to severe hydrocephalus, intracranial compli-
ance and diastolic flow decrease and RIs increase (207209).
In healthy infants, there is a small increase in CSF volume
when the anterior fontanelle is compressed by the transducer.
Intracranial pressure does not increase significantly because
the CSF can be readily displaced, compensating for the
increased volume. In infants with hydrocephalus, the CSF is
not displaced during fontanelle compression, which leads to
a transient increase in intracranial pressure, concomitant
decrease in cerebral perfusion pressure, and increase in the
RI (207).
Color flow Doppler imaging has been used to distin-
guish between communicating and noncommunicating
hydrocephalus (210). In communicating or nonobstructive
hydrocephalus, there is retrograde flow of CSF from the
fourth ventricle into the third ventricle immediately fol-
lowing rapid manual release of fontanelle compensation.
On color flow imaging, this appears as blue or mixed color
signal in the third ventricle. With intraventricular obstruc-
tion, there is no retrograde flow during release of com-
pression.
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A B
Benign extra-axial hydrocephalus. Coronal (A) and left parasagittal (B) scans show symmetric extra-axial fluid collections in the inter-
Fig. 3.99
hemispheric space (IH) and over the convexities (arrows). The ventricles are normal. Doppler imaging showed a vessel crossing within
the fluid, consistent with subarachnoid fluid (not shown).
Benign External Hydrocephalus
Benign enlargement of the extra-axial spaces is a relatively
common condition in infants between 2 months and
7 months of age. This disorder, also known as benign
macrocrania of infancy, benign hydrocephalus-megalo-
cephaly, and benign extraventricular obstructive hydro-
cephalus, is thought to be a result of inadequate CSF
absorption by immature arachnoid villi. Affected infants
are usually neurologically normal and typically present
with a head circumference above the 95th percentile
(211,212). There is often a family history of macro-
cephaly.
Sonographic findings include bilaterally symmetric
extra-axial subarachnoid fluid collections, normal brain
parenchyma, and normal to minimally enlarged lateral and
third ventricles (Fig. 3.99). Doppler sonography shows
veins crossing the subarachnoid space and entering the
superior sagittal sinus. Asymmetry is unusual and should
raise suspicion of traumatic extra-axial hematomas. Infan-
tile hydrocephalus is a self-limiting disorder and the sub-
arachnoid and ventricular dilatation usually resolves by
the second year of life. Occasionally patients with benign
enlargement of the subarachnoid spaces develop superim-
posed subdural hematomas (213).
INTRACRANIAL CYSTS AND NEOPLASMS
Arachnoid Cysts
Arachnoid cysts account for only 1% of all intracranial
masses in childhood (214). Congenital or primary cysts
are believed to be due to abnormal splitting of the lep-
Chapter 3 B R A I N 109
tomeninges with CSF collecting between the two layers of
the arachnoid membrane. They do not communicate with
the surrounding subarachnoid CSF or the ventricles.
Most congenital cysts (50% to 65%) are located in the
sylvian fissures and cerebellar-medullary angle cistern.
Other sites, in order of decreasing frequency, are the cere-
bral convexity, suprasellar region, interhemispheric and
quadrigeminal regions, and cerebellopontine angle cistern
(214). Arachnoid cysts usually are asymptomatic,
although large cysts may compress adjacent structures,
causing hydrocephalus and signs of intracranial hyper-
tension.
Acquired or secondary cysts are the result of entrap-
ment of CSF between arachnoid adhesions. They may be
secondary to infection, inflammation, or trauma. They
also lack a communication with the subarachnoid space.
Sonographically, arachnoid cysts appear as anechoic
lesions with indiscernible walls (see Fig. 3.75). The con-
tents may be echogenic if there is superimposed hemor-
rhage or infection. Large cysts may compress adjacent
brain and cause midline shift. Cysts near the midline can
compress the foramina of Monro, aqueduct of Sylvius, or
third ventricle, causing hydrocephalus.
The arachnoid cyst needs to be differentiated from nor-
mal extracerebral cystic areas, including the cisterna
magna and cava septa pellucidi and vergae. The normal
cisterna magna and cava usually do not alter brain archi-
tecture or produce mass effect. Differentiation from the
Dandy-Walker complex is made by determining whether
the cyst is separate from the fourth ventricle (arachnoid
cyst) or whether the cyst is the dilated fourth ventricle
(Dandy-Walker complex).
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110 P E D I AT R I C S O N O G R A P H Y
A B
Choroid plexus cyst in a patient with trisomy 13. Coronal (A) and right parasagittal (B) images demonstrate a large cyst (C) in the
Fig. 3.100
choroid plexus. Also noted is ventricular dilatation.
Other Cystic Lesions
Porencephalic cysts and encephalomalacia, areas of focal
brain destruction early and late in gestation, respectively,
are discussed earlier.
Subependymal cysts are most often a result of ger-
minal matrix hemorrhage in premature neonates (see
Fig. 3.37). Other causes include ischemia and TORCH
infections (see Fig. 3.88). They also can be an isolated
finding, unassociated with other neurologic or systemic
diseases. Sonographically, they appear as discrete ane-
choic lesions in the subependymal lining of the ventri-
cles.
Small cysts are common in the choroid plexus of the
trigones. They have no clinical significance and no associa-
tion with other CNS abnormalities (27). They tend to be
single and less than 1 cm (usually 4 to 7 mm) in diameter.
Large (1 cm) or bilateral cysts can be associated with
chromosomal disorders, particularly trisomies 9 and 18
(Fig. 3.100). At sonography, a choroid cyst appears as a
cystic mass with well-defined walls within the choroid
plexus.
Brain Neoplasms
Brain tumors in neonates are rare, accounting for
approximately 0.5% to 2.0% of all pediatric brain
tumors (214217). They have supratentorial predomi-
nance in contrast to the infratentorial predominance in
later infancy and childhood (214217). Teratomas, prim-
itive neuroectodermal tumors, astrocytomas, and choroid
plexus papillomas are the most frequent tumors in the
first year of life. Ependymomas, medulloepitheliomas,
germinomas, gangliogliomas, and meningiomas have
been reported on rare occasions. The clinical features
include increasing head circumference, vomiting and
lethargy, and neurologic signs related to the location of
the tumor.
MRI or CT is usually the initial imaging studies in
infants with signs and symptoms of increased intracranial
pressure. However, when clinical findings are nonspecific,
such as an enlarging head size, sonography may be the
initial imaging study. Intraoperative sonography can guide
localization of the tumor for biopsy or excision, thereby
reducing the extent of exploration and decreasing damage
to normal brain.
The sonographic features of intracranial tumors are
not specific for a particular type of neoplasm, but the
location of the tumor can help to suggest a histologic
diagnosis. Teratomas and astrocytomas are supratentorial
tumors. Teratomas are commonly located in the pineal
and suprasellar areas. Astrocytomas usually arise from the
optic chiasm or hypothalamus. Both tumors appear as
large echogenic masses. They may cause hydrocephalus
and displace midline structures. Calcifications and cystic
areas of degeneration and necrosis are typical of ter-
atomas (218,219).
Gliomas, ependymomas, and gangliomas typically
involve the brainstem. Posterior fossa tumors appear as
hyperechoic lesions (Fig. 3.101). They may contain cystic
spaces.
Choroid plexus papillomas arise in the ventricles, most
often in the trigones of the lateral ventricles (218). They
are large echogenic masses and they may obstruct the ven-
tricular system. Pulsed Doppler imaging shows increased
vascularity with low-velocity shifts and bidirectional flow
during diastole.
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Chapter 3 B R A I N 111

A B

Brainstem astrocytoma. Coronal (A) and midline sagit-

Fig. 3.101
tal (B) sonograms show a poorly defined echogenic
mass (arrows) in the brainstem displacing the fourth (4) ventricle
posteriorly. C: Magnetic resonance imaging confirms a prepontine
C mass, proven at operation to be an astrocytoma.

SUTURE EVALUATION
Conventional skull radiographs are the standard imaging
study for evaluating patency of the calvarial sutures. Ultra-
sonography is an alternative method of assessing sutural
patency when radiographs are indeterminate. Craniosynos-
tosis presents as an abnormally shaped head. Isolated sagit-
tal synostosis produces a long, narrow head (scapho-
cephaly). Isolated coronal or lambdoid synostosis produces
an asymmetric cranium with frontal or occipital flattening
(plagiocephaly). Isolated metopic synostosis produces a
pointed frontal region or forehead (trigonocephaly).
The sonographic diagnosis of suture patency is based
on the demonstration of a hypoechoic band extending Normal suture, lambdoid suture. The normal suture
from the inner to the outer tables of the skull along the Fig. 3.102
appears as a hypoechoic tract (arrow) extending between
expected course of a suture (Fig. 3.102). The diagnosis of the inner and outer table of the echogenic calvarium.
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112 P E D I AT R I C S O N O G R A P H Y

Sutural synostosis, left coronal suture. There is absence

Fig. 3.103
of the normal hypoechoic suture. Instead, hyperechoic
bone (*) bridges the two calvarial surfaces.

craniosynostosis is suggested when this hypoechoic zone is

Dermoid cyst. Longitudinal view of the left frontal region
not seen along the entire length of the suture or if it does Fig. 3.104
shows a well-defined hypoechoic mass (arrows) in the
not cross through both the inner and outer tables of the soft tissues overlying the calvarium (open arrows).
skull (220) (Fig. 3.103). False-positive diagnoses are
related to difficulty in identifying the margins of sutures
that course obliquely.

Sinus pericranii is a venous lesion characterized by

CALVARIAL MASSES
Calvarial masses include encephaloceles (see above dis-
cussion), dermoid inclusion cysts, hemangioma, and sinus
pericranii. Dermoid cysts are epithelial-lined cysts contain-
ing epidermal appendages such as hair, sebum, and seba-
ceous and apocrine glands. They present as soft, rubbery,
mobile scalp masses. Sonography shows a well-defined,
hypoechoic mass overlying an intact calvarium (Fig. 3.104).
Hemangiomas are soft scalp masses. Sonographic findings
are a well-defined hypoechoic mass with arterial flow.
dilated extracranial veins that adhere to the outer surface
of the calvarium and communicate with the dural sinuses
via transosseous diploic and epidural veins. Clinical find-
ings are a soft scalp mass that enlarges when the patient
cries or is in a supine position and spontaneously decreases
in size when the patient is quiet and erect. The lesion is
commonly located in the frontal region close to the mid-
line. Doppler imaging shows enlarged scalp veins commu-
nicating with the dural sinus via transosseous veins (221)
(Fig. 3.105).

A B
Sinus pericranii in a 6-month-old boy with a soft parietal scalp mass since birth. A: Sagittal image shows a hypoechoic mass (arrows)
Fig. 3.105
superficial to the right parietal bone (arrowheads). Note a small defect in the calvarium (open arrow). B: Color Doppler image shows
a dilated superficial vein (*) extending through the calvarial defect (arrowhead ) to enter the superior sagittal sinus (arrows). The lesion showed a
venous waveform on spectral imaging.
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REFERENCES
1. Babcock DS. Sonography of the brain in infants: role in evaluat-
ing neurologic abnormalities. AJR Am J Roentgenol 1995;165:
417423.
2. Barr LL. Neonatal cranial ultrasound. Radiol Clin North Am
1999;37:11271146.
3. Benson JE, Bishop MR, Cohen HL. Intracranial neonatal neu-
rosonography: an update. Ultrasound Q 2002;18:89114.
4. Veyrac C, Couture A, Saguintaah M, et al. Brain ultrasonogra-
phy in the premature infant. Pediatr Radiol 2006;36:626635.
5. Anderson N, Allan R, Darlow B, et al. Diagnosis of intraventric-
ular hemorrhage in the newborn: value of sonography via the
posterior fontanelle. AJR Am J Roentgenol 1994;163:893896.
6. Buckley KM, Taylor GA, Estroff JA, et al. Use of the mastoid
fontanelle for improved sonographic visualization of the neona-
tal midbrain and posterior fossa. AJR Am J Roentgenol 1997;
168:10211025.
7. Correa F, Enriquez G, Rossello J, et al. Posterior fontanelle
sonography: an acoustics window into the neonatal brain.
AJNR Am J Neuroradiol 2004;25:12741282.
8. Di Salvo DN. A new view of the neonatal brain: clinical utility
of supplemental neurologic US imaging windows. Radiograph-
ics 2001;21:943955.
9. Enriquez G, Correa F, Aso C, et al. Mastoid fontanelle approach
for sonographic imaging of the neonatal brain. Pediatr Radiol
2006;36:532540.
10. Steggerda SJ, Leijser LM, Wiggers-deBrune FT, et al. Cerebellar
injury in preterm infants: incidence and findings on US and MR
images. Radiology 2009;2525:190199.
11. Thomson GD, Teele RL. High-frequency linear array transduc-
ers for neonatal cerebral sonography. AJR Am J Roentgenol
2001;176:9951001.
12. Barkovich AJ. Concepts of myelin and myelination in neurora-
diology. AJNR Am J Neuroradiol 2000;21:10991109.
13. Huang C-C. Sonographic cerebral sulcal development in prema-
ture newborns. Brain Dev 1991;13:2731.
14. Naidich TP, Grant JL, Altman N, et al. The developing cerebral
surface. Preliminary report on the patterns of sulcal and gyral
maturation-anatomy, ultrasound, and magnetic resonance imag-
ing. Neuroimaging Clin N Am 1994;4:201240.
15. Worthen NJ, Gilbertson V, Lau C. Cortical sulcal development
seen on sonography: relationship to gestational parameters.
J Ultrasound Med 1986;5:153156.
16. Bowerman RA. Tangential sulcal echoes. Potential pitfall in the
diagnosis of parenchymal lesions on cranial sonography. J Ultra-
sound Med 1987;6:685689.
17. Enriquez G, Correa F, Lucaya J, et al. Potential pitfalls in cranial
sonography. Pediatr Radiol 2003;33:110117.
18. Davies MW, Swaminathan M, Chuang SL, et al. Reference
range for the linear dimensions of the intracranial ventricles in
preterm neonates. Arch Dis Child Fetal Neonatal Ed 2000;
82:F218F223.
19. Poland RL, Slovis TL, Shankaran S. Normal values for ventric-
ular size as determined by real time sonographic techniques.
Pediatr Radiol 1985;15:1214.
20. Patel MD, Cheng AG, Callen PW. Lateral ventricular effacement
as an isolated sonographic finding in premature infants: prevalence
and significance. AJR Am J Roentgenol 1995;165:155159.
21. Nelson MD, Tavare CJ, Petrus L, et al. Changes in the size of the
lateral ventricles in the normal-term newborn following vaginal
delivery. Pediatr Radiol 2003;33:831835.
22. Siegel MJ, Shackelford GD, Perlman JM, et al. Hypoxic
ischemic encephalopathy in term infants: diagnosis and progno-
sis evaluated by ultrasound. Radiology 1984;152:395399.
23. Koeda T, Ando Y, Takashima S, et al. Changes in the lateral ven-
tricle with the head position: ultrasonographic observation.
Neuroradiology 1988;30:315318.
Chapter 3 B R A I N 113
24. Rosenfeld DL, Schonfeld SM, Underberg-Davis S. Coarctation
of lateral ventricles: an alternative explanation for subependy-
mal pseudocysts. Pediatr Radiol 1997;27:895897.
25. Shaw C, Alvord E. Cava septi pellucidi et vergae: their normal
and pathologic states. Brain 1969;92:213224.
26. Epelman M, Daneman A, Blaser SI, et al. Differential diagnosis
of intracranial cystic lesions at head US: correlation with CT
and MR imaging. Radiographics 2006;26:173196.
27. Riebel T, Nasir R, Weber K. Choroid plexus cysts: a normal
finding on ultrasound. Pediatr Radiol 1992;22:410412.
28. Leijser LM, Srinivasan L, Rutherford MA. Frequently encoun-
tered cranial ultrasound features in the white matter of preterm
infants: Correlation with MRI. Eur J Paediatr Neurol 2009;13:
317326.
29. Goodwin L, Quisling RG. The neonatal cisterna magna: ultra-
sonic evaluation. Radiology 1983;149:691695.
30. Armstrong DL, Bagnall C, Harding JE, et al. Measurement of
the subarachnoid space by ultrasound in preterm infants. Arch
Dis Child Fetal Neonatal Ed 2002;86:F124F126.
31. Frankel DA, Fessell DP, Wolfson WP. High resolution sono-
graphic determination of the normal dimensions of the intracra-
nial extraaxial compartment in the newborn infant. J Ultra-
sound Med 1998;17:411415.
32. Libicher M, Trger J. US measurement of the subarachnoid
space in infants: normal values. Radiology 1992;184:749751.
33. Schlesinger AE, Munden MM, Hayman LA. Hyperechoic foci in
the thalamic region imaged via the posterior fontanelle: a potential
mimic of thalamic pathology. Pediatr Radiol 1999;29:520523.
34. Dean LM, Taylor GA. The intracranial venous system in infants:
normal and abnormal findings on duplex and color Doppler
sonography. AJR Am J Roentgenol 1995;164:151156.
35. Horgan JG, Rumack CM, Hay T, et al. Absolute intracranial
blood-flow velocities evaluated by duplex Doppler sonography
in asymptomatic preterm and term neonates. AJR Am J
Roentgenol 1989;152:10591064.
36. Mitchell DG, Merton DA, Mirsky PJ, et al. Circle of Willis in
newborns: color Doppler imaging of 53 healthy full-term
infants. Radiology 1989;172:201205.
37. Taylor GA. Intracranial venous system in the newborn: evalua-
tion of normal anatomy and flow characteristics with color
Doppler US. Radiology 1992;183:449452.
38. Seibert JJ, Avva R, Hronas TN, et al. Use of power Doppler in
pediatric neurosonography: a pictorial essay. Radiographics
1998;18:879890.
39. Bezinque SL, Slovis TL, Touchette AS, et al. Characterization of
superior sagittal sinus blood flow velocity using color flow Doppler
in neonates and infants. Pediatr Radiol 1995;25:175179.
40. Winkler P, Helmke K. Duplex-scanning of the deep venous
drainage in the evaluation of blood flow velocity of the cerebral
vascular system in infants. Pediatr Radiol 1989;19:7990.
41. Wong WS, Tsuruda JS, Liberman RL, et al. Color Doppler imag-
ing of intracranial vessels in the neonate. AJR Am J Roentgenol
1989;152:10651070.
42. Lupetin AR, Davis DA, Beckman I, et al. Transcranial Doppler
sonography. Part 1. Principles, techniques, and normal appear-
ances. Radiographics 1995;15:179191.
43. Lupetin AR, Davis DA, Beckman I, et al. Transcranial Doppler
sonography. Part 2. Evaluation of intracranial and extracranial
abnormalities and procedural monitoring. Radiographics
1995;15:193209.
44. Seibert JJ, Glasier CM, Leithiser RE, et al. Transcranial Doppler
using standard duplex equipment in children. Ultrasound Q
1990;8:167196.
45. Allison JW, Faddis LA, Kinder DL, et al. Intracranial resistive
index (RI) values in normal term infants during the first day of
life. Pediatr Radiol 2000;30:618620.
46. Deeg KH, Rupprecht TH. Pulsed Doppler sonographic measure-
ment of normal values for the flow velocities in the intracranial
arteries of healthy newborns. Pediatr Radiol 1989;19:7178.
LWBK505-C03_p43-117.qxd 7/7/10 1:24 PM Page 114 Aptara Inc
114 P E D I AT R I C S O N O G R A P H Y
47. Horgan JG, Rumack CM, Hay T, et al. Absolute intracranial
blood-flow velocities evaluated by duplex Doppler sonography
in asymptomatic preterm and term neonates. AJR Am J
Roentgenol 1989;152:10591064.
48. Seibert JJ, McCowan T, Chadduck WM, et al. Duplex pulsed
Doppler US versus intracranial pressure in the neonate: clinical
and experimental studies. Radiology 1989;171:155159.
49. Goh D, Minns RA, Hendry GMA, et al. Cerebrovascular resis-
tive index assessed by duplex Doppler sonography and its rela-
tionship to intracranial pressure in infantile hydrocephalus.
Pediatr Radiol 1992;22:246250.
50. Taylor GA. Effect of scanning pressure on intracranial hemo-
dynamics during transfontanellar duplex US. Radiology 1992;
185:763766.
51. Nishimaki S, Shima H, Yoda H, et al. Blood flow velocities in
the cerebral arteries and descending aorta in small-for-dates
infants. Pediatr Radiol 1993;23:575577.
52. Taylor GA. Regional cerebral blood flow estimates in newborn
lamb using amplitude-mode color Doppler ultrasound. Pediatr
Radiol 1996;26:282286.
53. Volpe JJ. Intracranial hemorrhage: germinal matrixintraven-
tricular hemorrhage of the premature infant. In: Volpe JJ, ed.
Neurology of the newborn. 5th ed. Philadelphia, PA: Saunders,
2008:517588.
54. Ghazi-Birry JS, Brown WR, Moody DM, et al. Human germinal
matrix: venous origin of hemorrhage and vascular characteris-
tics. AJNR Am J Neuroradiol 1997;18:219229.
55. Hambleton G, Wigglesworth JS. Origin of intraventricular
haemorrhage in the preterm infant. Arch Dis Child 1976;51:
651659.
56. Taylor GA. Effect of germinal matrix hemorrhage on terminal
vein position and patency. Pediatr Radiol 1995;25:S37S40.
57. Hill A. Current concepts of hypoxic-ischemic cerebral injury in
the term newborn. Pediatr Neurol 1991;7:317325.
58. Del Toro J, Louis PT, Goddard-Finegold J. Cerebrovascular reg-
ulation and neonatal brain injury. Pediatr Neurol 1991;7:312.
59. Boylan G, Young K, Panerai R, et al. Dynamic cerebral autoreg-
ulation in sick newborn infants. Pediatr Res 2000;48:1217.
60. Funato M, Tamai H, Noma K, et al. Clinical events in associa-
tion with timing of intraventricular hemorrhage in preterm
infants. J Pediatr 1992;121:614619.
61. Taylor GA. New concepts in the pathogenesis or germinal
matrix hemorrhage in premature infants. AJNR Am J Neurora-
diol 1997;18:231232.
62. Perlman JM, Rollins N. Surveillance protocol for the detection
of intracranial abnormalities in premature neonates. Arch Pedi-
atr Adolesc Med 2000;254:822826.
63. Rumack CM, Manco-Johnson ML, Manco-Johnson MJ, et al.
Timing and course of neonatal intracranial hemorrhage using
real-time ultrasound. Radiology 1985;154:101105.
64. Boal DKB, Watterberg KL, Miles S, et al. Optimal cost-effective
timing of cranial ultrasound screening in low-birth-weight
infants. Pediatr Radiol 1995;25:425428.
65. Papile LA, Munsick-Bruno G, Schaefer A. Relationship of cere-
bral intraventricular hemorrhage and early childhood neuro-
logic handicaps. J Pediatr 1983;103:273277.
66. Lemons JA, Bauer CR, Oh W, et al. Very low-birth weight out-
comes of the National Institute of Child Health and Human
Development Neonatal Research Network, January 1995
through December 1996. Pediatrics 2001;107:E1.
67. Herman TE, Siegel MJ. Intracranial hemorrhage in the neonate.
Neuroimaging Clin North Am 1992;2:107117.
68. Bellah RD. Intracranial hemorrhage and ischemia in the prema-
ture infant. In: Bluth EI, Arger PH, Benson CB, et al., eds. Ultra-
sound: a practical approach to clinical problems. 2nd ed. New
York: Thieme Medical Publishers, 2008:439458.
69. Larcos G, Gruenewald SM, Lui K. Neonatal subependymal cysts
detected by sonography: prevalence, sonographic findings, and
clinical significance. AJR Am J Roentgenol 1994;162: 953956.
70. Luisiri A, Sotelo-Avila C, Silberstein MJ, et al. Sonography of
the Zellweger syndrome. J Ultrasound Med 1988;7:169173.
71. Sudakoff GS, Mitchell DG, Stanley C, et al. Frontal periventric-
ular cysts on the first day of life. A one-year clinical follow-up
and its significance. J Ultrasound Med 1991;10:2530.
72. Rypens F, Avni EF, Dussaussois L, et al. Hyperechoic thickened
ependyma: sonographic demonstration and significance in
neonates. Pediatr Radiol 1994;24:550553.
73. Murphy BP, Inder TE, Rooks V, et al. Posthaemorrhagic ven-
tricular dilatation in the premature infant: natural history and
predictors of outcome. Arch Dis Child Fetal Neonatal Ed 2002;
87:F37F41.
74. Gould SJ, Howard S, Hope PL, et al. Periventricular intra-
parenchymal cerebral haemorrhage in preterm infants: the role
of venous infarction. J Pathol 1987;151:197202.
75. Takashima S, Mito T, Ando Y. Pathogenesis of periventricular
white matter hemorrhages in preterm infants. Brain Dev 1986;
8:2530.
76. Hall TR, Choi A, Schellinger D, et al. Isolation of the fourth ven-
tricle causing transtentorial herniation: neurosonographic findings
in premature infants. AJR Am J Roentgenol 1992;159:811815.
77. Rosenfeld DL, Lis E, DeMarco K. Transtentorial herniation of
the fourth ventricle. Pediatr Radiol 1995;25:436439.
78. Volpe JJ. Intracranial hemorrhage: subdural, primary subarach-
noid, intracerebellar, intraventricular (term infant), and miscel-
laneous. In: Volpe JJ, ed. Neurology of the newborn. 5th ed.
Philadelphia, PA: Saunders, 2008:483516.
79. Limperopoulos C, Bension CB, Bassan H, et al. Cerebellar hem-
orrhage in the preterm infant: ultrasonographic findings and
risk factors. Pediatrics 2005;116:717724.
80. Merrill JD, Piecuch RE, Fell SC, et al. A new pattern of cere-
bellar hemorrhages in preterm infants. Pediatrics 1998;102:
E62.
81. Kazam E, Rudelli R, Monte W, et al. Sonographic diagnosis of
cisternal subarachnoid hemorrhage in the premature infant.
AJNR Am J Neuroradiol 1994;15:10091020.
82. Mocharia R, Schexnayder SM, Glasier CM. Fatal cerebral
edema and intracranial hemorrhage associated with hyperna-
tremic dehydration. Pediatr Radiol 1997;27:785787.
83. Huang CC, Shen EY. Tentorial subdural hemorrhage in term
newborns: ultrasonographic diagnosis and clinical correlates.
Pediatr Neurol 1991;7:171.
84. Chen-Yu C, Chou T-Y, Zimmerman RA, et al. Pericerebral fluid
collection: differentiation of enlarged subarachnoid spaces from
subdural collections with color Doppler US. Radiology 1996;
201:389392.
85. Barkovich AJ. Brain and spine injuries in infancy and childhood.
In: Barkovich AJ, ed. Pediatric neuroimaging. Philadelphia, PA:
Lippincott Williams & Wilkins, 2005:190290.
86. Jones BV. Lobar hemorrhage from thrombosis of the vein of
Labbe. Radiology 2003;228:693696.
87. Bulas DI, Taylor GA, ODonnell RM, et al. Intracranial abnor-
malities in infants treated with extracorporeal membrane oxy-
genation: update on sonographic and CT findings. AJNR Am J
Neuroradiol 1996;17:287294.
88. Chao CP, Zaleski CG, Patton AC. Neonatal hypoxic-ischemic
encephalopathy: multimodality imaging findings. Radiographics
2006;26:S169S172.
89. Volpe JJ. Hypoxic-ischemic encephalopathy: neuropathology
and pathogenesis. In: Volpe JJ, ed. Neurology of the newborn.
5th ed. Philadelphia, PA: W.B. Saunders, 2008:347399.
90. Perlman JM. White matter injury in the preterm infant: an
important determination of abnormal neurodevelopment out-
come. Early Hum Dev 1998;53:99120.
91. Bracci R, Buonocore G. Chorioamnionitis: a risk factor for fetal
and neonatal morbidity. Biol Neonate 2003;83:8596.
92. Wu YW, Escobar GJ, Grether JK, et al. Chorioamnionitis and
cerebral palsy in term and near-term infants. JAMA 2003;290:
26772684.
LWBK505-C03_p43-117.qxd 7/7/10 1:24 PM Page 115 Aptara Inc
93. Takashima S, Tanaka K. Development of cerebrovascular archi-
tecture and its relationship to periventricular leukomalacia.
Arch Neurol 1978;35:1116.
94. Sie LTL, van der Knaap MS, van Wezel-Meijler G, et al. Early
MR features of hypoxic-ischemic brain injury in neonates with
periventricular densities on sonograms. AJNR Am J Neurora-
diol 2000;21:852861.
95. Bass WT, Jones MA, White LE, et al. Ultrasonographic differ-
ential diagnosis and neurodevelopmental outcome of cerebral
white mater lesions in premature infants. J Perinatal 1999;19:
330336.
96. Paneth N, Rudelli R, Monte W, et al. White matter necrosis in
very low birth weight infants: neuropathologic and ultrasono-
graphic findings in infants surviving six days or longer. J Pediatr
1990;116:975984.
97. Chamnanvanakij S, Rogers CG, Luppino C, et al. Linear hyper-
echogenicity within the basal ganglia and thalamus of preterm
infants. Pediatr Neurol 2000;23:129133.
98. Soghier LM, Vega M, Aref K, et al. Diffuse basal ganglia or
thalamus hyperechogenicity in preterm infants. J Perinatol
2006;26:230236.
99. Adcock LM, Moore PJ, Schlesinger AE, et al. Correlation of
ultrasound with postmortem neuropathologic studies in
neonates. Pediatr Neurol 1998;19:263271.
100. Kubota T, Okumura A, Hayakawa F, et al. Relation between
the date of cyst formation observable on ultrasonography and
the timing of injury determined by serial electroencephalogra-
phy in preterm infants with periventricular leukomalacia. Brain
Dev 2001;23:390394.
101. Coley BD, Hogan MJ. Cystic periventricular leukomalacia of
the corpus callosum. Pediatr Radiol 1997;27:583585.
102. Inder T, Anderson N, Spencer C, et al. White matter injury in
the premature infant: a comparison between serial cranial
sonographic and MR findings are term. AJNR Am J Neurora-
diol 2003;24:805809.
103. Miller S, Cozzio C, Goldstein R, et al. Comparing the diagno-
sis of white matter injury in premature newborns with serial
MR imaging and transfontanel ultrasonography findings.
AJNR Am J Neuroradiol 2003;24:16611669.
104. Volpe JJ. Hypoxic-ischemic encephalopathy: clinical aspects. In:
Volpe JJ, ed. Neurology of the newborn. 5th ed. Philadelphia,
PA: W.B. Saunders, 2008:400480.
105. Ancel PY, Livinec F, Larroque B, et al. Cerebral palsy among
very preterm children in relation to gestation age and neonatal
ultrasound abnormalities. The EPIPAGE cohort study. Pedi-
atrics 2006;117:828835.
106. De Vries LS, Van Haastert ILK, Rademaker KJ, et al. Ultra-
sound abnormalities preceding cerebral palsy in high-risk
preterm infants. J Pediatr 2004;144:815820.
107. Leijser LM, Liauw L, Veen S, et al. Comparing brain white mat-
ter on sequential cranial ultrasound and MRI in very preterm
infants. Neuroradiology 2008;50:799811.
108. Van Wezel-Meijler G, van der Knaap MS, Oosting J, et al. Pre-
dictive value of neonatal MRI as compared to ultrasound in
premature infants with mild periventricular white matter
changes. Neuropediatrics 1999;30:231238.
109. Mercuri E, He J, Curati WL, et al. Cerebellar infarction and
atrophy in infants and children with a history of premature
birth. Pediatr Radiol 1997;27:139143.
110. Barkovich AJ, Truwit CL. Brain damage from perinatal
asphyxia: correlation of MR findings with gestational age.
AJNR Am J Neuroradiol 1990;11:10871096.
111. Blankenberg FG, Loh N-N, Norbash AM, et al. Impaired cere-
brovascular autoregulation after hypoxic-ischemic injury in
extremely low-birth-weight neonates: detection with power and
pulsed wave Doppler US. Radiology 1997;205:563568.
112. Deeg KH, Rupprecht TH, Zeilinger G. Doppler sonographic
classification of brain edema in infants. Pediatr Radiol 1990;20:
509514.
Chapter 3 B R A I N 115
113. Stark JE, Seibert JJ. Cerebral artery Doppler ultrasonography
for prediction of outcome after perinatal asphyxia. J Ultra-
sound Med 1994;13:595600.
114. Connolly B, Kelehan P, OBrien N, et al. The echogenic thala-
mus in hypoxic ischaemic encephalopathy. Pediatr Radiol
1994;24:268271.
115. Coley BD, Rusin JA, Boue DR. Importance of hypoxic/ischemic
conditions in the development of cerebral lenticulostriate vas-
culopathy. Pediatr Radiol 2000;30:846855.
116. Wang HS, Kuo MF, Chang TC. Sonographic lenticulostriate
vasculopathy in infants: some associations and a hypothesis.
AJNR Am J Neuroradiol 1995;16:97102.
117. Chiu NC, Shen EY, Ho CS. Outcome in children with signifi-
cantly abnormal cerebral blood flow detected by Doppler ultra-
sonography. Focus on the survivors. J Neuroimaging 2003;13:
5356.
118. Barmada MA, Moossy J, Shuman RM. Cerebral infarcts
with arterial occlusion in neonates. Ann Neurol 1979;6:
495502.
119. Rosman NP, Roberts DJ. Respiratory distress and seizure in a
neonate. N Engl J Med 1997;336;14391446.
120. Dogra VS, Shyken JM, Menon PA, et al. Neurosonographic
abnormalities associated with maternal history of cocaine use in
neonates of appropriate size for their gestational age. AJNR Am
J Neuroradiol 1994;15:697702.
121. Heier LA, Carpanzano CR, Mast J, et al. Maternal cocaine
abuse: the spectrum of radiologic abnormalities in the neonatal
CNS. AJNR Am J Neuroradiol 1991;12:951956.
122. Bryant SO, Drose JA, Rubinstein D, et al. Unusual appearance
of a neonatal brain lesion. J Diag Med Sonogr 2000;16:
194197.
123. Steventon DM, John PR. Power Doppler ultrasound appear-
ances of neonatal ischaemic brain injury. Pediatr Radiol
1997;27:147149.
124. Taylor GA. Alterations in regional cerebral blood flow in
neonatal stroke: preliminary findings with color Doppler
sonography. Pediatr Radiol 1994;24:111115.
125. Matsumoto JS, Babcock DS, Brody AS, et al. Right common
carotid artery ligation for extracorporeal membrane oxygena-
tion: cerebral blood flow velocity measurement with Doppler
duplex US. Radiology 1990;175:757760.
126. Mitchell DG, Merton DA, Graziani JL, et al. Right carotid
artery ligation in neonates: classification of collateral flow with
color Doppler imaging. Radiology 1990;175:117123.
127. Taylor GA, Fitz CR, Kapur S, et al. Cerebrovascular accidents
in neonates treated with extracorporeal membrane oxygena-
tion: sonographic-pathologic correlation. AJR Am J Roentgenol
1989;153:355361.
128. Taylor GA, Short BL, Glass P, et al. Cerebral hemodynamics in
infants undergoing extracorporeal membrane oxygenation: fur-
ther observations. Radiology 1988;168:163167.
129. Taylor GA, Walker LK. Intracranial venous system in newborns
treated with extracorporeal membrane oxygenation: Doppler
US evaluation after ligation of the right jugular vein. Radiology
1992;183:453456.
130. Ohene-Frempong K, Winer S, Sleeper L, et al. Cerebrovascular
accidents in sickle cell disease: rates and risk factors. Blood
1998;91:188194.
131. Huttenlocher PR, Moohr JW, Johns I, et al. Cerebral blood flow
in sickle cell cerebrovascular disease. Pediatrics 1984;73:
615621.
132. Moran CJ, Siegel MJ, DeBaun MR. Sickle cell disease: imaging
of cerebrovascular complications. Radiology 1998;206:
311321.
133. Pegelow CH, Wang W, Granger S, et al. Silent infarcts in chil-
dren with sickle cell anemia and abnormal cerebral artery veloc-
ity. Arch Neurol 2001;58:20172021.
134. Adams RJ. TCD in sickle cell disease: an important and useful
test. Pediatr Radiol 2005;35:229234.
LWBK505-C03_p43-117.qxd 7/7/10 1:24 PM Page 116 Aptara Inc
116 P E D I AT R I C S O N O G R A P H Y
135. Pegelow CP, Adams RJ, McKie V, et al. Risk of recurrent stroke
in patients with sickle cell disease treated with erythrocyte
transfusions. J Pediatr 1995;126:896899.
136. Adams R, McKie, Nicholas F, et al. The use of transcranial
ultrasonography to predict stroke in sickle cell disease. N Eng J
Med 1992;42:699704.
137. Adams R, McKie V, Hsu L, et al. Long-term stroke risk in chil-
dren with sickle cell disease screened with Doppler. Ann Neurol
1997;42:699704.
138. Adams R, McKie V, Hsu L, et al. Prevention of a first stroke by
transfusion in children with sickle cell anemia and abnormal
results of transcranial Doppler ultrasonography. N Engl J Med
1998;339:511.
139. Bulas D. Screening children for sickle cell vasculopathy: guide-
lines for transcranial Doppler evaluation. Pediatr Radiol
2005;35:235241.
140. Lee MT, Piomelli S, Granger S, et al. Stroke Prevention Trial in
Sickle Cell Anemia (STOP): extended follow-up and final
results. Blood 2006;108:847852.
141. Malouf AJ, Jamrick-Turner JE, Coherty MC, et al. Implemen-
tation of the STOP protocol for stroke prevention in sickle cell
anemia by using duplex power Doppler imaging. Radiology
2001;219:359356.
142. Neish AS, Blews DE, Simms CA, et al. Screening for stroke in
sickle cell anemia: comparison of transcranial Doppler imaging
and nonimaging US techniques. Radiology 2002;222:709714.
143. Siegel MJ, Luker GD, Glauser TA, et al. Cerebral infarction in
sickle cell anemia: correlation of transcranial Doppler ultra-
sonography versus neurologic examination and MRI. Radiol-
ogy 1995;197:191194.
144. Adams RJ, McKie VC, Brambilla DJ, et al. Stroke Prevention
Trial in Sickle Cell Anemia (STOP) study design. Control
Clin Trials 1997;19:110129.
145. deVeber G, Andrew M, Adams C, et al. Cerebral sinovenous
thrombosis in children. N Engl J Med 2001;345:417423.
146. Van der Knaap MS, Valk J. Classification of congenital abnor-
malities of the CNS. AJR Am J Roentgenol 1988;9:315326.
147. Brunelle F. Arteriovenous malformation of the vein of Galen in
children. Pediatr Radiol 1997;27:501513.
148. Gailloud P, Riordan DP, Burger I, et al. State of the art. Diag-
nosis and management of vein of Galen aneurysmal malforma-
tions. J Perinatol 2005;25:542551.
149. Horowitz MB, Jungreis CA, Quisling RG, et al. Vein of Galen
aneurysms: a review and current perspective. AJNR Am J Neu-
roradiol 1994;15:14861496.
150. Chapman S, Hocklely AD. Calcification of an aneurysm of the
vein of Galen. Pediatr Radiol 1990;19:541542.
151. Tessler FN, Dion J, Vinuela F, et al. Cranial arteriovenous mal-
formations in neonates: color Doppler imaging with angiographic
correlation. AJR Am J Roentgenol 1989;153:1027 1030.
152. Westra SJ, Curran JG, Duckwiler GR, et al. Pediatric intracra-
nial vascular malformations: evaluation of treatment results
with color Doppler US. Radiology 1993;186:775783.
153. Meyers PM, Halbach VD, Barkovich AJ. Anomalies of cerebral
vasculature: diagnostic and endovascular considerations. In:
Barkovich AJ, ed. Pediatric neuroimaging. 4th ed. Philadelphia,
PA: Lippincott Williams & Wilkins, 2005:869918.
154. Herman TE, Siegel MJ. Congenital dural arteriovenous fistula
at torcula herophili. J Perinatol 2007;27:730731.
155. Barkovich AJ. The phakomatoses. In: Barkovich AJ, ed. Pedi-
atric neuroimaging. 4th ed. Philadelphia, PA: Lippincott
Williams & Wilkins, 2005:440505.
156. Baskin HJ. The pathogenesis and imaging of the tuberous scle-
rosis complex. Pediatr Radiol 2008;38:936952.
157. Pont MS, Elster AD. Lesions of skin and brain: modern imag-
ing of the neurocutaneous syndromes. AJR Am J Roentgenol
1992;158:11931203.
158. Barkovich AJ. Congenital malformations of the brain and skull.
In: Barkovich AJ, ed. Pediatric neuroimaging. 4th ed. Philadel-
phia, PA: Lippincott Williams & Wilkins, 2005:291439.
159. McLone DG, Naidich TP. Developmental morphology of the
subarachnoid space, brain vasculature and contiguous struc-
tures, and the cause of the Chiari II malformation. AJNR Am J
Neuroradiol 1992;13:463482.
160. Naidich TP, McLone DG, Fulling, KH. The Chiari II malfor-
mation: part IV. The hindbrain deformity. Neuroradiology
1983;25:170197.
161. Funk KC, Siegel MJ. Sonography of congenital midline brain
malformations. Radiographics 1988;8:1125.
162. Mikulis DJ, Diaz O, Egglin TK, et al. Variance of the position
of the cerebellar tonsils with age: preliminary report. Radiology
1992;183:725772.
163. Coley BD. Ultrasound diagnosis of luckenschadel (lacunar
skull). Pediatr Radiol 2000;30:8284.
164. Barkovich AJ, Kjos BO, Norman D, et al. Revised classification
of posterior fossa cysts and cystlike malformations based on the
results of multiplanar MR imaging. AJNR Am J Neuroradiol
1989;10:977988.
165. Kollias SS, Ball WS Jr, Prenger EC. Cystic malformations of the
posterior fossa: differential diagnosis clarified through embry-
ologic analysis. Radiographics 1993;13:12111231.
166. Nelson MD, Maher K, Gilles FH. A different approach to cysts
of the posterior fossa. Pediatr Radiol 2004;34:720732.
167. Truwit CL, Barkovich AJ. Pathogenesis of intracranial lipoma: an
MRstudyin42patients.AJNRAmJNeuroradiol1990;11:665657.
168. Fisher RM, Cremin BJ. Lipoma of the corpus callosum: diag-
nosis by ultrasound and magnetic resonance. Pediatr Radiol
1988;18:409410.
169. Lin K-L, Wang H-S, Lui T-N. Sonographic diagnosis of a cor-
pus callosum lipoma with extracranial extension in an infant. J
Ultrasound Med 1995;14:537541.
170. Fitz CR. Holoprosencephaly and septo-optic dysplasia. Neu-
roimaging Clin N Am 1994;4:263281.
171. Herman TE, Siegel MJ. Neurosonographic abnormalities in
chromosomal disorders. Pediatr Radiol 1991;21:398401.
172. McGahan JP, Nyberg DA, Mack LA. Sonography of facial fea-
tures of alobar and semilobar holoprosencephaly. AJR Am J
Roentgenol 1990;154:143148.
173. Rubinstein D, Cajade-Law AG, Youngman V, et al. The devel-
opment of the corpus callosum in semilobar and lobar holo-
prosencephaly. Pediatr Radiol 1996;26:839844.
174. Kuban KCK, Teele RL, Wallman J. Septo-optic-dysplasia-
schizencephaly: radiographic and clinical features. Pediatr
Radiol 1989;19:145150.
175. Klucznik RL, Wolpert SM, Anderson ML. Congenital and
developmental abnormalities. In: Wolpert SM, Barnes PD, ed.
MRI in pediatric neuroradiology. St. Louis, MO: Mosby Year
Book, 1992:83120.
176. Broumandi DD, Hayward UM, Benzian JM, et al. Hemimega-
lencephaly. Radiographics 2004;24:843848.
177. Babyn P, Chuang S, Daneman A, et al. Sonographic recognition of
unilateral megalencephaly. J Ultrasound Med 1992;11:563566.
178. Fariello G, Malena S, Lucigrari G, et al. Hemimegalencephaly:
early sonographic pattern. Pediatr Radiol 1993;23:151152.
179. Lam AH, Villanueva AC, de Silva M. Hemimegalencephaly. Cra-
nial sonographic findings. J Ultrasound Med 1992;11:241244.
180. Byrd SE, Naidich TP. Common congenital brain anomalies.
Radiol Clin North Am 1988;26:755772.
181. Herman TE, Siegel MJ. Miller-Dieker syndrome, type 1
lissencephaly. J Perinatol 2008;28:313315.
182. Cioffi V, Bossi MC, Ballarati E, et al. Lissencephaly in two
brothers detected by US. A pseudo-liver pattern. Pediatr
Radiol 1991;21:512514.
183. Pilz DT, Quarrel OWJ. Syndromes with lissencephaly. J Med
Genet 1996;33:319323.
184. Kurtz AB, Johnson PT. Hydranencephaly. Radiology 1999;210:
419422.
185. Doi H, Tatsuno M, Mizushima H, et al. The use of two-dimen-
sional Doppler sonography (color Doppler) in the diagnosis of
hydranencephaly. Childs Nerv Syst 1990;6:456458.
LWBK505-C03_p43-117.qxd 7/7/10 1:24 PM Page 117 Aptara Inc
186. Barkovich AJ. Infections of the central nervous system. In:
Barkovich AJ, ed. Pediatric neuroimaging. Philadelphia, PA:
Lippincott Williams & Wilkins, 2005:801868.
187. Volpe JJ. Viral, protozoan, and related intracranial infections.
In: Volpe JJ, ed. Neurology of the newborn. 5th ed. Philadel-
phia, PA: Saunders; 2008:851915.
188. Ben-Ami T, Yousefzadeh D, Backus M, et al. Lenticulostriate
vasculopathy in infants with infections of the central nervous
system sonographic and Doppler findings. Pediatr Radiol 1990;
20:575579.
189. Hughes P, Weinberger E, Shaw DWW. Linear areas of
echogenicity in the thalami and basal ganglia of neonates: an
expanded association. Radiology 1991;179:103105.
190. Rosenberg HK, Kesslar A. Sonography of neonatal intracranial
infection. In: Sanders RC, Hill MC, eds. Ultrasound quarterly.
New York: Raven Press, 1993:125.
191. Shaw DWW, Cohen WA. Viral infections of the CNS in children:
imaging features. AJNR Am J Neuroradiol 1993;160:125133.
192. Virkola K, Lappalainen M, Valanne L, et al. Radiologic signs in
newborns exposed to primary Toxoplasma infection in utero.
Pediatr Radiol 1997;27:133136.
193. Yamashita Y, Matsuishi T, Murakami Y, et al. Neuroimaging
findings (ultrasonography, CT, MRI) in 3 infants with congeni-
tal rubella syndrome. Pediatr Radiol 1991;21:547549.
194. Gray PH, Tudehope DI, Masel J. Cystic encephalomalacia and
intrauterine herpes simplex virus infection. Pediatr Radiol
1992;22:529532.
195. Ayoubi ME, de Bethmann O, Monset-Couchard M. Lenticulo-
striate echogenic vessels: clinical and sonographic study of 70
neonatal cases. Pediatr Radiol 2003;33:697703.
196. Kriss VM, Kriss TC. Doppler sonographic confirmation of thal-
amic and basal ganglia vasculopathy in three infants with tri-
somy 13. J Ultrasound Med 1996;15:523526.
197. Yikilmaz A, Taylor GA. Sonographic findings in bacterial
meningitis in neonates and young infants. Pediatr Radiol
2008;38:129137.
198. Chen-Yu C, Huang C-C, Chang Y-C, et al. Subdural empyema
in 10 infants: US characteristics and clinical correlates. Radiol-
ogy 1998;207:609617.
199. Babcock DS, Han BK. Sonographic recognition of gyral infarc-
tion in meningitis. AJR Am J Roentgenol 1985;144:833836.
200. Meier A, Chusid MJ, Sty JR. Neonatal Citrobacter meningitis:
neurosonographic observations. J Ultrasound Med 1998;17:
399401.
201. Messerschmidt A, Prayer D, Olischar M, et al. Brain abscesses
after Serratia marcescens infection on a neonatal intensive care
unit: differences on serial imaging. Neuroradiology 2004;46:
148152.
202. Barkovich AJ. Hydrocephalus. In: Barkovich AJ, ed. Pediatric
neuroimaging. Philadelphia, PA: Lippincott Williams &
Wilkins, 2005:659703.
203. Chow PP, Horgan JG, Burns PN, et al. Choroid plexus papil-
loma: detection by real-time and Doppler sonography. AJNR
Am J Neuroradiol 1986;7:168170.
Chapter 3 B R A I N 117
204. Schellhas KP, Siebert RC, Heithoff KB, et al. Congenital
choroid plexus papilloma of the third ventricle: diagnosis with
real-time sonography and MR imaging. AJNR Am J Neurora-
diol 1988;9:797798.
205. Karnaze MG, Shackelford GD, Abramson CL. Atrial ventricu-
lar diverticulum: sonographic diagnosis. AJNR Am J Neurora-
diol 1987;8:721723.
206. Cohen HL, Haller JO, Pollack A. Ultrasound of the septum pel-
lucidum: recognition of evolving fenestrations in the hydro-
cephalic infant. J Ultrasound Med 1990;9:377383.
207. Taylor GA, Madsen JR. Neonatal hydrocephalus: hemody-
namic response to fontanelle compressioncorrelation with
intracranial pressure and need for shunt placement. Radiology
1996;201:685689.
208. Taylor GA, Phillips MD, Ichord RN, et al. Intracranial compli-
ance in infants: evaluation with Doppler US. Radiology
1994;191:787791.
209. Westra SJ, Lazareff J, Curran JG, et al. Transcranial Doppler
ultrasonography to evaluate need for cerebrospinal fluid
drainage in hydrocephalic children. J Ultrasound Med
1998;17:561569.
210. Winkler P. Colour-coded echographic flow imaging and spectral
analysis of cerebrospinal fluid (CSF) in infants. Part II. CSF-
dynamics. Pediatr Radiol 1992;22:3142.
211. Alvarez LA, Maytal J, Shinnar S. Idiopathic external hydro-
cephalus: natural history and relationship to benign familial
macrocephaly. Pediatrics 1986;77:901907.
212. Babcock DS, Han BK, Dine MS. Sonographic findings in infants
with macrocrania. AJR Am J Roentgenol 1988;150:13591365.
213. Amodio J, Spektor V, Prmanik B, et al. Spontaneous develop-
ment of bilateral subdural hematomas in an infant with benign
infantile hydrocephalus: color Doppler assessment of vessels
traversing extra-axial spaces. Pediatr Radiol 2005;35:1113
1117.
214. Barkovich AJ. Intracranial, orbital and neck masses in children.
In: Barkovich AJ, ed. Pediatric neuroimaging. Philadelphia, PA:
Lippincott Williams & Wilkins, 2005:506658.
215. Buetow PC, Smirniotopoulos JG, Done S. Congenital brain
tumors: a review of 45 cases. AJR Am J Roentgenol 1990;155:
587593.
216. Isaacs H Jr. I. Perinatal brain tumors: a review of 250 cases.
Pediatr Neurol 2002;27:249261.
217. Isaacs H Jr. II. Perinatal brain tumors: a review of 250 cases.
Pediatr Neurol 2002;27:333342.
218. Simanovsky N, Taylor GA. Sonography of brain tumors in
infants and children. Pediatr Radiol 2001;31:392398.
219. Sandow BA, Dory CE, Aguiar MA, et al. Congenital intracra-
nial teratoma. Radiographics 2004;24:11651170.
220. Soboleski D, McCloskey D, Mussari B, et al. Sonography of
normal cranial sutures. AJR Am J Roentgenol 1997;168:
819821.
221. Luker GD, Siegel MJ. Sinus pericranii: sonographic findings.
AJR Am J Roentgenol 1995;165:175176.
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CHAPTER

4 Head and Neck

MARILYN J. SIEGEL

Salivary Glands Malignant Neck Masses Indications for Thyroid Ultrasonography

Technique Inflammatory Neck Masses Congenital Hypothyroidism
Normal Anatomy Thyroid Nodules
Great Vessels
Neoplasms Diffuse Thyroid Disease
Technique
Ranulas
Normal Sonographic Anatomy Parathyroid Glands
Inflammatory Disease
Internal Jugular Vein Thrombosis Normal Development and Anatomy
Sialolithiasis
Arterial Thrombosis and Stenosis Normal Parathyroid Function
Neck Aneurysms and Varices Normal Sonographic Anatomy
Technique Indications for Parathyroid
Thyroid Gland
Normal Gross Anatomy Ultrasonography
Normal Thyroid Development
Normal Sonographic Anatomy Hyperparathyroidism
and Anatomy
Congenital Neck Masses Parathyroid Cysts
Thyroid Function
Cystic Masses
Normal Sonographic Anatomy
Benign Noncystic Neck Masses

igh-resolution ultrasonography plays a role in the the salivary glands and any associated pathology. The

H evaluation of the soft tissue structures of the head and

neck. With this imaging modality, it is possible to
confirm the clinical impression of a neck mass as well as
demonstrate a lesion that is not detectable on physical
examination. Moreover, ultrasonography can provide
valuable information about the tissue characteristics of the
lesion, its anatomic location, and its effect on adjacent
structures (1,2).
This chapter will discuss techniques for imaging the
salivary glands, lateral neck, major vessels, and thyroid
and parathyroid glands and the normal anatomy and
common pathologic lesions in these areas.
SALIVARY GLANDS
The salivary glands are the major sonographic landmarks
in the face and submandibular area. There are three major
groups: the parotid, submandibular, and sublingual glands
(Fig. 4.1).
Technique
The parotid glands are superficial structures and are best
evaluated by high-frequency, 7- or 12-MHz, linear or curvi-
linear array transducers, with or without a stand-off pad
(35). Similar to other organs, images should be acquired in
axial and longitudinal planes. The positioning of the trans-
ducer for evaluation of each specific gland is discussed later
in this chapter. As part of the routine study, the neck should
be scanned to evaluate for lymphadenopathy or other
related disease.
Doppler interrogation should be performed to evaluate
vascularity and the feeding arteries and draining veins of
118
Doppler examination should be performed with color and
spectral techniques using the lowest repetition frequency
and Doppler gain settings that do not cause aliasing.
Normal Anatomy
PAROTID GLAND
The parotid gland, the largest of the salivary glands, is
bounded anteriorly by the ramus of the mandible and mas-
seter muscle and posteriorly by the mastoid process and
sternocleidomastoid muscle. The gland is subdivided into
superficial (lateral) and deep (medial) lobes, which are sep-
arated on anatomic studies by the facial nerve. The super-
ficial lobe is the larger portion of the parotid, accounting
for approximately 80% of the gland. The deep lobe
accounts for about 20% of the gland. The facial nerve usu-
ally is not seen by sonography. Instead, the retromandibu-
lar vein, which usually courses above the body of the facial
nerve, is used as the sonographic landmark to separate the
superficial and deep lobes (3). The substance of the gland
contains acini that are connected by small ducts. These
smaller ducts drain into the larger duct of Stensen. The
Stensen duct is found along the anterior border of the
parotid gland below the zygoma. It crosses the masseter
muscle and then pierces the muscle to enter the oral cavity.
Branches of the external carotid artery supply the gland
and the retromandibular (posterior facial) vein drains it.
Transverse or axial views of the parotid gland are
obtained by placing the transducer perpendicular and infe-
rior to the earlobe. Longitudinal images are obtained by
placing the transducer parallel and anterior to the ear. The
parotid gland lies anterior to the mandible and inferior to
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Chapter 4 H E A D A N D N E C K 119

Soft palate
Hard palate

Teeth

Parotid gland

Tongue Oropharynx

Parotid gland Epiglottis

Mandible

Esophagus
Sublingual gland Sublingual gland
Submandibular gland
Submandibular gland
Trachea
A B
Diagrams of normal salivary gland anatomy: parotid gland, submandibular gland, and sublingual gland (Courtesy of Anatomical Chart
Fig. 4.1
Company).

the masseter muscle. It has a round or oval shape on trans-
verse scans and an elliptical shape on coronal images (Fig.
4.2). The normal gland is usually homogeneous and hyper-
echoic relative to the adjacent masseter muscle, reflecting
the presence of fatty glandular tissue. However, in very
young children, the echogenicity may be similar to that of
muscle (35). Small lymph nodes are an occasional finding.
These are hypoechoic and oval or longitudinal in shape,
measuring less than 5 to 6 mm in longest diameter, with a
short axis-to-long axis ratio greater than 0.5 (3). A nondi-
lated Stensen duct is usually not visible on sonography.
The retromandibular vein and external carotid artery
are best seen on long-axis views of the gland (Fig. 4.3)
(3,6). The retromandibular vein enters the superficial lobe
of the gland and longitudinally crosses it to merge at the
inferior margin of the gland, where it continues as the
external jugular vein. The external carotid artery follows
the course of the vein, but it runs in a deeper plane, close
to the medial border of the gland. The two vessels can be
distinguished on the basis of their location, flow direction,
and waveform. In the upper third of the gland, branches
of the artery and vein run orthogonally to the longitudi-
nal axis in an orderly fashion (Fig. 4.3C). In the middle
and lower one third of the gland, intraparenchymal ves-
sels appear mostly as dots randomly scattered in the
parenchyma (Fig. 4.3B).

A B
Normal parotid gland anatomy. A: Transverse scan (perpendicular to the earlobe). The parotid gland (arrows) has an ovoid shape and is
Fig. 4.2
slightly hyperechoic to adjacent masseter muscle (M). Open arrows indicate the echogenic mandibular condyle. B: Longitudinal scan
parallel to the earlobe. In this plane, the gland has an elliptical shape (arrows). Note also normal hypoechoic intraparotid lymph nodes (N). The retro-
mandibular vein (V) divides the gland into the superficial lobe anteriorly and deep lobe posteriorly.
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120 P E D I AT R I C S O N O G R A P H Y

A B

Parotid gland, color flow sonography. A: Longitudinal color

Fig. 4.3
Doppler sonogram shows the retromandibular vein (arrow-
heads) coursing through the parenchyma. The superficial (S) lobe is
anterior to the vein and the deep (D) lobe is posterior. B: Longitudinal
color Doppler scan of the lower third of the parotid gland (arrows)
in another patient. The parenchymal vessels appear as random dots.
C: Longitudinal power Doppler sonogram of the upper third of the gland
in another patient shows the external carotid artery (arrows) and multi-
C ple branches running orthogonally to the long axis of the artery.

An accessory parotid gland is seen in up to 20% of
individuals. It lies superficial to the masseter muscle and
anterior to the main parotid gland and drains directly into
the main parotid gland (4).
SUBMANDIBULAR GLAND
The submandibular gland is bordered laterally by the
body of the mandible and superiorly and medially by the
mylohyoid muscle. A small portion of the gland may
course posteriorly to the mylohyoid muscle and lie within
the sublingual space. The gland is drained by the Whar-
ton duct, which courses between the mylohyoid muscle
laterally and hypoglossus muscle medially. The facial
artery and vein run superficially, providing branches to
the parenchyma. The submandibular gland is evaluated
by placing the transducer in a submental position.
The transducer is then angled coronally and sagittally
(Fig. 4.4).

A B
Normal submandibular gland. A: Transverse sonogram. The left submandibular gland (SM) is oval shaped and hyperechoic to the mylo-
Fig. 4.4
hyoid muscle (arrow). The open arrow indicates air in oral cavity. T  tongue. B: Longitudinal image shows the facial artery (arrowheads)
crossing the parenchyma of the submandibular gland (arrows).
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Sublingual gland. Transverse sonogram shows the normal
Fig. 4.5
oval shape of the sublingual gland (arrow) and slightly
increased echogenicity relative to adjacent digastric (DM), geniohyoid
(GH), and genioglossus (GG) muscles. T  tongue.
The submandibular glands are oval or triangular
shaped, homogeneous, and hyperechoic to adjacent mus-
cles (Fig. 4.4A). The facial artery and vein can be seen on
long-axis views (3,6) (Fig. 4.4B). A nondilated Wharton
duct is usually not seen on sonography.
SUBLINGUAL GLANDS
The sublingual glands, the smallest of the major salivary
glands, lie below the floor of the mouth between the
mandible and muscles of the floor of the oral cavity and
anterior to the submandibular glands. The lateral border
of the glands is adjacent to the mandible. The excretory
duct courses along the medial part of the gland. The sub-
lingual glands are imaged with the transducer perpendicu-
lar and parallel to the submental mandible.
The sublingual gland is oval shaped on transverse
images (perpendicular to the mandible) and rectangular
shaped on longitudinal sections parallel to the mandibular
body (3) (Fig. 4.5). Branches of the lingual artery and vein
may be seen within the gland on color Doppler imaging (6).
Neoplasms
Tumors of the parotid gland account for 90% to 95% of
all salivary gland neoplasms in children with the remaining
tumors arising in the submandibular glands (710). Most
salivary gland neoplasms (65% to 70%) are benign and
usually vascular lesions (711).
BENIGN TUMORS
Vascular Neoplasms
Congenital vascular lesions are of two types: hemangiomas
and vascular malformations. Vascular malformations are a
Chapter 4 H E A D A N D N E C K 121
spectrum of lesions that include arteriovenous, venous,
capillary, and lymphatic malformations. Hemangiomas
and lymphatic malformations are the most common vas-
cular lesions in the parotid gland and are discussed next.
The other vascular malformations are more likely to arise
in the head or neck and are discussed in more detail in the
section on neck masses.
Hemangioma
Hemangiomas are congenital vascular masses composed of
thin-walled, endothelial-lined vascular channels. Most
parotid hemangiomas present at birth or within a few
weeks or months of birth as a nontender mass at the angle
of the mandible, occasionally with bluish discoloration of
the overlying skin. They have a characteristic early prolif-
erating phase and a late involuting stage, undergoing spon-
taneous resolution in childhood or adolescence.
Sonography shows an enlarged parotid gland with
hypoechoic tubular areas representing dilated vascular
channels (1215) (Fig. 4.6). Focal areas of increased
echogenicity may be observed secondary to vessel throm-
bosis or calcification. Hemangiomas are hypervascular on
color Doppler imaging. Pulsed Doppler analysis shows a
low-resistance flow pattern, systolic Doppler shift greater
than 2 kHz, and absence of arteriovenous shunting. Most
vascular tumors are treated conservatively since they often
involute in early childhood.
Lymphangioma
Lymphangiomas, also termed cystic hygromas, are con-
genital malformations characterized by dilated lymphatic
channels. Approximately 50% are present at birth and
90% are identified by 1 year of age (8). They present as a
soft, asymptomatic mass in the area of the salivary glands.
Treatment includes surgical resection or debulking, scle-
rotherapy, and interferon injection.
Lymphangiomas are thin-walled, multilocular, predom-
inantly fluid-filled masses with echogenic septations. The
fluid-filled locules may appear echogenic if there is super-
imposed hemorrhage or infection. Smaller lesions are well
marginated, while larger lesions often are infiltrative and
have ill-defined borders. Color flow Doppler imaging
shows flow in the soft tissue septations, but not in the
fluid-filled locules.
First Branchial Cleft Cysts
The term branchial apparatus refers to the embryologic
precursors that develop into the tissues of the neck. Devel-
opmental anomalies of the branchial apparatus include
cysts, fistulas, and sinuses. The most common abnormality
of the branchial apparatus is the branchial cleft cyst. First
brachial cleft cysts account for about 8% of branchial
cleft cysts. They are typically located inferior and posterior
to the tragus (base of the ear), but they may also be in the
parotid gland or at the angle of the mandible. Second
branchial clefts are the most common of the cysts and are
found lower in the neck just below the angle of the
mandible (discussed later). Third and fourth branchial
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122 P E D I AT R I C S O N O G R A P H Y

Fig. 4.6 Parotid hemangioma. Neonate with a nontender mass at the left mandibular angle and bluish discoloration of the overlying skin. A: Long-
axis split-screen view. The left parotid gland (arrows) is enlarged and contains hypoechoic spaces representing dilated vascular chan-
nels. The normal right parotid gland (open arrows) is shown for comparison. B: Color Doppler image of the left parotid gland shows flow within
dilated vascular channels. Normal vascularity is noted in the right parotid gland.

cleft cysts are very rare and found near the hyoid bone or
thyroid gland.
Branchial cleft cysts usually present as painless, fluctu-
ant swelling, but they can be painful if they are infected.
Sonographic findings are typical of a cyst, including well-
defined borders, anechoic contents, posterior sound trans-
mission, and no internal vascularity. On occasion, the
contents are echogenic due to hemorrhage or infection.
hypoechoic echotexture (Fig. 4.7). However, they can
appear heterogeneous and contain anechoic cystic spaces,
secondary to hemorrhage or cystic degeneration, and
hyperechoic foci, corresponding to calcifications (35,7).
Color Doppler imaging shows mild or moderate vascular-
ity, which may have a central, peripheral, or combined dis-
tribution (3,6). Peak systolic velocities are usually below
50 cm/sec (16,17).

Other Benign Neoplasms MALIGNANT NEOPLASMS

Benign epithelial neoplasms of the salivary glands are rel-
atively rare in childhood and usually are pleomorphic
adenomas. Less common tumors include cystadenomas,
Warthin tumors, lymphoepithelial tumors, neurofibro-
mas, and xanthomas (711). Benign tumors occur in
older children and adolescents and present as slowly
growing, hard, painless masses. Treatment is partial or
total parotidectomy.
Pleomorphic adenomas, as well as other benign sali-
vary gland tumors, tend to be round or oval masses with
well-circumscribed, smooth margins and homogeneous,
Malignant lesions comprise 30% to 35% of salivary
gland tumors in children, and the most common malig-
nant tumors are low-grade mucoepidermoid and acinar
cell carcinomas (711). Rhabdomyosarcoma, undifferen-
tiated cancer, adenocarcinoma, malignant mixed tumor,
adenoid cystic cancer, squamous cell cancer, embryoma,
and sialoblastoma are less common. Patients usually
present with a painless, enlarging lump in the salivary
gland. Rapidly growing tumors may be tender or painful
on palpation. Other clinical features include facial nerve
weakness or paralysis, fixation to skin or deep tissues,
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Chapter 4 H E A D A N D N E C K 123

A B
Pleomorphic adenoma. Fifteen-year-old girl with a palpable mass over the area of the left parotid gland. A: Transverse sonogram shows
Fig. 4.7
a 14  18-mm homogeneously hypoechoic mass with smooth, well-defined borders (calipers). B: Color Doppler image shows flow
around the periphery of the tumor.

and lymphadenopathy. Mucoepidermoid carcinoma, ade-
nocarcinoma, and squamous cell carcinoma have the
highest incidence of regional nodal spread. Distant
metastases are uncommon.
At sonography, primary carcinomas tend to have
irregular margins and homogeneous or heterogeneous,
hypoechoic echotexture (Fig. 4.8) (35,7). Regional
lymph node enlargement, encasement of adjacent vessels,
and invasion of surrounding soft tissues are other findings
suggesting malignancy. Color Doppler sonography shows
moderate or marked flow, with single or multiple feeding
vessels entering the tumor and branching irregularly
within it (Fig. 4.8B). Pulsed Doppler imaging can show
high peak systolic velocities exceeding
60 cm/sec (6,16,17). It is important to recognize that
benign neoplasms can have an aggressive appearance and
malignant lesions can have features suggesting a benign
nodule, so that tissue sampling is required for a definitive
diagnosis.
Ranulas
A ranula is a mucus retention cyst that arises from an
obstructed sublingual or minor salivary duct in the floor of
the oral cavity. Causes of obstruction include postinflam-
matory stricture, trauma, or calculus. There are two types
of ranulas: simple and plunging. The more common simple
type is restricted to the sublingual space, usually presenting
as a painless, bluish, intraoral mass beneath the tongue.
The plunging or deep ranula extends beyond the sublingual
space through the mylohyoid muscle. It presents as a pain-
less submandibular or submental neck mass with or with-
out an associated mass in the floor of the mouth.
On sonography, simple ranulas appear as well-defined,
thin-walled lesions above the mylohyoid muscle in the

A B
Acinar cell carcinoma. Twenty-five-year-old woman with a mass at the angle of the mandible. A: Longitudinal sonogram shows a 3 
Fig. 4.8
1.5-cm oval, homogeneous tumor with hypoechoic matrix and well-defined, lobulated borders (calipers). B: Color Doppler sonogram
shows internal vascularity and a feeding artery (arrow). The findings mimic a benign tumor and biopsy is needed for diagnosis.
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124 P E D I AT R I C S O N O G R A P H Y
B tesy of Brian Coley, MD.)
floor of the mouth (Fig. 4.9A). Plunging ranulas may have
more irregular contours, infiltrate soft tissues, and cross
the midline (Fig. 4.9B). Most ranulas demonstrate homo-
geneous, hypoechoic or anechoic contents. The lesions
may have increased echogenicity and a thick wall if they
become infected. The location of this lesion in the floor of
the mouth is a clue to the diagnosis.
Inflammatory Disease
ACUTE INFECTION
Nonsuppurative Viral Inflammation
Inflammatory lesions are the most common cause of
salivary gland enlargement in children (8,18). Affected
patients present with a painful swollen salivary gland. The
inflammation is usually unilateral, but it can be bilateral.
Viral infections are more common than bacterial infec-
tions. Common viruses include cytomegalovirus, Epstein-
Barr virus (infectious mononucleosis), and human immu-
nodeficiency virus (HIV) (8,9). Mumps virus can be a cause
Ranula. A: Simple ranula. Transverse
Fig. 4.9
scan beneath the left mandibular
ramus shows a thin-walled, cystic mass (C) in the
floor of the mouth close to the mandible (MAND).
B: Plunging ranula. Longitudinal image in another
patient shows a hypoechoic mass with well-
defined margins and through-transmission in con-
tinuity with the sublingual gland (*). (Cases cour-
in infants and children who have not been immunized with
the mumps vaccine.
The sonographic findings of acute nonsuppurative
inflammation are an enlarged, heterogeneous gland con-
taining multiple hypoechoic nodules, representing enlarged
intraparotid nodes(35) (Fig. 4.10). The salivary glands
may have increased blood flow on Doppler imaging (Fig.
4.10C) and the nodes may show central hilar flow.
Parotid involvement occurs in up to 30% of children
with HIV infection and is usually bilateral (8,19). Sono-
graphically, the parotid glands are heterogeneous and con-
tain multiple hypoechoic or anechoic areas that are sur-
rounded by thickened septa (4,5,19,20) (Fig. 4.11). The
sonographic pattern reflects the presence of lymphoid infil-
tration and lymphoepithelial cysts (20). Associated cervical
lymphadenopathy is common (4).
Bacterial Infection
Acute bacterial parotitis is rare and is usually seen in
neonates and immunosuppressed children (18,21).
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Chapter 4 H E A D A N D N E C K 125

A B

Acute parotiditis. Transverse (A) and longitudinal (B) image

Fig. 4.10
of a 7-year-old boy with tender swelling at the angle of the
right mandible shows an enlarged parotid gland (arrows) with hypoe-
choic nodules, representing enlarged lymph nodes. V  retromandibu-
lar vein. C: Transverse color Doppler sonography shows increased
C parenchymal vascularity. Open arrow indicates the mandible.

A B
Human immunodeficiency virus infection. Transverse (A) and longitudinal (B) images show an enlarged, heterogeneous parotid gland
Fig. 4.11
(arrows) containing multiple hypoechoic foci. Open arrow indicates the mandible.
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126 P E D I AT R I C S O N O G R A P H Y
Bacterial parotiditis, abscess formation. Transverse sono-
Fig. 4.12
gram shows a hypoechoic mass with internal debris, con-
sistent with abscess formation (A). Also note enlarged intraparotid
lymph nodes (N). Arrows indicates margins of the parotid gland.
Staphylococcus aureus and Streptococcus species are the
common organisms. Abscess formation occurs in bacterial
infections. At sonography, abscesses appear as round of
oval, hypoechoic masses with well-defined walls and
internal septations, debris, or fluid-fluid levels (Fig. 4.12).
Intracavitary gas, appearing as highly echogenic bubbles
with posterior acoustic shadowing and reverberation arti-
facts, may also be seen in the abscess cavity. Enlarged
intraparotid lymph nodes, parenchymal or ductal calculi,
and cervical adenopathy are other findings. Doppler imag-
ing shows hyperemia in the wall of the abscess and in
adjacent soft tissues.
Recurrent parotiditis. Two-year-old boy with 1-year history of recurrent left parotid swelling. Split-screen view of the normal right
Fig. 4.13
parotid gland (RP) and abnormal left parotid gland (LP). The left parotid gland is normal size and slightly heterogeneous with small
hypoechoic areas. Increased blood flow was noted on Doppler imaging (not shown).
RECURRENT AND CHRONIC INFECTION/INFLAMMATION
Recurrent Sialadenitis
Chronic recurrent sialadenitis is characterized by intermit-
tent, unilateral or bilateral swelling of the parotid glands,
which can be accompanied by pain and fever (3,4,2224).
The etiology is usually unknown, but known causes
include drug sensitivity, food intolerance, and cystic fibro-
sis (9). In some cases, it may be due to infection. Bilateral
involvement of the parotid and submandibular glands is
not uncommon in cystic fibrosis (22).
Sonographic features of chronic recurrent, idiopathic
parotitis are a normal-sized or small, heterogeneous
gland (Fig. 4.13). The parenchyma may contain punctate
echogenic foci, hypoechoic areas measuring 2 to 4 mm in
diameter, or a combination of both (15,2224). The punc-
tate densities represent calcifications or mucus within areas
of ductal ectasia (sialectasis) or the actual walls of the
ectatic ducts. The hypoechoic areas represent sialectasis
and/or lymphocytic infiltration. Calculi also can be seen
within the parenchyma of the gland. Cervical lymph nodes
may be enlarged. Normal or increased flow can be
observed on color Doppler sonography. The differential
diagnosis of recurrent infection includes granulomatous
diseases, Sjgren syndrome (see following discussion), HIV
infection, and lymphoma (3).
Granulomatous Disease and Sjgren Syndrome
Autoimmune diseases, such as Sjgren syndrome, and
granulomatous diseases, including sarcoidosis, tuberculo-
sis, and cat-scratch fever, are rare causes of sialadenitis in
children. Sjgren syndrome is a chronic autoimmune dis-
ease characterized by lymphocytic and plasma cell infiltra-
tion, glandular destruction, and ductal dilatation. Clinical
findings include bilateral, nontender parotid swelling and
dry eyes and mouth (35). Granulomatous diseases are
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Sialolithiasis. A, B: Two transverse
Fig. 4.14
scans of the left parotid gland show
an enlarged gland with hypoechoic foci (arrows)
representing dilated ducts and echogenic foci
(arrowheads) representing calculi. Open arrow
indicates the mandible. (Case courtesy of Brian
Coley, MD.) B
characterized pathologically by tissue destruction and
inflammatory changes and clinically by parotid swelling.
Sonographic features of Sjgren syndrome and granulo-
matous sialadenitis are an enlarged or normal-sized gland
with heterogeneous parenchyma containing multiple hypo-
echoic areas (35,15). Increased blood flow may be noted in
both disorders on color Doppler imaging (6). The imaging
findings overlap with those of chronic recurrent idiopathic
sialadenitis.
Sialolithiasis
Approximately 80% to 90% of salivary gland calculi
occur in the submandibular gland, with the remainder
occurring in the parotid gland. Sialolithiasis has been
associated with cystic fibrosis, but it also may be an iso-
lated finding. Most parotid gland calculi are opaque, but
they can be difficult to see on plain radiographs if they are
superimposed on bone. The common symptom is painful
enlargement of the salivary gland. Sonographic findings
include dilated ducts with highly echogenic foci associated
with acoustic shadowing (calculi) (Fig. 4.14).
NECK
Technique
Cervical sonography is performed with the patient in the
supine position and the neck hyperextended by a sponge or
Chapter 4 H E A D A N D N E C K 127
pad placed under the upper back. This optimizes anterior
neck exposure and allows examination of the neck from
the mandible to the thoracic inlet. Images are obtained in
sagittal, transverse, and, if necessary, oblique positions. In
cooperative patients with suspected thyroid or parathyroid
disease, additional scans are obtained with the patient
swallowing during the examination. This maneuver facili-
tates detection of masses in the upper and lower poles of
the thyroid gland.
A high-frequency (7.5- to 12-MHz) real-time trans-
ducer provides optimal spatial resolution. The higher-
megahertz transducers improve resolution of the superfi-
cial tissue layers, but penetration into the deeper soft
tissues is limited. Lower-megahertz transducers provide
deeper penetration of the soft tissues, but resolution of the
superficial soft tissues decreases. Linear or curved array
transducers are preferred to sector scanners because they
provide a wider field of view and facilitate visualization of
structures in the near field. Spectral and color flow
Doppler imaging have a role in evaluating the hemody-
namics of the larger blood vessels and in characterizing the
vascularity of cervical masses.
Normal Gross Anatomy
The neck spans the distance between the mylohyoid mus-
cle superiorly and the first rib inferiorly. The mylohyoid
muscle is the dividing line between the floor of the mouth
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128 P E D I AT R I C S O N O G R A P H Y
and the neck. Structures above the mylohyoid muscle are
in the floor of the mouth and those below the muscle are
in the neck. Traditionally, the neck has been divided by the
sternocleidomastoid muscle into paired anterior and pos-
terior triangles (Fig. 4.15) (2527). Structures anterior to
the sternocleidomastoid muscle lie within the anterior tri-
angle and those behind the muscle lie within the posterior
triangle.
ANTERIOR TRIANGLE
The anterior triangles meet in the midline and are bordered
by the body of the mandible superiorly, the midline of the
neck medially, and the sternocleidomastoid muscle posteri-
orly. Each anterior triangle is divided into suprahyoid and
infrahyoid divisions by the hyoid bone. The suprahyoid
division is further subdivided into submental and sub-
mandibular triangles by the digastric muscle. The submen-
tal triangle is a midline unpaired triangle, bordered by the
anterior belly of the digastric muscle and the hyoid bone.
It contains small lymph nodes and branches of the facial
artery and vein. The submandibular triangle, formed by
the anterior and posterior bellies of the digastric muscles
and the mandibular rami, contains lymph nodes and the
submandibular gland.
The infrahyoid portion of the anterior cervical triangle
contains the cervical part of the trachea, esophagus, thy-
roid and parathyroid glands, vagus nerve, carotid artery,
and internal jugular vein.
POSTERIOR TRIANGLE
The posterior triangle is bordered by the sternocleidomas-
toid muscle anteriorly, the trapezius muscle posteriorly,
the deep cervical fascia superiorly, and the clavicle inferi-
orly. The posterior triangle contains lymph nodes, the
spinal accessory nerve, parts of the subclavian artery and
Triangles of the neck. The sternocleido-
Fig. 4.15
mastoid muscle divides the neck into
anterior and posterior triangles. The hyoid bone sep-
arates each anterior triangle into a suprahyoid and
infrahyoid division (C). The suprahyoid segment is
divided into submandibular triangles (A) and the sub-
mental (B) triangles by the digastric muscle. The pos-
terior triangle (D) is bordered by the sternocleido-
mastoid muscle anteriorly, the trapezius muscle
posteriorly, the deep cervical fascia superiorly, and
the clavicle inferiorly.
vein, and portions of the brachial plexus and phrenic
nerve.
LYMPH NODES
The lymph nodes are divided into two groups: superficial
(e.g., parotid, submandibular, facial, occipital) and deep
(sublingual, retropharyngeal, and lateral cervical). The
nodes of the lateral cervical group can be further subdi-
vided into superficial (external jugular) and deep (inter-
nal jugular, spinal accessory, and transverse cervical)
groups (Fig. 4.16). The superficial group of nodes fol-
lows the course of the external jugular vein, extending
from the base of the skull to its junction with the bra-
chiocephalic vessels. The nodes of the internal jugular
chain follow the course of the internal jugular vein. They
are the largest in the upper neck, and the jugulodigastric
node is the largest node in this chain (28,29) (Fig. 4.16).
The importance of these nodes lies in the fact that they
drain the nasopharynx, oropharynx, tonsils, hypophar-
ynx, and larynx and are the ones most often involved by
disease processes.
Small lymph nodes, 5 mm or less in short-axis diame-
ter, can be seen in the neck of asymptomatic children.
They appear as flattened or oval, hypoechoic structures
with an echogenic linear hilum. The hilum is vascular on
color Doppler imaging (28,29). The length exceeds the
width by 2:1.
Normal Sonographic Anatomy
Constant landmarks seen on all sonograms of the neck are
the strap muscles, anterior wall of the trachea, carotid
sheath, and thyroid gland (Fig. 4.17). The review of the
normal sonographic anatomy of the thyroid and parathy-
roid glands and vessels will be presented in more detail
later in this chapter. The strap muscles (sternohyoid,
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Schematic drawing of the deep lateral
Fig. 4.16
cervical lymph nodes. The deep cervical
nodes include the internal jugular, spinal accessory,
and transverse cervical nodes. The largest node in
the upper portion of the internal jugular chain is the
jugulodigastric node.
sternothyroid, thyrohyoid, and omohyoid muscles) of the
neck are located anterior and lateral to the thyroid gland
and appear hypoechoic compared to the thyroid gland.
The anterior wall of the trachea is readily identified as a
well-defined echogenic band. The posterior cartilaginous
wall is obscured by air in the trachea (Fig. 4.17), but the
cartilaginous cricoid ring laterally may be visualized (30).
In young children, the cricoid cartilage has a homogenous,
hypoechoic texture relative to the adjacent thyroid gland.
Calcifications increase with age and appear as echogenic
foci that may or may not cast an acoustic shadow.
Normal sonographic neck anatomy. Transverse sonogram
Fig. 4.17
at the midlevel of the thyroid gland demonstrates normal
sonographic landmarks: trachea (Tr), thyroid lobes (Th), thyroid isth-
mus (I), strap muscles (S), carotid artery (C), and esophagus (E). The
anterior tracheal wall posterior to the isthmus is strongly echogenic
and casts an acoustic shadow, which obscures the posterior tracheal
wall.
Chapter 4 H E A D A N D N E C K 129
Congenital Neck Masses
Congenital cystic masses (vascular lesions, thyroglossal
duct cysts, branchial cleft cysts, teratomas, dermoids, con-
genital thymic cysts) and lymphadenopathy account for
nearly all benign neck lesions (3133). Primary malignant
tumors in children are usually neuroblastoma, lymphoma,
or rhabdomyosarcoma.
Vascular lesions are of two types: hemangiomas and
vascular malformations. Vascular malformations are fur-
ther classified as arteriovenous, venous, capillary, or lym-
phatic malformations.
Cystic Malformations
LYMPHANGIOMAS
Lymphangiomas, also known as cystic hygromas, are
endothelial-lined, dilated lymphatic spaces separated by
connective tissue stroma. They result from congenital
blockage of lymphatic drainage. About 75% are found in
the neck, characteristically in the posterior triangle. The
remainder are found in the axilla, mediastinum, retroperi-
toneum, bone, and abdominal viscera (4,13,3237).
Cervical lymphangiomas are usually recognized on
physical examination, presenting as an asymptomatic soft
tissue mass, but they may present as a painful mass due to
inflammation or hemorrhage. Approximately 90% are
detected in the first 2 years of life. Large ones may fill one
side of the neck and extend into the mediastinum, produc-
ing esophageal or airway compression. Although usually
discovered in an otherwise healthy infant, they can be
associated with Noonan, Turner, fetal alcohol, Robert, and
trisomy 21, 13, and 18 syndromes. Treatment includes
surgical resection or debulking, sclerotherapy, and inter-
feron injection (13,35).
On sonography, lymphangioma appears a thin-
walled, unilocular or multilocular mass with acoustic
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130 P E D I AT R I C S O N O G R A P H Y

A B
Lymphangioma (cystic hygroma). Longitudinal (A) and transverse (B) scans of a newborn girl with a neck mass show a large, multiloc-
Fig. 4.18
ular mass (arrows). The posterior part of the mass contains echogenic internal contents (*) secondary to hemorrhage.

enhancement (Figs. 4.18 and 4.19). The septa are of HEMANGIOMAS

variable thickness (32,3439). Similar to other cystic
lesions, the echogenicity can increase secondary to hem-
orrhage, infection, or high lipid content. The cyst walls
also become thicker with infection. The margins of
smaller lesions may be well circumscribed, but infiltration
into adjacent soft tissues is common with larger lesions.
On Doppler imaging, the fluid-filled spaces are avascular;
low-velocity arterial or venous flow may be observed in
the septa or soft tissues (Fig. 4.19B). The posterior trian-
gle location, multiseptated appearance, and young
patient age help differentiate lymphangioma from other
cervical lesions.
Hemangiomas are congenital masses composed of vascular
channels lined by proliferating endothelial cells (13,40).
Most are clinically evident before patients are 6 months of
age. They typically present as soft cutaneous or subcuta-
neous masses with bluish discoloration and occasionally
bruits. Hemangiomas elsewhere in the body also may be
noted. Hemangiomas often undergo a period of initial
growth before spontaneously involuting in early childhood.
At sonography, hemangiomas appear as homogeneous
or heterogeneous, hypoechoic or isoechoic masses with
well-defined borders (40,41). Occasionally, they contain
punctate hyperechoic areas, representing phleboliths. The

A B
Lymphangioma. A: Transverse sonogram shows a unilocular cystic lymphangioma (C) with posterior enhancement. B: Color Doppler
Fig. 4.19
image shows flow in the surrounding soft tissues. The cyst (C) is avascular. SCM  sternocleidomastoid.
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Chapter 4 H E A D A N D N E C K 131

A B

C D
Hemangioma, spectrum of sonographic findings. A: Longitudinal sonogram shows a small (1-cm diameter) homogeneous, hypoechoic
Fig. 4.20
mass (arrows) anterior to the carotid sheath. CA  carotid artery; IJ  internal jugular vein. B: Pulsed Doppler image shows arterial
flow. C: Longitudinal sonogram of another patient shows a heterogeneous echogenic mass (calipers, 4-cm longest diameter) in the superficial soft
tissues. D: Longitudinal color Doppler image shows a hypervascular lesion.

echogenicity increases as the channels become smaller and
undergo thrombosis during involution. Hypervascularity,
a high systolic Doppler shift greater than 2 kHz (12), and
feeding arteries and veins can be documented on Doppler
imaging (Fig. 4.20). Arteriovenous shunting is absent.
Vascular Malformations
Vascular malformations include arteriovenous, venous,
capillary, and lymphatic malformations. Arteriovenous
malformations are high-flow anomalies characterized by
an abnormal connection between arteries and veins and
absence of a capillary network. Instead, a network of small
vessels (the nidus) is interposed between the supplying
artery and draining vein (12). Clinical findings include a
pulsatile mass with a bruit or thrill. At sonography, arteri-
ovenous malformations are poorly defined. Doppler imag-
ing shows a mass of vessels with arteriovenous shunting
characterized by low-resistance arterial blood flow, high
diastolic flow (resistive index 0.5), and pulsatile venous
flow (arterialized waveforms in the draining veins) (12). A
surrounding soft tissue mass is absent (Fig. 4.21).
The arteriovenous fistula is a form of arteriovenous
malformation, which has a single communication inter-
posed between a feeding artery and a draining vein. Other
than the number of channels, the features of the arteriove-
nous fistula and malformation are similar.
Venous malformations are slow-flow vascular lesions
characterized by abnormal venous spaces and a normal
arterial component (13,40). Venous malformations may
involve skin, muscle, or both tissues. Most present as
superficial, compressible masses with bluish discoloration
of the overlying skin. On sonography, they are usually
hypoechoic, but they may be isoechoic or hyperechoic to
subcutaneous soft tissues (41). Doppler evaluation
demonstrates either low-resistance monophasic venous
flow or no flow. The absence of flow may reflect throm-
bosis (12).
Capillary malformations (i.e., port wine stain) are
characterized by a collection of small vascular channels in
the dermis. Sonography is usually normal, although
increased thickness of the subcutaneous fat and prominent
venous channels may be seen in some patients.
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132 P E D I AT R I C S O N O G R A P H Y
B Coley, MD.)
THYROGLOSSAL DUCT CYSTS
Thyroglossal duct cysts arise from remnants of the embry-
onic thyroglossal duct that connects the foramen cecum at
the base of the tongue to the thyroid gland. Ductal enlarge-
ment occurs as a result of accumulation of secretions pro-
duced by the epithelial lining.
Approximately 65% are located below the level of the
hyoid bone, 20% are suprahyoid, and 15% are at the level
of the hyoid bone (32,35,36,39,42). Infrahyoid cysts can
be embedded within the strap muscles of the neck. Most
thyroglossal duct cysts present during the first decade of
life as midline or slightly off-midline masses in the anterior
part of the neck. Characteristically, they move with swal-
lowing (43). Treatment is surgical resection because of the
risk of infection and malignancy, most commonly papillary
carcinoma (35,44). The cysts also may contain ectopic thy-
roid tissue anywhere along the course of the duct.
The sonographic appearance of an uncomplicated thy-
roglossal duct cyst is a well-defined, thin-walled, anechoic
mass with acoustic enhancement in a midline or just off-mid-
line position (Fig. 4.22) (32,33,3842,45). The internal
Arteriovenous malformation. A: Trans-
Fig. 4.21
verse sonogram shows multiple hypo-
echoic spaces (calipers). B: Transverse color Doppler
sonogram shows vascular channels without an asso-
ciated soft tissue component. (Case courtesy of Brian
echogenicity increases if the cyst contains highly proteina-
ceous contents, blood, or purulent material. Thick walls and
thin internal septa also can be identified. Suprahyoid cysts are
usually midline in location, while cysts below the hyoid bone
tend to have midline and off-midline components. Extension
into the hyoid bone may occur. Thyroglossal duct cysts are
avascular unless infected (Fig. 4.22C). Infected cysts can show
flow in the wall of the cyst or in surrounding soft tissues.
The midline location of thyroglossal duct cysts helps to
differentiate them from other anterior triangle masses.
BRANCHIAL CLEFT CYSTS
The branchial network consists of a series of six paired
mesodermal arches that are separated externally by five
ectodermal-lined branchial clefts (grooves) and internally
by five endodermal-lined pouches (35,36,39,46). The first
four arches are visible externally on the surface of the
embryo and give rise to the major structures of the neck.
The fifth and sixth arches give rise to cartilages of the neck.
As the branchial apparatus develops, the first and second
arches grow in a caudal direction, covering the third and
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Chapter 4 H E A D A N D N E C K 133

A B

Thyroglossal duct cyst. A: Suprahyoid cyst. Transverse

Fig. 4.22
sonogram of an 8-year-old girl beneath the chin shows a
midline cystic mass (C) just anterior to the trachea (Tr). B: Subhyoid cyst.
Transverse sonogram of a 15-year-old girl shows an off-midline well-
defined cystic mass (C) anterior to the left lobe of the thyroid gland (Th).
C: Longitudinal color Doppler imaging demonstrates no internal flow,
C typical of a cyst (C).

fourth arches and their clefts, which become recessed in a At sonography, uncomplicated branchial cleft cysts
deep pit, known as the cervical sinus of His. The cervical appear as sharply marginated, thin-walled, hypoechoic or
sinus becomes obliterated during subsequent development. anechoic masses in the lateral neck, anterior to the stern-
Branchial cysts, sinuses, or fistulas develop when there is ocleidomastoid muscle (Fig. 4.23) (32,35,36,38,39). With
failure of obliteration of the cervical sinus or first or second
clefts or pouches. A branchial sinus opens externally to the
skin and a fistula communicates externally to the skin and
internally to the pharynx. A cyst has no internal or external
openings. Approximately 90% of all branchial abnormali-
ties arise from the second branchial cleft, 8% from the first
branchial cleft, and the remainder from the third branchial
cleft (32,35,36,39,46). Branchial cleft cysts are the most
common of the branchial apparatus abnormalities.
Second branchial cleft cysts are located in the lateral
part of the anterior triangle of the neck, anterior to the
sternocleidomastoid muscle, lateral to the thyroid gland,
and anterolateral to the carotid artery and jugular vein.
Rarely, they arise posterior to the sternocleidomastoid
muscles or in the parapharyngeal spaces. First branchial
cleft cysts are located in or around the parotid gland (see
previous discussion). Second branchial cleft cysts typically
present as nontender masses in the upper neck and are usu-
ally found in patients between 10 and 40 years of age.
These cysts do not communicate with either the skin or the Branchial cleft cyst. Longitudinal sonogram of a girl with a
pharynx and hence do not drain. Infected cysts may be ten- Fig. 4.23
painless, left-sided, lateral neck mass shows a thin-walled,
der and painful. They may be bilateral. anechoic mass (calipers) anterior to the common carotid artery (CA).
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134 P E D I AT R I C S O N O G R A P H Y
A B
Infected branchial cleft cyst. Eighteen-year-old female with swelling of the left lateral neck. A: Longitudinal scan shows a cystic mass
Fig. 4.24
(C) with internal echoes, lying anterior to the carotid artery (CA). B: Transverse color Doppler image shows flow in vessels with no flow
in the cyst (C), which is lateral to the vessels, typical of this anomaly.
infection, the wall of the cyst may become irregular and
thick, and the echogenicity of the fluid increases (Fig.
4.24). Cholesterol crystals are another cause of internal
debris and increased echogenicity. Branchial cleft cysts are
avascular unless infected. Infected cysts can show flow in
the wall of the cyst or in surrounding soft tissues. Occa-
sionally, sonography can show branchial cleft sinuses and
fistulas (Fig. 4.25), although these are evaluated better by
contrast fistulograms.
The upper lateral neck position helps differentiate
branchial cleft cysts from other anterior triangle lesions.
Branchial cleft cysts with complex echotexture secondary
to debris can mimic lymphadenopathy. Lymph nodes tend
to have an echogenic center, whereas cysts do not.
TERATOMAS AND DERMOID CYSTS
A teratoma is a congenital lesion arising from pluripoten-
tial germ cells (47). Up to 90% contain tissue from all three
Branchial cleft sinus. Longitudinal scan of the left neck
Fig. 4.25
shows an anechoic tract (arrows) extending toward the
skin surface.
embryonic germ layers (ectoderm, mesoderm, endoderm).
The remainder contains a single germ layer that shows his-
tologically divergent differentiation (48). The dermoid cyst
is a unilocular sac lined only by mature ectodermal tissue
(i.e., skin), with hair follicles, sweat glands, and sebaceous
glands (47).
Cervical teratomas are usually large bulky masses that
are clearly recognizable at birth. Large lesions may cause
stridor, dyspnea, or dysphagia. Maternal polyhydramnios
has been reported in about 20% of affected neonates
(9,47,48). Most teratomas arise in the anterior suprahy-
oid neck. They may be midline or off midline in location
and adjacent to or within a thyroid lobe. At sonography,
they appear as heterogeneous masses with cystic compo-
nents representing sebum or fluid and echogenic foci rep-
resenting fat, calcification, or soft tissue (38,47,48) (Fig.
4.26). They are relatively avascular on Doppler imaging.
Their upper anterior neck location and complex
echogenicity help to differentiate them from other cervical
lesions.
Dermoid cysts are slowly expanding and usually pres-
ent as a small midline neck mass. At sonography, the cysts
appear as well-defined, homogeneous, echogenic masses
that are isoechoic or hypoechoic to adjacent soft tissues.
The internal echogenicity reflects the presence of kerati-
nous or sebaceous debris (Fig. 4.27). Calcifications can be
present in the wall.
CERVICAL THYMIC CYSTS
As the thymus descends from the neck into the mediastinum,
it maintains a connection to the third branchial pouch. This
connection, termed the thymopharyngeal duct, usually
involutes during embryonic life. Cervical thymic cysts
develop from vestiges of the thymopharyngeal ducts or from
areas of cystic degeneration of the thymus gland. About two
thirds of cysts are diagnosed in the first decade of life, with
the remaining cases being diagnosed in the second and third
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Chapter 4 H E A D A N D N E C K 135

A B

Teratoma. Newborn male with a cervical mass seen on a

Fig. 4.26
fetal sonogram. Transverse midline scan (A) and longitu-
dinal scan (B) show a heterogeneous mass (white arrows) with multi-
ple anechoic areas. A hyperechoic area with acoustic shadowing
(open arrow), representing calcification, is seen on the transverse
view. SP  spine. C: Transverse midline color Doppler sonogram
C demonstrates an avascular mass.

A B
Dermoid cyst. Seven-year-old girl with a midline mass. Transverse (A) and longitudinal midline (B) scans show a midline mass (arrows)
Fig. 4.27
with internal echoes and well-defined, smooth borders. The mass is separate from the thyroid gland (Th) and anterior to the trachea
(Tr). Color Doppler sonogram (not shown) demonstrated absence of internal vascularity, confirming the cystic nature of the mass. Pathologic exam-
ination demonstrated keratinous debris.
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136 P E D I AT R I C S O N O G R A P H Y

Thymic cyst. Fifteen-year-old boy with a lateral

Fig. 4.28
neck mass. A: Transverse mage shows a cystic
mass (C), which was just below the right lobe of the thyroid
gland (TY). B: Longitudinal extended field-of-view sonogram of
the lateral neck in another patient shows a well-circumscribed
cystic mass (C) arising from the superior mediastinum (M) and
extending into the base of the neck. (Case courtesy of Brian
B Coley, MD.)

decades. Most present as slowly enlarging, nontender masses

in the lower third of the lateral neck (9,49), although they
can occur anywhere in the neck from the angle of the
mandible to the sternum. The cysts occur more often on the
left than the right side.
The thymic cyst is a well-marginated, unilocular or
multilocular, hypoechoic mass (Fig. 4.28). The echogenic-
ity increases if the contents contain blood or protein. Most
thymic cysts are located anterior to the sternocleidomas-
toid muscle, but they can extend posterior to it. There is an
intimate association with the carotid sheath, with lesions
often splaying the carotid artery and jugular vein (35).
Approximately 50% extend into the mediastinum (9,49).
The close association with the carotid sheath or mediasti-
nal extension should suggest the diagnosis of thymic cyst.

DUPLICATION CYSTS
Esophageal duplication or bronchogenic cysts can occasion-
ally be found in the lower neck. Bronchogenic cysts may com-
press the trachea, causing stridor (9). The sonographic
appearance is similar to that of cysts elsewhere in the body (i.e.,
a thin-walled, anechoic or hypoechoic mass). Internal debris,
fluid-fluid level, and thick walls can be seen if the cystic con-
tents are hemorrhagic, proteinaceous, or purulent (Fig. 4.29).
Ectopic bronchogenic cyst. Two-year-old girl with a
Fig. 4.29
midline mass in the lower neck. Transverse midline sono-
gram just above the sternoclavicular notch shows a well-defined
cystic mass (M) with internal debris secondary to proteinaceous
contents.
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Chapter 4 H E A D A N D N E C K 137

A B

Ectopic thymus. Neonate with a palpable left-sided neck mass at

Fig. 4.30
birth. A: Transverse view of the left neck shows a mass (M) rep-
resenting the thymus, medial to the carotid artery (C), internal jugular vein (J),
and sternocleidomastoid muscle (SCM). The thin echogenic linear densities
are typical of normal thymus. B: On a longitudinal image, the thymic tissue (T)
lies anterior to the carotid artery (C). C: Longitudinal color Doppler image
shows internal vascularity. The mass had no connection with the mediastinal
thymus. Histologic examination of the resected mass demonstrated ectopic
C hyperplastic cervical thymus.

Benign Noncystic Neck Masses
ECTOPIC THYMUS
Failure of complete descent of the embryonic thymus can
result in an ectopic thymus. The ectopic thymus presents as
a midline or lateral neck mass (4951) and is slightly more
common on the right than the left. Most patients are
asymptomatic, although hoarseness, dysphagia, and stri-
dor can occur (50). At sonography, ectopic thymic tissue is
isoechoic or hypoechoic to muscle, has linear echogenic
foci characteristic of normal thymus, and shows mild to
moderate vascularity (Fig. 4.30) (5052). It usually extends
anteromedial to the carotid sheath and has no connection
with mediastinal thymic tissue.
CERVICAL EXTENSION OF NORMAL THYMUS
The normal mediastinal thymus can intermittently herniate
into the neck. The thymic tissue lies above the level of the
left brachiocephalic vein and presents as a lateral or mid-
line neck mass. Sonographic features of the herniated
mediastinal thymus are an echogenicity similar to that of
the normal mediastinal thymus and anatomic continuity
with the mediastinal thymus (Fig. 4.31).
FIBROMATOSIS COLLI
Fibromatosis colli is a benign lesion resulting from con-
tracture of the sternocleidomastoid muscle, causing the
head to tilt to the ipsilateral side and the chin to rotate to
the opposite side (43). Patients present shortly after birth
with torticollis and a painless, firm mass, which is most
commonly on the right side (75% of cases). A history of a
traumatic breech or forceps delivery is frequent. The lesion
frequently regresses over 4 to 8 months with conservative
therapy.
Sonography shows fusiform enlargement of the stern-
ocleidomastoid muscle (Fig. 4.32) (5355). The echogenic-
ity is usually isoechoic or hypoechoic to normal muscle.
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138 P E D I AT R I C S O N O G R A P H Y
Herniated mediastinal thymus. Longitudinal scan just
Fig. 4.31
below the level of the thyroid gland shows thymus (T)
extending from the superior mediastinum (M) into the lower neck ante-
rior to the carotid artery (CA). Again, note the thin echogenic linear foci
typical of normal thymus.
Occasionally, bright punctate foci with acoustic shadow-
ing, representing calcifications, may be noted.
AGGRESSIVE FIBROMATOSIS
Fibromatosis is a histologically benign, but locally aggres-
sive lesion characterized by fibrous tissue proliferation, an
invasive growth pattern, and a tendency to recur locally
after surgical excision, but no tendency for distant spread
(9,32,56). It usually occurs after puberty, but it has been
reported in infants and children. Patients present with a
firm neck mass. At sonography, it appears as a poorly
A B
Fibromatosis colli. Two-week-old boy with torticollis. A: Longitudinal scan of the left side of the neck demonstrates fusiform enlarge-
Fig. 4.32
ment (arrows) of the sternocleidomastoid muscle (SCM). The echogenicity of the enlarged muscle is normal. B: Split-screen image in
another patient shows a normal right (RT) sternocleidomastoid muscle and a diffusely enlarged left (LT) sternocleidomastoid muscle (arrows).
circumscribed, isoechoic or hypoechoic mass with minimal
to moderate Doppler flow (12). The tumor matrix may be
homogeneous or heterogeneous, containing areas of tumor
necrosis or calcification.
Malignant Neck Masses
Hodgkin and non-Hodgkin lymphomas account for
about 50% to 60% of pediatric neck malignancies
(3133,57). Rhabdomyosarcoma accounts for 10% to
15% of cervical tumors. The remaining malignancies
include neuroblastoma, other sarcomas (fibrosarcoma,
neurofibrosarcoma), and Langerhans cell histiocytosis.
Squamous cell carcinoma is a rare head and neck tumor
in children.
LYMPHOMA
Lymphoma is the third most common malignant tumor
in children. Cervical involvement is more common in
Hodgkin than in non-Hodgkin lymphoma. Affected chil-
dren present with painless, enlarged cervical adenopathy
(5860). The lymph nodes in the upper neck, especially
the internal jugular and spinal accessory nodes, are more
frequently involved than those in the lower neck. Extran-
odal involvement in the head and neck region is unusual
in Hodgkin disease but frequent in non-Hodgkin lym-
phoma. Both tumors occur most commonly in the second
decade of life.
Involved lymph nodes may be discretely enlarged or
appear as a conglomerate soft tissue mass (Fig. 4.33). Lym-
phomatous nodes are typically hypoechoic to muscle and
homogeneous, and they may have a round rather than oval
shape. Bilateral involvement is common. Doppler imaging
can show central and/or peripheral flow (61). The sono-
graphic appearance can be similar to that of inflammatory
adenopathy, and correlation with clinical findings and/or
tissue sampling is required for diagnosis.
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Chapter 4 H E A D A N D N E C K 139

A B

Lymphoma. Nineteen-year-old girl with a palpable left

Fig. 4.33
neck mass. Transverse (A) and longitudinal (B) sonograms
show enlarged hypoechoic lymph nodes (N) without echogenic cen-
tral hila. Th  right lobe of thyroid gland. C: Transverse color Doppler
C image of the node in panel A shows peripheral flow.

NEUROGENIC TUMORS
Neuroblastomas and neurofibromas are the most common
neurogenic tumors in the neck. Ganglioneuromas and
schwannomas can occur, but are less common. Approxi-
mately 5% of all neuroblastomas arise in the neck (6264).
Neuroblastomas are usually found in children younger
than 5 years of age. Affected children typically present with
a painless, firm, lateral neck mass. Other presenting find-
ings include airway obstruction, dysphagia, hoarseness,
Horner syndrome (ptosis, myosis, and anhidrosis), and
paralysis of the lower cranial nerves. Neurofibromas are
more common in the second decade of life in the pediatric
population.
At sonography, neuroblastoma appears as an elliptical or
round, echogenic mass in a paraspinal location (Fig. 4.34)
(65). It may be isoechoic or hyperechoic to adjacent muscle
and the echotexture may be homogeneous or heterogeneous.
Scattered hyperechoic foci, representing calcifications, are Neuroblastoma. Longitudinal view of the right side of the
common. Mild to moderate vascularity can be noted on Fig. 4.34
neck demonstrates a large soft tissue mass (arrowheads)
Doppler imaging. Other findings include soft tissue infiltra- adjacent to the cervical spine (SP). The mass invades the canal
tion and vascular encasement. Because of their origin from (arrow). Hyperechoic foci represent calcifications.
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140 P E D I AT R I C S O N O G R A P H Y
Cervical rhabdomyosarcoma. Longitudinal sonogram of
Fig. 4.35
the left side of the neck shows a large, heterogeneous
mass (arrows). The appearance is nonspecific and similar to that of
other malignant masses.
neural tissue, neuroblastomas have a tendency to invade the
spinal canal. Recognition of intraspinal extension is impor-
tant because such involvement necessitates a laminectomy or
radiation therapy prior to tumor debulking. The paraspinal
location of neuroblastoma is a clue to the diagnosis.
Nerve root tumors, such as neurofibroma, have an
appearance similar to that of neuroblastoma. Differenti-
ating among the various neural tumors requires tissue
sampling.
RHABDOMYOSARCOMA
Rhabdomyosarcoma is the most common soft tissue
sarcoma of childhood and 35% to 40% of all rhab-
A B
Metastatic rhabdomyosarcoma. A: Longitudinal view of the neck in a child with a primary intracranial rhabdomyosarcoma shows an
Fig. 4.36
enlarged, round, homogenous, hypoechoic lymph node (N) anterior to the carotid sheath (arrows). Note the absence of a central
echogenic hilum. B: Color Doppler image shows flow in the periphery of the node (N).
domyosarcomas arise in the head and neck (66,67).
Common sites of origin are the orbits and nasopharynx,
each accounting for 25% of tumors, with the paranasal
sinuses, ear, neck, and parotid gland each accounting for
about 10% (67). The embryonal form is the predominant
histologic subtype in the head and neck. Most patients
are under 10 years of age at diagnosis and present with
an enlarging painless mass. A smaller subset of patients
present in adolescence. Common sites of metastases
are lung, bone, bone marrow, lymph node, brain, and
liver.
The sonographic appearance of rhabdomyosarcoma is
similar to that of neuroblastoma. The tumor is usually
hypoechoic or isoechoic to normal muscle and the archi-
tecture may be homogeneous or heterogeneous (Fig. 4.35).
Other findings include parenchymal calcification, soft tissue
infiltration, vessel encasement, and regional lymph node
enlargement (68). Central or peripheral flow can be seen on
Doppler interrogation (1).
Fibrosarcoma, malignant fibrous histiocytoma,
myosarcoma, neurofibrosarcoma, and angiosarcoma are
less common malignant tumors (67). They have an appear-
ance similar to that of rhabdomyosarcoma and a specific
diagnosis usually requires histologic evaluation.
METASTASES
Metastatic nodal disease in children is usually from rhab-
domyosarcoma and less frequently from thyroid carci-
noma and neuroblastoma. Approximately one third of
patients with head and neck rhabdomyosarcoma have
regional lymph node metastases. The sonographic findings
of malignant nodes include a round shape, hypoechoic
echotexture, absent or eccentric hilum, and irregular mar-
gins (Fig. 4.36). The matrix can be homogeneous or het-
erogeneous. Nodal metastases from papillary thyroid
carcinoma may contain scattered calcifications. Color
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Chapter 4 H E A D A N D N E C K 141

A B

Inflammatory lymphadenitis. Longitudinal (A) and trans-

Fig. 4.37
verse (B) sonograms show multiple, enlarged nodes
(arrows) measuring 3.0 cm in long axis and 1.5 cm in short diameter. The
nodes are hypoechoic relative to surrounding tissues. Central (hilar)
areas of the nodes are echogenic. C: Transverse color Doppler image
C shows central vascularity.

Doppler imaging often shows peripheral flow (Fig. 4.36B).
Central or hilar flow is absent or minimal.
Inflammatory Neck Masses
The common inflammatory masses of the neck are lym-
phadenopathy and abscess. Occasionally, an infected
congenital lesion, such as a branchial cleft cyst, presents
as an inflammatory mass. Sonography usually suffices
for evaluation of lymph nodes in the anterior, lateral,
and posterior neck. Computed tomography (CT) is
the study of choice for evaluation of retropharyngeal
disease (72).
CERVICAL ADENITIS AND ABSCESS
Cervical adenitis is a common pediatric problem and is usu-
ally caused by viral (commonly adenovirus and enterovirus)
or bacterial infections (commonly Staphylococcus aureus or
group A Streptococcus) (69,70). Sources of infection include
upper respiratory tract infections, tonsillar and pharyngeal
infections, and recent dental work (71). These conditions
drain predominantly to the submandibular and deep cervi-
cal (jugular chain) nodes. Submental, posterior cervical, and
preauricular nodes comprise most of the other sites of
involvement. Enlarged cervical nodes present as painful
masses.
Sonography of infectious adenopathy shows a well-
defined, oval structure with a hypoechoic echotexture and
linear hyperechoic hilum, which is vascular on Doppler
imaging (12,61,73) (Fig. 4.37C). The long axis to short axis
ratio of 2:1 is often maintained (72,73).
The major complication of cervical adenitis is abscess
formation. Differentiation of the two conditions is impor-
tant because adenopathy is treated medically and abscess
requires surgical or percutaneous drainage. The sono-
graphic findings of abscess are a hypoechoic mass with
variable wall thickness and through-transmission. The cen-
tral hilar stripe is absent. Internal echoes, representing
purulent material and debris, and septations are common
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142 P E D I AT R I C S O N O G R A P H Y

A B

Cervical abscess. One-year-old boy with a tender left-sided

Fig. 4.38
neck mass. Transverse (A) and longitudinal (B) sonograms
show a hypoechoic mass (arrows) with internal debris and well-defined
walls. The central hilar stripe is absent. C: Color Doppler image shows
peripheral flow. Central flow is absent. Cultures from percutaneous
C aspirate grew Staphylococcus aureus.

(Fig. 4.38). Intensely echogenic foci with dirty shadowing

are highly suggestive of air. Color Doppler imaging shows
peripheral flow (Fig. 4.38B). Flow is not demonstrable
within the central cavity.

MYCOBACTERIUM INFECTION
Tuberculosis and atypical mycobacterial infection should
be included in the differential diagnosis of patients with
cervical nodal enlargement. Patients with mycobacterial
infections may have few constitutional symptoms, and the
nodes are often firm, nontender, and matted together. The
sonographic findings include discretely enlarged nodes or a
conglomerate nodal mass with hypoechoic echotexture,
calcifications, and inflammatory changes in the cutaneous
and subcutaneous tissues (Fig. 4.39). Color Doppler
sonography can show central, peripheral, or combined
flow (61). Differentiation from other inflammatory adenitis
requires tissue sampling.

ACQUIRED IMMUNODEFICIENCY SYNDROME

Cervical nodal enlargement in combination with parotid
lesions should suggest the possibility of HIV infection (21).
Lymph node enlargement has been correlated with decreas-
ing CD4 lymphocyte counts. Nodal enlargement in patients
with acquired immunodeficiency syndrome (AIDS) also can
be due to non-Hodgkin lymphoma.
Tuberculous adenopathy. Longitudinal sonogram of the
Fig. 4.39
left neck demonstrates a large, hypoechoic node
(calipers) anterior to the jugular vein (J). (Case courtesy of Nathan
Concepcion, MD, Manila, Philippines.)
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OTHER INFLAMMATORY NODAL DISEASES
Other infectious causes of enlarged cervical nodes include
mononucleosis and cat-scratch disease. Noninfectious
causes include sinus histiocytosis with massive lym-
phadenopathy, Kawasaki disease (mucocutaneous lymph
node syndrome), Langerhans histiocytosis, and sarcoido-
sis. In all these diseases, the nodes are enlarged and hypo-
echoic and may have a heterogeneous or homogeneous
matrix, indistinguishable from infectious or neoplastic
causes of lymph node enlargement. Laboratory tests
and/or biopsy are needed for specific diagnosis.
GREAT VESSELS
Technique
The carotid artery and jugular vein are scanned with the
neck extended and the head turned away from the side
being examined. Longitudinal and transverse scans are
obtained with gray-scale and pulsed and color flow Doppler
imaging using light transducer pressure on the neck to avoid
collapsing the vein. A coronal view through the supraclavic-
ular fossa can be useful to assess the lower segment of the
internal jugular vein and medial segment of the subclavian
vein at the point where they join to form the brachio-
cephalic vein.
The common indications for sonography of the internal
jugular vein are evaluation of suspected venous thrombosis
and evaluation of vessel patency for internal jugular or sub-
clavian vein cannulation. A less common indication is diag-
nosis of venous ectasia. The clinical indication for sonography
of the carotid artery is suspected occlusion or stenosis.
Normal Sonographic Anatomy
The common carotid artery and internal jugular vein, lying
within the carotid sheath, are anechoic structures, with the
walls of the carotid artery being more echogenic than those
A B
Normal carotid artery, spectral waveform. A: Internal carotid artery. Pulsed Doppler interrogation shows a low-resistance profile with
Fig. 4.40
broad systolic peaks, gradual diastolic decline, and continuous diastolic flow above the baseline. B: External carotid artery. The exter-
nal carotid waveform has a narrower systolic peak, faster systolic decline, and less end-diastolic flow.
Chapter 4 H E A D A N D N E C K 143
of the jugular vein. In the upper neck, the common carotid
artery and internal jugular vein lie medial and posterior to
the strap muscles. In the lower neck at the level of the thy-
roid gland, the carotid sheath structures lie posterior and
lateral to the thyroid gland and posterior to the sternoclei-
domastoid muscle (Fig. 4.17).
CAROTID ARTERIES
The external carotid artery supplies the high-resistance
vascular bed of the facial muscles and has a sharp rise dur-
ing systole, a sharp systolic peak, rapid systolic decline,
and low end-diastolic flow approaching zero or descending
transiently below the baseline (Fig. 4.40). In adults, flow
indices include peak systolic velocity (PSV) of 57 to 87
cm/sec, end-diastolic volume (EDV) of 11 to 21 cm/sec,
and resistive index (RI) of 0.72 to 0.84 (74).
The internal carotid artery supplies a low-resistance
cerebral circulation with a sharp rise during systole, a
sharp or slightly broad systolic peak, gradual systolic
deceleration into early diastole, and continuous forward
flow throughout diastole (Fig. 4.40) (74,75). In adults, flow
indices include PSV of 62 to 90 cm/sec, EDV of 23 to 37
cm/sec, and RI of 0.54 to 0.66 (74).
The common carotid artery displays components of
both internal and external carotid artery waveforms with a
sharp peak in systole as seen in the external carotid artery
and persistent diastolic flow above the baseline as seen in
the internal carotid artery. In adults, PSV is 78 to 118
cm/sec, EDV is 20 to 32 cm/sec, and RI is 0.72 to 0.84 (74).
Color flow Doppler imaging is useful to demonstrate
the presence and direction of flow and to assess the degree
of stenosis.
INTERNAL JUGULAR VEIN
The internal jugular veins are responsible for return
of venous blood from the brain to the heart. Doppler
sonography shows a pulsatile waveform related to cardiac
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144 P E D I AT R I C S O N O G R A P H Y
Normal jugular vein. Longitudinal Doppler sonogram of the
Fig. 4.41
internal jugular vein with the patient breathing quietly
shows a slightly pulsatile waveform, reflecting cardiac contractions
and respiratory motion.
contractions and intrathoracic pressure changes (Fig. 4.41).
During inspiration, venous flow is increased as a result of
negative intrathoracic pressure, leading to decreased diam-
eter of the jugular vein and a higher-amplitude spectral
waveform (74). During expiration and the Valsalva maneu-
ver, intrathoracic pressure increases, causing decreased
blood return and increased diameter of the jugular vein.
The walls of the vein collapse when moderate transducer
pressure is applied.
Color flow Doppler imaging is useful to demonstrate
the presence and direction of flow and to detect thrombus
(Fig. 4.42).
A B
Color flow Doppler image of the common carotid artery and jugular vein. Longitudinal (A) and transverse (B) images. Flow in the jugu-
Fig. 4.42
lar vein is assigned a blue color, because blood is moving away from the transducer. Flow in the carotid artery is toward the transducer
and is red. Color Doppler sonography helps to assess patency and luminal diameter.
NORMAL VARIANTS
A common normal variant is asymmetry in the size of the
internal jugular veins. It is not unusual for the right inter-
nal jugular vein to be larger than the left, presumably due
to predominance of the right cerebral venous drainage.
Internal Jugular Vein Thrombosis
Thrombosis of the internal jugular vein in childhood pres-
ents as cervical swelling or a palpable mass and is primarily
a complication of an indwelling central venous line (76).
Other predisposing conditions include neck surgery, intra-
venous drug abuse, head and neck neoplasms, mediastinal
tumor, and inflammatory conditions such as cervical lym-
phadenitis, abscess or cellulitis, and bacterial pharyngitis.
The sonographic findings of acute thrombosis include
an enlarged, noncompressible jugular vein with low-level
intraluminal echoes, absent or diminished flow on pulsed
and color Doppler imaging, and collateral vessel formation
(Fig. 4.43). Cardiorespiratory phasicity is absent. On occa-
sion, acute thrombus may be anechoic, mimicking flowing
blood. The lack of compressibility and absent flow on
Doppler examination can establish the correct diagnosis.
Findings of chronic thrombosis are hypoechoic or ane-
choic clot related to red blood cell lysis and collateral ves-
sel formation (Fig. 4.44).
Echogenic thrombus may be seen around the tip of an
indwelling catheter. The catheter is seen as two parallel
echogenic lines surrounding an anechoic lumen.
Complications of jugular vein thrombosis include sup-
purative thrombophlebitis and pulmonary embolism. A
rare cause of jugular thrombophlebitis is Lemierre syn-
drome, caused by Fusobacterium necrophorum, a gram-
negative anaerobic organism that normally inhabits the
oropharynx. The syndrome follows a primary oropharyn-
geal infection and results in a tonsillar or peritonsillar
abscess, jugular venous thrombosis, and septic emboli
(77,78).
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Chapter 4 H E A D A N D N E C K 145

A B

Acute jugular vein thrombosis. Patient with a previous

Fig. 4.43
indwelling catheter. Transverse (A) and longitudinal (B)
images show an enlarged left jugular vein (J) with low-level intraluminal
C echoes. C  carotid artery. C: Color Doppler image shows absent flow.

Arterial Thrombosis and Stenosis

Chronic venous thrombosis. Longitudinal image shows
Fig. 4.44
multiple round and tubular structures, representing collat-
eral vessels. The jugular vein is not identified.
Carotid artery thrombus and stenosis are rare in children
and usually due to trauma. A historical cause is extracor-
poreal membrane oxygenation (ECMO). When this proce-
dure was initially described, perfusion cannulas were
placed in the right jugular vein and in the right common
carotid artery. After the cannulas were removed, the carotid
and jugular vessels were ligated. Currently, ECMO is per-
formed via direct cannulation of the superior vena cava and
aortic arch, so that carotid artery thrombus formation and
stenosis are no longer complications of the procedure.
The sonographic findings of acute arterial thrombosis
are echogenic material filling the lumen and the absence of
flow on pulsed and color flow Doppler imaging. Findings
of chronic occlusion include small vessel size, hypoechoic
intraluminal clot, and collateral vessel formation.
The gray-scale finding of stenosis is vessel narrowing.
Although vessel narrowing may be seen on gray-scale
imaging, the diagnosis of stenosis is best based on Doppler
interrogation. Color Doppler interrogation shows the
stenotic zone and aliasing (i.e., Doppler spectrum with red,
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146 P E D I AT R I C S O N O G R A P H Y
Arterial stenosis. Longitudinal image shows a narrowed,
Fig. 4.45
irregular carotid artery with some aliasing (more than two
colors of the Doppler spectrum).
yellow, green, and blue colors) (Fig. 4.45). Aliasing at the
site of stenosis is also seen on pulsed Doppler imaging and
is a useful sign to locate the area of maximum velocity in
high-grade stenosis. Doppler waveform findings down-
stream from a stenosis include spectral broadening
(blunted systolic peaks) and reversal of flow (Fig. 4.46).
Three measurements are used to assess the degree
of stenosis: PSV, EDV, and the ratio of the peak systolic
velocities in the internal and common carotid arteries (IC/CC
systolic ratio). In vessels with less than 50% stenosis, the
PSV, EDV, and IC/CC ratio are less than 125 cm/sec, less
than 40 cm/sec, and less than 2.0, respectively. With 50% to
69% stenosis, the PSV, EDV, and IC/CC ratio are 125 to 230
cm/sec, 40 to 100 cm/sec, and 2 to 4, respectively. With 70%
stenosis but less than total occlusion, the PSV, EDV, and
IC/CC ratio are greater than 230 cm/sec, greater than
Carotid artery stenosis. Young adult. Pulsed Doppler
Fig. 4.46
waveform of the internal carotid artery shows high peak
systolic velocity flow (271 cm/sec), high end-diastolic velocity
(125 cm/sec), and spectral broadening (blunted, broad systolic peaks).
Luminal narrowing was greater than 70%.
Carotid artery aneurysm. Transverse sonogram of a
Fig. 4.47
15-year-old girl with Takayasu disease demonstrates a
large aneurysm (arrows) of the carotid artery (C). J  jugular vein.
100 cm/sec, and greater than 4, respectively (75). The veloc-
ity at the site of stenosis logarithmically decreases up to a
90% diameter reduction. After 95% diameter reduction, the
velocity rapidly decreases due to the high-flow resistance.
Aneurysms and Varices
Carotid artery aneurysms can result from an arteritis,
including Kawasaki disease, Takayasu disease, and giant cell
arteritis; infection; trauma; or Langerhans histiocytosis.
Sonographic findings include fusiform or saccular dilatation
of a segment of the carotid artery (Fig. 4.47), intraluminal
thrombus, and displacement of surrounding structures.
Jugular vein varices are rare. However, aneurysmal
dilatation has been described in association with cystic
hygroma (Fig. 4.48) (79).
Aneurysmal dilatation of the jugular vein. Nine-month-old
Fig. 4.48
girl with a large cystic hygroma of the right neck. Longitu-
dinal sonogram shows marked dilatation of the jugular vein (calipers).
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Chapter 4 H E A D A N D N E C K 147

THYROID GLAND Thyroid Function

Normal Thyroid Development and Anatomy The thyroid gland secretes two active hormones, T3 (tri-
iodothyronine) and T4 (thyroxine). The production and
The thyroid gland develops in the first trimester as a midline
secretion of T3 and T4 is mediated by thyroid-stimulating
ventral outgrowth from the floor of the embryonic pharynx
hormone (TSH), a glycoprotein hormone secreted by the
near the base of the tongue. As it descends caudally to reach
anterior lobe of the pituitary gland. Pituitary secretion of
its adult position in front of the larynx opposite C57, it
TSH is in turn regulated by thyrotropin-releasing hor-
retains its connection with the base of the tongue via a tubu-
mone (TRH), which is produced by the hypothalamus.
lar stalk, known as the thyroglossal duct. Once the gland
Within the gland, thyroid hormones are stored in thy-
reaches its final position in the neck, the duct usually atro-
roglobulin (TG), a glycoprotein. In the circulation, several
phies and disappears.
carrier proteins transport thyroid hormones. These
The thyroid gland is composed of paired right and left
include thyroid-binding globulin (TBG), thyroid-binding
lobes, one on each side of the trachea. The upper margin
preglobulin, and albumin. Iodine is essential in the pro-
extends to the level of the thyroid cartilage and the body of
duction of thyroid hormone. Deficiencies in TSH, TRH,
the gland is at the level of the cricoid cartilage. The lower
TG, and TBG produce changes in serum levels of the thy-
margin is at the level of the fifth or sixth tracheal rings. An
roid hormone levels. High levels of hormones inhibit TSH
isthmus joins the lobes and crosses the trachea anteriorly.
and TRH secretion and low levels stimulate their secretion
Occasionally, an extra lobe, the pyramidal lobe, extends
(81,82).
superiorly from the isthmus in the midline along the course
of the thyroglossal duct (80,81). The thyroid gland is cov-
ered by a fibrous capsule that is fixed to the deep pretracheal Normal Sonographic Anatomy
fascia, causing it to move upward with deglutition. The The normal thyroid gland is a homogeneous bilobed struc-
gland is bordered posterolaterally by the common carotid ture that is slightly hyperechoic relative to adjacent neck
artery and internal jugular vein and medially by the trachea muscles (4). The isthmus is anterior to the trachea and
on the right and esophagus on the left. Anterolateral to each the pyramidal lobe, when present, extends superiorly
thyroid lobe are the sternocleidomastoid and strap muscles. (Fig. 4.49). Colloid follicles, appearing as small cystic areas
Posterolateral to each lobe is the longus colli muscle. (1 cm in diameter), are commonly seen within the

A B

Normal thyroid gland. A: Transverse sonogram of the thyroid

Fig. 4.49
gland and B: longitudinal sonogram of the right lobe. The
lobes of the thyroid (Th) have a homogeneous echotexture. Note the isth-
mus (calipers) crossing the midline. C  common carotid artery; Arrows
indicate hypoechoic longus colli muscle posterior to the thyroid gland.
C C: Transverse scan in a young adult shows a pyramidal lobe (arrows).
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148 P E D I AT R I C S O N O G R A P H Y
A B
Normal thyroid gland. Transverse (A) and longitudinal (B) scans of the left thyroid lobe demonstrate normal homogeneous echogenic-
Fig. 4.50
ity and small hypoechoic colloid follicles (arrow, panel A; calipers, panel B), which is a normal finding and of no clinical significance.
The echogenicity within the follicles is inspissated colloid.
parenchyma (Fig. 4.50). They may contain echogenic mate-
rial representing inspissated colloid. The longus colli muscle
posterolateral to each lobe appears as a triangular-shaped
hypoechoic structure on transverse scans and as a long, slen-
der hypoechoic structure anterior to the cervical vertebrae
on longitudinal scans (Fig. 4.49).
Small vessels are noted in the parenchyma of the gland
on color Doppler imaging (Fig. 4.51). Occasionally, the
paired superior and inferior thyroid arteries (2 mm
diameter), which supply the gland, can be seen entering the
parenchyma.
The thickness and volumes of the thyroid lobes have
been reported as a function of body height (83,84). There
appears to be no significant correlation with birth weight.
Thyroid volume has also been reported as a function of age
(8587) (Tables 4.1).
Normal thyroid gland. Transverse color flow Doppler
Fig. 4.51
image of the right lobe (arrows) shows small vessels in the
substance of the gland. CA  carotid artery.
Indications for Thyroid Ultrasonography
Sonography is the primary imaging examination in chil-
dren for confirming suspected thyroid lesions and for
differentiating solid and cystic lesions. CT or magnetic
resonance imaging (MRI) is used in patients with malig-
nancy or abscesses to determine regional and distant
metastases.
The common clinical indications for thyroid sonogra-
phy are: congenital hypothyroidism, a suspected thyroid
nodule or mass, and an enlarged gland (goiter). Other indi-
cations include screening of patients with histories of head
and neck radiation; guidance of fine-needle aspiration
biopsy of a nodule; follow-up evaluation of changes in the
size of a nodule or the thyroid gland itself in patients
receiving replacement or suppressive therapy; and detec-
tion of recurrence in patients who have had prior surgery
for treatment of thyroid cancer.
Congenital Hypothyroidism
Congenital hypothyroidism is a relatively common anom-
aly occurring in approximately 1 in every 3000 to 4000
live birth (42). Therefore, screening is important because
mental retardation can be prevented by early treatment.
Congenital hypothyroidism can result from thyroid dys-
genesis (abnormality of structure), dyshormonogenesis
(error in hormone synthesis and secretion), and pituitary/
hypothalamic hypothyroidism.
DYSGENESIS
Thyroid dysgenesis, which refers to a developmental
defect in thyroid morphogenesis, is the most common
cause of neonatal hypothyroidism, accounting for about
85% to 90% of these cases (42). Neonates with thyroid
dysgenesis are usually asymptomatic at birth, because there
is sufficient transplacental passage of thyroid hormone,
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Chapter 4 H E A D A N D N E C K 149

Normal Dimensions of the Thyroid Gland as a Function of Height (Means  SD) from
Table 4.1 Neonates to Adolescence

No. of Subjects
Height (cm) (male:female) Thickness (cm) Width (cm)

4550 42 (20:22) 1.4  0.2 1.7  0.2

5070 42 (27:15) 1.4  0.1 1.8  0.2
7090 8 (6:2) 1.4  0.1 1.9  0.1
90100 8 (3:5) 1.4  0.1 1.8  0.2
100110 34 (12:22) 1.5  0.3 2.1  0.3
110120 35 (20:15) 1.7  0.3 2.3  0.3
120130 45 (23:22) 1.8  0.4 2.4  0.3
130140 36 (21:15) 1.9  0.5 2.7  0.2
140150 42 (20:22) 2.1  0.4 2.8  0.3
150160 59 (25:34) 2.2  0.4 2.8  0.4
160170 16 (14:2) 2.4  0.4 3.0  0.4

With permission from Ueda D, Mitamura R, Suzuki N, et al. Sonographic imaging of the thyroid gland in congenital
hypothyroidism. Pediatr Radiol 1992;22:102105.

and the abnormality is detected on routine neonatal
screening (42). Thyroid hormone levels (T3 and T4) are
decreased and thyroid-stimulating hormone levels are
increased. There are three main forms of dysgenesis:
aplasia, hypoplasia and ectopia. Aplasia is defined as
absence of any thyroid tissue. Thyroid hypoplasia results
in a small gland.
Ectopic thyroid tissue is the most frequent form of
dysgenesis and the most common congenital cause of
hypothyroidism (82). Arrest in descent of the thyroid
anlage results in ectopic thyroid tissue. Ectopic thyroid tis-
sue may be found anywhere along the migration course of
the thyroid primordium from the base of the tongue to the
intrathoracic trachea, but in most cases (90%), the ectopic
gland is located at the base of the tongue (termed the
lingual thyroid). Ectopic tissue can also be found in
the mediastinum, heart, esophagus, and diaphragm
(42,88,89). In approximately 75% of patients, the ectopic
tissue is the only functioning thyroid tissue (42,81). Thy-
roid hormone deficiency and elevation of thyroid-stimulat-
ing hormone are usually less marked in cases of thyroid
ectopia than in aplasia. Occasionally, the ectopic gland is
capable of secreting sufficient quantities of thyroid hor-
mone such that results of routine neonatal screening blood
tests are within normal limits. Such patients may present
later in childhood with signs of hypothyroidism or with
signs of airway compression or a mass at the base of the
tongue or in the upper neck if the hyperstimulated gland
enlarges.
Sonography in thyroid ectopia shows an empty thyroid
fossa. In neonates, the ectopic tissue has normal echotex-
ture and is hyperechoic relative to adjacent tissues and
highly vascular on Doppler sonography (88) (Fig. 4.52). In
older children, it may appear hypoechoic and hypovascu-
lar (89). The lingual thyroid gland is usually located close
to the hyoid bone.
DYSHORMONOGENESIS
Dyshormonogenesis is a less frequent cause of neonatal
hypothyroidism and is defined as an abnormality of one or
more of the enzymes involved in the pathway of thyroid
hormone synthesis and secretion. The enzymatic defect is
often a hereditary trait. The most common defect is thy-
roid peroxidase deficiency, which results in a failure of
oxidation of iodide to iodine. Iodide is trapped but not
organified. Clinical findings of dyshormonogenesis are a
palpable enlarged thyroid gland, the result of increased
levels of thyroid-stimulating hormone. Sonography shows
an enlarged, normally positioned thyroid gland. The isth-
mus is often enlarged and the pyramidal lobe may be
enlarged. The echogenicity is normal (Fig. 4.53).
CENTRAL HYPOTHYROIDISM
In patients with central (pituitary or hypothalamic) defects
in production of TSH or TRH, serum thyroid hormone
levels are low and TSH levels are low or normal (82). The
thyroid gland is small and normally positioned. Other rare
causes of congenital hypothyroidism include end-organ
unresponsiveness to thyrotropin or thyroid hormone and
maternal ingestion of medications.
Thyroid Nodules
Thyroid nodules are rare in children, compared to adults,
and are estimated to occur in 1% to 2% of the pediatric
population (42,9093). Most are benign, although a 30% to
40% incidence of malignancy has been reported (42,9093).
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150 P E D I AT R I C S O N O G R A P H Y

A B
Ectopic lingual thyroid gland. A: Transverse sonogram at the level of the base of the tongue demonstrates homogeneously hyperechoic
Fig. 4.52
thyroid tissue. B: It is highly vascular on Doppler imaging. (Reprinted from Babcock DS. Thyroid disease in the pediatric patient: empha-
sizing imaging with sonography. Pedatr Radiol 2006;36:299308, with permission.)

Most thyroid nodules are detected by palpation of the neck.
Treatment is nodule resection or lobectomy in limited benign
or malignant disease and total or near-total thyroidectomy in
extensive malignant disease.
THYROID ADENOMAS
Adenoma is the most frequent benign neoplasm of the
thyroid gland. Pathologically, adenomas are solitary,
well-encapsulated lesions with a fibrous capsule; they
arise in glands that are otherwise normal. They can
present as slowly growing nodules, sometimes associ-
ated with hyperthyroidism, or they may be found inci-
dentally on imaging examinations performed for other
indications. Sudden enlargement of an adenoma is usu-
ally related to spontaneous hemorrhage within the
lesion.
Most adenomas are hyperechoic or isoechoic relative
to the normal thyroid gland. A thin (1- to 2-mm) hypoe-
choic halo or rim, which may represent the fibrous

A B
Goiter due to congenital error in hormone synthesis. One-year-old boy with enlarged thyroid gland on physical examination. Transverse
Fig. 4.53
(A) and longitudinal (B) images show an enlarged right lobe of the thyroid gland (Th) displacing the jugular vein (JV) and carotid artery
(CA) posteriorly and laterally. The echogenicity is normal.
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Chapter 4 H E A D A N D N E C K 151

A B

C D
Thyroid adenoma. A: Longitudinal image of the right lobe of the thyroid demonstrates an ovoid, nearly homogeneous mass (calipers)
Fig. 4.54
that is hyperechoic to normal thyroid tissue (Th). B: Color Doppler scan shows peripheral and central flow. C: Longitudinal scan in
another patient shows a nearly isoechoic mass with a hypoechoic rim (arrows). D: Color Doppler image shows predominantly peripheral flow.

capsule, compressed thyroid parenchyma, or pericapsu-

lar inflammatory infiltrate, has been described in about
60% of cases. Cystic changes due to hemorrhage or
necrosis and comet-tail artifacts produced by inspissated
colloid may be present (Figs. 4.54 and 4.55) (9497).
Comet-tail artifacts appear as small echogenic foci with
posterior reverberation artifacts (98). Although calcifica-
tion is relatively uncommon, it is usually curvilinear and
peripheral, a pattern referred to as eggshell calcifica-
tion. A vascular rim and in some cases central vascular-
ity may be noted on Doppler imaging (Figs. 4.54B and
4.54D) (99102).

Adenoma with hemorrhagic change. Longitudinal sono-
Fig. 4.55
gram of the left lobe of the thyroid gland demonstrates a
well-circumscribed complex mass (calipers) with cystic areas and
internal debris. Surgical exploration documented a thyroid adenoma
with extensive hemorrhage.
THYROID CYSTS
Colloid Cysts
Colloid cysts are large colloid follicles. They are thought to
be the result of cycles of hyperplasia and involution of thy-
roid follicles. They are predominantly anechoic, are soli-
tary or multiple, and may contain internal echoes or sep-
tations (Fig. 4.56).
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152 P E D I AT R I C S O N O G R A P H Y
A B
Colloid cyst. A: Transverse sonogram shows an anechoic nodule (arrows) with a few internal echoes and posterior septations. B: Lon-
Fig. 4.56
gitudinal sonogram of another patient shows a large anechoic cyst (C) in the upper pole of the thyroid. THY  normal thyroidal tissue.
Differentiation from a true cyst requires tissue sampling.
True Cysts
A true epithelial-lined cyst accounts for about 1% of thy-
roid masses. Sonographically, the true cyst appears as an
anechoic mass with smooth walls and through-sound
transmission. Cystic lesions are avascular on Doppler
imaging. Differentiation between a true cyst and colloid
cyst requires tissue sampling.
Hemorrhagic Cysts
Hemorrhagic cysts are usually the result of bleeding into a fol-
licular adenoma. The hemorrhage may occur spontaneously
or as the result of blunt trauma to the neck. The acute lesion
appears as a hyperechoic or complex mass with internal sep-
tations or debris and irregular walls. Over time, the lesion
becomes hypoechoic and develops a more circumscribed bor-
der. The septations may or may not persist, and a fluid-fluid
level can develop (see Fig. 4.55).
MALIGNANT THYROID NODULES
Thyroid Cancer
Carcinoma of the thyroid gland is rare in children, consti-
tuting 1% to 1.5% of all malignancies before the age of 15
years (42,57,80,82,103). There is a female predominance
and the peak incidence in childhood is between 7 and 18
years (90,103). Patients are usually euthyroid and present
with a palpable thyroid nodule, regional adenopathy, or a
combination of findings. Large tumors can cause hoarse-
ness from pressure on the recurrent laryngeal nerve or air-
way obstruction. There is a higher frequency of advanced
disease, including regional nodal involvement and distant
metastases to lung or bone, in children compared with
adults (42,90,103107).
Papillary thyroid carcinoma is the most common sub-
type of thyroid cancer in children, accounting for 70% to
90% of all thyroid cancers (90,92,103107). It spreads by
direct invasion or nodal metastases. Follicular carcinoma
accounts for 10% to 20% of thyroid malignancies
(90,92,103107). It spreads hematogenously and may
metastasize to lung, bone, or cervical nodes. Medullary car-
cinoma represents 5% to 10% of pediatric thyroid cancers
(57,90). Metastases are to regional lymph nodes, lung, and
bone and occasionally to liver and brain (42,107,108).
Anaplastic carcinomas and sarcomas are extremely rare in
children.
Medullary carcinoma arises from parafollicular cells
or C-cells and secretes the hormone calcitonin. It may
be familial, with an autosomal dominant inheritance
pattern, and it can be associated with multiple endocrine
neoplasia (MEN) type IIa (medullary thyroid carcinoma,
parathyroid hyperplasia, and pheochromocytoma) or IIb
(medullary thyroid carcinoma, mucosal neuromas, and
pheochromocytoma) (108,109). Serum calcitonin is ele-
vated and a marker of disease. There is a high incidence
of bilateral disease (42).
On sonography, thyroid cancers can be hypoechoic,
isoechoic, or hyperechoic relative to normal parenchyma.
Other findings include cystic changes due to necrosis or
hemorrhage; punctate calcifications (psammomatous cal-
cifications), which may or may not demonstrate acoustic
shadowing; irregular or ill-defined margins; and a thick
or irregular hypoechoic rim or halo (Figs. 4.57 to 4.59)
(9497,99102). Calcifications are common in papillary
and medullary cancers. The hypoechoic rim or halo is
usually partial and thicker than the thin 1- to 2-mm halo
surrounding a benign-appearing lesion. Color Doppler
imaging shows increased internal and/or peripheral flow
(Fig. 4.58B).
Nodal metastases secondary to thyroid cancer range in
diameter from 4 mm to 30 mm. The echotexture is similar
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Chapter 4 H E A D A N D N E C K 153

Papillary thyroid cancer. Transverse (A) and longitudi-

Fig. 4.57
nal (B) images show a complex mass (arrows) con-
taining cystic areas from necrosis and punctate echogenic foci
A representing calcifications.

A B

Follicular thyroid cancer. Transverse scan shows a minimally heterogeneous mass (arrows) anterior to the trachea (Tr). B: Color Doppler
Fig. 4.58
image shows scattered internal and peripheral flow (arrows).

Papillary thyroid cancer. Eighteen-year-old male. Longitu-

Fig. 4.59
dinal sonogram of the right lobe of the thyroid shows an
echogenic mass (arrows) with echogenic punctuate calcifications and
poorly defined posterior borders. Punctate calcifications are a strong
sign of malignancy.
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154 P E D I AT R I C S O N O G R A P H Y

Sonographic Features of Benign and Malignant cer (111114). Nuclear fallout exposure also increases the
Table 4.2 Thyroid Nodules incidence of thyroid carcinoma (115,116). Radiation-
related cancers have a high frequency of multicentricity
Feature Pathologic Diagnosis
(55%) and bilaterality (35%) (112).
Size 1.0 cmincreased likelihood of The sonographic findings of thyroid irradiation include
malignancy unilateral parenchymal atrophy, solitary or multiple nod-
Internal matrix
ules, and gland heterogeneity with calcifications (117,118).
Cystic Benign (often adenomatous The nodules are usually hypoechoic to normal thyroid tis-
nodule) sue, but they may be isoechoic with a hypoechoic halo,
Comet-tail artifact Benign cystic, or complex. Although sonography cannot separate
benign and malignant thyroid lesions in patients who have
Echogenicity
undergone radiation, it can be used to identify nonpalpa-
Hypoechoic Benign and malignant
Halo 60%80% benign if smooth
ble nodules, assess changes in the echotexture of the thy-
roid gland, follow the course of parenchymal abnormali-
Margin ties, and direct the site of biopsy (117,118).
Irregular Increased risk of malignancy Papillary cancers have been associated with abnormal-
Calcifications ities on chromosome arm 10q and follicular tumors with
Benign Eggshell, large and coarse abnormalities on chromosome 3. The ras proto-oncogene
Malignant Fine (microcalcifications) and has been associated with follicular and papillary tumors
punctate (psammoma bodies) and the ret proto-oncogene with papillary and medullary
Other Findings cancers.
Lymph nodes Malignant
Internal and/or peripheral flow Benign and malignant lesions
Diffuse Thyroid Disease
Causes of diffuse thyroid enlargement (also known as goi-
Adapted from Babcock DS. Thyroid disease in the pediatric patient: emphasizing
ter) include inflammatory conditions, such as acute suppu-
imaging with sonography. Pedatr Radiol 2006;36:299308.
rative and subacute thyroiditis; autoimmune processes
including chronic lymphocytic (Hashimoto thyroiditis)
to that of the primary tumor. Nodal metastases may show and Graves disease; and multinodular goiter.
calcification, necrosis, or hemorrhage (110).
INFECTIOUS CONDITIONS
Lymphoma Acute Suppurative (Bacterial) Thyroiditis
Thyroid involvement by lymphoma is rare in children and Acute suppurative thyroiditis is usually caused by a bacter-
adolescents. The sonographic findings vary from a solitary, ial infection of the gland. The common inciting organisms
hypoechoic mass to multiple hypoechoic and anechoic are Streptococcus hemolyticus and Staphylococcus pneu-
masses replacing the thyroid gland (81). moniae. A rare cause of infection is a congenital fistula
between the pyriform sinus and the ipsilateral lobe of the
OVERVIEW OF SONOGRAPHIC CRITERIA OF MALIGNANT AND BENIGN NODULES thyroid gland or the perithyroidal space (119121). Con-
An overview of the sonographic criteria of malignant and genital fistulas are more common on the left than on the
benign nodules is given in Table 4.2. The findings that are right side. Children with suppurative thyroiditis are usu-
more suggestive of malignancy are a minimally cystic ally euthryoid and present with painful enlargement of the
lesion, fine punctate calcifications, irregular contours and thyroid gland and fever. Sonographic findings include an
poor margination, and nodal metastases. Findings that are enlarged thyroid gland containing a single or multiple
more indicative of a benign lesion include very extensive hypoechoic or complex masses, representing abscess for-
cystic components (usually seen in adenomas or colloid mation (Fig. 4.60). Abscess and cellulitis also may occur in
cysts), peripheral rim-like calcifications, and comet-tail the perithyroid area (Fig. 4.61). Increased vascularity is
artifacts. However, there is overlap in the sonographic fea- noted on Doppler imaging.
tures of benign and malignant nodules, and definite diag-
nosis requires biopsy. Subacute (De Quervain) Thyroiditis
Subacute thyroiditis is a transient inflammatory disease, usu-
RISK FACTORS FOR THYROID NODULES AND CANCER ally caused by a viral infection (82,122). Histologic exami-
Radiation exposure in childhood is a risk factor for the nation reveals granulomas and epithelioid cells. Patients
development of thyroid disease, including both hypothy- present with fever, painful thyroid enlargement, and labora-
roidism and neoplasia. A latent period of 6 to 40 years fol- tory findings of mild thyrotoxicosis. Serum T3 and T4 levels
lowing irradiation precedes the appearance of the tumors. are elevated; the levels of thyroid-stimulating hormone are
About 30% to 40% of patients with a history of head and decreased (82). Sonography shows an enlarged gland with
neck radiation will develop nodular thyroid disease and lobulated margins. Echogenicity is decreased, either diffusely
between 6% and 9% of patients will develop thyroid can- or focally (Fig. 4.62). Focal hypoechoic areas are often
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Chapter 4 H E A D A N D N E C K 155

A B
Acute suppurative thyroiditis with abscess formation. A: Longitudinal sonogram shows a hypoechoic mass (arrows) with internal debris
Fig. 4.60
in an enlarged left lobe of the thyroid. B: Lateral radiograph from a barium study demonstrates a fistula tract (arrowheads) between the
pyriform sinus and the area of the thyroid gland.

poorly defined (123,124). The echopattern usually reverts to
normal as the patient becomes euthyroid.
AUTOIMMUNE-MEDIATED PROCESSES
Hashimoto Thyroiditis
Hashimoto thyroiditis, also known as chronic lymphocytic
thyroiditis, is an organ-specific autoimmune disease occur-
ring most frequently in adolescent girls and women over 40
years of age. It is the most common thyroiditis in children
and the most common cause of acquired hypothyroidism.
The pathogenesis involves both cellular and humoral mech-
anisms resulting in autoantibodies that attack thyroglobulin
and TSH receptors. Histologically, the thyroid gland is infil-
trated by lymphocytes, and the follicles are atrophic or

Acute suppurative thyroiditis with abscess formation.

Fig. 4.61
Transverse sonogram shows an abscess (A) in the soft tis-
sue of the anterior neck and a second abscess (arrowheads) in the left
thyroid lobe (LT). Arrow indicates the fistulous tract between the left
thyroid lobe and soft tissue abscess. RT  normal right thyroid lobe;
Tr  trachea.
Subacute thyroiditis. Sixteen-year-old girl with a tender
Fig. 4.62
right neck mass. Longitudinal scan shows a poorly
defined hypoechoic area (arrows) in an enlarged right thyroid
lobe. Follow-up sonogram showed complete resolution of the
inflammation.
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156 P E D I AT R I C S O N O G R A P H Y

A B

C D

Hashimoto thyroiditis. Transverse (A) and longitudinal (B)

Fig. 4.63
images in a 14-year-old girl with hyperthyroidism show an
enlarged thyroid gland with a heterogeneous echotexture. C  carotid
artery; Tr  trachea. Transverse (C) and longitudinal (D) images in a
10-year-old boy show an enlarged thyroid gland including the isthmus
(arrows) with multiple small, hypoechoic nodules. Tr  trachea. E: Color
E Doppler image in the same patient shows markedly increased vascularity.

fibrotic. Affected children present with painless enlarge-
ment of the thyroid gland. Most patients are initially
euthyroid and slowly become hypothyroid. About 10%
are hyperthyroid (82). A family history of thyroid dis-
ease is common and the incidence of the disease is
increased in patients with chromosomal disorders,
including Turner, Down, and Klinefelter syndromes.
There is also an association with autoimmune diseases,
including rheumatoid arthritis, lupus erythematosus, and
Jorgenson syndrome, and with other endocrine disorders,
including Addison disease, hypoparathyroidism, and
diabetes mellitus (82).
The sonographic findings are glandular enlargement;
diffuse parenchymal heterogeneity; and multiple hypoe-
choic nodules, reflecting infiltration by lymphoid tissue
and follicular degeneration (125,126) (Fig. 4.63). There
may be parenchymal calcifications and lymph node
enlargement. Marked hyperemia is noted on color flow
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Chapter 4 H E A D A N D N E C K 157

A B

Graves disease. Transverse (A) and left longitudinal (B)

Fig. 4.64
scans show an enlarged thyroid gland with normal echo-
texture. Tr  trachea. C: Color Doppler sonogram shows intensely
hyperemic glandular parenchyma, an appearance termed thyroid
C inferno.

imaging. In end-stage disease, the gland may be small and
hyperechoic, reflecting atrophy and fibrosis.
Graves Disease
Graves disease or thyrotoxicosis is an autoimmune disease
caused by thyroid-stimulated immunoglobulin, which binds
to the receptors for thyroid-stimulating hormone, leading to
increased synthesis of thyroid hormone (127). Pathologi-
cally, there is diffuse hyperplasia of follicular epithelial cells,
depletion of colloid, and increased vascularity. Graves
disease is more frequent in girls than boys and peaks in
adolescence (82). There is an increased incidence in
patients with McCune-Albright syndrome. Congenital
hyperthyroidism occurs in about 1% of infants born to
mothers with Graves disease (42), due to placental transfer
of thyroid-stimulating immunoglobulin. Hereditary auto-
somal dominant hyperthyroidism is another rare cause of
congenital hyperthyroidism.
The clinical findings of Graves disease include diffuse
thyroid gland enlargement and thyrotoxicosis, manifested
by jitteriness, nervousness, weight loss, sweating, palpita-
tions, heat intolerance, infiltrative ophthalmopathy
(proptosis) and, rarely, infiltrative dermopathy. Serum T4
and T3 levels are increased and levels of serum thyroid-
stimulating hormone are decreased. Treatment includes
antithyroid medications or thyroid ablation with radioac-
tive iodine-131.
Sonography shows a diffusely enlarged gland, often
with lobulated contours (Fig. 4.64). The echogenicity may
be normal or hypoechoic (128). Nodule formation is not a
feature of Graves disease. Doppler findings include marked
parenchymal hypervascularity (termed the thyroid
inferno), arteriovenous shunting, and high systolic and
diastolic flow velocities, ranging between 50 and 120
cm/sec (Fig. 4.64C) (129).
MULTINODULAR GOITER
Multinodular goiter, also referred to as adenomatous goi-
ter, simple colloid goiter, or nodular hyperplasia, may be
sporadic, congenital due to defects in thyroid synthesis,
or secondary to inadequate dietary iodine intake
(endemic goiter) or ingestion of iodine or antithyroid
medications. This condition also has been associated with
renal and digital anomalies, McCune-Albright syndrome,
Hashimoto thyroiditis, and thyroid carcinoma. Patholog-
ically, the nodules in multinodular goiter are not true ade-
nomas, but rather are adenomatous tissue. Patients with
goiters may be euthyroid or hypothyroid. The pituitary
secretion of thyroid-stimulating hormone is increased
in response to decreased circulatory levels of thyroid
hormone.
Sonography shows an enlarged, heterogeneous, echogenic
gland with multiple hypoechoic nodules, some of which may
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158 P E D I AT R I C S O N O G R A P H Y

A B

Multinodular goiter. Transverse (A) and longitudinal (B)

Fig. 4.65
scans of the right thyroid lobe (calipers) demonstrate
hypoechoic parenchymal nodules (arrows). The surrounding thyroid tis-
sue (Th) is normal. CA  carotid artery; Tr  trachea. C: Color Doppler
C scan of the right lobe shows areas of both normal and increased flow.

show cystic degeneration (Fig. 4.65) (130). The nodules
can be hyperechoic if they contain inspissated colloid or
hemorrhage. Color Doppler imaging demonstrates normal
or mildly increased vascularity.
Normal Parathyroid Function
The parathyroid glands secrete parathyroid hormone
(PTH) and are responsible for maintaining calcium and
phosphate homeostasis. The target organs of PTH are the
kidneys and liver.

PARATHYROID GLANDS Normal Sonographic Anatomy

Normal Development and Anatomy
The parathyroid glands are derived from the third and
fourth pharyngeal pouches. There are usually four
glands. The paired superior glands arise from the fourth
branchial pouch and have a fairly constant position
near the upper surface of the thyroid lobes. The inferior
parathyroid glands arise from the third branchial pouch
and are found in close proximity to the lower pole of
the thyroid gland (131,132). Similar to the thyroid
gland, the migration of the parathyroid glands may be
arrested or the glands may migrate below the level of
the thyroid gland into the mediastinum. In general, less
than 5% are found in ectopic locations in the neck or in
a substernal position (131,132). Occasionally, there are
more than four parathyroid glands. Supernumerary
glands are usually located in the superior mediastinum
close to the thymus.
The normal parathyroid glands are difficult to visualize by
sonography because of their small size (5 mm in length)
and an echotexture that is similar to that of adjacent thy-
roid parenchyma. The glands, however, may be seen
as separate oval structures near the thyroid gland when
their echogenicity is less than that of the thyroid
parenchyma.
Indications for Parathyroid Ultrasonography
Indications for parathyroid imaging include preoperative
evaluation of primary hyperparathyroidism for localiza-
tion of an adenoma or hyperplastic glands; guidance of
fine-needle aspiration biopsy; and postoperative evaluation
of persistent or recurrent hyperparathyroidism. Ultra-
sonography is usually the initial study of choice to detect a
parathyroid lesion because of its ease of performance and
availability. If the sonographic study of the neck is negative
or ambiguous and there is still a high suspicion of disease,
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other localizing studies such as sestamibi scintigraphy, CT,
or MRI are indicated.
Hyperparathyroidism
PRIMARY HYPERTHYROIDISM
Hyperparathyroidism results from excess parathormone
production. Primary hyperparathyroidism is diagnosed
when serum calcium is elevated and PTH is increased. It
is usually due to a solitary, benign hyperfunctioning ade-
noma (80% of cases) and less often due to diffuse glan-
dular hyperplasia (about 20% of cases) (57,103).
Rarely, it results from glandular hyperplasia associated
with MEN type I or II or from a functioning parathy-
roid carcinoma or parathyroid cyst. Clinical findings
include polydipsia, polyuria, pruritus, keratitis, and
bone pain.
The treatment for primary hyperparathyroidism is sur-
gical exploration with resection of an adenomatous gland.
The treatment for multiglandular disease is a subtotal
resection or a total parathyroidectomy with autotrans-
plantation into the forearm or neck muscle (133,134). The
success rate of surgical exploration exceeds 90% and pre-
operative localization with imaging is rarely needed. Imag-
ing of the parathyroid glands may be useful in patients in
whom only a unilateral neck exploration is planned and in
postoperative patients with persistent or recurrent hyper-
parathyroidism.
SECONDARY HYPERTHYROIDISM
Secondary hyperparathyroidism is due to multiglandu-
lar hyperplasia in response to chronic hypercalcemia,
usually from chronic renal disease or intestinal malab-
sorption. Typically all four parathyroid glands are
enlarged. Hyperparathyroidism also occurs in MEN
A B
Parathyroid adenomas. A: Transverse sonogram of a 16-year-old boy with hyperparathyroidism shows an oval hypoechoic mass (M)
Fig. 4.66
behind the right lobe of the thyroid (Th) gland. CA  carotid artery; Tr  trachea. B: Power Doppler sonography shows a feeding artery
(arrows) coursing around the periphery of the mass before entering the upper pole of the adenoma.
Chapter 4 H E A D A N D N E C K 159
types I and II. Secondary hyperparathyroidism is treated
medically.
ADENOMA
The parathyroid adenoma appears as a well-marginated,
oval hypoechoic mass located along the posterior surface
of the thyroid gland (Fig. 4.66) (134). On occasion, ade-
nomas are entirely cystic, contain calcifications, or have a
multilobulated configuration. Color Doppler imaging
characteristically demonstrates a tortuous extrathyroidal
artery (usually off the inferior thyroidal artery) feeding the
tumor. The vessel courses 90 to 270 degrees around the
periphery of the adenoma before entering the lesion
(135137). Sonographically, it can be difficult to differen-
tiate adenoma from carcinoma.
Cervical lymph nodes may mimic parathyroid adeno-
mas. Lymph nodes have an echogenic center, which is vas-
cular on Doppler imaging, and are commonly found
beneath the thyroid gland. Parathyroid adenomas are uni-
formly hypoechoic, show peripheral flow, and are poste-
rior or lateral to the thyroid gland.
HYPERPLASIA
In multiglandular hyperplasia, all four glands are enlarged
(134). The enlarged glands are separated from the thyroid
gland by a highly echogenic line, believed to represent the
fibrous capsule. The echogenicity is less than that of the adja-
cent thyroid tissue. On occasion, hyperplastic glands appear
as multiple solid nodules with homogeneous low-level echoes.
Parathyroid Cysts
Parathyroid cysts arise from remnants of the third and
fourth pharyngeal pouches or from cystic degeneration of
LWBK505-C04_p118-163.qxd 7/7/10 1:25 PM Page 160 Aptara Inc
160 P E D I AT R I C S O N O G R A P H Y
A B
Parathyroid cyst. Transverse (A) and longitudinal (B) sonograms of the left neck show a fluid-filled mass, with dependent debris, lateral
Fig. 4.67
to the left lobe of the thyroid (TH) gland.
parathyroid adenomas. Most are located in the inferior
parathyroid glands, although they can occur anywhere
from the angle of the mandible to the superior medi-
astinum. Patients are usually normocalcemic and present
with a palpable neck mass. They may be signs of hyper-
parathyroidism if the cysts are functional.
Parathyroid cysts appear as unilocular, smooth-walled,
anechoic lesions with through-sound transmission. They
are found lateral to the thyroid gland (Fig. 4.67). Because
of their relationship to the thyroid gland, separating
parathyroid from thyroid cysts can be difficult without
analysis of the cyst fluid. Percutaneous aspiration of the
cyst with assay of parathyroid hormone is helpful to
establish the diagnosis of a parathyroid cyst. Parathyroid
hormone levels in the fluid are elevated when compared
with serum parathyroid hormone levels.
REFERENCES
1. Lewis GJS, Leithiser RE Jr, Glasier CM, et al. Ultrasonography
of pediatric neck masses. Ultrasound Q 1989;7:315355.
2. Solbiati L, Cioffi V, Ballarati E. Ultrasonography of the neck.
Radiol Clin North Am 1992;30:941954.
3. Bialek EJ, Jakubowski W, Zajkowski P, et al. US of the major
salivary glands: anatomy and spatial relationship, pathologic
conditions, and pitfalls. Radiographics 2006;26:745763.
4. Garcia CJ, Flores PA, Arce JD, et al. Ultrasonography in the
study of salivary gland lesions in children. Pediatr Radiol 1998;
28:418425.
5. Lowe LH, Stokes LS, Johnson JE, et al. Swelling at the angle of
the mandible: imaging of the pediatric parotid and periparotid
region. Radiographics 2001;21:12111227.
6. Martinoli C, Derchi LE, Solbiati L, et al. Color Doppler sonog-
raphy of salivary glands. AJR Am J Roentgenol 1994;163:
933941.
7. Bialek EJ, Jakubowski W, Karpinska G. Role of ultrasonogra-
phy in diagnosis and differentiation of pleomorphic adenomas.
Arch Otolaryngol Head Neck Surg 2003;129:929933.
8. Boyd ZT, Goud AR, Lowe LH, Shao L. Pediatric salivary gland
imaging. Pediatr Radiol 2009;39(7):71022.
9. Fallat ME, Bryant KA. Neck. In: Oldham KT, Colombani PM,
Folgia RP, et al., eds. Surgery of infants and children. Philadel-
phia, PA: Lippincott Williams & Wilkins, 2005:863890.
10. Orvidas LJ, Kasperbauer JL, Lewis JE, et al. Pediatric parotid
masses. Arch Otolaryngol Head Neck Surg 2000;126:177184.
11. Pappo AS, Furman WL. Management of infrequent cancers in
childhood. In: Pizzo PA, Poplack DG, eds. Principles and prac-
tice of pediatric oncology. Philadelphia, PA: Lippincott
Williams & Wilkins, 2006:11721201.
12. Dubois J, Patriquin H. Doppler sonography of head and neck
masses in children. Neuroimaging Clin N Am 2000;10:215252.
13. Robertson RL, Robson CD, Barnes PD, et al. Head and neck
vascular anomalies of childhood. Neuroimaging Clin N Am
1999;9:115132.
14. Roebuck DJ, Ahuja AT. Hemangioendothelioma of the parotid
gland in infants: sonography and correlative MR imaging.
AJNR Am J Neuroradiol 2000;21:219223.
15. Seibert RW, Seibert JJ. High resolution ultrasonography of the
parotid gland in children. Part II. Pediatr Radiol 1988;19:
1318.
16. Schick S, Steiner E, Gahleitner A, et al. Differentiation of benign
and malignant tumors of the parotid gland: value of pulsed
Doppler and color Doppler sonography. Eur Radiol 1998;8:
14621467.
17. Bradley MJ, Durham LH, Lancer JM. The role of colour flow
Doppler in the investigation of the salivary gland tumour. Clin
Radiol 2000;55:759762.
18. McQuone SJ. Acute viral and bacterial infections of the salivary
glands. Otolaryngol Clin North Am 1999;32:793811.
19. Goddart D, Francois A, Ninane J, et al. Parotid gland abnor-
mality found in children seropositive for the human immunod-
eficiency virus (HIV). Pediatr Radiol 1990;20:355357.
20. Soberman N, Leonidas JC, Berdon WE, et al. Parotid enlarge-
ment in children seropositive for human immunodeficiency
virus: imaging findings. AJR Am J Roentgenol 1991;157:
553556.
21. Chiu CH, Lin TY. Clinical and microbiological analysis of six
children with acute suppurative parotitis. Acta Paediatr
1996;85:106108.
22. Nozaki H, Harasawa A, Hara A, et al. Ultrasonographic fea-
tures of recurrent parotitis in childhood. Pediatr Radiol
1994;24:98100.
LWBK505-C04_p118-163.qxd 7/7/10 1:25 PM Page 161 Aptara Inc
23. Nolasco AM, Oxer SA. Ultrasonographic features of recurrent
parotitis in childhood. Pediatr Radiol 1995;25:402.
24. Shimizu M, Ussmller J, Donath K, et al. Sonographic analysis
of recurrent parotitis in children: a comparative study with
sialographic findings. Oral Surg Oral Med Oral Pathol Oral
Radiol Endod 1998;86:606615.
25. Bielamowicz SA, Storper IS, Jabour BA, et al. Spaces and trian-
gles of the head and neck. Head Neck 1994;16:383388.
26. Som PM, Smoker RK, Balboni A, et al. Embryology and
anatomy. In: Som PM, Curtin HD, eds. Head and neck imaging.
4th ed. St. Louis, MO: Mosby, 2003:17571804.
27. Evans RM. Anatomy and technique. In: Ahuja AT, Evans RM,
eds. Practical head and neck ultrasound. London, UK: Green-
wich Medical Media Limited, 2000:316.
28. Som PM, Brandwein MS. Lymph nodes. In: Som PM, Curtin
HD, eds. Head and neck imaging. 4th ed. St. Louis, MO:
Mosby, 2003:18651934.
29. Evans RM. Lymph nodes. In: Ahuja AT, Evans RM, eds. Prac-
tical head and neck ultrasound. London, UK: Greenwich Med-
ical Media Limited, 2000:6583.
30. Strauss S. Sonographic appearance of cricoid cartilage calcifica-
tion in healthy children. AJR Am J Roentgenol 2000;174:
223228.
31. Turkington JRQA, Paterson A, Sweeney LE, et al. Neck masses
in children. Br J Radiol 2005;78:7585.
32. Castellote A, Vaazquez E, Vera J, et al. Cervicothoracic lesions
in infants and children. Radiographics 1999;19:583600.
33. Telander RL, Filston HC. Review of head and neck lesions in
infancy and childhood. Surg Clin North Am 1992;72:14291447.
34. Borecky N, Gudinchet F, Laurini R, et al. Imaging of cervico-
thoracic lymphangiomas in children. Pediatr Radiol 1995;25:
127130.
35. Koch BL. Cystic malformations of the neck in children. Pediatr
Radiol 2005;35:463477.
36. Koeller KK, Alamo L, Adair CF, et al. Congenital cystic masses
of the neck: radiologic-pathologic correlation. Radiographics
1999;19:121146.
37. Zadvinskis DP, Benson MT, Kerr HH, et al. Congenital malfor-
mations of the cervico-thoracic lymphatic system: embryology
and pathogenesis. Radiographics 1992;12:11751189.
38. Siegel MJ. Neck. In: Siegel MJ, Coley BD, eds. Core curriculum:
pediatric imaging. Philadelphia, PA: Lippincott Williams &
Wilkins, 2006:130.
39. Som PM, Sacher M, Lanzieri CF, et al. Parenchymal cysts of the
lower neck. Radiology 1995;157:399406.
40. Burrows P, Laor T, Paltiel H, et al. Diagnostic imaging in the
evaluation of vascular birthmarks. Dermatol Clin 1998;16:
455488.
41. Meuwly J-Y, Lepori D, Theumann N, et al. Multimodality
imaging evaluation of the pediatric neck: techniques and spec-
trum of findings. Radiographics 2005;25:931948.
42. Som PM, Smoker RK, Curtin HD, et al. Neck: congenital
lesions. In: Som PM, Curtin HD, eds. Head and neck imaging.
4th ed. St. Louis: Mosby, 2003:18281864.
43. Karmody CS. Developmental anomalies of the neck. In: Bluestone,
CD, Stool SE, Alper CM, et al., eds. Pediatric otolaryngology. 4th
ed. Philadelphia, PA: Saunders Company, 2003:16481663.
44. Maddalozzo J, Bennett E. Thyroid. In: Bluestone CD, Stool SE,
Alper CM, et al., eds. Pediatric otolaryngology. 4th ed.
Philadelphia, PA: Saunders Company, 2003:17371745.
45. Wadsworth DT, Siegel MJ. Thyroglossal duct cysts: variability
of sonographic findings. AJR Am J Roentgenol 1994;163:
14751477.
46. Benson MT, Dalen K, Mancuso AA, et al. Congenital anomalies
of the branchial apparatus: embryology and pathologic
anatomy. Radiographics 1992;12:943960.
47. Smitniotopoulos JG, Chiechi MV. Teratomas, dermoids and
epidermoids of the head and neck. Radiographics 1995;15:
14371455.
Chapter 4 H E A D A N D N E C K 161
48. Herman TE, Siegel MJ. Perinatal/neonatal casebook. Cervical
teratoma. J Perinatol 2008;28:649651.
49. Nguyen Q, deTar M, Wells W, et al. Cervical thymic cyst: case
reports and review of the literature. Laryngoscope 1996;106:
247252.
50. Herman TE, Siegel MJ. Cervical ectopic thymus. J Perinatol
2009;29:173174.
51. Fitoz S, Atasoy C, Turkoz E, et al. Sonographic findings in
ectopic cervical thymus in an infant. J Clin Ultrasound 2001;29:
523526.
52. Koumanidou C, Vakaki M, Theophanopoulou M, et al. Aber-
rant thymus in infants: sonographic evaluation. Pediatr Radiol
1998;28:987989.
53. Chan YL, Cheng JCY, Metreweli C. Ultrasonography of con-
genital muscular torticollis. Pediatr Radiol 1992;22:356360.
54. Cheng JC, Metreweli C, Chen TM, et al. Correlation of ultra-
sonographic imaging of congenital muscular torticollis with
clinical assessment in infants. Ultrasound Med Biol 2000;26:
12371241.
55. Lin JN, Chou ML. Ultrasonographic study of the sternocleido-
mastoid muscle in the management of congenital muscular tor-
ticollis. J Pediatr Surg 1997;32:16481651.
56. Koujok K, Ruiz RE, Hernandez RJ. Myofibromatosis: imaging
characteristics. Pediatr Radiol 2005;35:374380.
57. Whittemore KR, Cunningham MJ. Malignant tumors of the
head and neck. In: Bluestone CD, Stool SE, Alper CM, et al.,
eds. Pediatric otolaryngology. 4th ed. Philadelphia, PA: Saun-
ders Company, 2003:17031736.
58. Link MP, Weinstein HJ. Malignant non-Hodgkin lymphomas in
children. In: Pizzo PA, Poplack DG, eds. Principles and practice
of pediatric oncology. Philadelphia, PA: Lippincott Williams &
Wilkins, 2006:722747.
59. LaQuaglia MP. Non-Hodgkin lymphoma of the head and neck
in childhood. Semin Pediatr Surg 1994;3:207215.
60. Hudson MM, Onciu M, Donaldson SS. Hodgkin lymphoma.
In: Pizzo PA, Poplack DG, eds. Principles and practice of pedi-
atric oncology. Philadelphia, PA: Lippincott Williams &
Wilkins, 2006:695721.
61. Na DG, Lim HK, Byun HS, et al. Differential diagnosis of cer-
vical lymphadenopathy: usefulness of color Doppler sonogra-
phy. AJR Am J Roentgenol 1997;168:13111316.
62. Brodeur GM, Maris JM. Neuroblastoma. In: Pizzo PA, Poplack
DG, eds. Principles and practice of pediatric oncology. 5th ed.
Philadelphia, PA: Lippincott Williams & Wilkins, 2006: 933970.
63. Haase GM. Head and neck neuroblastoma. Semin Pediatr Surg
1994;3:194202.
64. Lonergan GJ, Schwab CM, Suarez ES, et al. Neuroblastoma,
ganglioneuroblastoma, and ganglioneuroma: radiologic-patho-
logic correlation. Radiographic 1992;22:911934.
65. Siegel MJ. Neuroblastoma. In: Husband JE, Reznek RH, eds.
Imaging in oncology. 2nd ed. London, UK: Taylor & Francis,
2004:953971.
66. Wexler LH, Meyer WH, Helman LJ. Rhabdomyosarcoma and
the undifferentiated sarcomas. In: Pizzo PA, Poplack DG, eds.
Principles and practice of pediatric oncology. 5th ed. Philadel-
phia, PA: Lippincott Williams & Wilkins, 2006:9711001.
67. Wiener ES. Head and neck rhabdomyosarcoma. Semin Pediatr
Surg 1994;3:203206.
68. Siegel MJ. Uncommon pediatric neoplasms. In: Husband JE,
Reznek RH, eds. Imaging in oncology. 2nd ed. London, UK:
Taylor & Francis, 2004:973996.
69. Bodenstein L, Altman RP. Cervical lymphadenitis in infants and
children. Semin Pediatr Surg 1994;3:134141.
70. Rosenfeld RM. Cervical adenopathy. In: Bluestone CD, Stool
SE, Alper CM, et al., eds. Pediatric otolaryngology. 4th ed.
Philadelphia, PA: Saunders Company, 2003:16651680.
71. Yellon RF. Head and neck space infections. In: Bluestone CD,
Stool SE, Alper CM, et al, eds. Pediatric otolaryngology. 4th ed.
Philadelphia, PA: Saunders Company, 2003:16811701.
LWBK505-C04_p118-163.qxd 7/7/10 1:25 PM Page 162 Aptara Inc
162 P E D I AT R I C S O N O G R A P H Y
72. Glasier CM, Stark JE, Jacobs RF, et al. CT and ultrasound
imaging of retropharyngeal abscesses in children. AJNR Am J
Neuroradiol 1992;13:11911195.
73. Restrepo R, Oneto J, Lopez K, et al. Head and neck lymph
nodes in children: the spectrum from normal to abnormal. Pedi-
atr Radiol 2009;39:836846.
74. Chavhan GB, Parra DA, Mann A, et al. Normal Doppler spec-
tral waveforms of major pediatric vessels: specific patterns.
Radiographics 2008;28:691706.
75. Grant EG, Benson CB, Moneta GL, et al. Carotid artery stenosis:
gray-scale and Doppler US diagnosisSociety of Radiologists in
Ultrasound Consensus Conference. Radiology 2003;229:340346.
76. Rand T, Kohlhauser C, Popow C, et al. Sonographic detection of
internal jugular vein thrombosis after central venous catheteri-
zation in the newborn period. Pediatr Radiol 1994;24:577580.
77. DeSena S, Rosenfeld DL, Santos S, et al. Jugular throm-
bophlebitis complicating bacterial pharyngitis (Lemierres syn-
drome). Pediatr Radiol 1996;26:141144.
78. Gudinchet F, Maeder P, Neveceral P, et al. Lemierres syndrome
in children: high-resolution CT and color Doppler sonography
patterns. Chest 1997;112:271273.
79. Joseph AE, Donaldson JS, Reynolds M. Neck and thorax
venous aneurysm: association with cystic hygroma. Radiology
1989;170:109112.
80. Babcock DS. Thyroid disease in the pediatric patient: empha-
sizing imaging with sonography. Pedatr Radiol 2006;36:
299308.
81. Loevner LA. Thyroid and parathyroid: anatomy and pathology.
In: Som PM, Curtin HD, eds. Head and neck imaging. 4th ed.
St. Louis: Mosby, 2003;21342171.
82. Rossi WC, Caplin N, Alter CA. Thyroid disorders in children.
In: Moshang T, ed. Pediatric endocrinology: the requisites in
pediatrics. St. Louis, MO: Elsevier Mosby, 2005:171190.
83. Ueda D. Normal volume of the thyroid gland in children. J Clin
Ultrasound 1990;18:455462.
84. Ueda D, Mitamura R, Suzuki N, et al. Sonographic imaging of
the thyroid gland in congenital hypothyroidism. Pediatr Radiol
1992;22:102105.
85. Chanoine JP, Toppet V, Lagasse R, et al. Determination of thy-
roid volume by ultrasound from the neonatal period to late
adolescence. Eur J Pediatr 1991;150:395399.
86. Vade A, Gottschalk ME, Yetter EM, et al. Sonographic mea-
surements of the neonatal thyroid gland. J Ultrasound Med
1997;16:395399.
87. Perry RJ, Hollman AS, Wood AM, et al. Ultrasound of the thy-
roid gland in the newborn: normative data. Arch Dis Child
Fetal Neonatal Ed 2002;87:F209F211.
88. Ueda D, Yoto Y, Sato T. Ultrasonic assessment of the lingual
thyroid gland in children. Pediatr Radiol 1998;28:126128.
89. Marinovic D, Garel C, Czernichow P, et al. Ultrasonographic
assessment of the ectopic thyroid tissue in children with con-
genital hypothyroidism. Pediatr Radiol 2004;34:109113.
90. Hung W, Anderson KD, Chandra RS, et al. Solitary thyroid nod-
ules in 71 children and adolescents. J Pediatr Surg 1992;27:
14071409.
91. Koch CA, Pacak K, Chrousos GP. Endocrine tumors. In: Pizzo
PA, Poplack DG, eds. Principles and practices of pediatric
oncology. 3rd ed. Philadelphia, PA: Lippincott Williams &
Wilkins, 2006:11391172.
92. Lafferty AR, Batch JA. Thyroid nodules in childhood and ado-
lescence: thirty years of experience. J Pediatr Endocrinol Metab
1997;10:479486.
93. Raab SS, Silverman JF, Elsheikh TM, et al. Pediatric thyroid
nodules: disease demographics and clinical management by fine
needle aspiration biopsy. Pediatrics 1995;95:4649.
94. Ahuja AT, Metreweli C. Ultrasound of thyroid nodules. Ultra-
sound Q 2000;16:111121.
95. Gooding GA. Sonography of the thyroid and parathyroid.
Radiol Clin North Am 1993;31:967989.
96. Reading CC. Palpable neck mass. In: Bluth EI, Benson CB,
Ralls RW, et al., eds. Ultrasound a practical approach to clini-
cal problems. 2nd ed. New York, NY: Thieme, 2007:657667.
97. Sillery JC, Reading CC, Charboneau JW, et al. Thyroid follicu-
lar carcinoma: sonographic features of 50 cases. AJR 2010;
194:4454.
98. Ahuja A, Chick W, King W, et al. Clinical significance of the
comet-tail artifact in thyroid ultrasound. J Clin Ultrasound
1996;24:129133.
99. Clark KJ, Cronan JJ, Scola FH. Color Doppler sonography:
anatomic and physiologic assessment of the thyroid. J Clin
Ultrasound 1995;23:215223.
100. Frates MC, Benson CB, Doubilet PM, et al. Can color Doppler
sonography aid in the prediction of malignancy of thyroid nod-
ules? J Ultrasound Med 2003;22:127131.
101. Kerr L. High resolution thyroid ultrasound: the value of color
Doppler. Ultrasound Q 1994;12:2143.
102. Lyshchik A, Drozd V, Demidchik Y, et al. Diagnosis of thyroid
cancer in children: value of gray scale and power Doppler US.
Radiology 2005;235:604613.
103. Skinner MA. Surgical diseases of the thyroid and parathyroid
glands. In: Oldham KT, Colombani PM, Folgia RP, et al., eds.
Surgery of infants and children. Philadelphia, PA: Lippincott
Williams & Wilkins, 2005:671684.
104. Campo M, Vela AC, Oleaga L, et al. Thyroid follicular carci-
noma: a case report. Pediatr Radiol 2000;30:358359.
105. Danese D, Gardini A, Farsetti A, et al. Thyroid carcinoma in
children and adolescents. Eur J Pediatr 1997;156:190194.
106. Moir CR, Telander RL. Papillary carcinoma of the thyroid in
children. Semin Pediatr Surg 1994;3:182187.
107. Segal K, Arad-Cohen A, Mechlis S, et al. Cancer of the thyroid
in children and adolescents. Clin Otolaryngol 1997;22:525528.
108. Samaan NA, Draznin MB, Halpin RE, et al. Multiple endocrine
syndrome type IIb in early childhood. Cancer 1990;19:
18321834.
109. Telander RL, Moir CR. Medullary thyroid carcinoma in chil-
dren. Semin Pediatr Surg 1994;3:188193.
110. Ahuja AT, Chow L, Chick W, et al. Metastatic cervical nodes in
papillary carcinoma of the thyroid: ultrasound and histological
correlation. Clin Radiol 1995;50:229231.
111. Acharya S, Sarafoglou K, LaQuaglia M, et al. Thyroid neo-
plasms after therapeutic radiation for malignancies during
childhood or adolescence. Cancer 1993;97:23972403.
112. Favus MJ, Schneider AB, Stachura ME, et al. Thyroid cancer
occurring as a late consequence of headandneck irradiation.
evaluation of 1056 patients. N Engl J Med 1976;294:10191025.
113. Schneider AB, Pinsky S, Bekerman, et al. Characteristics of 108
thyroid cancers detected by screening in population with a his-
tory of head and neck irradiation. Cancer 1980;46:12181227.
114. Shafford EA, Kingston JE, Healy JC, et al. Thyroid nodular dis-
ease after radiotherapy to the neck for childhood Hodgkins
disease. Br J Cancer 1999;80:808814.
115. Chiesa F. Thyroid disease in northern Italian children born
around the time of the Chernobyl nuclear accident. Ann Oncol
2004;15:18421846.
116. Stezhko VA, Buglova EE, Danilova LI. A cohort study of thy-
roid cancer and other thyroid diseases after the Chernobyl acci-
dent: objectives, design and methods. Radiat Res 2004;161:
481489.
117. Soberman N, Leonidas JC, Cherrick I, et al. Sonographic
abnormalities of the thyroid gland in long term survivors of
Hodgkin disease. Pediatr Radiol 1991;21:250253.
118. Stewart RR, David CL, Eftekhari F, et al. Thyroid gland: US in
patients with Hodgkin disease treated with radiation therapy in
childhood. Radiology 1989;172:159163.
119. Ahuja AT, Griffiths JF, Roebuck DJ, et al. The role of ultra-
sound and oesophagography in the management of acute sup-
purate thyroiditis in children associated with congenital pyri-
form fossa sinus. Clin Radiol 1998;53:209211.
LWBK505-C04_p118-163.qxd 7/7/10 1:25 PM Page 163 Aptara Inc
120. Hatabu H, Kasagi K, Yamamoto K, et al. Acute suppurative
thyroiditis associated with piriform sinus fistula: sonographic
findings. AJR Am J Roentgenol 1990;155:845847.
121. Lucaya J, Berdon WE, Enriquez G, et al. Congenital pyriform
sinus fistula: a cause of acute left-sided suppurative thyroiditis
and neck abscess in children. Pediatr Radiol 1990;21:2729.
122. Ogawa E, Katsushima Y, Fujiwara I, et al. Subacute thyroiditis
in children: patient report and review of the literature. J Pedi-
atr Endocrinol Metab 2003;16:897900.
123. Bennedbaek FN, Hegedus L. The value of ultrasonography in
the diagnosis and follow-up of subacute thyroiditis. Thyroid
1997;7:4550.
124. Birchall IWJ, Chow CC, Metreweli C. Ultrasound appearances
of de Quervains thyroiditis. Clin Radiol 1990;41:5759.
125. Ivarsson SA, Ericsson UB, Fredriksson B, et al. Ultrasonic imag-
ing in the differential diagnosis of diffuse thyroid disorders in
children. Am J Dis Child 1989;143:13691372.
126. Yeh HC, Futterweit W, Gilbert P. Micronodulation: ultrasono-
graphic sign of Hashimoto thyroiditis. J Ultrasound Med
1996;15:813819.
127. Kraiem Z, Newfield RS. Graves disease in childhood. J Pediatr
Endocrinol Metab 2001;14:229243.
128. Cappelli C, Pirola I, De Martino E, et al. The role of imaging
in Graves disease: a cost-effectiveness analysis. Eur J Radiol
2007;65:99103.
Chapter 4 H E A D A N D N E C K 163
129. Ralls PW, Mayekawa DS, Lee KP, et al. Color-flow Doppler
sonography in Graves disease: thyroid inferno. AJR Am J
Roentgenol 1988;150:781784.
130. Garcia CJ, Daneman A, Thorner P, et al. Sonography of multin-
odular thyroid gland in children and adolescents. Am J Dis
Child 1992;146:811816.
131. Akerstrom G, Malmaeus J, Bergstrom R. Surgical anatomy of
human parathyroid glands. Surgery 1984;95:1421.
132. Wang CA. The anatomic basis of parathyroid surgery. Ann
Surg 1976;183:271275.
133. Chen H. Surgery for primary hyperparathyroidism: what is the
best approach? Am Surg 2002;236:552553.
134. Johnson NA, Tublin ME, Ogilvie JB. Parathyroid imaging:
technique and role in the preoperative evaluation of primary
hyperparathyroidism. AJR Am J Roentgenol 2007;188:1706
1715.
135. Lane MJ, Desser TS, Weigel RJ, et al. Use of color and power
Doppler sonography to identify feeding arteries associated with
parathyroid adenomas. AJR Am J Roentgenol 1998;171:819823.
136. Reeder SB, Desser TS, Weigel RJ, et al. Sonography in primary
hyperparathyroidism: review with emphasis on scanning tech-
nique. J Ultrasound Med 2002;21:539555.
137. Wolf RJ, Cronan JJ, Monchik JM. Color Doppler sonography:
an adjunctive technique in assessment of parathyroid adeno-
mas. J Ultrasound Med 1994;13:303308.
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CHAPTER

5 Chest
MARILYN J. SIEGEL

Technique Parenchymal Disease Arterial Stenosis and Aneurysm

Transducers Atelectasis and Consolidation Internal Mammary Compartment
Imaging Approaches Parenchymal or Pleural Disease
Esophagus and Trachea
Lung Necrosis and Abscess
Normal Anatomy Esophagus
Thymus Congenital Lung Anomalies Tracheobronchial Tree
PleuraLung Interface Anomalies with Normal Vasculature
Diaphragmatic Lesions
Trachea Anomalies with Abnormal Vasculature
Diaphragmatic Hernias
Esophagus
Pulmonary Neoplasm Eventration
Great Vessels and Internal Mammary
Paralysis
Compartment Mediastinum
Inversion
Diaphragm Anterior Mediastinal Masses
Juxtadiaphragmatic Masses
Middle Mediastinal Masses
Clinical Indications
Posterior Mediastinal Masses Chest Wall Lesions
Pleural Diseases Cardiophrenic Angle Masses Soft Tissue Masses
Pleural Effusion Osseous Lesions
Vascular Abnormalities
Fibrothorax
Venous Thrombosis and Stenosis
Pleural Masses
Congenital Arch Anomalies
Pneumothorax

iseases of the pediatric chest are initially evaluated A lower-frequency transducer (5.0 MHz) may be needed

D with chest radiography. However, when the location

or nature of an area of increased opacity remains
uncertain, sonography may help establish a diagnosis.
Sonography is particularly useful in differentiating between
pulmonary and pleural lesions. It also allows characteriza-
tion of pleural fluid collections as simple or complicated,
which can help in planning thoracentesis or thoracotomy.
Computed tomography (CT) and magnetic resonance
imaging (MRI) are superior to sonography in assessing
mediastinal widening or a mass, but sonography can pro-
vide clinically relevant information in selected situations,
namely, the evaluation of the normal thymus and vascular
lesions. In patients with chest wall lesions, sonography
allows localization and characterization of the mass.
Finally, the real-time imaging capability of sonography is
valuable in evaluating the diaphragm and juxtadiaphrag-
matic abnormalities.
This chapter reviews the technique of chest sonogra-
phy, the diagnostic applications of sonography in a wide
variety of disease processes of the chest, and the sono-
graphic features of the normal anatomy and common
pathologic lesions of the chest in infants and children.
TECHNIQUE
Transducers
A 7.5- or 10.0-MHz transducer usually suffices for the
evaluation of near-field structures in infants and children.
164
for evaluation of larger patients and the deep pleural
space, lung, or mediastinum. Curved or linear array trans-
ducers are used for most sonographic examinations of the
lung, pleura, mediastinum, and chest wall, although sector
or small-footprint transducers with a narrow field of view
are often preferred for insonation of the suprasternal,
intercostal, and subxiphoid spaces.
Doppler sonography is used to characterize flow in
mediastinal vessels; detect anomalous vessels, particularly
those associated with pulmonary sequestration; and
demonstrate the relationship of lesions to major vessels
and the heart. Gray-scale and color Doppler images are
obtained in both transverse and sagittal planes. These are
supplemented by oblique planes when needed to increase
lesion conspicuity.
Imaging Approaches
The windows for chest sonography are (i) supraclavicu-
lar, (ii) suprasternal, (iii) parasternal, (iv) transsternal,
(v) intercostal, (vi) subxiphoid, (vii) subdiaphragmatic,
and (viii) posterior paraspinal approaches (Fig. 5.1)
(17).
Supraclavicular views (Fig. 5.1, number 1) are obtained
with the transducer positioned above the clavicle.
Suprasternal views (Fig. 5.1, number 2) are acquired with
the transducer placed above the manubrium in the
suprasternal notch and angled caudally. These views are
used to evaluate the lung apices, upper mediastinum, and
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Acoustic windows for chest sonographic examination: (1 )
Fig. 5.1
supraclavicular, (2 ) suprasternal, (3 ) parasternal, (4 )
transsternal, (5) intercostal, (6) subxiphoid, (7) subdiaphragmatic, and
(8 ) posterior paraspinal. (Adapted from Coley BD, Pediatric chest
ultrasound. Radiol Clin N Am. 2005;43:405418.)
great vesselsaorta, superior vena cava, brachiocephalic
veins, and subclavian arteries.
Parasternal views (Fig. 5.1, number 3) are acquired
with the transducer paralleling the sternum and the
patient in the lateral decubitus position, which shifts the
mediastinum downward, enlarging the acoustic window.
The main pulmonary artery and left side of the anterior
mediastinum are imaged via the left parasternal window
with the patient in the left lateral decubitus position. The
ascending aorta and right side of the anterior medi-
astinum are imaged with a right parasternal approach
and the patient in the ipsilateral decubitus position.
The parasternal view is also used to image the mammary
vessels.
Transsternal views (Fig. 5.1, number 4) can be
obtained with the transducer directly over the sternum. In
neonates, this view is useful to image the thymus. In this
age group, the sternum is predominantly cartilaginous,
thus allowing transmission of the sound beam.
Intercostal views (Fig. 5.1, number 5) are acquired
with the transducer directly positioned on the chest and
the patient in a supine or oblique position. This approach
improves access to the pleural space and peripheral lung
parenchyma.
The subxiphoid (Fig. 5.1, number 6) and subdi-
aphragmatic (Fig. 5.1, number 7) views are obtained
with the transducer placed beneath the xiphoid and mar-
gins of the lower ribs, respectively, and angled cephalad,
using the liver or spleen as an acoustic window. These
views can facilitate the evaluation of abnormalities in the
deep sulcal spaces (lower lung and pleural space) and the
diaphragm. The posterior paraspinal approach (Fig. 5.1,
number 8), with the transducer paralleling the spine,
may improve visualization of posterior mediastinal
masses.
Chapter 5 C H E S T 165
NORMAL ANATOMY
Thymus
The appearance of the thymus changes with patient age.
Recognition of variations in size, consistency, and posi-
tion is important for proper sonographic interpretation.
The thymus is a bilobed structure. Each lobe has a sepa-
rate fibrous capsule. The thymus is largest, with respect
to whole-body weight, in neonates and young infants
and increases in size in childhood to reach a maximum
weight at puberty. Prior to puberty, the thymus is com-
posed of parenchymal elements and contains a large lym-
phocyte population separated by thin connective tissue
septa. At puberty, the lymphocytes begin a gradual invo-
lution and there is progressive replacement of the thymic
follicles by adipose tissue. The thymus produces hor-
mones that stimulate maturation of T cells, playing an
important role in maintaining immune competency
(811).
The thymus lies anterior to the great vessels. In infants
and young children, it usually extends from the horizon-
tal portion of the left brachiocephalic vein cephalad to the
origin of the great vessels caudally. On occasion, one or
both thymic lobes extend almost to the level of the
diaphragm. Inferior extension decreases with increasing
patient age.
Because it has a broad anterior margin that abuts the
chest wall and sternum, the thymus is easily demonstrable
by sonography in nearly all neonates and is often visible in
many infants and young children in the first decade of life
(sensitivity  / 95%) (12,13). It is best demonstrated
using suprasternal, transsternal, or parasternal approaches.
The thymus is more difficult to visualize in older children
and adolescents because of the aerated lung in the anterior
mediastinum and the ossified sternum, which impair trans-
mission of the sound beam, and the relatively small size of
the gland.
SONOGRAPHIC APPEARANCE
The normal thymus in infants and neonates has a quadri-
lateral shape and sharply defined, smooth, convex or
straight margins. It is hypoechoic to subcutaneous tissue
and nearly isoechoic to liver. It has a characteristic echo-
texture, with regular linear and punctate echodensities that
allow confident recognition and differentiation from medi-
astinal pathology (Fig. 5.2) (17,12,13). Even when large,
the normal thymus drapes around adjacent mediastinal
structures without displacing or deforming them. With
rare exception, the left lobe is larger than the right. Color
Doppler sonography can show small vessels in the
parenchyma of the gland (Fig. 5.2C). In older children, the
thymus assumes a triangular or arrowhead configuration
with straight or concave margins.
Measurements of thymic size have been reported for
infants and young children (1). The right lobe measures
between 0.81 and 2.35 cm (mean, 1.4 cm) in anteroposte-
rior dimension and between 1.54 and 4.02 cm (mean, 2.5
cm) in the longitudinal dimension. The left lobe measures
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166 P E D I AT R I C S O N O G R A P H Y

A B

Normal thymus. Mediastinal windows. A: Parasternal view showing

Fig. 5.2
the right thymic lobe with well-circumscribed borders (arrows) and
characteristic echotexture with regular linear and punctate echogenicities. V 
brachiocephalic vein. B: Suprasternal view in another patient showing both
thymic lobes (arrows). The thymus has a quadrilateral shape with smooth convex
margins. Again, note the characteristic echotexture. V  brachiocephalic vein.
C: Transverse color Doppler image shows small vessels coursing through the
C thymic (TY) parenchyma.

between 0.78 and 2.47 cm (mean, 1.4 cm) in the antero-

posterior dimension and between 1.79 and 4.1 cm (mean,
2.9 cm) in the longitudinal dimension. Thymic measure-
ments may change with respiratory motion, reflecting the
pliability of the organ.
The thymus may extend into the superior mediastinum,
simulating adenopathy (Fig. 5.3), or into the posterior
mediastinum, simulating neuroblastoma (14,15). Demon-
stration of continuity between the aberrant thymus and the
thymic tissue in the anterior mediastinum, an echotexture
similar to that of normal thymic tissue, and lack of com-
pression of adjacent mediastinal structures supports the
diagnosis of an ectopic thymus.
PleuraLung Interface
The normal pleuralung interface appears as a hyperechoic
line beneath the chest wall and ribs (Fig. 5.4A). The vis-
ceral pleura and aerated lung move freely along the pari-
etal pleural layer with respiration, termed the gliding
sign.
The acoustic interface of the pleura with the normal aer-
ated lung provides a strong reflective surface and produces
characteristic reverberation artifacts (Fig. 5.4B). These arti-
facts diminish in intensity with increasing distance from the
transducer. The thinner chest wall and pleura of infants may
not produce this artifact.
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Chapter 5 C H E S T 167

A B

Thymic extension into the neck. A: Transverse view to the left of midline
Fig. 5.3
shows thymus (THY) extending into the lower neck, medial to the carotid
artery and sternocleidomastoid muscle (SCM). B: Longitudinal scan. The aberrant
thymic tissue is contiguous with mediastinal thymus (THY) and has an echotexture
similar to mediastinal thymus. Linear and punctate echogenicities are typical of nor-
mal thymus. C: Longitudinal image with color Doppler imaging shows multiple small
C vessels in the ectopic tissue. CA  carotid artery.

A B
Normal pleuralung interface. A: Longitudinal image via an intercostal approach shows the strong echogenic pleural surface (arrows)
Fig. 5.4
and aerated echogenic lung (L) beneath the pleura. B: Longitudinal intercostal sonogram in another patient shows the echogenic
pleuralung interface (arrowheads) and reverberation artifacts (arrows) in distal aerated lung. R  cartilaginous ribs. (Panel B courtesy of Brian
Coley, MD.)
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168 P E D I AT R I C S O N O G R A P H Y
When the pleuralung interface is imaged using the
liver or spleen as an acoustic window, the curved surface
of the diaphragm can reflect the sound waves, producing a
mirror image of the interface between the liver or spleen
and the diaphragm (Fig. 5.5) (17,16).
Trachea
The trachea is difficult to visualize because of the
absence of an acoustic window and the air-filled lumen,
which produces reverberation artifacts. However, the
anterior wall of the trachea can be visualized when the
thymus or thyroid gland serves as an acoustic window.
Sonographically, the anterior wall of the trachea appears
as an echogenic curvilinear midline band (Fig. 5.6). The
posterior and lateral walls of the trachea are obscured by
the air-filled lumen. Because of this limitation, sonogra-
phy has no practical role in the evaluation of tracheal
abnormalities.
Pleuralung interface, mirror-image artifact. Transverse
Fig. 5.5
subcostal sonogram shows the interface between the liver
and diaphragm (1) and the hypoechoic muscular tissue of the
diaphragm (d). The second line (2) represents a mirror image of the
interface between the liver and diaphragm.
Esophagus
The esophagus is difficult to delineate by sonography
because it is usually collapsed. Sonographic demonstration
of the esophagus can be improved by having the patient
drink fluid. This is occasionally useful in establishing the
presence of gastrointestinal reflux. Although sonography is
not the primary study for documenting reflux, reflux can be
diagnosed as the cause of vomiting in some patients who
are referred for evaluation of suspected pyloric stenosis.
The diagnosis of gastroesophageal reflux is based on the
demonstration of retrograde flow of fluid and air bubbles
into the esophageal lumen (for a more detailed discussion,
see Chapter 9).
Great Vessels and Internal Mammary Compartment
The aortic arch and the brachiocephalic arteries and veins
are best seen with a suprasternal approach, while the
Normal trachea. The anterior wall of the trachea appears as
Fig. 5.6
a curvilinear echogenic band (arrow). The tracheal lumen
(Tr) is air filled, impeding sound transmission. Thy  thyroid lobes.
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Chapter 5 C H E S T 169

C
Normal mediastinal vessels. A: Transverse color flow Doppler scan through a suprasternal approach. SVC  superior vena cava; arrow 
Fig. 5.7
brachiocephalic vein. A  aortic arch. Color signal in BCV is red because blood is flowing toward the transducer. Color signal in the supe-
rior vena cava and aorta is blue because blood is flowing away from the transducer. B: Pulsed Doppler waveform of the superior vena cava shows pul-
satility due to cardiac contractions or respiratory-related motion. (Panel B courtesy of Brian Coley). C: Pulsed Doppler image of the aortic arch shows
a triphasic waveform with a sharp upswing, sharp systolic peak and early diastolic reversal.

ascending and descending aorta and main pulmonary artery
are better delineated with parasternal scans (Fig. 5.1).
Pulsed and color flow Doppler sonography are useful to
document whether a vascular structure is arterial or
venous (Fig. 5.7) (17,18). Normal veins have anechoic
lumina and imperceptible walls. Doppler waveforms in
the superior vena cava and brachiocephalic vein show
phasic changes due to right atrial contractions and respi-
ratory-related motion (Fig. 5.7B) (17,18). The luminal
diameter and flow increase with inspiration as negative
intrathoracic pressure increases and decreases during
expiration.
The aorta and major branch arteries are anechoic struc-
tures, with the walls being more echogenic than those of the
veins. Doppler waveforms in the ascending and transverse
aorta and brachiocephalic artery are characterized by a
triphasic waveform with a steep systolic rise, narrow sys-
tolic peak, early diastolic flow reversal, and forward flow at
end diastole.
The internal mammary artery and vein lie within the
adipose and connective tissue of the chest wall. They are
bordered anteriorly by intercostal muscles and costal carti-
lage and posteriorly by fascia and lung (Fig. 5.8). The ves-
sels are located within 2.5 cm of the lateral sternal border.
Above the level of the second or third rib, the vein is a sin-
gle vessel lying medial to the artery. Below this level there
are two veins, one on either side of the single artery. Exam-
ination of these vessels is best performed in the longitudinal
plane.
Diaphragm
The diaphragm is the dome-shaped musculotendinous struc-
ture that separates the thoracic and abdominal cavities, and
it is also the primary muscle of respiration. It is composed of
a central tendon and peripheral muscle leaflets. The anterior
portion of the diaphragm attaches to the posterior surfaces
of the sternum and lower six costal cartilages. The posterior
portion of the diaphragm, including the crural parts, attaches
to the anterolateral surfaces of the upper lumbar vertebral
bodies and the medial and lateral arcuate ligaments, which
cover the anterior surfaces of the psoas and quadratus
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170 P E D I AT R I C S O N O G R A P H Y
B and minimal flow at end diastole.
lumborum muscles. The central portion of the diaphragm is
attached to the pericardium. The lungs and pleura lie periph-
eral and lateral to the hemidiaphragms, while the abdominal
viscera lie central to the hemidiaphragms.
The right hemidiaphragm is usually easy to image
because the right lobe of the liver provides an excellent
acoustic window. The left hemidiaphragm is more difficult
to delineate because gas in the subadjacent stomach and
splenic flexure of the colon impedes sound transmission.
Use of the spleen or left lobe of the liver as an acoustic win-
dow or distention of the stomach with fluid, administered
orally or through a nasogastric tube, can improve delin-
eation of the left hemidiaphragm. The diaphragm is best
imaged with a subxiphoid or subdiaphragmatic approach.
The normal diaphragm appears as a relatively smooth,
slightly undulating echogenic band (Fig. 5.9). The echogenic-
ity represents a combination of echoes produced by the
lungdiaphragm, liverdiaphragm, or spleendiaphragm
Normal mammary vessels. A: Longitudinal
Fig. 5.8
parasternal image of the anterior chest
wall demonstrates the internal mammary artery
(arrow) beneath the costochondral cartilage (C) and
chest wall muscles. The hypoechoic costochondral
cartilages allow imaging through the chest wall.
B: Pulsed Doppler sonogram shows a normal wave-
form with a steep systolic rise, narrow systolic peak,
interfaces. Less commonly, the diaphragm has a scalloped or
lobulated appearance (19). The crural parts appear as rela-
tively hypoechoic, linear structures near the midline close to
the upper lumbar vertebral bodies. The larger right crus
attaches to the first three lumbar vertebrae. The smaller left
crus attaches to the first two lumbar vertebrae.
Diaphragmatic motion is assessed on images obtained
during deep inspiration and expiration (20). The transverse
plane allows simultaneous identification of both hemidi-
aphragms and thus a comparison of diaphragmatic excur-
sion, which is useful for assessing paralysis or paresis. The
longitudinal plane allows visualization of the relationship
between the diaphragm and intrathoracic structures (e.g.,
lungs and heart) and of intra-abdominal structures (e.g.,
liver and spleen), and is helpful for assessing structural
integrity and diaphragmatic hernias (1925).
Measurements for normal diaphragmatic excursion on
longitudinal scans have been established in the neonate
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A B
Normal diaphragm. Transverse (A) and longitudinal subcostal (B) scans using the liver (LIV) as an acoustic window demonstrate an
Fig. 5.9
echogenic, slightly undulating diaphragm (arrows).
(26). The excursion of the middle and posterior thirds of
the diaphragm is greater than that of the anterior third. In
the longitudinal plane, the mean excursion (and standard
deviation) for anterior, middle, and posterior thirds of the
diaphragm is 2.6  0.1, 3.6  0.2, and 4.5  0.2 mm,
respectively (26).
CLINICAL INDICATIONS
Sonography is usually performed to evaluate an abnormal-
ity seen on plain chest radiography. The common indica-
tions for sonography of the chest include (a) differentiation
of simple and complex pleural effusions; (b) differentiation
of pleural from parenchymal disease in a child with a
peripheral opacity on plain chest radiography; (c) charac-
terization of focal parenchymal masses; (d) evaluation of
an abnormal mediastinal contour, which often is a normal
thymus, (e) assessment of vascular abnormalities, such as a
superior vena caval thrombosis or an anomalous vessel in
a pulmonary sequestration; (f) evaluation of diaphrag-
matic motion and peridiaphragmatic masses; (g) charac-
terization of palpable chest wall lesions; and (h) localiza-
tion of pleural fluid for thoracentesis or a mass for biopsy.
PLEURAL DISEASES
Pleural Effusion
In evaluation of a small amount of pleural effusion, sonog-
raphy is more sensitive than supine or decubitus radi-
ographs (27). Sonography is also superior to computed
tomography (CT) in demonstrating septations within the
fluid collections (28). Recognition of the presence of sep-
tations and loculated fluid collection is important because
it means that the fluid may not be amenable to aspiration
or chest tube drainage (28).
Chapter 5 C H E S T 171
PARAPNEUMONIC EFFUSIONS
Most pleural effusions in childhood are of parapneumonic
origin (2830). A parapneumonic effusion is a pleural
effusion adjacent to infected lung. Parapneumonic effu-
sions can be further classified as exudative (i.e., purulent)
or transudative (i.e., serous). Exudates are high in protein
and lactate dehydrogenase, while transudates are low in
protein. The common causes of both types of effusions are
bacterial pneumonias and the common inciting organisms
are Staphylococcus aureus and Streptococcus pneumoniae.
Transudative effusion also can occur with other condi-
tions, including congestive heart failure, renal failure,
acute glomerulonephritis, nephrotic syndrome, cirrhosis,
hypoalbuminemia, overhydration, and pancreatitis.
HEMORRHAGIC AND CHYLOUS EFFUSIONS
Hemorrhagic effusions (hemothorax) contain a high
hematocrit level and usually follow blunt or penetrating
chest trauma, but they may be secondary to a bleeding
diathesis. Chylous effusions (chylothorax) contain intes-
tinal lymph (i.e., chyle) composed of high protein and fatty
acid and usually are a complication of thoracic or cardiac
surgery, but they can be idiopathic. Left-sided chylous effu-
sion occurs when there is an injury of the upper thoracic
duct, while right-sided chylous effusion is more often asso-
ciated with injury of the distal duct. Other causes of pleu-
ral fluid include esophageal or hypopharyngeal rupture,
inadvertent placement of a central venous catheter into the
pleural space, and direct erosion of the wall of the superior
vena cava by a total parenteral nutrition catheter.
SONOGRAPHIC EVALUATION
Pleural effusions can range from completely anechoic
to complex collections containing internal echoes,
swirling debris, and septations (Figs. 5.10 and 5.11).
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172 P E D I AT R I C S O N O G R A P H Y

Transudate. Subdiaphragmatic longitudinal sonogram

Fig. 5.10
demonstrates a large anechoic left pleural effusion (E).
The spleen (SP) serves as an acoustic window.

A B

C D
Exudates. Transverse (A) and longitudinal (B) sonograms show a large pleural effusion (E) with multiple internal echoes along with
Fig. 5.11
atelectatic lung (L). LIV  liver. C: Transverse view in another patient demonstrates a large complex pleural effusion (E) with multiple
septations adjacent to atelectatic left lower lobe (L). D: Coronal view in another patient shows a large septated effusion (E) and thickened echogenic
pleura (arrows).
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Fluid color sign. Transverse color Doppler image shows
Fig. 5.12
color signal (arrowhead) anteriorly between the visceral
and parietal pleura. Absence of flow in the remainder of the effusion
suggests high-viscosity fluid. Diagnostic percutaneous aspiration of
the anterior collection was successful.
Anechoic effusions represent exudative and transuda-
tive processes with almost equal frequency. Complex
effusions are more likely to be exudates or hemorrhagic
effusions. With moderate- or large-size pleural effu-
sions, volume loss (compressive atelectasis) occurs in
the adjacent lung (Fig. 5.10). The collapsed lobe is dis-
placed anteriorly and toward the hilum. On occasion,
large effusions can invert the diaphragm or cause
mediastinal shift. Chylous effusions can be anechoic or
complex.
Nonloculated pleural effusion changes shape and loca-
tion with patient breathing or changes in patient position-
ing (30). The normal gliding motion between the visceral
and parietal pleural surface also persists, whereas it disap-
pears in patients with loculated effusions or hydropneu-
mothorax. Mobile fluid collections show color signal dur-
ing respiratory excursions with color Doppler imaging,
termed the fluid color sign, whereas nonmobile effusions
do not (Fig 5.12). The color fluid sign is useful to distin-
guish echogenic but still fluid collections from solid organ-
ized empyema or fibrothorax (3133).
Sonography can be used to guide percutaneous
drainage and determine treatment, which is largely based
on determining whether the pleural fluid is exudative or
transudative. Simple fluid collections that change shape
with inspiration and expiration or patient positioning,
Chapter 5 C H E S T 173
Quantification of pleural fluid. Transverse view of the left
Fig. 5.13
chest shows a large pleural effusion (calipers) measuring
approximately 48 mm in both long and short axes, which corresponds
to a mean volume of slightly greater than 1000 mL.
have mobile echodensities, or show color signal are likely
to be amenable to percutaneous aspiration and conserva-
tive management (17,3133). These findings generally
indicate a relatively low-viscosity fluid collection. The
presence of septations, a honeycomb appearance, and
fixed configuration with no change in respiration or
patient position are not necessarily a contraindication to
percutaneous drainage, but they often indicate that fibri-
nolytic therapy may be required to achieve complete
drainage (1). Not unexpectedly, the length of hospitaliza-
tion is reduced when empyemas are treated early by
intervention (30).
The quantity of pleural fluid can be estimated by mea-
suring the largest perpendicular distance between the chest
wall and the lung surface, ideally during maximum inspi-
ration (34). Measurements should be made just above or
near the diaphragm. A 20-mm width corresponds approx-
imately to a mean volume of 380 mL (130 mL, standard
deviation). A 40-mm thickness corresponds to a mean vol-
ume of 1000 mL (330 mL) (34) (Fig. 5.13). Sonography
also can help guide percutaneous drainage and thoracos-
tomy tube placement (Fig. 5.14).
Fibrothorax
If incompletely treated, empyemas can progress to a
fibrothorax, characterized by extensive fibrin deposition on
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Pleural effusion aspiration. Longitudinal sonogram shows

Fig. 5.14
the aspiration catheter (arrows) in the center of a large Fibrothorax. Transverse subcostal sonogram shows a
effusion (E ). The tube was placed under ultrasound visualization. Fig. 5.15
heterogeneous, predominantly solid-appearing mass
LIV  liver. (arrowheads). LIV  liver.

A B

Pleural metastases. Chest radiograph in a 9-year-old girl

Fig. 5.16
with metastatic osteosarcoma showed an opacified left
hemithorax. A: Longitudinal sonogram shows a pleural effusion (E )
and multiple echogenic, pleural-based metastases (arrows). B: More
medial view shows effusion (E), atelectatic lung (L), and an echogenic
nodule (arrow) with acoustic shadowing representing a calcified
parenchymal metastasis. C: Computed tomography (CT) scan con-
firms pleural-based metastases (M). The pleural effusion had been
C partially drained prior to the CT scan.
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Chapter 5 C H E S T 175

A B

Hemangioma. Transverse gray-scale (A) and longitudinal

Fig. 5.17
color Doppler (B) images in a newborn girl with respiratory
distress show a large mass (arrows) with internal flow at the right
lung base. C: Axial computed tomography scan shows a vascular
mass abutting the chest wall. At surgery, the mass was separate from
the lung and chest wall and probably arose from the pleura or soft
C tissues.

the pleural surface and loculated fluid. Sonographic
findings are a homogeneous or heterogeneous, solid-
appearing, echogenic mass encasing the underlying lung
(Fig. 5.15).
Pleural Masses
Metastases to the lung can occur with Wilms tumor or
sarcomas. Sonographic findings include solid masses
adjacent to the parietal or visceral pleura and pleural
effusion (Fig. 5.16). The effusion is often hemorrhagic and
contains echogenic debris. Other findings include medi-
astinal lymph node enlargement, lung metastases, and
chest wall invasion. Benign causes of pleural thickening
include hemangioma and lymphangioma (Fig. 5.17).
Pneumothorax
Sonography does not have a role in the diagnosis of
pneumothorax, but knowledge of the sonographic
appearance of pneumothorax is important because it
may be detected incidentally during an examination per-
formed for another clinical indication. When air is pres-
ent in the pleural space, the expected gliding motion
between the visceral and parietal pleura can no longer be
seen and the expected reverberations are replaced by
homogeneous posterior acoustic shadowing (35,36). An
air-fluid level may be demonstrated in patients with
hydrothorax (37).
PARENCHYMAL DISEASE
Atelectasis and Consolidation
Atelectatic or consolidated lung allows transmission of the
ultrasound beam (3840). The echogenicity of nonaerated
lung appears similar to the liver, termed hepatization.
Bronchi are commonly seen in areas of consolidation.
Air-filled bronchi appear as branching linear echogenici-
ties with acoustic shadowing, the sonographic air
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176 P E D I AT R I C S O N O G R A P H Y
A B
Consolidated lung with sonographic air bronchograms. A, B: Transverse scans in two different patients show echogenic lower lobe
Fig. 5.18
consolidations (arrows) with bright echogenic reflections representing air bronchograms (open arrows). E  pleural effusion.
bronchogram (3840) (Fig. 5.18). Fluid- or mucoid-filled
bronchi appear as hypoechoic branching structures, the
sonographic fluid bronchogram (Fig. 5.19). Pulmonary
flow is preserved in uncomplicated pneumonic consolida-
tion and is easily seen with color Doppler imaging. With
atelectasis, the vessels are more closely apposed and have
a more parallel orientation than they do in consolidated
lung.
Consolidated lung with sonographic fluid bronchogram.
Fig. 5.19
Longitudinal sonogram of the lower right chest demon-
strates hypoechoic consolidated lung (arrowheads) with an anechoic
tubular structure representing a fluid-filled bronchus (arrows).
Parenchymal or Pleural Disease
The sonographic features that are helpful in separating a
pleural effusion and lung consolidation or atelectasis are
the shape of the lesion, the margins, the echotexture, and
the presence of air or fluid bronchograms. Fluid collections
usually have an elliptical or lenticular shape, a sharp inter-
face with the chest wall and adjacent lung, and an anechoic
or hypoechoic echotexture. Bronchi and vessels are not
seen in the pleural space. Consolidated and atelectatic lung
are often poorly defined, wedge shaped, and solid appear-
ing and may contain bronchi and vessels.
Lung Necrosis and Abscess
In children, primary lung abscesses are due to necrotizing
pneumonia. Secondary lung abscesses are associated with
sequestration, cystic adenomatoid malformation, lung
cyst, or pneumatocele (4146).
Necrotizing pneumonia develops when the infected
lung compresses and occludes alveolar capillaries, leading
to decreased perfusion of the pulmonary parenchyma
(42,44). Areas of necrosis may appear as poorly mar-
ginated hypoechoic areas showing decreased or absent
flow on color Doppler imaging (Fig. 5.20).
The sonographic findings of an abscess are a spherical
or ovoid hypoechoic mass with thick, irregular walls and
central echogenic debris or brightly reflective foci with
acoustic shadowing representing air bubbles (Figs. 5.21
and 5.22). An air-fluid level may be observed, particu-
larly if the patient is scanned in an erect or semierect
position (46). When the abscess adheres to the pleura, the
normal hyperechoic pleural line and gliding motion of
the lung are no longer seen (46). If an abscess is identi-
fied, sonography can be used to guide percutaneous nee-
dle aspiration.
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Chapter 5 C H E S T 177

A B
Necrotizing pneumonia A: Transverse sonogram of the right lower hemithorax in a 4-year-old boy demonstrates heterogeneous lung
Fig. 5.20
parenchyma with poorly defined, hypoechoic areas surrounded by consolidated lung (L). B: Axial computed tomography scan shows
low-attenuation foci of necrosis (arrows), decreased contrast enhancement in the consolidated lung, and a right pleural effusion. (Case courtesy of
Edward Lee, MD.)

CONGENITAL LUNG ANOMALIES veins in these disorders are demonstrable by pulsed or

color flow Doppler imaging, especially in neonates.
Congenital pulmonary anomalies represent a continuum of
Congenital lesions can be detected prenatally on sonog-
maldevelopment that involves the pulmonary parenchyma,
raphy or magnetic resonance imaging (MRI), appearing as
the pulmonary vessels, or a combination of both (47,48).
solid or cystic masses. Postnatally the lesions can be inci-
Congenital lobar emphysema, bronchogenic cyst, and cys-
dental findings on chest radiography or detected on studies
tic adenomatoid malformation are abnormalities with
performed for evaluation of respiratory distress. Plain radi-
abnormal lung parenchyma and normal pulmonary ves-
ographs are often diagnostic. However, immediately after
sels. Pulmonary sequestration and hypogenetic lung syn-
birth, congenital anomalies can appear opaque secondary
drome have a combination of pulmonary and vascular
to retained fetal lung fluid, mimicking an intrathoracic
abnormalities. Pulmonary arteriovenous malformation is
characterized by abnormal vessels within normal lung
parenchyma. The anomalous feeding arteries or draining

Abscess. Transverse view of the right upper lung in an

Lung abscess. Transverse sonogram of the left lower lobe
Fig. 5.21
shows an oval-shaped hypoechoic mass with thick and
irregular walls (arrows). (Case courtesy of Edward Lee, MD.)
Fig. 5.22
immunocompromised patient shows a hypoechoic, thick-
walled mass (arrows) containing hyperechoic focus, representing gas
(arrowheads). (Case courtesy of Brian Coley, MD.)
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178 P E D I AT R I C S O N O G R A P H Y
Congenital lobar emphysema. Anteroposterior chest radi-
Fig. 5.23
ograph (not shown) revealed an opacified right upper
hemithorax. Transverse sonogram shows acoustic enhancement
(sound transmission) (*) in the near field consistent with a fluid-filled
right upper lobe. (Normally aerated lung would show loss of sound
transmission distal to the pleuralung interface.) The ribs (R) produce
acoustic shadowing.
mass or pleural effusion. In this circumstance, sonography
can be useful in characterization and diagnosis.
Anomalies with Normal Vasculature
CONGENITAL LOBAR EMPHYSEMA
Congenital lobar emphysema is a condition characterized
by hyperinflation of a lobe without destruction of alveolar
septa. Bronchial obstruction, likely due to primary carti-
lage deficiency, is thought to be the cause of emphysema.
The left upper lobe is involved in about 45% of cases, the
right middle lobe in 30%, the right upper lobe in 20%,
and two lobes in 5% of cases (49).
Fluid-filled lobar emphysema appears as a homoge-
neous, hypoechoic lobe with enhanced sound transmission
and atelectasis of the ipsilateral lobe (Fig. 5.23). Color
Doppler sonography can demonstrate attenuated vessels in
the periphery of the hyperexpanded lobe.
INTRAPULMONARY BRONCHOGENIC CYST
Intrapulmonary bronchogenic cyst results when there is
failure of incorporation of part of the fetal lung bud into
the primitive lung tissue (50). It may contain air or serous
or mucoid fluid. The sonographic appearance is that of a
unilocular, rounded mass with sharply marginated smooth
walls (51). Predominantly fluid-filled cysts appear hypo-
echoic (Fig. 5.24), while cysts containing fluid and air have
Bronchogenic cyst. Chest radiography in a newborn boy
Fig. 5.24
with mild dyspnea showed a left apical opaque mass.
Transverse sonogram shows a smoothly marginated, fluid-filled cyst
(C) just beneath the rib (arrow).
a complex pattern with both hypoechoic and echogenic
components. Color signal may be present in the cyst wall.
CYSTIC ADENOMATOID MALFORMATION
Cystic adenomatoid malformation is a mass of disorgan-
ized pulmonary tissue that has a normal communication
with the bronchial tree and normal vascular supply and
drainage (52). The cause is believed to be an overgrowth of
distal bronchiolar structures (53). It may involve a lobe or
part of a lobe. Pathologically, three major histologic types
are recognized: type I (50% of cases) contains a single or
multiple large cysts (2 meters in diameter); type II (41%)
contains multiple small cysts (1 to 10 mm in diameter); type
III (9%) is a solid lesion to visual inspection, but contains
microscopic cysts (53). Associated anomalies of the kid-
neys, bowel, heart, and skeletal system are common in
types II and III malformations (52,53).
The sonographic features of cystic adenomatoid mal-
formation correspond to the histologic types. Types I and
II appear as a complex mass containing fluid-filled spaces
and echogenic septations (Figs. 5.25 and 5.26). Type III
malformations appear solid (Fig. 5.27). Acoustic shadow-
ing occurs when the cysts contain air. Pulsed and color
flow Doppler imaging show an avascular mass. The major
differential diagnostic considerations are pleuropulmonary
blastoma and mesenchymal hamartoma (see discussions
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Cystic adenomatoid malformation, type I. Transverse view
Fig. 5.25
of the right lower lung in a 1-week-old girl with an abnormal
chest radiograph obtained for respiratory distress demonstrates a fluid-
filled cystic lesion with thin walls (Case courtesy Edward Lee, MD.)
later in this chapter). Both lesions appear as complex cys-
tic masses.
Anomalies with Abnormal Vasculature
BRONCHOPULMONARY SEQUESTRATION
Bronchopulmonary sequestration is a mass of nonfunc-
tioning pulmonary tissue that has no normal connection
with the tracheobronchial tree and is supplied by an anom-
alous systemic artery, usually arising from the aorta
(54,55). The sequestered lung is termed intralobar or
acquired confined when it enclosed by the normal vis-
ceral pleura and has venous drainage to the pulmonary
veins. The arterial supply is usually from the descending
thoracic aorta (about 75% of cases) and occasionally from
Cystic adenomatoid malformation, type III. Longitudinal
Fig. 5.27
sonogram shows an echogenic mass in the lower lobe
without demonstrable cysts causing mass effect on the adjacent
diaphragm (arrowhead).
Chapter 5 C H E S T 179
Cystic adenomatoid malformation, type II. Longitudinal
Fig. 5.26
view of the right lower chest in a newborn boy with a pre-
natal diagnosis of a right lower lobe mass shows an echogenic mass
containing multiple small cysts (1 cm in diameter). LIV, Liver.
intercostal, subclavian internal thoracic, or pericardio-
phrenic arteries. About 10% of patients have other con-
genital anomalies, including esophagobronchial fistulas,
cystic adenomatoid malformation, and congenital lobar
emphysema.
The sequestered lung is termed extralobar or con-
genital when it has its own pleura and venous drainage to
systemic veins. Extralobar sequestrations may arise above
or below the diaphragm. The arterial supply is often from
the thoracoabdominal aorta or upper abdominal aorta,
but it may be from splenic, gastric, or celiac arteries. About
65% of extralobar sequestrations have associated anom-
alies, including cystic adenomatoid malformation, usually
type II; pulmonary hypoplasia; diaphragmatic eventration
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180 P E D I AT R I C S O N O G R A P H Y

A B

Intralobar sequestration. A: Transverse sonogram of the

Fig. 5.28
right lower hemithorax shows an echogenic mass (arrow-
heads) with an anomalous arterial supply (A) above the right hemidi-
aphragm (curved arrow). LIV  liver. B: Longitudinal sonogram of the left
lower chest in another infant shows an echogenic mass (arrows) with
highly reflective linear structures that represent air bronchograms.
SPL  spleen. C: Color Doppler sonogram of the patient in panel B shows
the feeding vessel (straight arrows) arising from the aorta and supplying
C the sequestered lung (open arrows).

and hernia; esophagobronchial fistula; and skeletal and
cardiac anomalies (55).
Patients with intralobar sequestrations usually present
in childhood or later in life with signs of chronic or recur-
rent segmental or subsegmental pneumonitis, especially at
a lung base. By comparison, approximately 60% of
extralobar sequestrations are diagnosed in infancy, usu-
ally in the first 6 months of life (55). They may cause res-
piratory distress or present as abdominal masses or
incidental findings on chest radiographs. Extralobar
sequestration has also been associated with maternal
polyhydramnios and hydrops and neonatal anasarca (56).
Typically, sequestrations appear as solid echogenic
masses (Figs. 5.28 and 5.29) (5759). Intralobar seques-
tration can show cystic changes due to superimposed infec-
tion (5759) and in both types there may be cystic compo-
nents if there is an associated cystic adenomatoid
malformation (Fig. 5.30) (60,61). Sequestered lung may
also contain small fluid- or air-filled bronchi (Fig. 5.28).
The key diagnostic feature of sequestration is the presence
of systemic arterial supply (55,56,62) (Figs. 5.28C, 5.29B,
and 5.30B). Color Doppler sonography can show the feed-
ing vessel in neonates and infants. In older patients, CT
and MRI are often required for diagnosis.
HYPOGENETIC LUNG SYNDROME
Hypogenetic lung syndrome, also known as congenital
venolobar syndrome and scimitar syndrome, refers to pul-
monary hypoplasia, usually right sided, accompanied by
ipsilateral anomalous pulmonary venous return. The
anomalous return is commonly into the inferior vena cava,
but it may also drain into the right atrium, superior vena
cava, azygous vein, portal vein, or hepatic vein. Other vari-
able features include an absent or small ipsilateral pul-
monary artery; anomalous arterial supply to the hypoplas-
tic lung; ipsilateral diaphragmatic abnormalities, including
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C D
Extralobar sequestration. Two-week old boy with a left lower lobe density seen on chest radiography. A: Longitudinal sonogram shows
Fig. 5.29
an echogenic mass (calipers) above the left kidney (LK). B: Color Doppler sonogram shows a large feeding artery (arrow) arising from
the upper abdominal aorta (A) feeding the sequestration. LK  left kidney. C: Pulsed Doppler sonogram shows a low-resistance arterial waveform.
D: Contrast-enhanced computed tomography scan shows the feeding artery (arrow) arising from the upper abdominal aorta.

A B
Extralobar sequestration with cystic adenomatoid malformation. A: Transverse sonogram shows an echogenic paraspinal mass
Fig. 5.30
(arrows) with cystic and solid components. SP  spine. B: Transverse Doppler image shows a large feeding vessel (arrowhead) with
an arterial waveform arising from the aorta (A).
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182 P E D I AT R I C S O N O G R A P H Y

A B
Scimitar syndrome. Longitudinal gray-scale (A) and color Doppler (B) sonograms show an anomalous vein (arrows) draining into the
Fig. 5.31
right atrium (RA). Color signal is red because the flow is toward the transducer.

accessory hemidiaphragm and diaphragmatic hernia; and PULMONARY NEOPLASM

pulmonary isomerism resulting in a left bronchial branch-
Primary lung neoplasms are rare in children. Pleuropul-
ing pattern (63,64). Cardiovascular anomalies occur in
monary blastoma (also known as pulmonary blastoma) is
approximately 25% of patients, the most common being
the most common. It is a malignant tumor occurring pri-
atrial septal defect, followed by ventricular septal defect,
marily in children younger than 5 years of age. Histologi-
tetralogy of Fallot, and patent ductus arteriosus.
cally, it contains primitive blastemal and sarcomatous
Patients with marked pulmonary hypoplasia are often
symptomatic in early infancy or childhood and present
with dyspnea or cyanosis. Patients with milder degrees of
hypoplasia may be asymptomatic. In these patients, the
lesion is detected incidentally on chest radiography done
for investigation of a heart murmur or respiratory infec-
tion. Sonography can confirm the diagnosis by demon-
strating the anomalous vein (Fig. 5.31).

PULMONARY ARTERIOVENOUS MALFORMATION

Pulmonary arteriovenous malformation (AVM) is charac-
terized by a direct communication between a pulmonary
artery and vein without an intervening capillary bed. It is
usually supplied by one artery and drained by one vein,
although multiple feeding arteries and draining veins may
be present (65,66). Most occur in the lower lobes, and both
lungs are involved with equal frequency. Approximately
60% occur in patients with Rendu-Osler-Weber disease
(hereditary hemorrhagic telangiectasia). Conversely, about
15% of patients with this condition have pulmonary arte-
riovenous malformations. Symptoms include cyanosis,
polycythemia, dyspnea, and clubbed fingers, caused by
arteriovenous shunting.
Vascular malformations appear on gray-scale images as
hypoechoic round or tubular structures (Fig. 5.32). Pulsed Pulmonary arteriovenous malformation. Transverse view
Doppler imaging shows elevated systolic and diastolic flow Fig. 5.32
in a cyanotic infant girl with a right lower lobe mass on
velocities and arterialization in the draining vein. Color chest radiography shows a complex mass with multiple anechoic
Doppler imaging demonstrates turbulent flow within the channels (arrows) at the right lung base. Doppler waveform shows
malformation. The pulmonary parenchyma is normal. high diastolic arterial flow.
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Chapter 5 C H E S T 183

A B
Normal thymus. A: Frontal radiograph of a 4-month-old girl with fever shows right upper hemithorax opacity (arrow). B: Transverse
Fig. 5.33
sonogram demonstrates a normal right thymic lobe (TY) with linear and punctate echogenicities and smooth, well-defined borders
conforming to the contours of the superior vena cava (SVC).

tissue. It can arise from the lung, pleura, or both and it
can be cystic or solid or mixed on imaging studies
(6769). Other rare tumors include rhabdomyosarcoma,
leiomyosarcoma, hemangiopericytoma, and bronchogenic
carcinoma. Although sonography can confirm the
presence of a mass, definitive diagnosis requires tissue
sampling.
can confidently exclude pathology and obviate further
imaging evaluation.
TERATOMA
Teratoma is a complex mass with well-defined walls and
an admixture of tissues, including sebum or serous fluid,
which appears hypoechoic, and hair, calcifications, bone,
or fat, which appears hyperechoic (Fig. 5.34) (7072).

MEDIASTINUM
Chest masses in infants and children are most commonly
located within the mediastinum (70). The plain chest
radiograph remains the imaging study of choice for
detecting mediastinal masses. CT and MRI are the pro-
cedures of choice to follow chest radiography for further
evaluation of the nature, site of origin, and extent of a
mediastinal lesion. Sonography is not routinely used for
evaluation of the mediastinum, although in the neonate
or young infant, sonography can characterize the cystic,
solid, or vascular nature of the lesion if it is located close
to the diaphragm or thymus, which can serve as an
acoustic window. Masses also can be detected inciden-
tally on examinations performed for other clinical
indications.

Anterior Mediastinal Masses

NORMAL THYMUS
An abnormally shaped or enlarged thymus can mimic a
mediastinal mass or upper lobe consolidation or atelecta-
sis on conventional radiography. In these cases, the char-
acteristic sonographic findings of normal thymic tissue,
which are an echogenic mass with linear and punctate
echogenicities draping over the great vessels (Fig. 5.33),
Mediastinal teratoma. Transverse sonogram in a neonate
Fig. 5.34
at the level of the diaphragm shows a complex lesion
(arrows) with cystic and solid components. (Case courtesy of Brian
Coley, MD.)
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184 P E D I AT R I C S O N O G R A P H Y
A B
C anterior mediastinal nodes (arrows) and also thymic (TY) infiltration.
Because teratomas are nonpliable, they compress and dis-
place adjacent structures. They are typically avascular or
hypovascular on Doppler interrogation.
LYMPHOMA
Lymphoma, especially Hodgkin disease, is the most com-
mon malignant tumor involving the mediastinum in chil-
dren and adolescents (73). Mediastinal involvement may
appear as discrete lymph node enlargement, diffuse thymic
infiltration, or both. Lymphoma tends to be hypoechoic
(Fig. 5.35). The infiltrated thymus is commonly heteroge-
neous with convex or lobulated borders. An infiltrated thy-
mus loses its pliability, and it may deform and displace
adjacent structures instead of normally conforming to
their shape. Lymphoma is relatively avascular on Doppler
Hodgkin lymphoma. A: Left anterior parasternal view in a
Fig. 5.35
21-year-old woman demonstrates small hypoechoic lymph
node (arrows) in the anterior mediastinum. The sonogram was per-
formed to localize a site for biopsy. PA  pulmonary artery. B: Color
Doppler sonogram shows no flow in the nodes. C: Computed tomogra-
phy image at the level of the pulmonary outflow tract shows multiple
imaging compared with inflammatory and malignant
adenopathy secondary to metastases, which are often
hypervascular.
CYSTIC LESIONS
Thymic cysts arise from remnants of the thymopharyngeal
duct or from cystic degeneration of the thymus itself
secondary to mediastinal trauma or surgery. They can occur
anywhere along the course of thymic descent from the
mandible to the diaphragm. Typically, thymic cysts are
unilocular masses with thin walls and anechoic contents,
but they can be septated or contain internal echoes if the
contents are hemorrhagic or proteinaceous. Cysts associated
with human immunodeficiency virus infection are often
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Chapter 5 C H E S T 185

A B
Cystic hygroma. Two-month-old girl with a neck mass and mediastinal widening on chest radiography. A: Transverse sonogram using
Fig. 5.36
the suprasternal notch as a window shows a septated cystic mass (calipers) anterior to superior vena cava (SVC). B: Coronal Half
Fourier Acquisition Single Shot Turbo Spin Echo (HASTE) magnetic resonance image shows a complex cystic mass superior to the heart (H).

multiseptated and may cause diffuse thymic enlargement
(74,75).
Lymphangiomas are congenital malformations of the
lymphatic channels. Pathologically, they contain dilated lym-
phatic spaces separated by connective tissue. Most affected
children present in the first year of life with a posterior cer-
vical mass. Approximately 10% of these tumors extend into
the anterior mediastinum (76). Sonography shows multiple
cysts with intervening echogenic septa (Fig. 5.36). The cyst
contents are usually anechoic, but increased echogenicity or
solid areas may be noted if there is superimposed hemor-
rhage or infection. Color Doppler imaging shows a predom-
inantly avascular mass with scattered flow in the soft tissue
components. Aneurysmal dilatation of the jugular vein,
innominate vein, axillary vein, or superior vena cava also
may be noted (77).
Middle Mediastinal Masses
Middle mediastinal masses are usually adenopathy sec-
ondary to infection, lymphoma, or metastatic disease, and
foregut malformations.
ADENOPATHY
Enlarged lymph nodes appear as multiple discrete or con-
fluent hypoechoic or isoechoic masses relative to adjacent
muscle. Flow in the central hilar area can be seen on color
Doppler sonography.
FOREGUT CYSTS
Foregut cysts are classified as bronchogenic, enteric, or
neurenteric. Bronchogenic cysts are lined by respiratory
epithelium and most are located in the subcarinal or right
paratracheal regions. Enteric duplications are lined by gas-
trointestinal mucosa and usually are located close to or within
the esophageal wall. Neurenteric cysts are lined by gastroin-
testinal epithelium and are connected to the meninges
through a midline defect in one or more vertebral bodies.
Foregut cysts, regardless of type, appear as well-
circumscribed, thin-walled hypoechoic lesions with
increased sound transmission (Fig. 5.37). The echogenicity
increases if the cysts contain mucoid or proteinaceous
material, debris, or air. Uncomplicated cysts are avascular.
Flow may be noted within the wall or surrounding soft tis-
sues if the cyst is infected.
Posterior Mediastinal Masses
NEUROBLASTOMA
Posterior mediastinal masses usually arise from neural
crest cells within the sympathetic ganglia. In order of
decreasing frequency, they include neuroblastoma,
ganglioneuroblastoma, and ganglioneuroma. Posterior
mediastinal masses are best visualized using a posterior
thoracic or subxiphoid approach. Neuroblastoma tends to
affect infants and children younger than 5 years of age. It
appears as a sharply marginated, fusiform paraspinal
mass. It is commonly isoechoic or hyperechoic relative to
the thymus or chest wall muscle and it may contain hypo-
echoic areas representing cystic necrosis or degeneration
and highly reflective areas due to calcification (Fig. 5.38).
Peripheral or central flow may be noted on color Doppler
evaluation. Neuroblastoma can extend through the neural
foramina causing extradural cord compression, which can
be recognized by sonography.
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A B
Esophageal duplication cyst. A: Anteroposterior chest radiographs in a 3-year-old boy with wheezing and cough shows a right-sided
Fig. 5.37
mediastinal mass (arrows). B: Longitudinal sonogram shows a right paratracheal cyst (C). Tr  trachea.

A B

Neuroblastoma. Two-week-old girl with a right apical

Fig. 5.38
mass. A: Transverse scan through the upper chest
shows a solid mass (arrows) adjacent to a rib (R). B: Color Doppler
image shows internal flow. C: Axial computed tomography scan
C shows an apical paraspinal mass with faint calcifications.
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Chapter 5 C H E S T 187

Pericardial cyst. Transverse sonogram in a neonate with a

Fig. 5.39
right cardiophrenic mass on chest radiography demon-
strates a complex pericardial cyst (PC) adjacent to the heart (H). The
echoes posteriorly represent blood.
Acute venous thrombosis. Infant with a swollen upper
Fig. 5.40
extremity and a previous indwelling catheter in the supe-
rior vena cava. Transverse sonogram shows echogenic thrombus
Cardiophrenic Angle Masses (calipers) in the left brachiocephalic vein.
Pericardial cysts arise from remnants of the coelomic ven-
tral parietal recesses that fail to fuse with the pericardial
cavity. They are commonly located in the right cardio-
phrenic angle, but they can be found anywhere along the
pericardium (78). They typically are unilocular, round or
ovoid shaped, well marginated, and anechoic or hypo-
echoic (Fig. 5.39). The echogenicity increases if the fluid is
hemorrhagic or proteinaceous. Pericardial cysts are pliable
and usually do not displace or compress adjacent struc-
tures. Most are incidental findings on chest radiographs.

VASCULAR ABNORMALITIES
Venous Thrombosis and Stenosis
The most common indication for sonography of the
intrathoracic vessels is suspected venous thrombosis, which
is usually due to an indwelling vascular catheter (79). Acute
thrombus appears as echogenic material partially or com-
pletely filling the vessel lumen (Fig. 5.40). The echogenicity
of the thrombus decreases as the hemoglobin is resorbed
and the clot involutes and retracts. The sonographic findings
of chronic thrombus are an anechoic or hypoechoic clot and
collateral vessel formation. Because clot can be hypoechoic
or anechoic, Doppler imaging is important for diagnosis.
Patent central veins show marked phasicity due to car-
diac and respiratory activity and even reversed flow during Superior vena cava stenosis. Pulsed Doppler sonogram of
atrial systole (see Fig. 5.7). Doppler findings of stenosis Fig. 5.41
the superior vena cava (arrow) shows a patent vessel
include absence of flow, loss or dampened phasicity, with loss of normal phasicity. A subsequent venogram (not shown)
increased downstream flow velocity, and decreased upstream demonstrated stenosis of the superior vena cava, attributed to use of
velocity (Fig. 5.41) (17). indwelling vascular catheters. (Case courtesy of Brain Coley, MD.)
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188 P E D I AT R I C S O N O G R A P H Y
Congenital Arch Anomalies
Anomalies of arch position, such as double- or right-sided
arch, can alter the mediastinal contour on plain chest radi-
ographs and mimic a mass (80,81). Sonography can
demonstrate the nature of these findings if the abnormali-
ties are near an acoustic window. Following surgical repair
of congenital heart disease, sonography has also been used
to evaluate vascular patency.
Arterial Stenosis and Aneurysm
Arterial stenosis and aneurysm formation can occur in asso-
ciation with vascular disorders, such as Kawasaki disease,
Takayasu disease, and giant cell arteritis; with infection; or
as a complication of vascular access procedures. Arterial
stenoses produce delayed systolic upstroke, elevated peak
systolic flow, and decreased diastolic flow. The sonographic
findings of aneurysm include vessel dilatation and turbulent
flow in the enlarged segment on Doppler imaging.
Internal Mammary Compartment
The internal mammary artery and vein can act as path-
ways of collateral vascular flow. Dilatation of the internal
mammary artery has been associated with aortic coarcta-
tion and palliative surgical shunts for cyanotic heart dis-
ease (6). Gray-scale sonography can show the dilated
mammary artery. Doppler interrogation of collateral arte-
rial formation shows flow reversal and a broadened sys-
tolic peak with high diastolic flow velocity (6).
Dilatation of the internal mammary vein and collateral
vessel formation has been associated with obstruction of
the superior vena cava by thrombosis or compression by a
mediastinal mass. Blood flow becomes retrograde. Gray-
scale imaging can detect the dilated internal mammary
vein and Doppler sonography can confirm reversed venous
flow (6).
ESOPHAGUS AND TRACHEA
Esophagus
Sonography can be used to diagnose esophageal atresia
when there is both esophageal and gastric atresia without
fistula formation. The diagnosis is based on the demonstra-
tion of a distended fluid-filled proximal esophageal segment.
Tracheobronchial Tree
Sonography has been used to evaluate endotracheal
tube malpositioning (82) and vocal cord anatomy (83).
Endotracheal tubes appear as continuous, circumferential
linear echodensities in comparison to the anterior curvilin-
ear echogenic band seen in nonintubated patients. The dis-
tal end of the tube can be easily recognized by gently mov-
ing the tube in the airway.
Sonographic images of the true cords can be obtained
using a phased array transducer and the thyroid cartilage
as an acoustic window (83). The true cords are hypoechoic
since they contain mostly muscle, while the false cords are
echogenic due to the presence of fibrofatty tissue. The
abduction/adduction movements of the cords can be seen
during respiration on real-time imaging. Normal cord
motion is rapid and symmetric (83). In general, as sonog-
raphy is time consuming and does not provide detailed
anatomic data, it has not gained widespread acceptance in
evaluation of the airway.
DIAPHRAGMATIC LESIONS
The common indications for sonography of the diaphragm
are evaluation of a suspected diaphragmatic hernia or
eventration, delineation of juxtadiaphragmatic masses,
and evaluation of diaphragmatic motion.
Diaphragmatic Hernias
BOCHDALEK HERNIA
A Bochdalek hernia is a congenital defect resulting from
incomplete closure of the embryonic pleuroperitoneal
membrane. It is posterolateral in location and is left sided
in about 80% of patients and right sided in the remainder.
The left-sided predominance is attributed to the protective
effect of the liver on the right side. Bilateral hernias occur
but are extremely rare (84).
The diagnosis of Bochdalek hernia is often made by
prenatal sonography. Postnatally, neonates with Bochdalek
hernia present with tachypnea, dyspnea, and cyanosis at
birth. Classically, they have a scaphoid abdomen and an
asymmetric chest. The diagnosis can easily be established
when the chest radiograph demonstrates air-filled loops of
intestine in the thorax. Sometimes, however, the diagnosis
is not obvious because the bowel loops contain fluid rather
than air. In these instances, sonography becomes a valu-
able diagnostic tool to show the diaphragmatic disruption.
Occasionally, the diagnosis is not made until later in the
neonatal period when patients present with dyspnea or
vomiting. Delayed-onset Bochdalek hernias have been
associated with group B streptococcal pneumonia and are
more often right than left sided (85).
Left-sided defects can contain the left lobe of the liver, the
spleen, the stomach, the large or small bowel, or the kidney.
Right-sided defects contain the large right lobe of the liver
and occasionally other abdominal viscera. Right-sided defects
can be associated with hydrothorax, ascites, and Budd-Chiari
syndrome, the latter occurring secondary to compression or
occlusion of lymphatic vessels or hepatic veins by the free
edge of the diaphragmatic defect. Other anomalies associated
with Bochdalek hernia include congenital heart disease, mal-
rotation, and malformation syndromes including trisomy 18,
trisomy 21, Fryn syndrome (diaphragmatic hernia, coarse
facies, macrostomia, pulmonary hypoplasia, and distal limb
defects), and tetrasomy 12p mosaicism (craniofacial, cuta-
neous, and neurologic manifestations) (84). The major com-
plications associated with Bochdalek hernia are pulmonary
hypoplasia and persistent fetal circulation.
MORGAGNI HERNIA
Morgagni hernia occurs in the anterior muscular part of
the diaphragm. It results from failure of fusion of the
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Chapter 5 C H E S T 189

costal and xiphoid fibrotendinous components of the ACQUIRED HERNIA

diaphragm and is commonly right sided because the left-
sided defects are covered by the heart and pericardium.
Bilateral lesions can occur. Infants with Morgagni hernias
can be symptomatic and present with acute respiratory dis-
tress and cyanosis. Older children are usually asympto-
matic, and the diagnosis is made on a chest radiograph
obtained for other clinical indications.
The Morgagni hernia typically contains omentum,
transverse colon, and liver. Small bowel and stomach
rarely comprise the hernia contents. Anomalies associated
with Morgagni hernia include Down syndrome and
Cantrell pentad (upper midline omphalocele syndrome)
(84).
Acquired hernias are the result of penetrating or blunt
abdominal trauma. The left hemidiaphragm is more often
involved in blunt trauma, because the liver protects the right
side. Most tears involve the peripheral portion of the
diaphragm at the junction of the tendon and posterior leaves.
SONOGRAPHIC FINDINGS OF DIAPHRAGMATIC HERNIA
The characteristic sonographic findings of congenital and
acquired diaphragmatic hernias are discontinuity of the
normal linear diaphragmatic echoes and the presence of
abdominal contents (i.e., bowel, liver, spleen, kidney, and
omentum) in the ipsilateral hemithorax (Figs. 5.42 and

A B

Bochdalek hernia. A: Frontal chest radiograph of a new-

Fig. 5.42
born boy with respiratory distress shows opacity in the left
lower hemithorax. B: Longitudinal sonogram shows herniated bowel
(arrows) in the lower hemithorax. The echogenic foci represent intralu-
minal meconium. Aerated lung (L) is displaced away from the chest
wall. C: Transverse view in another infant shows a defect in the right
hemidiaphragm (arrow) with herniation of liver (LIV) and bowel (B) into
C the chest adjacent to the heart (H).
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190 P E D I AT R I C S O N O G R A P H Y
C permission.)
5.43) (86). The echogenicity of the hernia varies with its
contents. A hernia containing predominantly solid organs
such as the liver or spleen or air-filled bowel loops appears
echogenic, while one that contains fluid-filled bowel
appears hypoechoic. Sonographic findings that may be
present when there is incarceration of the liver include
absent intrahepatic venous waveforms, hydrothorax,
ascites, and a fluid-filled peritoneal sac.
Herniated omentum can appear hypoechoic, iso-
echoic, or hyperechoic relative to the liver. Pulsed or color
flow Doppler imaging shows omental vessels in the lower
chest.
Eventration
Eventration of the diaphragm is the result of a congenital
weakness or thinness of the central tendon or muscle (87).
The cause is thought to be hypoplasia of the diaphragmatic
muscle. Eventration is more often left sided than right
sided and the defect is usually focal, affecting the antero-
medial portion of the diaphragm. Occasionally, it involves
the entire hemidiaphragm. Most eventrations are clinically
insignificant and detected incidentally on chest radi-
Morgagni hernia. Newborn boy with an abnormal
Fig. 5.43
fetal sonogram showing right hemithorax mass.
A: Chest radiograph demonstrates a right cardiophrenic mass.
B: Longitudinal sonogram shows liver (LIV) anterior to the lung
(L). Arrow indicates the hepatic vein. C: Sagittal color Doppler
sonogram in a 7-day-old boy shows herniation of the liver (L)
through an anterior defect in the diaphragm (arrow). Note the
abnormal course of the hepatic vein. A  intra-abdominal part
of the liver; T  intrathoracic part of the liver. (Panel C reprinted
from Taylor GA, Atalabi OM, Estroff JA. Imaging of congenital
diaphragmatic hernias. Pediatr Radiol 2009;39:116, with
ographs. Large eventrations in neonates may cause respi-
ratory distress.
Sonographic findings of eventration include a focally
thinned but intact diaphragm that protrudes cephalad into
the ipsilateral hemithorax and is adjacent to the liver or
spleen (Fig. 5.44). Diaphragmatic motion is decreased or
absent. When the diaphragmatic muscle is extremely thin,
it may not be possible to distinguish between eventration
and true diaphragmatic herniation based on sonographic
findings.
Paralysis
Diaphragmatic paralysis is usually a result of phrenic nerve
injury following cardiothoracic surgery, birth injury, or
trauma. Less common causes include subpulmonic effu-
sion, subphrenic abscess, pneumonia, and diaphragmatic
eventration. The sonographic finding of paralysis is absent
or paradoxical diaphragmatic excursion during deep inspi-
ration and expiration. When motion is paradoxical, the
paralyzed hemidiaphragm moves cranially during inspira-
tion and caudally during expiration. The degree of excur-
sion of the anterior, middle, and posterior portions of the
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Diaphragmatic eventration. Longitudinal sonogram demon-
Fig. 5.44
strates a focal diaphragmatic bulge (arrows) containing
liver (LIV). The diaphragm is intact.
diaphragm is similar, in contrast to the normal situation
where the excursion of the middle and posterior thirds is
greater than that of the anterior third. Transverse imaging
allows comparison of both hemidiaphragms and is particu-
larly helpful for evaluation of paradoxical motion (Fig. 5.45).
Inversion
Inversion of the diaphragm has been associated with large
amounts of fluid and large intrathoracic masses. Sono-
graphic evaluation during deep inspiration shows the
inverted diaphragm and the associated pleural effusion or
mass. Diaphragmatic excursion may be normal, paradoxi-
cal, or absent (19).
A B
Diaphragmatic paralysis. A: Transverse view of the diaphragm in a 6-month-old boy during inspiration demonstrates symmetric posi-
Fig. 5.45
tioning of right (curved arrow) and left (straight arrow) hemidiaphragms. B: Transverse sonogram during expiration shows anterior
movement of the left hemidiaphragm (straight arrow) and no excursion of the right hemidiaphragm (curved arrow), which is paralyzed.
Chapter 5 C H E S T 191
Juxtadiaphragmatic Masses
Juxtadiaphragmatic masses are uncommon and include
lipoma, hemangioma, primitive neuroectodermal tumor,
and rhabdomyosarcoma (88). Abnormalities, such as sub-
phrenic abscess, subpulmonic effusion, and hepatic or
retroperitoneal tumors, are more common than diaphrag-
matic tumors. The role of sonography is to differentiate
primary diaphragmatic from peridiaphragmatic abnormal-
ities and characterize the echotexture of the mass.
CHEST WALL LESIONS
Soft Tissue Masses
Soft tissue masses in the chest wall in children are more
commonly benign than malignant (89,90). Cystic and vas-
cular masses are more often benign than solid masses,
which have a higher likelihood of malignancy.
BENIGN SOFT TISSUE MASSES
Vascular Lesions
Vascular lesions include hemangioma, vascular malforma-
tion, and lymphangioma (91). Hemangioma is the most
common soft tissue tumor of infancy, usually presenting in
the first few months of life with bluish discoloration of the
skin. Hemangiomas are composed of vascular channels
lined by flattened endothelium. They typically show an
early proliferative phase, usually between 3 and 9 months
of life; a variable phase of stability; and a phase of
involution. Most hemangiomas resolve by age 10 years
(91,92).
On gray-scale imaging, hemangiomas commonly
appear as well-defined masses in the superficial soft tissues.
They can be hypoechoic, isoechoic, or hyperechoic to sur-
rounding tissue and homogeneous or heterogeneous
depending on the size of the vascular channels and the
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192 P E D I AT R I C S O N O G R A P H Y

A B

Hemangiomas. A: A transverse view of a palpa-

Fig. 5.46
ble mass over the right anterior chest wall in an
11-month-old girl shows a well-marginated heterogeneous
mass (arrowheads) containing anechoic spaces. B: Trans-
verse color Doppler image demonstrates multiple vascular
channels. C: Transverse sonogram in a 1-year-old girl shows
a well-marginated, relatively homogeneous echogenic mass
(arrows). D: Color Doppler image demonstrates vascular
D channels within the mass.

amount of thrombus and fatty stroma (Fig. 5.46). Color
Doppler sonography shows the vascular channels and
feeding vessels. Pulsed Doppler interrogation shows high
Doppler frequency shifts (93,94).
Vascular malformations present at birth and grow with
the patient, unlike hemangiomas, which show rapid early
growth and subsequent involution. Vascular malformations
are characterized by their predominant vascular channel as
arteriovenous or venous. Arteriovenous malformations are
high-flow vascular lesions. Pathologically, they contain an
abnormal vascular network (the nidus), which connects
enlarged feeding arteries and draining veins. The normal
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Chapter 5 C H E S T 193

Lymphangioma. A transverse view of the right lateral

Fig. 5.47
chest wall in a 3-month-old girl demonstrates a poorly
defined, multiloculated, hypoechoic mass with internal septa.

capillary bed is absent. Sonography shows a high-flow
lesion with multiple vascular channels. There is absence of
surrounding echogenic stroma, which helps to differentiate
them from hemangiomas.
Venous malformations are slow-flow vascular lesions
characterized by abnormal venous spaces and a normal
arterial component. Venous vascular malformations include
such lesions as nevus flammeus, which is seen in patients
with Klippel-Trenaunay syndrome, and port wine stains,
seen in patients with Sturge-Weber syndrome. Phleboliths
are common in venous vascular malformations. Sonography
shows an echogenic mass with venous waveforms.
Lymphangiomas are composed of sequestered noncom-
municating lymphoid channels lined by lymphatic endothe-
lium. At sonography, they appear as multilocular masses
with variable-sized cystic spaces and interspersed echogenic
septa (Fig. 5.47). The cyst fluid is usually anechoic, but
it may contain low-level echoes if it is hemorrhagic or
infected. The margins may be well-defined or poorly cir-
cumscribed. Doppler imaging shows flow in the septa, but
not in the cystic components.
Other Benign Lesions
Lipomas are benign tumors containing fat. Sonography
shows a well-circumscribed, homogeneous mass, usually
located within the subcutaneous tissues, with an echogeni-
city similar to subcutaneous fat (Fig. 5.48). Color Doppler
shows minimal or absent flow.

Lipoma. Transverse sonogram of the upper

Fig. 5.48
back shows a well-marginated, homoge-
neous echogenic mass.
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194 P E D I AT R I C S O N O G R A P H Y
Hematomas are relatively common soft tissue masses
in children. They are usually a sequela of trauma, but
they can occur spontaneously or be associated with
bleeding diatheses. An acute hematoma has ill-defined
margins and a heterogeneous, hyperechoic matrix, due
to the presence of fibrin. Subacute hematomas contain
both hypoechoic and echogenic components and have a
well-defined periphery or capsule. Chronic hematomas
are well-circumscribed hypoechoic masses. At this stage,
they may not be readily differentiated from an abscess or
cyst.
Cellulitis is an acute infection of the subcutaneous
tissues. The common inciting organisms are S. aureus
and group A Streptococcus. Sonographic findings
Cellulitis. Longitudinal view of the left
Fig. 5.49
lateral chest wall in an 8-year-old girl
with an area of erythematous soft tissue swelling
shows thickened and hyperechoic subcutaneous tis-
sues with reticular hypoechoic striations (arrows)
secondary to edema.
include increased echogenicity of the subcutaneous tis-
sues, a reticular pattern of anechoic or hypoechoic stria-
tions related to edema dissecting along the fascial inter-
faces, and increased flow on color Doppler images
(Fig. 5.49).
Abscesses occasionally present as palpable chest wall
masses. At sonography, they appear as hypoechoic complex
masses with internal echoes or septations and thick hyper-
vascular walls (Fig. 5.50). In the absence of percutaneous
or surgical intervention, the presence of gas, appearing as
highly echogenic foci with acoustic shadowing in the
abscess cavity, supports the diagnosis of an abscess. Associ-
ated cellulitis is common. Doppler imaging shows flow in
the periphery of the abscess and in the surrounding soft
Soft tissue abscess. Transverse view of
Fig. 5.50
left anterior chest wall over an area of
soft tissue swelling associated with erythema and
tenderness shows a complex hypoechoic fluid collec-
tion (arrows) with echogenic debris. Purulent material
was aspirated.
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Chapter 5 C H E S T 195

A B
Soft tissue abscess with osteomyelitis. A: Transverse sonogram of the left chest wall over an area of soft tissue swelling shows a hypo-
Fig. 5.51
echoic mass (M) immediately anterior to the left ninth rib (arrows). The cortex of the rib is irregular and thickened, consistent with
osteomyelitis. B: Color Doppler image shows flow in soft tissues around the abscess and minimal flow in the abscess cavity.

tissues. Irregular thickening or disruption of the cortex of Osseous Lesions

adjacent ribs should suggest associated osteomyelitis
(Fig. 5.51) (95).
MALIGNANT SOFT TISSUE NEOPLASMS
Malignant soft tissue neoplasms include lymphoma, rhab-
domyosarcoma, fibrosarcoma, and the Ewing family of
tumors (96,97). The echogenicity is variable, ranging from
hypoechoic to highly echogenic, and the margins may be well
defined or infiltrative (Fig. 5.52). Color Doppler imaging
often shows increased central or peripheral flow. Associated
findings include rib destruction and pleural effusion. The
sonographic findings are not specific for malignancy and some
benign lesions, such as acute hematomas and abscesses, may
have aggressive sonographic findings. Tissue sampling, which
can be guided by sonography, is required for diagnosis (98).
Chest wall masses may be secondary to osseous or cartilagi-
nous lesions. Mesenchymal hamartoma is a rare benign
chest wall lesion of infancy and childhood (99,100). It is not
considered a true neoplasm and is composed of maturing,
proliferating normal skeletal elements with no propensity
for invasion or metastasis (99). Pathologically, it contains
proliferating bone, cartilage, and fibroblasts, along with
hemorrhagic cystic cavities representing secondary aneurys-
mal bone cyst formation. It arises from the central portions
of ribs and is associated with erosion of adjacent ribs. It
commonly presents as a palpable mass at birth. Plain radi-
ographic findings are expanded or destroyed ribs and a large
extrapleural soft tissue mass. Sonography is not needed for
diagnosis, but it can clarify findings and help guide diag-
nostic needle aspiration. Sonography shows a complex mass

Non-Hodgkin lymphoma. Longitudinal gray scale of the

Fig. 5.52
left lateral chest shows a heterogeneous, echogenic
mass with poorly defined margins.
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196 P E D I AT R I C S O N O G R A P H Y

Mesenchymal hamartoma. A: Chest radiograph in a

Fig. 5.53
3-month-old boy shows marked deformity of several right-
sided ribs and a soft tissue mass. B: Transverse view from a sonogram
performed for biopsy guidance shows an expanded, irregular rib (R)
with an adjacent fluid collection (arrows). C: Axial computed tomogra-
phy scan demonstrates expansion of the rib (arrow) and an extrapleural
C mass with fluid and soft tissue density.

A B
Mesenchymal hamartoma. A: Transverse sonogram of the left lower chest wall in a neonate shows a complex mass (arrows) with cys-
Fig. 5.54
tic and highly echogenic areas, some of which shadow. B: Computed tomography scan with bone windows shows a complex mass
(arrow) with areas of fluid density and calcification expanding the left seventh rib. Pathologic examination showed proliferating bone and
hemorrhagic cystic cavities.
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Prominent costal cartilage. A 7-year-old boy who presents with a nontender, left chest wall mass, which had been present for several
Fig. 5.55
years. Transverse scan demonstrates enlargement of the left fifth rib (arrows). The cartilaginous part of the rib is hypoechoic, while the
cortex is echogenic.
containing hypoechoic areas (representing hemorrhagic
cystic regions) and echogenic components, which may
shadow (representing expanded or destroyed ribs) (Figs.
5.53 and 5.54).
Cartilaginous rib abnormalities, such as asymmetric
cartilaginous costochondral junctions, osteochondromas,
and healing rib fractures, are other causes of firm chest
wall masses (101). These are readily visible sonographi-
cally. Cartilaginous abnormalities are typically hypoechoic
masses relative to the adjacent echogenic cortical surface
of the rib (Fig. 5.55). Rib fractures produce cortical dis-
ruption, and there may be an adjacent hematoma (Fig.
5.56). Healing fractures are associated with callous forma-
tion, which appears as thickened cortex.
Rib fracture. Longitudinal sonogram along a painful rib in
Fig. 5.56
a 5-year-old boy demonstrates cortical discontinuity
(arrows). The fragments are displaced anteriorly.
Chapter 5 C H E S T 197
REFERENCES
1. Coley BD. Pediatric chest ultrasound. Radiol Clin North Am
2005;43:405418.
2. Ben-Ami TE, ODonovan JC, Yousefzadeh DK. Sonography of
the chest in children. Radiol Clin North Am 1993;31:517531.
3. Kim H, Kim WS, Kim MJ, et al. Ultrasound in the diagnosis of
pediatric chest diseases. Radiographics 2000;20:653671.
4. Koh D, Burke S, Davies N, et al. Transthoracic US of the chest:
clinical uses and applications. Radiographics 2002;22:1e.
5. Lee EY, Siegel MJ. Pediatric chest. In: Meire HB, Cosgrove D,
Dewbury K, eds. Abdominal and general ultrasound. 3rd ed.
Oxford, UK: Elsevier, in press.
6. Kuzo RS, Ben-Ami TE, Yousefzadeh DK, et al. Internal mam-
mary compartment: window to the mediastinum. Radiology
1995;195:187192.
7. Scartarige JC, Hamper UM, Sheth S, et al. Parasternal sonogra-
phy of the internal mammary vessels: technique, normal
anatomy, and lymphadenopathy. Radiology 1989;172:453457.
8. Boehm T. Thymus development and function. Curr Opin
Immunol 2008;20:178184.
9. Nishino M, Ashiku SK, Kocher ON, et al. The thymus: a com-
prehensive review. Radiographics 2006;26:335348.
10. Jacobs MT, Frush DP, Donnelly LF. The right place at the wrong
time: historical perspective of the relation of the thymus gland
and pediatric radiology. Radiology 1999;210:1116.
11. Siegel MJ. Mediastinum. In: Siegel MJ, ed. Pediatric body CT. 2nd
ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:3367.
12. Adam EJ, Ignotus PI. Sonography of the thymus in healthy chil-
dren: frequency of visualization, size, and appearance. AJR Am
J Roentgenol 1993;161:153155.
13. Liang CD, Huang SC. Sonographic study of the thymus in
infants and children. J Formos Med Assoc 1997;96:700703.
14. Han B, Yoon H, Suh Y. Thymic ultrasound: diagnosis of aber-
rant cervical thymus. Pediatr Radiol 2001;31:480487.
15. Koumanidou C, Vakaki M, Theophanopoulou M, et al. Aberrant
thymus in infants: sonographic evaluation. Pediatr Radiol 1998;
28:987989.
16. Pozniak MA, Zagzebski JA, Scanlan KA. Spectral and color
Doppler artifacts. Radiographics 1992;12:3544.
LWBK505-C05_p164-199.qxd 7/7/10 1:27 PM Page 198 Aptara Inc
198 P E D I AT R I C S O N O G R A P H Y
17. Hammerli M, Meyer RA. Doppler evaluation of central venous
lines in the superior vena cava. J Pediatr 1993;122:S104S108.
18. Chavhan GB, Parra DA, Mann A, et al. Normal Doppler spec-
tral waveforms of major pediatric vessels: specific patterns.
Radiographics 2008;28:691706.
19. Yeh HC, Halton KP, Gray CE. Anatomic variations and abnor-
malities in the diaphragm seen with US. Radiographics 1990;10:
10191030.
20. Houston JG, Fleet M, Cowan MD, et al. Comparison of ultra-
sound with fluoroscopy in the assessment of suspected hemidi-
aphragmatic movement abnormality. Clin Radiol 1995;50:9598.
21. Gerscovich E, Cronan M, McGahan J, et al. Ultrasonographic
evaluation of diaphragmatic motion. J Ultrasound Med 2001;20:
597604.
22. Gottesman E, McCool FD. Ultrasound evaluation of the paralyzed
diaphragm. Am J Respir Crit Care Med 1997;155:15701574.
23. Houston JG, Angus RM, Cowan MD, et al. Ultrasound assess-
ment of normal hemidiaphragmatic movement: relation to
inspiratory volume. Thorax 1994;49:500503.
24. Patel AS, ODonnell C, Parker MJ, et al. Diaphragm paralysis
definitively diagnosed by ultrasonography and postural depen-
dence of dynamic lung volumes after seven decades of dysfunc-
tion. Lung 2007;185:1520.
25. Summerhill EM, El-Sameed YA, Glidden TJ, et al. Monitoring
recovery from diaphragm paralysis with ultrasound. Chest
2008;133:737743.
26. Laing IA, Teele RL, Stark AR. Diaphragmatic movement in
newborn infants. J Pediatr 1988;112:638643.
27. Kocijancic I, Vidmar K, Ivanovi-Herceg Z. Chest sonography
versus lateral decubitus radiography in the diagnosis of small
pleural effusion. J Clin Ultrasound 2003;31:6974.
28. Calder A, Owens CM. Imaging of parapneumonic pleural effu-
sions and empyema in children. Pediatr Radiol 2009;39:527537.
29. Donnelly LF. Maximizing the usefulness of imaging in children
with community-acquired pneumonia. AJR Am J Roentgenol
1999;172:505512.
30. Ramnath RR, Heller RM, Ben-Ami T, et al. Implications of early
sonographic evaluation with parapneumonic effusions in chil-
dren with pneumonia. Pediatrics 1998;101:6871.
31. Chen K, Liaw Y, Wang H, et al. Sonographic septations: a useful
prognostic indicator of acute thoracic empyema. J Ultrasound
Med 2000;19:837843.
32. Wu RG, Yang PC, Kuo SH, et al. Fluid color sign: a useful
indicator for discrimination between pleural thickening and
pleural effusion. J Ultrasound Med 1995;14:767769.
33. Yang P. Applications of colour Doppler ultrasound in the diag-
nosis of chest diseases. Respirology 1997;2:231238.
34. Eidenberger K, Dock WI, Ammann M, et al. Quantification of
pleural effusions: sonography versus radiography. Radiology
1994;191:681684.
35. Dulchavsky S, Schwarz R, Kirkpatrick A, et al. Prospective eval-
uation of thoracic ultrasound in the detection of pneumothorax.
J Trauma 2001;50:201205.
36. Rowan K, Kirkpatrick A, Liu D, et al. Traumatic pneumothorax
detection with thoracic US: correlation with chest radiography
and CT-initial experience. Radiology 2002;225:210214.
37. Targhetta R, Bourgeois M, Chavagneux R, et al. Ultrasonographic
approach to diagnosing hydropneumothorax. Chest 1992;101:
931934.
38. Targhetta R, Chavagneux R, Bourgeois JM, et al. Sonographic
approach to diagnosing pulmonary consolidation. J Ultrasound
Med 1992;11:667672.
39. Lichtenstein DA, Lascols N, Meziere G, et al. Ultrasound diag-
nosis of alveolar consolidation in the critically ill. Intensive Care
Med 2004;30:276281.
40. Mathis G. Thoraxsonographypart II: peripheral pulmonary
consolidation. Ultrasound Med Biol 1997;23:11411153.
41. Hogan MJ, Coley BD. Interventional radiology treatment of
empyema and lung abscesses. Paediatr Respir Rev 2008;9:
7784.
42. Hsieh YC, Hsiao CH, Tsao PN, et al. Necrotizing pneumococ-
cal pneumonia in children: the role of pulmonary gangrene.
Pediatr Pulmonol 2006;41:623629.
43. Lin CJ, Chen PY, Huang FL, et al. Radiographic, clinical,
and prognostic features of complicated and uncomplicated
community-acquired lobar pneumonia in children. J Microbiol
Immunol Infect 2006;39:489495.
44. Patradoon-Ho P, Fitzgerald DA. Lung abscess in children. Pae-
diatr Respir Rev 2007;8:7784.
45. Puligandla PS, Laberge JM. Respiratory infections: pneumonia,
lung abscess, and empyema. Semin Pediatr Surg 2008;17:4252.
46. Yang P, Luh K, Kee Y, et al. Lung abscesses: US examination and
US-guided transthoracic aspiration. Radiology 1991;80:
171175.
47. Berrocal T, Madrid C, Novo S, et al. Congenital anomalies of
the tracheobronchial tree, lung, and mediastinum: embryology,
radiology, and pathology. Radiographics 2004;24:e17.
48. Panicek DM, Heitzman ER, Randall PA, et al. The continuum
of pulmonary developmental anomalies. Radiographics
1987;7:747771.
49. Cleveland RH. Congenital lobar emphysema. In: Siegel BA,
Proto AV, eds. Pediatric disease (fourth series) test and syllabus.
Reston, VA: American College of Radiology, 1993:96129.
50. McAdams HP, Kirejczyk WM, Rosado-Christenson ML, et al.
Bronchogenic cyst: imaging features with clinical and
histopathologic correlation. Radiology 2000;217:441446.
51. Hendry PJ, Hendry GMA. Ultrasonic diagnosis of a bron-
chogenic cyst in a child with persistent stridor. Pediatr Radiol
1988;18:338.
52. Rosado-de-Christenson ML, Stocker JT. Congenital cystic ade-
nomatoid malformation. Radiographics 1991;11:865886.
53. Stocker JT. The respiratory tract. In: Stocker, JT, Dehner LP, eds.
Pediatric pathology. Philadelphia, PA: Lippincott Williams &
Wilkins, 2001:445517.
54. Frazier AA, Rosado de Christenson ML, Stocker JT, et al.
Intralobar sequestration: radiologic-pathologic correlation.
Radiographics 1997;17:725745.
55. Rosado-de-Christenson ML, Frazier AA, Stocker JT, et al.
Extralobar sequestration: radiologic-pathologic correlation.
From the archives of the AFIP. Radiographics 1993;13:
425441.
56. Dhingsa R, Coakley FV, Albanese CT, Prenatal sonography and
MR imaging of pulmonary sequestration. AJR Am J Roentgenol
2003;180:433437.
57. Ceola AF, Angtuaco TL. US case of the day: extralobar pul-
monary sequestration. Radiographics 1999;19:817819.
58. Schlesinger AE, DiPietro MA, Statter MB, et al. Utility of sonog-
raphy in the diagnosis of bronchopulmonary sequestration. J
Pediatr Surg 1994;29:5255.
59. Smart LM, Hendry GMA. Imaging of neonatal pulmonary
sequestration including Doppler ultrasound. Br J Radiol 1991;
64:324329.
60. Benya EC, Bulas DI, Selby DM, et al. Cystic sonographic
appearance of extralobar pulmonary sequestration. Pediatr
Radiol 1993;23:605607.
61. Conran RM, Stocker JT. Extralobar sequestration with fre-
quently associated congenital cystic adenomatoid malformation,
type 2: report of 50 cases. Pediatr Dev Pathol 1999;2:454463.
62. Hernanz-Schulman M, Stein SM, Neblett WW, et al. Pulmonary
sequestration: diagnosis with color Doppler sonography and a
new theory of associated hydrothorax. Radiology 1991;180:
817821.
63. Konen E, Raviv-Zilka L, Cohen RA, et al. Congenital pul-
monary venolobar syndrome: spectrum of helical CT findings
with emphasis on computerized reformatting. Radiographics
2003;23:11751184.
64. Woodring JH, Howard TA, Kanga JF. Congenital pulmonary
venolobar syndrome revisited. Radiographics 1994;14: 349369.
65. Hoffman LV, Kuszyk BS, Mitchell SE, et al. Angioarchitecture of
pulmonary arteriovenous malformation: characterization using
LWBK505-C05_p164-199.qxd 7/7/10 1:27 PM Page 199 Aptara Inc
volume-rendered 3D CT angiography. Cardiovasc Intervent
Radiol 2000;23:165170.
66. Jaskolka JL, Wu L, Chan RP, et al. Imaging of hereditary hemor-
rhagic telangiectasia. AJR Am J Roentgenol 2004;183:307314.
67. Naffa LN, Donnelly LF. Imaging findings in pleuropulmonary
blastoma. Pediatr Radiol 2005;35:387391.
68. Herman TE, Siegel MJ. Neonatal pleuropulmonary blastema,
type 1. J Perinatol 2008;28:8284.
69. Weldon CB, Shamberger RC. Pediatric pulmonary tumors: pri-
mary and metastatic. Semin Pediatr Surg 2008;17:1729.
70. Franco A, Mody NS, Meza MP. Imaging evaluation of pediatric
mediastinal masses. Radiol Clin North Am 2005;43:325353.
71. Rosado-de-Christenson ML, Templeton PA, Moran CA. Medi-
astinal germ cell tumors: radiologic and pathologic correlation.
Radiographics 1992;12:10131030.
72. Wu TT, Wang HC, Chang YC, et al. Mature mediastinal ter-
atoma: sonographic and imaging patterns and pathologic corre-
lation. J Ultrasound Med 2002;21:759765.
73. Hudson MM, Onciu M, Donaldson SS. Hodgkin lymphoma. In:
Pizzo PA, Poplack DG, eds. Principles and practice of pediatric
oncology. Philadelphia, PA: Lippincott Williams & Wilkins,
2006:695721.
74. Kontny H, Sleasman J, Kingma D, et al. Multilocular thymic
cysts in children with human immunodeficiency virus infection:
clinical and pathologic aspects. J Pediatr 1997;131:264270.
75. Leonidas JC, Berdon WE, Valderrama E, et al. Human immun-
odeficiency virus infection and multilocular thymic cysts. Radi-
ology 1996;198:377379.
76. Zadvinskis DP, Benson MT, Kerr HH, et al. Congenital malfor-
mations of the cervico-thoracic lymphatic system: embryology
and pathogenesis. Radiographics 1992;12:11751189.
77. Joseph AE, Donaldson JS, Reynolds M. Neck and thorax
venous aneurysm: association with cystic hygroma. Radiology
1989;170:109112.
78. Patel J, Park C, Michaels J, et al. Pericardial cyst: case reports
and a literature review. Echocardiography 2004;21:269272.
79. Babcock DS. Sonographic evaluation of suspected pediatric vas-
cular diseases. Pediatr Radiol 1991;21:486489.
80. Cole TJ, Henry DA, Jolles H, et al. Normal and abnormal vas-
cular structures that simulate neoplasms on chest radiographs:
clues to the diagnosis. Radiographics 1995;15:867891.
81. Siegel MJ. Great vessels. In: Siegel MJ, ed. Pediatric body CT.
2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2008:
121144.
82. Slovis TL, Poland RL. Endotracheal tubes in neonates: sono-
graphic positioning. Radiology 1986;160:262263.
83. Ueda D, Yano K, Okuno A. Ultrasonic imaging of the tongue,
mouth, and vocal cords in normal children: establishment of
basic scanning positions. J Clin Ultrasound 2005;21:431439.
Chapter 5 C H E S T 199
84. Lally KP. Congenital diaphragmatic hernia. In: Oldham KT,
Colombani PM, Folgia RP, et al., eds. Principles and practice of
pediatric surgery. Philadelphia, PA: Lippincott Williams &
Wilkins, 2005:897908.
85. Siegel MJ, Shackelford GD, McAlister WH. Left-sided congen-
ital diaphragmatic hernia: delayed presentation. AJR Am J
Roentgenol 1981;137:4346.
86. Taylor GA, Atalabi OM, Estroff JA. Imaging of congenital
diaphragmatic hernias. Pediatr Radiol 2009;39:116.
87. Deslauriers J. Eventration of the diaphragm. Chest Surg Clin N
Am 1998;8:315330.
88. Gupta AAK, Mitra DK, Berry M. Primary embryonal rhab-
domyosarcoma of the diaphragm in a child: case report. Pediatr
Radiol 1999;29:823825.
89. Tateishi U, Gladish GW, Kusumoto M, et al. Chest wall
tumors: radiologic findings and pathologic correlation: part 1.
Benign tumors. Radiographics 2003;23:14771490.
90. Watt AJ. Chest wall lesions. Paediatr Respir Rev 2002;3:
328338.
91. Burrows PE, Laor T, Paltiel H, et al. Diagnostic imaging in the
evaluation of vascular birthmarks. Dermatol Clin 1998;16:
455488.
92. Coffin CM, Dehner LP. The soft tissues. In: Stocker JT, Dehner
LP, eds. Pediatric pathology. Philadelphia, PA: Lippincott
Williams & Wilkins, 2002:11691171.
93. Dubois J, Patriquin HB, Garel L, et al. Soft-tissue hemangiomas
in infants and children: diagnosis using Doppler sonography.
AJR Am J Roentgenol 1998;171:247252.
94. Dubois J, Garel L, David M, et al. Vascular soft-tissue tumors
in infancy: distinguishing features on Doppler sonography. AJR
Am J Roentgenol 2002;178:15411545.
95. Herman TE, Siegel MJ. Osteopenia of prematurity, staphylo-
coccal rib osteomyelitis. J Perinatol 2009;29:254255.
96. Tateishi U, Gladish GW, Kusumoto M, et al. Chest wall
tumors: radiologic findings and pathologic correlation: part 2.
Malignant tumors. Radiographics 2003;23:14911508.
97. van den Berg H, van Rijn RR, Merks JH. Management of
tumors of the chest wall in childhood: a review. J Pediatr
Hematol Oncol 2008;30:214221.
98. Sistrom C, Wallace CK, Gay SB. Thoracic sonography for diag-
nosis and intervention. Curr Probl Diagn Radiol 1997;26:249.
99. Groom KR, Murphey Md, Howard LM, et al. Mesenchymal
hamartoma of the chest wall: radiologic manifestations with
emphasis on cross sectional imaging and histopathologic com-
parison. Radiology 2002;222:205211.
100. Herman TE, Siegel MJ. Chest wall mesenchymal hamartoma. J
Perinatol 2009;29:462463.
101. Donnelly LF, Frush DP. Abnormalities of the chest wall in pedi-
atric patients. AJR Am J Roentgenol 1999;173:15951601.
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CHAPTER
6 Breast
ELLEN CHUNG AND MARILYN J. SIEGEL
Technique Premature Thelarche
Gynecomastia
Normal Anatomy
Juvenile (Virginal) Hypertrophy
Clinical Indications for Breast Sonography
Cystic Lesions
Breast Sonography: General Principles
Mammary Duct Ectasia
Shape
Retroareolar (Montgomery) Cysts
Orientation
Galactocele
Margins Fibrocystic Disease
Echotexture Hematoma
Acoustic Enhancement Mastitis and Abscess
Effect on Surrounding Tissues
Benign Masses
Variants and Developmental Abnormalities
Fibroadenoma
Anomalous Nipple and Breast Development Hemangioma
ltrasonography has become a widely used study to
U evaluate breast lesions in children, including masses,
infection, and trauma (1,2). Knowledge of the sono-
graphic spectrum of conditions that affect the pediatric
breast is important in establishing a diagnosis and guiding
management. The vast majority of breast masses in the
pediatric population are benign, and a conservative
approach to diagnosis and management is usually prudent.
This chapter addresses the sonographic features of the
normal prepubertal and pubertal breast and common
pathologic lesions that affect the breast in children. The
sonographic features are also correlated with important
clinical features.
TECHNIQUE
Breast sonography requires a high-resolution, linear
array, real-time transducer (7.0 to 15.0 MHz). In general,
the highest-frequency transducer that penetrates the
breast should be used. With the use of very high frequen-
cies (15 MHz), evaluation of masses as small as 2 to
4 mm in diameter is possible. If the lesion is superficial, a
stand-off pad may improve conspicuity by positioning
the lesion in the focal zone of the transducer. Gain set-
tings must be optimized to allow differentiation of fluid-
filled and solid masses. This is important because a low
gain can prevent identification of low-level echoes in a
solid mass and a high gain may produce artifactual
echoes in a cystic mass.
In some cases, Doppler evaluation may help increase
diagnostic specificity. The presence of internal flow sup-
ports the diagnosis of a solid mass or complicated cyst,
while absence of flow favors a simple cyst.
200
Lactating Adenoma
Granular Cell (Myoblastoma) Tumor
Juvenile Papillomatosis
Pseudoangiomatous Stromal
Hyperplasia
Intraductal Papilloma
Intramammary Lymph Nodes
Malignant Tumors
Phyllodes Tumor
Carcinoma
Metastatic Disease and Hematologic
Malignancy
NORMAL ANATOMY
The sonographic appearance of the breast varies with age.
The human female breast undergoes two stages of devel-
opment (1). The first stage occurs in utero, usually in the
fifth to sixth week, resulting in the formation of a rudi-
mentary organ containing primary mammary ridges and
ducts (2). After birth and until the time of puberty, the
breast is composed of epithelial-lined ducts surrounded by
connective tissue (2,3). These ducts are commonly
enlarged immediately after birth in both female and male
neonates due to stimulation by maternal hormones. This
occurrence results in palpable subareolar nodules, which
may persist up to 1 year of age (3). In the period between
infancy and puberty, the female breasts show very little
development. The prepubertal breast consists of simple
branched ducts and connective tissue.
At puberty, the breasts increase in size. The second
stage of growth occurs at puberty related to increases in
estrogen and progesterone levels. In response to hormonal
stimulation, the ducts elongate, branch, and form terminal
duct lobular units. The onset of pubertal breast develop-
ment is termed thelarche, which normally occurs after
age 8 and prior to age 13 (2).
Pubertal breast development is divided into five stages,
called Tanner stages (2). In Tanner stage I, sonography
shows hyperechoic retroareolar tissue (Fig. 6.1A). In Tanner
stage II, the breast bud forms. Sonography at this stage
shows a hyperechoic retroareolar nodule with small
branching hypoechoic tubular structures representing ducts
(Fig. 6.1B) (4). Tanner stage III is clinically characterized by
obvious enlargement and elevation of the breast tissue.
Sonography shows a larger hypoechoic subareolar nodule
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Chapter 6 B R E A S T 201

A B

C D
Normal breast tissue versus Tanner stages. A: Tanner stage I showing a small area of echogenic retroareolar breast tissue (arrows).
Fig. 6.1
B: Tanner stage II showing ill-defined, echogenic breast tissue (arrows) along with branching hypoechoic structures (asterisk), repre-
senting developing ducts. C: Tanner stage III showing more fibrofatty and glandular tissue (arrows) extending away from the areolar area, a larger
central subareolar nodule (asterisk), and more ducts extending deeper into the parenchyma compared with Tanner stage II. D: Tanner stage IV
showing even more fibrofatty and glandular tissue (arrows) and a central hypoechoic nodule (asterisk). The ducts are less prominent. P  pectoralis
muscle; S  subcutaneous tissue.

with multiple linear ducts, which are elongated and extend
away from the retroareolar area. There is more echogenic
glandular tissue extending away from the retroareolar area
compared with Tanner stage II (Fig. 6.1C). Tanner stage IV
is characterized clinically by areolar mounding. This stage
is very transient and it may not always be apparent. Sonog-
raphy shows a hypoechoic subareolar nodule and more
fibroglandular tissue compared with Tanner stage IV
(Fig. 6.1D). The prominent ducts seen in the other stages
are not as apparent in this stage.
Tanner stage V is the mature breast. It is composed of a
framework of fibrous connective tissue (Cooper ligaments)
that provides support for the fatty tissue and glandular ele-
ments (acini) (2) (Fig. 6.2). Sonography shows the subcuta-
neous fat layer and subadjacent parenchymal lobules con-
taining fibrofatty and glandular tissue. Normal lobules are
hypoechoic, have an ovoid or polyhedral shape, and are sur-
rounded by echogenic fibrous tissue (Fig. 6.3) (4). Linear
branching structures, about 2 mm in diameter, representing
ducts, may be seen in the fibrous connective tissue. The large
hypoechoic central nodule and large ducts in Tanner stages
II, III, and IV are no longer seen. The nipple, which contains
fibrous tissue, can be seen, appearing as an echogenic struc-
ture just below the skin. It may produce shadowing, which
can impair visualization of deeper structures. The mammary
tissue is covered by subcutaneous fat and a thin (1- to 2-mm)
layer of skin. Normal breast tissue is avascular on Doppler
imaging (Fig. 6.3C).
The pectoralis muscle is deep to the mammary tissue. It
has a linear orientation, paralleling the chest wall. The
muscle bundles in the substance of the muscle are separated
by thin echogenic septa. The ribs and costal cartilages are
subadjacent to the pectoralis muscles.
CLINICAL INDICATIONS FOR BREAST SONOGRAPHY
The common indication for sonography is a palpable breast
mass, which may be due to normal and abnormal breast
development in boys and girls as well as infection, trauma,
and tumors (1,2,4,5). Thelarche is commonly asymmetric or
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202 P E D I AT R I C S O N O G R A P H Y

Diagram of breast in sagittal section. Curve arrow indi-

Fig. 6.2
cates the subareolar draining ducts, and arrowheads
indicate the pectoralis muscle. P  parenchymal lobule containing
fibrofatty and glandular tissue; R  ribs.

A B

C D
Normal mature breast tissue, Tanner V stage. Transverse (A) and longitudinal (B) sonogram show subcutaneous fat (S) anteriorly, innu-
Fig. 6.3
merable fibroglandular lobules (arrowheads), and the pectoralis (P) muscle posteriorly. Normal lobules are hypoechoic, have an ovoid
or polyhedral shape, and are surrounded by echogenic fibrous tissue (Cooper ligament). Normal ducts (arrows), which have a linear rather than an
ovoid shape, are seen in panel B. C: Transverse sonogram in another patient shows normal mammary tissue (arrowheads) and the echogenic nip-
ple (asterisk). D: Color Doppler image in another patient shows flow around the nipple. The subcutaneous (S) fatty tissue and subadjacent mammary
tissue are avascular.
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unilateral, and the normal breast bud can be mistaken for a
mass. Sonography can show the presence of normal devel-
oping breast tissue and the absence of a mass lesion.
BREAST SONOGRAPHY: GENERAL PRINCIPLES
In the case of nodules, the most important issue is char-
acterization of the mass. The features that need to be
evaluated are shape, orientation, margins, echotexture,
acoustic enhancement, and effect on surrounding tissues
(6).
Shape
Masses can have round, oval, or irregular shapes. Cysts are
usually round in shape, while fibroadenomas often have an
oval contour. Cancers are typically irregular.
Orientation
Orientation refers to positioning with reference to the skin
surface. Lesions may be parallel or not parallel. Fibroade-
nomas typically have a parallel orientation, while cysts and
malignancies usually are not parallel to the skin surface
(equal width and anteroposterior diameter, or anteropos-
terior diameter greater than width).
Margins
Lesion margins are defined as smooth or irregular, and well
defined or indistinct. Cysts and fibroadenomas have
smooth, well-defined contours. Malignancies often demon-
strate ill-defined, irregular margins.
Echotexture
Echotexture, referring to the echogenicity of the matrix of
the lesion relative to surrounding tissue, may be anechoic,
hypoechoic, or hyperechoic. Anechoic lesions are usually
simple cysts. Hypoechoic lesions can be benign or malig-
nant. Hyperechoic lesions are often benign, with the
echogenicity indicating blood, fat, or fibrous tissue.
Acoustic Enhancement
Cysts show the greatest acoustic enhancement. Fibroade-
nomas also may show some enhancement, although the
degree is less than that associated with a simple cyst. Other
solid tumors may or may not show enhancement.
Effect on Surrounding Tissues
Effects on adjacent structures include edema, skin thicken-
ing, and distortion of normal vessels. Most benign lesions
do not distort surrounding structures. By comparison,
malignancies are more likely to distort surrounding tissues.
VARIANTS AND DEVELOPMENTAL ABNORMALITIES
Anomalous Nipple and Breast Development
Amastia, or absence of the breast, is rare and may be asso-
ciated with Poland syndrome (unilateral pectoral muscle
agenesis) (3). Supernumerary nipple, or polythelia, occurs
Chapter 6 B R E A S T 203
in 1% to 2% of the population (2). This anomaly is usually
unilateral and 95% of supernumerary nipples are found
along the milk line (3). Accessory breast tissue, or poly-
mastia (presence of more than two breasts), is less common
and is most often found in the axilla (3).
Premature Thelarche
Premature thelarche is the onset of female breast develop-
ment prior to the age of 7 to 8 years. It may be an isolated
event or associated with true precocious puberty. Isolated
premature thelarche commonly occurs in girls between 1 and
3 years of age. It may be asymmetric, unilateral, or bilateral.
Sonography shows normal developing breast tissue without
a discrete mass.
Gynecomastia
Gynecomastia is overdevelopment of the male breast, which
clinically presents as a tender, firm subareolar nodule. Breast
enlargement occurs in two thirds to three fourths of healthy
boys, beginning about 1 year after the onset of puberty and
resolving within 1 to 2 years (2,7). It is usually bilateral, but
it may be unilateral and it may be familial. The cause is
thought to be a decrease in the ratio of testosterone to
estrogen levels.
Gynecomastia also can be secondary to conditions asso-
ciated with increased levels of estrogens, including adreno-
cortical tumors and hyperplasia, testicular tumors (Sertoli
or Leydig cell), hepatoblastoma, prolactinomas, Klinefelter
syndrome, testicular feminization syndrome, and neurofi-
bromatosis type 1. Drugs, including exogenous estrogens,
anabolic steroids, digitalis, corticosteroids, tricyclic antide-
pressants, and marijuana, are other causes of increased
breast tissue (2).
Bilateral breast development is common in neonates
due to maternal hormone stimulation. Regardless of patient
age, sonography shows increased subareolar breast tissue
similar to the appearance of early developing breast
(Tanner stage I) (Fig. 6.4) (7,8).
Juvenile ( Virginal) Hypertrophy
Juvenile hypertrophy, also known as virginal hypertrophy
or macromastia, is characterized by very marked female
breast enlargement occurring over a relatively short period
of weeks to months. It commonly begins soon after menar-
che. The condition is usually symmetric and bilateral, but
it may be asymmetric or even unilateral. Patients often are
symptomatic, presenting with breast discomfort or pain
related to the large size of the breasts.
Sonographically, the findings are similar to those of
gynecomastia. Treatment is antiestrogen drugs, such as
tamoxifen, and if needed, reduction mammoplasty after
growth has stabilized (9).
CYSTIC LESIONS
Mammary Duct Ectasia
Ductal ectasia usually involves the retroareolar ducts.
Affected patients present with bloody nipple discharge or,
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204 P E D I AT R I C S O N O G R A P H Y

Gynecomastia. Sixteen-year-old boy with right breast development. Longitudinal split-screen image sonogram shows prominent subareolar
Fig. 6.4
tissue (arrows) in the right (RT) breast, similar to Tanner stage I. The normal left (LT) breast is shown for comparison. P  pectoralis muscle.

less often, with tender or nontender palpable masses related
to inflammation. Stasis of secretions can lead to secondary
infection with Staphylococcus aureus or Bacteroides species
(1,2,8).
The ectatic ducts appear as hypoechoic, round or tubu-
lar subareolar structures (Fig. 6.5), which may contain
internal echoes due to debris (8). The cysts are avascular
on Doppler imaging. The ectatic ducts may resolve with
antibiotic therapy, although surgical excision may be
needed if there is persistent drainage.
Retroareolar (Montgomery) Cysts
Retroareolar cysts result from obstruction of the glands of
Montgomery at the edge of the areola. Affected patients,

A B

Retroareolar duct ectasia. A: Transverse sonogram

Fig. 6.5
shows dilated anechoic ducts (arrowheads) in the
subareolar area. B: Transverse split-screen sonogram shows the
duct ectasia in the right (RT) breast and the normal left (LT)
breast for comparison. C: Color Doppler image shows flow in the
C surrounding tissues but not in the cysts.
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Chapter 6 B R E A S T 205

A B
Galactoceles. A: Longitudinal sonogram in a 15-year-old postpartum girl shows a well-circumscribed, cystic mass (calipers) with some
Fig. 6.6
internal echoes (arrow) and acoustic enhancement. Cyst aspiration yielded serous fluid with minimal fat. B: Transverse sonogram in a
25-year-old female shows a well-circumscribed, round mass with homogeneous internal echogenicity (arrowheads), indicating a predominance of fat.

usually adolescents, can present with signs of inflammation
or a painless mass (10). The cysts may be solitary or
multiple.
Sonography shows single or multiple, anechoic, thin-
walled, retroareolar cysts, which may contain debris, sep-
tations, or a fluid-fluid level. They usually measure 2 cm or
less in diameter and are often bilateral (10). Simple cysts
are avascular on color Doppler imaging, although flow
may be noted in the wall if the cyst is infected. Most
resolve with conservative management.
changes. Affected patients present with cyclically tender
breasts that are nodular on palpation (2). In the pediatric
population, solitary cysts are more common than multiple
cysts.
Sonographic findings are nonspecific and include single
or multiple cysts of varying size, dilated ducts, and highly
echogenic areas with posterior acoustic shadowing repre-
senting fibrous tissue (Fig. 6.7) (12).

Galactocele
Galactoceles usually develop in lactating women, but they
may occur in infants of either gender (3,11). The cause is
an obstructed milk duct. Galactoceles typically present as
enlarging unilateral or bilateral painless masses. Patholog-
ically, they are lined by epithelium and filled with milky
fluid, which contains fat and water.
Sonography shows a complex cystic mass containing
hypoechoic areas related to the water component and
echogenic areas related to the fat component (8). Galacto-
celes also can appear homogeneous and echogenic due to a
predominance of fat (Fig. 6.6). Occasionally, a fat-fluid
level is seen. Cyst aspiration yields a milky substance, lead-
ing to a definitive diagnosis. Aspiration also can be thera-
peutic.

Fibrocystic Disease Fibrocystic disease in a 15-year-old girl. Longitudinal view

Fibrocystic disease is seen in adolescent girls. Histologically, Fig. 6.7
of the left breast demonstrates an anechoic cyst with pos-
it is characterized by benign cystic and proliferative terior acoustic enhancement.
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206 P E D I AT R I C S O N O G R A P H Y
Hematoma, 14-year-old girl with a painful breast mass.
Fig. 6.8
Longitudinal sonogram shows a well-defined, cystic mass
(calipers) with internal septations and posterior acoustic enhance-
ment. Aspiration yielded bloody fluid.
A B
C shows peripheral flow around the abscess of the same patient.
Hematoma
Hematomas most often result from blunt trauma, either the
sequelae of blunt trauma or diagnostic or therapeutic inter-
ventions (2). The sonographic appearance varies with the
age of the hemorrhage. The acute hematoma is hyperechoic
to surrounding tissues, becoming complex with internal
echoes and septations, and eventually anechoic as the clot
retracts and lyses before resolving (Fig. 6.8). The walls of
the hematoma may be indistinct initially, becoming more
defined over time. Differentiation among hematoma and
abscess requires clinical history and often lesion aspiration.
Mastitis and Abscess
Mastitis most often affects lactating women, but it can
occur in infants and adolescents. The causative factors
include mammary duct obstruction or ectasia, cellulitis,
immunocompromised states, and nipple injury. Breast
abscess is the sequela of acute mastitis (2,8,13). Affected
patients present with a tender, indurated erythematous
Mastitis and abscess. A: Longitudinal sonogram in a
Fig. 6.9
13-year-old girl shows a hypoechoic mass with internal
echoes, representing an abscess (A) and surrounding thickened,
echogenic breast tissue, indicating mastitis. B: Longitudinal sono-
gram in a 4-year-old girl shows a thick-walled complex mass with
internal debris and through-transmission. C: Color Doppler image
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Chapter 6 B R E A S T 207

breast. Staphylococcus aureus is the most common
pathogen (3,11).
Sonographic findings of mastitis are thickened and
echogenic breast tissue due to edema and cellular infiltrate.
Sonographic findings of abscess are a hypoechoic complex
mass with internal echoes, septations, or fluid-fluid levels,
and posterior acoustic enhancement (Fig. 6.9). Other findings
of abscess include a thick wall and skin thickening. Color
Doppler imaging shows flow at the periphery of the abscess
and in the adjacent breast tissue. Sonography can be used to
guide needle aspiration of the abscess.
BENIGN MASSES
Fibroadenoma
Fibroadenoma is a benign fibroepithelial tumor and is the
most common solid breast tumor in the pediatric popula-
tion (3,13). The typical fibroadenoma contains a predom-
inance of stromal elements. When ductal elements pre-
dominate, the lesion is referred to as a tubular adenoma.
Fibroadenomas usually range between 2 and 5 cm in diam-
eter and they are multiple in 15% to 20% of patients. The
mean patient age at diagnosis is 15 to 17 years (3). Most
patients present with a slowly enlarging, painless mass. At
physical examination, the mass is well marginated, rubbery,
and mobile.
The typical sonographic appearance of fibroadenomas is
a smoothly marginated, oval mass with a homogeneous,
hypoechoic matrix containing low-level echoes (1214) (Fig.
6.10). Fibroadenomas also may appear almost anechoic.
Rarely the matrix is heterogeneous due to necrosis or dys-
trophic calcification. Both posterior acoustic enhancement
and shadowing have been reported; the latter may be due to
infarction (15). The growth pattern is typically parallel to the
chest wall. At Doppler sonography, the lesions can be avas-
cular or show internal vascularity (Figs. 6.10c and 6.11).
The juvenile or giant fibroadenoma is a histologic vari-
ant of fibroadenoma that is characterized by rapid growth,
large size (5 to 10 cm), and highly cellular stroma; the stro-
mal elements dominate. Like the classic fibroadenoma, the
clinical course is benign. Except for the large size, the sono-
graphic appearance usually is similar to that of the typical

A
B

Fibroadenoma. A: Longitudinal view of the left breast of a

Fig. 6.10
15-year-old girl with a palpable mass shows a sharply
marginated, hypoechoic lesion (calipers) with homogeneous low-level
internal echoes. The long axis of the mass is parallel to the chest wall
(arrows). B: Color Doppler image shows that the mass is avascular.
C: Transverse color Doppler sonogram in a 13-year-old girl shows an
ovoid mass with homogeneous, hypoechoic matrix and central vascu-
C larity.
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208 P E D I AT R I C S O N O G R A P H Y

A B
Fibroadenoma in a 15-year-old girl. A: Transverse sonographic image shows a homogeneous mass with a hypoechoic curvilinear struc-
Fig. 6.11
ture (arrowhead). B: Color Doppler image shows that the curvilinear structure is a central vessel.

fibroadenoma (Fig. 6.12). In addition, slender, fluid-filled
clefts may be seen within juvenile fibroadenomas (14).
The natural history of fibroadenoma is one of slow
growth and eventual regression. Surgical excision may be
needed for symptomatic or rapidly growing masses.
Hemangioma
Infantile or capillary hemangioma is a common breast
mass in infancy and childhood. Similar to hemangiomas
elsewhere, the lesion usually presents early in the first few
months of life as a growing mass. Infantile hemangiomas
typically undergo a phase of initial growth, usually until the
infant is 11 to 12 months of age, followed by slow involu-
tion over months to several years (16,17). There may be
associated bluish discoloration of the overlying skin (so-
called strawberry nevus). Histologically, infantile heman-
giomas contain dilated vascular channels, which are sur-
rounded by fibrous septa.
On gray-scale sonography, hemangioma is usually
hypoechoic relative to surrounding normal tissue. More
anechoic areas representing dilated sinusoids or vascular
channels may be present. The margins can be well circum-
scribed or infiltrating. Color Doppler imaging shows a vas-
cular lesion (Fig. 6.13) (18,19).
Lactating Adenoma
Lactating adenoma is a benign tumor occurring late in preg-
nancy or during lactation in response to the physiologic
changes of pregnancy (3). Pathologically, it consists of
secretory lobules with intervening stroma and pregnancy-
associated changes. Most are often located in the anterior
portion of the breast and are firm, mobile, and nontender
on physical examination.
Sonography shows a sharply circumscribed solid mass
with homogeneous echotexture, posterior acoustic enhance-
ment, and a long axis parallel to the chest wall (Fig. 6.14).

Juvenile fibroadenoma in a 15-year-old girl. Extended

Fig. 6.12
field-of-view sonogram shows a homogeneous, hypo-
echoic, well-marginated mass (arrows) with a hyperechoic septation
(arrowhead). P  pectoralis muscle.
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Chapter 6 B R E A S T 209

A B
Hemangioma in a 3-year-old girl with a small palpable breast mass. A: Transverse scan of the left breast demonstrates increased soft
Fig. 6.13
tissue thickness with several anechoic channels (arrowheads). P  pectoralis muscles. B: Color Doppler image shows intense color
signal within dilated vascular channels.

However, some tumors may have irregular margins or small
central hyperechoic foci, which may represent fat in the milk
produced by the tumor (Fig. 6.14C) (15). Lactating adeno-
mas usually resolve at delivery or upon cessation of
lactation.
Granular Cell (Myoblastoma) Tumor
Granular cell tumor is an uncommon benign tumor that
most often arises in the skin and tongue, but it can occur
at other sites, including the breast (20). Approximately 5%

A B

Lactating adenoma in a 17-year-old female. A: Transverse

Fig. 6.14
sonogram shows a homogeneous mass (arrowheads) that
is isoechoic to normal breast tissue. There is slight acoustic enhance-
ment (arrow). B: Color Doppler image demonstrates no flow within the
mass. C: Sonographic image of another patient shows a hypoechoic
mass (calipers) containing multiple small hyperechoic foci that repre-
C sent fat in the milk produced by the tumor.
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210 P E D I AT R I C S O N O G R A P H Y

Granular cell tumor in an 18-year-old woman. Longitudinal

Fig. 6.15 Juvenile papillomatosis in a 16-year-old girl. Transverse
sonogram shows a hypoechoic mass with irregular, ill- Fig. 6.16
defined borders (arrowheads). image shows a well-circumscribed, complex mass
(arrowheads) containing innumerable small anechoic cysts.

to 6% of these tumors arise in the breast. Granular cell dense collagenous stroma. The anastomosing spaces resem-
tumor is believed to be of neural origin (Schwann cells) ble vascular channels, but they do not contain red blood cells.
and has a predilection for premenopausal African Ameri- The sonographic appearances are variable, but most
can women (20). Clinically, the tumor presents as a palpa- PASH tumors appear as well-circumscribed, hypoechoic,
ble, firm superficial mass, occasionally associated with skin ovoid masses with their long axis paralleling the chest
retraction (21). wall, findings similar to those of fibroadenomas (Fig. 6.17)
The sonographic appearance is variable and includes a (2527). Posterior acoustic enhancement is variable but
well-circumscribed hypoechoic mass with posterior acoustic usually absent. PASH tumors are treated with simple sur-
enhancement and an ill-defined hyperechoic mass with pos- gical excision because of their tendency to enlarge slowly.
terior acoustic shadowing (Fig. 6.15) (2022). A hypere-
choic rim is often present. Intraductal Papilloma
Intraductal papilloma is a benign proliferation of ductal
Juvenile Papillomatosis epithelium (28). It can arise in central ducts (subareolar
Juvenile papillomatosis is a localized proliferative disorder ducts) or in terminal ducts. Large lesions may dilate the duct.
of adolescents and young women. The mean patient age at Clinically, patients present with serous or serosanguineous
diagnosis is 19 years (3). Affected patients present with a
firm, well-defined, mobile mass, commonly in the periph-
ery of the breast. Histologic examination shows multiple
macrocysts and dilated ducts within a fibrous stroma.
Although it is benign, it is associated with familial breast
cancer. Affected patients have an increased family history
of breast cancer (33% to 58% of cases) (1). About 5% to
15% have concurrent breast cancer.
At sonography, juvenile papillomatosis appears as a
complex mass with multiple small cysts, particularly at the
periphery, and well-circumscribed or ill-defined margins
(Fig. 6.16) (15,23,24). Small echogenic foci, representing
microcalcifications, may be seen (15).

Pseudoangiomatous Stromal Hyperplasia

Pseudoangiomatous stromal hyperplasia (PASH) is a
benign, hormonally stimulated myofibroblastic prolifera-
tion that is usually found in premenopausal women, but it
can be seen in adolescent girls (25). Affected patients pres-
ent with a painless, firm, rubbery, movable mass. The con- Pseudoangiomatous stromal hyperplasia in an 18-year-old
dition has been reported in boys and men with gynecomas- Fig. 6.17
girl. Longitudinal image shows a large, well-defined,
tia (26). The histologic findings of PASH are anastomosing homogeneous mass. The long axis parallels the chest wall. P  pec-
channels lined with flat myofibroblastic cells surrounded by toralis muscle.
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Intraductal papilloma. Sonographic image shows a dilated
Fig. 6.18
duct (arrowhead) with an irregular, echogenic mass (curved
arrow) partially filling the lumen.
nipple discharge. Three basic patterns of intraductal papillo-
mas are recognized on sonography: an intraductal mass with
minimal or no ductal dilatation, a small mass partially filling
a dilated duct, and a large intraductal mass totally filling a
dilated duct (Fig. 6.18) (28). Intraductal papillomas can con-
tain calcifications that tend to be dense and coarse. The
tumors are highly vascular and can show hyperemia on color
Doppler imaging.
Intramammary Lymph Nodes
Intramammary lymph nodes are most often found in the
upper outer quadrant of the breast. They have a sono-
graphic appearance similar to nodes elsewhere in the body,
manifesting as a well-delineated ovoid structure with a cen-
tral echogenic hilum that is vascular on Doppler imaging.
MALIGNANT TUMORS
Malignant breast tumors in the pediatric age group are
extremely rare and account for less than 5% of breast
masses (2,3,5,29). These include phyllodes tumor, primary
cancer, and metastases from another primary tumor.
Phyllodes Tumor
Phyllodes tumor, or cystosarcoma phyllodes, is a fibroep-
ithelial neoplasm composed of cellular stroma and branch-
ing, epithelial-lined cystic spaces. It accounts for only 1%
of all breast lesions in children and adolescents, but it is
the most common primary breast malignancy in this pop-
Chapter 6 B R E A S T 211
Malignant phyllodes tumor in a 26-year-old woman. Trans-
Fig. 6.19
verse image demonstrates a sharply marginated, hypo-
echoic, heterogeneous mass (arrowheads) with anechoic cysts and
clefts (curved arrows) and posterior acoustic enhancement. The pres-
ence of fluid-filled cystic spaces is suggestive of the diagnosis of phyl-
lodes tumor.
ulation (2,3,13). Approximately 5% of all phyllodes
tumors occur in girls and women younger than 20 years of
age. Affected patients present with a painless, rapidly
growing, rubbery mass, often larger than 6 cm at presen-
tation (3). Phyllodes tumors range in size from 1 to 20 cm,
but most are 8 to 10 cm (2).
The biologic behavior varies from benign to intermedi-
ate to malignant depending on stromal cellularity, infiltra-
tion at the edge of the tumor, and mitotic activity. Most
phyllodes tumors in adolescents are histologically benign.
However, all forms are considered as having malignant
potential. Metastases are rare in the pediatric population
and most often go to the lungs. The prognosis is usually
favorable following wide local excision.
The sonographic features of phyllodes lesions are non-
specific and similar to those of fibroadenomas. The tumor
usually appears as a well-circumscribed, round or ovoid,
hypoechoic mass, often with lobulated borders and posterior
acoustic enhancement (3033). The internal matrix is het-
erogeneous, a finding that is less frequent in fibroadenoma.
The finding of anechoic cysts or clefts is very suggestive of
phyllodes tumor but not pathognomonic, and it can also be
seen in juvenile fibroadenoma (Fig. 6.19) (14). Tissue sam-
pling is needed to differentiate between benign and malignant
tumors.
Carcinoma
Adenocarcinoma is exceedingly rare in children, accounting
for less than 1% of breast lesions (11). The age-adjusted
incidence is 0.03 cases per 100,000 in patients younger
than 20 years of age (34). Secretory (juvenile) carcinoma is
the main subtype in children and adolescents and is associ-
ated with a favorable prognosis (11,13,35). Breast cancer
in young patients can be associated with hereditary cancer
syndromes, such as BRCA1 and BRCA2 gene mutations
(3). It also can occur as a secondary malignancy in patients
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212 P E D I AT R I C S O N O G R A P H Y

common tumors to metastasize to the breast in children,

and approximately 6% of children with rhabdomyosar-
coma have breast metastases (3941). Breast metastases
are much more common in girls but can occur in boys
(42). Clinically, they present as mobile, rapidly enlarging
masses that may be painful (4143).
Breast metastases are most commonly large, solitary
masses, but they can be bilateral and multiple (3). They
usually demonstrate irregular or lobulated margins and het-
erogeneous, hypoechoic, internal echotexture (Fig. 6.21)
(37,41). Hyperechoic foci related to calcification and pos-
terior acoustic shadowing are also common findings.
Leukemia and lymphoma usually appear as hypoechoic,
homogeneous masses with well-defined or poorly circum-
scribed margins (4143). Metastatic neuroblastoma may
appear as a hyperechoic mass (44).

REFERENCES
Invasive ductal carcinoma in a young adult woman. Trans- 1. Chang E, Cube R, Hall GJ, et al. Breast masses in children and
Fig. 6.20
verse sonogram shows a hypoechoic nodule with internal adolescents: radiologic-pathologic correlation. Radiographics
heterogeneity, irregular margins (arrowheads), and posterior acoustic 2009;29:907931.
shadowing (arrow). 2. Greydanus DE, Matytsina L, Gains M. Breast disorders in chil-
dren and adolescents. Prim Care 2006;33:455502.
3. Coffin CM. The breast. In: Stocker JT, Dehner LP, eds. Pediatric
treated for childhood cancer (2,3). Patients present with a pathology. 2nd ed. Philadelphia, PA: Lippincott Williams &
painless, firm mass (35). Secretory carcinomas are usually Wilkins, 2002:9931015.
less than 3 cm in diameter at presentation (3). 4. Garcia CJ, Espinoza A, Dinamarca V, et al. Breast US in chil-
The sonographic features of malignancy are variable dren and adolescents. Radiographics 2000;20:16051612.
5. Bock K, Duda VF, Hadji P, et al. Pathologic breast conditions in
and nonspecific. Carcinoma most commonly appears as a
childhood and adolescence: evaluation by sonographic diagno-
hypoechoic mass with irregular or spiculated margins, sis. J Ultrasound Med 2005;24:13471354.
internal heterogeneity, and a long axis perpendicular to the 6. Merrritt CRB. Breast nodule. In: Bluth EI, Arger PH, Benson
chest wall (Fig. 6.20) (12,36). Posterior acoustic shadow- CB, et al., eds. Ultrasound: a practical approach to clinical
ing also may be seen. problems. 2nd ed. New York: Thieme Press, 2000:668679.
7. Welch ST, Babcock DS, Ballard ET. Sonography of pediatric
Metastatic Disease and Hematologic Malignancy male breast masses: gynecomastia and beyond. Pediatr Radiol
2004;34:952957.
Metastatic tumors include lymphoma, leukemia, and solid 8. Weinstein SP, Conant EF, Orel SG, et al. Spectrum of US find-
neoplasms, such as rhabdomyosarcoma, neuroblastoma, ings in pediatric and adolescent patients with palpable breast
and renal carcinoma (3,11,13,37,38). Rhabdomyosar- masses. Radiographics 2000;20:16131621.
coma, particularly the alveolar subtype, is one of the more 9. OHare PM, Frieden IJ. Virginal breast hypertrophy. Pediatr
Dermatol 2000;17:277281.
10. Huneeus A, Schilling A, Horvath E, et al. Retroareolar cysts in
the adolescent. J Pediatr Adolesc Gynecol 2003;16:4549.
11. Pettinato G, Manivel JC, Kelly DR, et al. Lesions of the breast
in children exclusive of typical fibroadenoma and gynecomas-
tia. A clinicopathologic study of 113 cases. Pathol Annu
1989;24(Pt 2):296328.
12. Venta LA, Dudiak CM, Salomon CG, et al. Sonographic evalu-
ation of the breast. Radiographics 1994;14:2950.
13. West KW, Rescorla FJ, Scherer LR III, et al. Diagnosis and treat-
ment of symptomatic breast masses in the pediatric population.
J Pediatr Surg 1995;30:182186.
14. Kronemer KA, Rhee K, Siegel MJ, et al. Gray scale sonography
of breast masses in adolescent girls. J Ultrasound Med
2001;20:491496.
15. Sabate JM, Clotet M, Torrubia S, et al. Radiologic evaluation of
breast disorders related to pregnancy and lactation. Radi-
ographics 2007;27:S101.
16. Burrows PE, Laor T, Paltiel H, et al. Diagnostic imaging in the eval-
uation of vascular birthmarks. Dermatol Clin 1998;16:455488.
17. Coffin CM, Dehner LP. The soft tissues. In: Stocker JT, Dehner
Metastatic malignant melanoma. Transverse sonogram LP, eds. Pediatric pathology. 2nd ed. Philadelphia, PA: Lippin-
Fig. 6.21
reveals an irregularly shaped, hypoechoic mass. cott Williams & Wilkins, 2002:11691171.
LWBK505-C06_p200-213.qxd 7/7/10 2:04 PM Page 213 Aptara Inc
18. Dubois J, Garel L. Imaging and therapeutic approach of heman-
giomas and vascular malformations in the pediatric age group.
Pediatr Radiol 1999;29:879893.
19. Paltiel HJ, Burrows PE, Kozakewich HP, et al. Soft-tissue vas-
cular anomalies: utility of US for diagnosis. Radiology
2000;214:747754.
20. Adeniran A, Al-Ahmadie H, Mahoney MC, et al. Granular cell
tumor of the breast: a series of 17 cases and review of the liter-
ature. Breast J 2004;10:528531.
21. Yang WT, Edeiken-Monroe B, Sneige N, et al. Sonographic and
mammographic appearances of granular cell tumors of the
breast with pathological correlation. J Clin Ultrasound 2006;34:
153160.
22. Feder JM, de Paredes ES, Hogge JP, et al. Unusual breast
lesions: radiologic-pathologic correlation. Radiographics
1999;19(Spec No):S11S26.
23. Han BK, Choe YH, Ko YH, et al. Benign papillary lesions of the
breast: sonographic-pathologic correlation. J Ultrasound Med
1999;18:217223.
24. Kersschot EA, Hermans ME, Pauwels C, et al. Juvenile papillo-
matosis of the breast: sonographic appearance. Radiology
1988;169:631633.
25. Wieman SM, Landercasper J, Johnson JM, et al. Tumoral
pseudoangiomatous stromal hyperplasia of the breast. Am Surg
2008;74:12111214.
26. Ferreira M, Albarracin CT, Resetkova E. Pseudoangiomatous
stromal hyperplasia tumor: a clinical, radiologic and pathologic
study of 26 cases. Mod Pathol 2008;21:201207.
27. Cohen MA, Morris EA, Rosen PP, et al. Pseudoangiomatous
stromal hyperplasia: mammographic, sonographic, and clinical
patterns. Radiology 1996;198:117120.
28. Ganesan S, Karthik G, Joshi M, et al. Ultrasound spectrum in
intraductal papillary neoplasms of breast. Br J Radiol 2006;79:
843849.
29. Rogers DA, Lobe TE, Rao BN, et al. Breast malignancy in chil-
dren. J Pediatr Surg 1994;29:5255.
30. Liberman L, Bonaccio E, Hamele-Bena D, et al. Benign and
malignant phyllodes tumors: mammographic and sonographic
findings. Radiology 1996;198:121124.
Chapter 6 B R E A S T 213
31. Rajan PB, Cranor ML, Rosen PP. Cystosarcoma phyllodes in
adolescent girls and young women: a study of 45 patients. Am
J Surg Pathol 1998;22:6469.
32. Vade A, Lafita VS, Ward KA, et al. Role of breast sonography
in imaging of adolescents with palpable solid breast masses.
AJR Am J Roentgenol 2008;191:659663.
33. Yilmaz E, Sal S, Lebe B. Differentiation of phyllodes tumors
versus fibroadenomas. Acta Radiol 2002;43:3439.
34. Gutierrez JC, Housri N, Koniaris LG, et al. Malignant breast
cancer in children: a review of 75 patients. J Surg Res 2008;147:
182188.
35. Murphy JJ, Morzaria S, Gow KW, et al. Breast cancer in a 6-year-
old child. J Pediatr Surg 2000;35:765767.
36. Stavros AT, Thickman D, Rapp CL, et al. Solid breast nodules:
use of sonography to distinguish between benign and malignant
lesions. Radiology 1995;196:123134.
37. Chateil J-F, Arboucalot F, Perel Y, et al. Breast metastases
in adolescent girls: US findings. Pediatr Radiol 1998;28:
832835.
38. Pursner M, Petchprapa C, Haller JO, et al. Renal carcinoma:
bilateral breast metastases in a child. Pediatr Radiol 1997;27:
242243.
39. Howarth CB, Caces JN, Pratt CB. Breast metastases in children
with rhabdomyosarcoma. Cancer 1980;46:25202524.
40. Hays DM, Donaldson SS, Shimada H, et al. Primary and
metastatic rhabdomyosarcoma in the breast: neoplasms of ado-
lescent females, a report from the Intergroup Rhabdomyosar-
coma Study. Med Pediatr Oncol 1997;29:181189.
41. Yang WT, Metreweli C. Sonography of nonmammary malig-
nancies of the breast. AJR Am J Roentgenol 1999;172:343348.
42. Cunningham I. A clinical review of breast involvement in acute
leukemia. Leuk Lymphoma 2006;47:25172526.
43. Kumar PRG, Grossman Z, Scorza L, et al. Isolated extramedullary
relapse of acute leukemia in the breast of an adolescent girl:
radiologic findings and discussion. Pediatr Radiol 2010;40:
773776.
44. Boothroyd A, Carty H. Breast masses in childhood and adoles-
cence: a presentation of 17 cases and a review of the literature.
Pediatr Radiol 1994;24:8184.
LWBK505-C07_p214-274.qxd 7/7/10 1:28 PM Page 214 Aptara Inc

CHAPTER

7 Liver
MARILYN J. SIEGEL

Scanning Technique Infections Portal Vein Thrombosis

Viral Hepatitis Budd-Chiari Syndrome
Normal Anatomy and Fissures
Pyogenic Abscess Hepatic Veno-occlusive Disease
Lobar and Segmental Anatomy and Fissures
Fungal Abscess Arteriovenous Malformations
Hepatic Ligaments
Hydatid Disease Hepatic Infarction
Normal Vascular Anatomy: Gray Scale Amebic Abscess Peliosis Hepatis
Imaging Ascariasis Passive Venous Congestion
Portal Veins Schistosomiasis
Portal Venous Gas
Hepatic Veins Chronic Granulomatous Disease
Hepatic Artery Cat-Scratch Disease Radiation Effects
Normal Doppler Anatomy Acquired Immunodeficiency Hepatic Trauma
Portal Veins Syndrome Acute Injuries
Hepatic Veins Diffuse Parenchymal Diseases Complications
Hepatic Artery Steatosis Liver Transplantation
Hepatic Parenchyma Focal Fatty Sparing Preoperative Evaluation
Anatomic Variants Hepatic Fibrosis Surgical Anatomy
Hemochromatosis Imaging Guidelines
Hepatic Neoplasms Cirrhosis Normal Posttransplantation Liver
Ultrasound Techniques for Tumor Metabolic Liver Diseases Postoperative Vascular Complications
Imaging
Disorders of Hepatic Vessels Parenchymal Complications
Overview of Hepatic Tumors
Portal Hypertension Biliary Complications
Malignant Hepatic Neoplasms
Surgical Portosystemic Shunts Miscellaneous Complications
Secondary Hepatic Neoplasms
Benign Neoplasms Transjugular Intrahepatic Portosystemic
Cysts Shunts

onography has become established as the imaging very superficial lesions. Longitudinal, transverse, and coro-

S method of choice for screening the liver for both focal

and diffuse pathologic processes (1,2). With the addi-
tion of Doppler flow imaging, sonography also has proven
to be effective in the evaluation of hepatic vascular abnor-
malities.
This chapter addresses sonographic techniques for
evaluating the liver and the sonographic appearances of
important focal and diffuse hepatic diseases in children.
The clinically and pathologically relevant features of the
common pathologic processes are also highlighted to pro-
vide a basis for understanding the sonographic features.
SCANNING TECHNIQUE
The sonographic examination of the liver is best per-
formed when the patient has fasted for 4 to 6 hours so that
the gallbladder is distended and the amount of bowel gas
is minimized. A 5- or 7.5-MHz linear or curved linear
array transducer usually provides optimal images of the
liver in infants and smaller children. In larger patients, a
2.5- or 3.0-MHz transducer may be needed to penetrate
the larger right lobe. A 7.5 to 12 MHz may help define
nal scans should be obtained with the patient in the supine
and left posterior oblique positions.
Most of the liver can be imaged by a subcostal approach,
but an intercostal approach with a small-footprint trans-
ducer may be necessary for evaluation of the cranial parts of
the liver, especially the subdiaphragmatic part of the right
lobe. The incorporation of pulsed and color flow Doppler
imaging can help to differentiate blood vessels from bile
ducts and characterize vascular abnormalities.
NORMAL ANATOMY AND FISSURES
Lobar and Segmental Anatomy and Fissures
The nomenclature of Couinaud and Bismuth is most com-
monly used for defining segmental anatomy and localizing
hepatic lesions and has replaced the traditional classifica-
tion (3). Each segment contains a branch or branches of the
portal vein in the center and a hepatic vein at the periphery.
Distinguishing hepatic segments is important since surgical
techniques have been developed that allow resection of such
subdivisions (47). There are eight segments, with each

214
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Couinaud hepatic segmental anatomy. The diagram shows
Fig. 7.1
the segmental anatomy of the liver and the portal veins. The
Couinaud classification of liver anatomy divides the liver into eight
functionally independent segments. In the center of each segment
there is a branch of the portal vein, hepatic artery, and bile duct. In the
periphery of each segment there is a branch of the hepatic vein. The
hepatic veins divide the liver into four sections. The right and left por-
tal veins divide the sections into cranial and caudal segments. The
numbering of the segments is in a clockwise manner. Segment 1 (cau-
date lobe) is located posteriorly. The left lobe of the liver is made up of
segments 2, 3, and 4. The right lobe consists of segments 5, 6, 7, and 8.
The cranially located segments are 2, 7, and 8; the caudally located
segments are 3, 5, and 6. The left portal vein divides segment 4 into two
segments (4a and 4b). (Figure courtesy of Robin Smithus.)
hepatic lobe containing four segments. The liver is divided
longitudinally into four sections by the right, middle, and
left hepatic veins, and each of these sections is divided trans-
versely by the right and left portal veins. The caudate lobe is
segment 1, and the other segments, 2 through 7, are num-
bered in a clockwise direction when the liver is viewed from
its ventral aspect (Figs. 7.1 and 7.2). Segment 4 is divided
into segment 4a and 4b.
In the traditional segmental nomenclature, the liver was
divided into right and left lobes, with each lobe divided into
two segments. In this system the main hepatic veins were used
to define the major hepatic segments. The right and left lobes
were defined by a plane passing through the middle hepatic
vein and gallbladder fossa. The anterior and posterior seg-
ments of the right lobe were divided by a plane drawn through
the right hepatic vein, and the medial and lateral segments of
the left lobe were divided by a plane drawn through the left
hepatic vein. In this traditional system, no distinction was
made between superior and inferior subsegments.
Hepatic Ligaments
Several ligaments of the liver can be identified on sonographic
examination when they contain fibrofatty tissue, or when
they are surrounded by ascites. Ligaments containing fibro-
fatty tissue appear highly echogenic relative to surrounding
parenchyma and they may cast an acoustic shadow.
The falciform ligament is an anteroposterior fold of
peritoneum that courses over the anterior surface of the
Chapter 7 L I V E R 215
liver and extends from the diaphragm or anterior body
wall to the lower hepatic margin (Fig. 7.3). It attaches the
liver to the anterior body wall and courses between seg-
ments 3 and 4 in the Couinaud system. Its base or free edge
contains between its layers the round ligament and umbil-
ical vein. On transverse images, the ligament appears as a
hyperechoic, vertically oriented structure extending to the
anterior hepatic surface (Fig. 7.3B).
The ligamentum teres (also known as the round liga-
ment of the liver) contains the remnant of the fetal umbil-
ical vein. It runs within the posteroinferior free edge of the
falciform ligament extending to the origin of the left por-
tal vein within the porta hepatis (Fig. 7.3A). On transverse
images, it appears as a round hyperechoic area to the right
of midline (Fig. 7.4). On longitudinal views, it is seen as a
hyperechoic linear structure extending from the inferior
surface of the liver to the left portal vein. Slow flow, either
hepatofugal or hepatopetal, can be noted in paraumbilical
vessels within the ligamentum teres in healthy individuals
and does not necessarily indicate portal hypertension (8).
Mean hepatofugal flow velocity is approximately 3 cm/sec
and mean hepatopetal flow velocity is about 4 cm/sec. The
waveform in these vessels is monophasic or mildly undu-
lating, similar to normal portal venous waveforms (8).
The ligamentum venosum is the fibrous remnant of the
obliterated ductus venosus of the fetal circulation. In utero,
the ductus venosus shunts blood from the umbilical vein
to the inferior vena cava. It courses along the inferior surface
of the liver between segments 1 and 2 (caudate lobe and lat-
eral segment of the left lobe). It may be continuous with the
ligamentum teres. On transverse images, the ligament appears
as a hyperechoic, transverse linear structure anterior to the
caudate lobe and posterior to the left portal vein (Fig. 7.5).
Other ligaments, such as the coronary and triangular
ligaments, can only be recognized when they are sur-
rounded by ascites. The coronary ligament is a reflection of
peritoneum that extends from the diaphragm to the super-
oposterior surface of the right hepatic lobe. The right and
left triangular ligaments course between the lateral por-
tions of the right and left hemidiaphragms and the superior
surfaces of the right and left hepatic lobes, respectively.
NORMAL VASCULAR ANATOMY: GRAY SCALE IMAGING
Portal Veins
Portal veins carry blood from the splenic and mesenteric
circulation to the liver and they supply 70% to 75% of
the livers blood supply (Figs. 7.1 and 7.2).
In the porta hepatis, the main portal vein divides into a
more caudad and posterior right portal vein and a more
cephalad and anterior left portal vein. The right portal vein
divides into anterior and posterior branches, and each of
these branches in turn divides into superior and inferior
branches, which supply their corresponding segments of
the right hepatic lobe. The initial horizontal portion of the
left portal vein gives branches to the caudate lobe and then
courses along the anterior surface of the caudate lobe. The
vein ascends anteriorly and then divides into medial and
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216 P E D I AT R I C S O N O G R A P H Y

A B

C D

E F
Hepatic Couinaud segmental and venous anatomy, ultrasound demonstration with computed tomography comparison. Axial images AF.
Fig. 7.2
Hepatic segmental anatomy viewed in the transaxial plane. The hepatic veins divide the liver longitudinally into four sections. The left
and right portal vein branches separate the cranially located segments (2, 7, and 8) from the caudally located segments (3, 4, and 6). The medial
segment of the left lobe is divided into segments 4a and 4b by the plane of the left portal vein. IVC, inferior vena cava; L, left hepatic vein; LPV, left
portal vein; M, main hepatic vein; R, right hepatic vein; RPV, right portal vein.
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A B
Falciform ligament. Transverse view. A: Diagram of falciform ligament and ligamentum teres. The falciform ligament coures from the
Fig. 7.3
diaphragm or anterior body wall to the free edge of the liver. B: Transverse sonogram shows the hyperechoic band-like falciform liga-
ment (arrow), extending to the anterior-superior hepatic margin and abdominal wall. P  pancreas. (Panel A courtesy of Robin Smithus.)

Ligamentum teres. Transverse scan of the left lobe of the

Fig. 7.4
liver shows a round echogenic area (arrow), which is the
ligamentum teres. The ligament teres lies in the free inferior margin of
the falciform ligament. P  pancreas; St  stomach.

A B
Ligamentum venosum. A, B: Two transverse scans show a linear echogenic density (arrows), representing the ligamentum venosum, on
Fig. 7.5
the inferior surface of the liver anterior to the caudate lobe (CL). C  inferior vena cava; PV  left portal vein.
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218 P E D I AT R I C S O N O G R A P H Y
Portal vein anatomy. The right portal vein (R) divides into
Fig. 7.6
anterior (a) and posterior (p) branches, which course
through the anterior and posterior segments of the right lobe. The left
portal vein (L) gives off branches to segments 2, 3 (lateral segments)
(arrow), and 4 (medial segment) of the left lobe.
lateral branches, which supply the corresponding segments
of the left lobe (segments 2, 3, and 4) (Fig. 7.6).
The main, left, and right portal veins are easily recog-
nized at gray-scale sonography because they are relatively
large and have echogenic walls. The mean diameter of the
main portal vein is 8.5  2.7 mm in children under
10 years of age and 10  2 mm in individuals between 10
and 20 years of age (9). The portal veins increase in diame-
ter as they approach the porta hepatis. Portal vein diameter
also increases during inspiration and decreases during expi-
A B
Ductus venosum. Newborn infant. Transverse gray-scale (A) and color Doppler (B) sonograms show the patent ductus venosus (open
Fig. 7.7
arrow) coursing between the anterior hepatic surface and the inferior vena cava (C) at its junction with the portal vein (arrow).
ration. The normal intraparenchymal branches of the portal
veins are difficult to visualize because of their small size.
In utero, the ductus venosus originates from left portal
vein immediately opposite the insertion site of the umbilical
vein and courses cephalad to the inferior vena cava, shunting
oxygenated blood from the placenta directly to the inferior
vena cava. Flow can be seen in the ductus venosus and left
portal vein by sonography in nearly all neonates in the first
few days of life (10,11). The ductus closes within several days
to weeks after birth. On gray-scale sonography, the patent
ductus venosus appears as an anechoic channel joining with
the left portal vein and extending from the anterior surface of
the liver to the inferior vena cava (Fig. 7.7). Its length ranges
from 1.1 to 1.9 cm and its diameter from 1 to 2 mm. The
closed ductus appears as an echogenic channel that exhibits
neither color nor pulsed Doppler signal. After it involutes, the
obliterated remnant may calcify, producing an intrahepatic
linear echogenic focus with distal shadowing (12,13).
Variations in the intrahepatic branching of the portal
venous system include (a) absence of the portal vein with
diversion of portal blood into the vena cava (14); (b)
absence of the horizontal segment of the left portal vein
with blood supply from the right portal vein; (c) trifurca-
tion of the main portal vein; (c) origin of the right poste-
rior segmental branch from the main portal vein; (d) origin
of the right anterior segmental branch from the left portal
vein; and (f) absence of the main right, right anterior, and
right posterior portal branches (Fig. 7.8) (15,16). In the
latter anomaly, multiple vessels of variable size arise from
the main and left portal vein to supply the right lobe.
The coronary vein, also known as the left gastric vein
communicates with the superior aspect of the portal or
splenic vein in the region of the confluence. It arises along
the gastric pylorus and lesser curvature of the stomach and
proceeds toward the esophageal hiatus where it turns back
and runs inferiorly to drain into the portal splenic
confluence. Sonographically, the coronary vein is usually
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Chapter 7 L I V E R 219

A B

C D
Coronary vein A: Anatomy. Diagram shows the relationship of the portal vein (PV), splenic vein (SV), superior mesenteric vein (SMV),
Fig. 7.8
and coronary vein (CV). The coronary vein communicates with the superior aspect of the portal or splenic vein in the region of the
confluence. B: Magnified transverse view of the upper abdomen shows the celiac artery arising from the aorta (Ao) and bifurcating into the splenic
artery (SA) and hepatic artery (HA). The coronary vein (CV) is anterior to the bifurcation. Also seen is the portal vein (PV). C: Sagittal view shows the
splenic vein (SV), Ao, and celiac axis (CA). The CV arises from the superior aspect of the SV and travels anterior to the CA. D: Sagittal color Doppler
view flow in the CV directed inferiorly (black arrow) toward the SV. ( From Robinson KA, Middleton WD, AL-Sukaiti R, et al. Doppler Sonography of
Portal Hypertension. Ultrasound Quarterly. 2009; 25(1):313.)

seen anterior to the bifurcation of the celiac axis and then
it travels superiorly and to the left (Fig. 7.8). Occasionally,
it can be located posterior to either the common hepatic
artery or the splenic artery. Blood flow is normally directed
toward the portal vein. The importance of the coronary
vein is that it is the most prevalent portal systemic collat-
eral in patients with portal hypertension.
Hepatic Veins
The right, middle, and left hepatic veins are the efferent ves-
sels of the liver and transport blood from the hepatic
parenchyma into the systemic circulation, draining into the
inferior vena cava. The three major hepatic veins are found
between hepatic segments (Figs. 7.1 and 7.2). The right
hepatic vein separates segments 5 and 8 from segments
6 and 7. The middle hepatic vein, running in the interlobar
fissure, separates segment 4 from segments 5 and 8. The left
hepatic vein separates segment 4 from segments 2 and
3. The middle and left hepatic veins often merge to form a
common trunk before emptying into the inferior vena cava.
The hepatic veins are best recognized on images
through the cephalad portion of the liver (Fig. 7.9). They
become larger as they approach their junction with the
inferior vena cava. The walls of the hepatic veins are
imperceptible in contrast to the peripheral echogenicity
that is associated with the walls of the portal veins.
Accessory hepatic veins are a common anatomic vari-
ation. Up to 55% of individuals have more than three
hepatic veins. The accessory veins most commonly seen
are the right superior-anterior hepatic vein, which usually
enters the middle hepatic vein; the right and left marginal
veins, which drain into the right and left hepatic veins,
LWBK505-C07_p214-274.qxd 7/7/10 1:28 PM Page 220 Aptara Inc
220 P E D I AT R I C S O N O G R A P H Y
respectively (Fig. 7.10); and the accessory right hepatic
vein, which drains into the inferior vena cava (17).
Hepatic Artery
The celiac axis arises from the abdominal aorta and
divides into the hepatic, splenic, and left gastric arteries.
The hepatic artery courses anteriorly and to the right giv-
ing off right gastric and gastroduodenal branches, before
reaching the porta hepatis. In the porta hepatis, the hepatic
artery lies anterior and medial to the main portal vein and
medial to the common bile duct (Fig. 7.11). The hepatic
artery and bile duct can be differentiated by their relative
positions within the porta hepatis and their flow pattern
on Doppler imaging (see later discussion). The intrahepatic
arterial structures beyond the porta are difficult to recog-
nize because of their small size.
Variations in the origin of the hepatic arteries occur in
about 45% of the population and include replaced and
Hepatic veins. Transverse view shows three major hepatic
Fig. 7.9
veins. The right hepatic vein (R), middle hepatic vein (M),
and left hepatic vein (L) drain into the inferior vena cava (C). The mid-
dle hepatic vein courses within the interlobar fissure, which divides
the liver into right and left lobes.
accessory hepatic arteries. Common variations are (a) a
replaced right hepatic artery arising from the superior
mesenteric artery (Fig. 7.12), (b) a replaced left hepatic
artery arising from the left gastric artery, and (c) a replaced
common hepatic artery originating from the superior
mesenteric artery. Accessory arteries are supernumerary ves-
sels and may be the only vascular supply to part of the liver.
NORMAL DOPPLER ANATOMY
Pulsed and color flow Doppler imaging are useful tech-
niques in evaluating the presence and direction of blood in
the hepatic vessels. Each of the major hepatic vessels has a
unique Doppler signal.
Portal Veins
The Doppler characteristics of the main portal vein are
best evaluated on scans that parallel the long axis of the
Accessory hepatic vein. The right superior-anterior
Fig. 7.10
hepatic vein (arrowhead) joins the middle (M) hepatic
vein. The left marginal vein (arrow) drains into the left (L) hepatic vein.
C  inferior vena cava; R  right hepatic vein.
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A B

Normal arterial anatomy. A: Transverse scan. The celiac

Fig. 7.11
artery (open arrow) arises from the abdominal aorta (A)
and branches into the hepatic artery (arrow) and the splenic artery
(arrowhead). B: Transverse scan at the level of the portal hepatis. The
hepatic artery (HA) proper lies anteromedial to the main portal (PV)
vein and medial to the common bile duct (BD). GB  gallbladder.
C: Longitudinal sonogram. The hepatic artery (HA) lies anterior to the
main portal (PV) vein and posterior to the common bile duct (BD).
C P  pancreas; C  inferior vena cava.

Replaced hepatic artery. Transverse view showing the

Fig. 7.12
right hepatic artery (arrowheads) arising from the supe-
rior mesenteric artery (S). A  aorta; C  inferior vena cava.
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222 P E D I AT R I C S O N O G R A P H Y

A B

Normal portal vein waveform, color Doppler sonogram.

Fig. 7.13
A: Nonpulsatile portal venous flow. B: Minimally pulsatile
flow related to respiration. The direction is antegrade (hepatopetal).
C: Flow in the ascending branch (white arrow) of the left portal vein is
red because flow is toward the transducer. Flow in the posterior
branch (open arrow) of the right portal vein is blue, reflecting flow
C away from the transducer.

vessel. The portal venous waveform is monophasic with
minimal if any pulsatility (Fig. 7.13) (18). Flow diminishes
slightly during inspiration, but the minimum velocity
should remain antegrade and should measure at least one
half to two thirds of the maximum velocity. Portal blood
flow increases after a meal (Fig. 7.14) (19).
Portal venous flow is toward the transducer, except in
the posterior branch of the right portal vein where flow is
away from the transducer. When flow toward the trans-
ducer is assigned a red color, the portal veins appear red.
The posterior branch has a blue color assignment because
flow is away from the transducer (Fig. 7.13C).
Tricuspid regurgitation and congestive heart failure
elevate right atrial pressure. The pressure elevation is
transmitted through the hepatic sinusoids to the portal
vein, altering portal venous waveforms. The changes in
flow patterns include: (a) monophasic forward flow with
gradual diminution of velocity throughout ventricular sys-
tole, (b) retrograde flow, and (c) vena cavalike biphasic
waveforms (20,21).
Hepatic Veins
The middle and left hepatic veins are best sampled with
Doppler interrogation from an anterior or subxiphoid
approach. Because the right hepatic vein is perpendicular
(90 degrees) to the transducer in the anterior approach,
this vein may be better evaluated through a right lateral
approach.
The typical hepatic venous waveform shows a triphasic
pattern: (a) an antegrade wave during right ventricular
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A B
Fig. 7.14 Portal vein flow. A: Fasting portal vein flow 0.28 meter/sec. B: Postprandial 0.53 meter/sec.
systole (S wave), (b) a second smaller antegrade pulse dur-
ing right atrial diastole (D wave), and (c) retrograde flow
during right atrial systole (A wave) (Fig. 7.15). Two addi-
tional small retrograde waves, V and C waves, are occa-
sionally seen. The small V wave is caused by right ventric-
ular diastole and atrial overfilling and the small C wave is
caused by closure of the tricuspid valve at the start of sys-
tole (22). A triphasic flow pattern in all three hepatic veins
is seen in about 40% of healthy children, with the remain-
ing children showing monophasic flow in one or more
hepatic veins. Neonates have the highest percentage of
monophasic flow in all three veins (23). Flow in the hepatic
Normal hepatic vein waveform. The typical triphasic wave-
Fig. 7.15
form reflects right atrial pressure changes, with antegrade
flow during right ventricular systole (S), smaller antegrade peak during
right atrial diastole (D), and retrograde flow during right atrial systole (A).
An additional retrograde waveform, the V wave, is seen during right ven-
tricular diastole. Flow is away from the transducer and is antegrade
below the baseline.
Chapter 7 L I V E R 223
veins is normally away from the transducer. The result is a
blue color assignment on Doppler Imaging.
Changes in intrathoracic pressure can alter the hepatic
venous waveform. During deep inspiration, systolic flow
decreases and diastolic flow increases, with the opposite
occurring during expiration. Tricuspid insufficiency can
also alter the waveform (Fig. 7.16). During right ventricu-
lar systole, regurgitant flow into the right atrium elevates
right atrial pressure, and this pressure elevation is transmit-
ted to the hepatic veins, causing a decrease or reversal of
the antegrade systolic wave. The systolic-to-diastolic flow
velocity ratio decreases (22).
Tricuspid regurgitation. Pulsed Doppler sonogram shows
Fig. 7.16
increased pulsatility with reversal of antegrade flow.
Hepatic venous flow is away from the transducer (blue signal) on the
color Doppler image.
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224 P E D I AT R I C S O N O G R A P H Y
Normal hepatic artery waveform. The waveform shows a
Fig. 7.17
low-resistance pattern with continuous antegrade flow
through diastole (RI  0.77).
Hepatic Artery
In the healthy fasting individual, the hepatic artery shows
a low-resistance waveform with continuous antegrade
flow throughout diastole (Fig. 7.17) (24,25). Peak sys-
tolic shift is usually less than 0.7 kHz (at 3 MHz
insonation). The normal resistive index is approximately
0.7.
Vasoconstriction of the hepatic artery occurs as a nor-
mal response to the increased portal venous flow induced
by eating. Approximately 30 minutes after a meal, hepatic
arterial diastolic flow decreases with a corresponding
A B
Normal liver echotexture. A: Neonate. Right hepatic lobe, longitudinal view. The echogenicity of the liver (L) and renal cortex of the right
Fig. 7.18
kidney (RK) are isoechoic. B: Fifteen-year-old girl. The liver is hyperechoic relative to kidney (calipers). L  liver.
increase in the hepatic arterial resistive index. The mean
postprandial increase in the resistive index in healthy indi-
viduals is about 40%, while in patients with liver disease it
is less than 10% (24,25). Recognition of this postprandial
increase in arterial resistance is important lest it be mis-
taken as a finding of liver disease.
HEPATIC PARENCHYMA
Normal hepatic parenchyma has a fine homogeneous
echotexture. In the neonate and young infant, the hepatic
parenchyma and renal cortex are equally echogenic. By 6
months of age, the liver is usually slightly hyperechoic
compared to the right kidney and is slightly hypoechoic
compared to the spleen (Fig. 7.18). Interspersed within
the hepatic parenchyma are small, round, hyperechoic
areas representing periportal fibrofatty tissue and hyper-
echoic linear structures representing fissures and liga-
ments.
The ligamentum teres and the ligamentum venosum
may cause acoustic shadowing so that the liver parenchyma
posterior to these ligaments appears hypoechoic, mimick-
ing a mass. Scanning in multiple planes can eliminate the
shadowing effect of the fissures and establish the presence
of a normal liver.
The papillary process is a thin protrusion arising from
the anteroinferior aspect of the caudate lobe. It lies to the
left of the tip of the caudate lobe, posterior to the left lobe,
and anterior to the main hepatic artery and portal vein
(26). If imaged obliquely, it may appear separate from the
caudate lobe and be confused for an enlarged lymph node
or mass. It should be recognizable by its characteristic
location and echotexture, which is similar to that of the
rest of the liver.
Diaphragmatic slips, caused by the diaphragmatic
insertions, can create hyperechoic bands within the cranial
parts of the right and left lobes. The slips appear linear or
wedge shaped on sagittal views and round on transverse
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Chapter 7 L I V E R 225

A B
Prominent left hepatic lobe. A: On a sagittal view, the left hepatic lobe (L) extends around the lateral margin of the spleen (S). The liver
Fig. 7.19
is hypoechoic to spleen. This variant needs to be recognized so that it is not mistaken for a subcapsular hematoma. B: Computed tomog-
raphy shows left lateral extension of the liver (L) around the spleen (S).

views. Scanning in multiple planes can confirm the origin
of these pseudomasses.
Anatomic Variants
VARIATIONS IN POSITION
The right lobe is normally larger than the left and usually
extends inferiorly to about the level of the right renal fossa.
However, in some individuals, the inferior tip of the right
lobe extends below the kidney. This extension is termed a
Riedel lobe.
Variations in position and size are more common in the
left than the right hepatic lobe. The left lobe may be located
entirely on the right side of the abdomen or a tongue-like
protrusion may cross the midline as far as the left lateral
abdominal wall, wrapping around the spleen (Fig. 7.19).
Recognition of this variant is important so that it is not
mistaken for a subcapsular fluid collection. Other varia-
tions include situs inversus (Fig. 7.20), where the liver is
located on the left side of the abdomen, and polysplenia or
asplenia, where the liver has a transverse lie and both lobes
are symmetric.
VARIATIONS IN SIZE
Normal longitudinal measurements of the liver have been
reported and correlated with the findings of sex, age,
weight, height, and body surface area in neonates, infants,

A B
Situs inversus. A: Transverse view of the upper abdomen showing the liver (L) in the left upper quadrant and the spleen (S) in the right
Fig. 7.20
upper quadrant. RK  right kidney. B: Computed tomography shows a left-sided liver and multiple right-sided spleens (S).
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226 P E D I AT R I C S O N O G R A P H Y
and children (27). These can be used as reference standards
to measure liver size.
Rarely, the left or right hepatic lobe is absent and there
is compensatory hypertrophy of the remaining hepatic seg-
ments (2830). Lobar agenesis can be associated with other
anomalies, including partial or complete absence of the
right hemidiaphragm, intestinal malrotation, and chole-
dochal cyst.
ACCESSORY FISSURES
Accessory fissures are caused by an infolding of peri-
toneum. A common accessory fissure is the inferior hepatic
fissure. It extends inferiorly from the posterior branch of
the right portal vein to the inferior surface of the right lobe
of the liver, dividing the posterior segment into anterolat-
eral and posteromedial parts (31). Accessory fissures and
lobes are nearly always asymptomatic. Rarely, an acces-
sory lobe will undergo torsion, causing acute abdominal
pain or vomiting (32,33). Sonographic findings of torsion
are a well-defined hypoechoic mass that is contiguous with
the liver and contains echogenic branching lines, repre-
senting vessels within the torsed hepatic tissue.
HEPATIC NEOPLASMS
Because of its ease of performance and ready availability,
ultrasonography is the initial examination of choice in con-
firming the presence and character of a suspected hepatic
mass. If a mass is identified or suspected on sonography,
computed tomography (CT) or magnetic resonance imag-
ing (MRI) is preferred for further characterizing the lesion
and determining extent and resectability (1,2,34,35).
Ultrasound Techniques for Tumor Imaging
Sonographic characterization of hepatic tumors is per-
formed with gray-scale and color or power Doppler imag-
ing (36). The use of contrast-enhanced sonography can
further help in characterizing and diagnosing hepatic
masses. Contrast-enhanced imaging increases visibility of
tumor vessels, and unlike Doppler imaging, it allows con-
tinuous visualization of blood flow, thereby improving the
functional characterization of liver lesions (37,38). Ultra-
sound contrast agents are composed of tiny bubbles of gas
contained within a stabilizing shell. These produce high
reflectivity and allow real-time imaging of the hepatic
microcirculation for up to several minutes after intra-
venous injection, which in turn allows assessment of lesion
vascularity and enhancement patterns. In adults, benign
hypervascular tumors (hemangioma and focal nodular
hyperplasia) enhance more than the liver in the portal
venous phase, while malignant lesions enhance less. In the
hepatic arterial phase, they all show greater enhancement
than normal liver. There is limited experience with
enhanced sonography in children (38).
Overview of Hepatic Tumors
Hepatic tumors are the third most frequent abdominal neo-
plasm in children after Wilms tumor and neuroblastoma.
Approximately two thirds of all primary hepatic tumors in
children are malignant, and most of these are hepatoblas-
tomas. Hepatocellular carcinoma, including the fibrolamel-
lar variant; undifferentiated sarcoma; and angiosarcoma
are less common malignant tumors. The common benign
hepatic tumors are hemangioendothelioma, hemangioma,
and mesenchymal hamartoma, with focal nodular hyper-
plasia and adenoma encountered less often (3942).
Hepatic tumors have a distinctive distribution by age,
which can help in the diagnosis. Hemangioendothelioma is
common in the first 6 months of life. Hepatoblastoma and
mesenchymal hamartoma usually present in the first 5
years of life. Undifferentiated sarcoma commonly presents
between 6 and 10 years of age, and hepatocellular carci-
noma, focal nodular hyperplasia, and hepatic adenoma are
seen in older children and adolescents.
Malignant Hepatic Neoplasms
HEPATOBLASTOMA
Hepatoblastoma is the most common malignant liver
tumor in children, and 90% are seen in infants and young
children under 5 years of age, with most presenting in the
first 2 years of life (3942). Hepatoblastoma is rare after
15 years of age. There is an association with Beckwith-
Wiedemann syndrome (macrosomia, macroglossia, vis-
ceromegaly, hemihypertrophy, and umbilical hernia or
omphalocele), isolated hemihypertrophy, fetal alcohol syn-
drome, familial polyposis coli, and Gardner syndrome.
Metastases, occurring in 10% to 20% of patients, are to
the lungs, brain, and skeleton. Hepatoblastoma most often
presents as an asymptomatic mass. Other features include
abdominal pain, anorexia, weight loss, jaundice, and pre-
cocious puberty (related to the secretion of chorionic
gonadotropins). Serum -fetoprotein levels are elevated in
80% to 90% of patients (3942).
Pathologically, hepatoblastoma contains small, primitive
epithelial cells, resembling fetal liver, and occasionally mes-
enchymal elements (3942). The tumor is usually unifocal
and the right lobe of the liver is most often affected, but
multifocal disease or diffuse infiltration can occur. There is
no association with cirrhosis. Vascular invasion is common,
and portal vein involvement is more common than hepatic
vein involvement. Tumors invading the hepatic veins may
extend into the right atrium or the inferior vena cava.
HEPATOCELLULAR CARCINOMA
Hepatocellular carcinoma is the second most common
pediatric liver malignancy after hepatoblastoma. In the
pediatric population, median patient age is 12 years, with
a range of 5 to 15 years. It is rare in children under 5 years
(3942). Preexisting liver disease, such as hepatitis B
infection, type I glycogen storage disease, tyrosinemia,
familial cholestatic cirrhosis, hemochromatosis, Wilson
disease, and 1-antitrypsin deficiency, is present in about
one half of affected children (4345). Right upper quad-
rant mass and abdominal distention are the most common
presenting features. Serum -fetoprotein levels are usually
elevated (40).
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Pathologically, hepatocellular carcinoma contains large,
pleomorphic, multinucleated cells with variable degrees of
differentiation (40). The tumor is usually solitary and con-
fined to a single lobe, with the right lobe affected twice as
often as the left, but it may be multifocal or diffusely infil-
trate the liver. Vascular invasion is common and distant
sites of metastases are the lungs, brain, and skeleton.
Sonographic Findings
Hepatoblastoma and hepatocellular carcinoma have simi-
lar findings. Both tumors are typically large masses that are
hyperechoic to normal liver and heterogeneous with areas
of calcification or necrosis (Figs. 7.21 to 7.24) (46,47).
Less commonly, they are predominantly isoechoic or
hypoechoic to normal liver. A hypoechoic rim representing
a fibrous capsule may be seen in hepatocellular carcinoma
(see Fig. 7.23A).
Multifocal disease appears as either multiple small
masses or as a large dominant mass with one or more
satellite nodules. Diffusely infiltrating tumors cause wide-
spread parenchymal heterogeneity. Secondary findings
include spread to portal lymph nodes and intravascular
extension. Tumor thrombus appears as an echogenic intra-
luminal focus. Color signal and arterial waveforms may be
noted within the thrombus (Fig. 7.25).
Pulsed Doppler insonation shows high-velocity blood
flow (48). Systolic Doppler shifts are equal to or greater
than 3 kHz at an insonating frequency of 3 or 3.5 MHz and
mean peak systolic flow velocity is greater than 0.5
meters/sec. Color Doppler imaging shows peripheral, cen-
tral, or combined flow (36,4852) (see Figs. 7.22 and 7.23).
On microbubble-enhanced sonography, both tumors
enhance more than normal liver in the hepatic arterial
phase and less than normal liver in the portal venous phase
of perfusion (37).
The treatment of hepatoblastoma and hepatocellular
carcinoma is chemotherapy and partial hepatectomy.
A B
Hepatoblastoma. Transverse (A) and longitudinal (B) scans show a large (4  5 cm), well-marginated echogenic mass (calipers) in the
Fig. 7.21
posterior right lobe.
Chapter 7 L I V E R 227
Determination of resectability depends on tumor extent,
particularly the presence or absence of vascular invasion
and extrahepatic spread. Imaging findings soon after par-
tial hepatectomy include a hypoechoic fluid collection at
the surgical margin representing transient accumulation of
blood and bile, pleural effusion, and extraluminal gas.
Later findings include shift of abdominal organs and
hepatic regeneration. Perihepatic or subphrenic fluid col-
lections not conforming to the margins of resection should
raise suspicion of an abscess, biloma, hematoma, or
seroma (53). Transcatheter arterial embolization and per-
cutaneous ethanol injection have not been widely used to
treat malignant hepatic tumors in children.
FIBROLAMELLAR HEPATOCELLULAR CARCINOMA
Fibrolamellar carcinoma is a histologic subtype of hepato-
cellular carcinoma with distinct pathologic and clinical
features. Histologically, it is characterized by eosinophilic-
laden hepatocytes and abundant fibrous bands arranged in
a parallel pattern around the hepatocytes, leading to the
term fibrolamellar (39). There is no coexisting liver dis-
ease. The tumor predominantly affects adolescents and
young adults with a peak incidence of approximately 25
years (5457). Hepatomegaly and abdominal pain are
common presenting features. Serum -fetoprotein levels
are usually normal. The prognosis for patients with fibro-
lamellar hepatocellular carcinoma is better than that for
patients with the more frequent subtype of hepatocellular
carcinoma. The median 5-year survival rate for patients
with resectable fibrolamellar hepatocellular carcinoma is
76% versus 37% to 56% for patients with hepatocellular
carcinoma (57).
Fibrolamellar carcinoma is usually solitary and well
marginated. The echogenicity is variable and the tumor
may be hyperechoic, isoechoic, or hypoechoic to normal
parenchyma (Fig. 7.26) (5457). A central scar is present
in up to 50% of patients and focal calcifications are seen
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228 P E D I AT R I C S O N O G R A P H Y

A B

Hepatoblastoma. Transverse (A) and longitudinal (B)

Fig. 7.22
scans show a large, heterogeneous echogenic mass in
C the posterior right lobe. C: Color Doppler image shows peripheral flow.

A B
Hepatocellular carcinoma. A: Longitudinal sonogram shows a well-circumscribed, heterogeneous, predominantly hyperechoic mass
Fig. 7.23
(arrows) with a hypoechoic periphery in the right lobe of the liver. The hypoechoic rim corresponded to the fibrous capsule. B: Trans-
verse color Doppler image shows peripheral and central neovascularity. Arrows indicate tumor.
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Hepatoblastoma. Transverse sonogram shows an echogenic

Fig. 7.24
mass with a central hyperechoic focus casting an acoustic
shadow, representing calcification.

A B
Hepatocellular carcinoma, portal vein invasion. A: Transverse scan shows echogenic tumor thrombus in the right portal vein (arrows).
Fig. 7.25
B: Color Doppler image through the portal vein (arrow) shows arterial waveforms in the thrombosed vessel consistent with neoplastic
rather than bland thrombus.

Fibrolamellar carcinoma. Transverse sonogram demon-

Fig. 7.26
strates an echogenic mass (arrows) in the left lobe of the
liver. The central area of increased echogenicity with acoustic shad-
owing represents calcification.
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230 P E D I AT R I C S O N O G R A P H Y
in 40% to 55% of lesions. The imaging features of fibro-
lamellar carcinoma and the classic form of hepatocellular
carcinoma are similar and tissue sampling is needed for
definitive diagnosis.
UNDIFFERENTIATED EMBRYONAL SARCOMA
Undifferentiated embryonal sarcoma (also known as
malignant mesenchymoma and hepatic mesenchymal sar-
coma) is a malignant tumor of mesenchymal origin.
Grossly, the tumor ranges from 7 to 20 cm in diameter and
contains cystic spaces and cellular areas. Histologically, it
contains primitive undifferentiated spindle cells in a myx-
oid matrix (39,42). It is thought to be the malignant coun-
terpart of mesenchymal hamartoma of the liver (see later
discussion). It is most commonly seen in children between
6 and 10 years of age and 90% occur by 15 years of age
(39,42,58). The usual presenting features are abdominal
mass and pain. Serum -fetoprotein levels are normal. The
prognosis is poor with a mean survival of less than 1 year.
Undifferentiated embryonal sarcoma is typically soli-
tary. At sonography, it has a nonspecific appearance, pre-
senting as a large, predominantly solid mass or as a com-
plex mass with cystic spaces and septations, mural nodules,
or other echogenic solid components (Fig. 7.27) (5961).
RARE MISCELLANEOUS TUMORS
Angiosarcoma
Primary angiosarcoma is a rare tumor derived from
endothelial cells. The pathologic appearance is that of mul-
tiple small nodules or a large mass with or without satel-
lite nodules (62,63). The sonographic findings are nonspe-
cific and are those of a heterogeneous mass with cystic and
solid components (64).
Hepatic Leiomyosarcoma
Leiomyosarcoma is a malignant mesenchymal tumor of the
liver (65). Isolated cases have been reported in patients with
acquired immunodeficiency syndrome (AIDS). The tumor
A B
Undifferentiated embryonal sarcoma. Longitudinal (A) and transverse (B) sonograms show a large, heterogeneous, predominantly
Fig. 7.27
echogenic mass (arrows) with some cystic areas in the right hepatic lobe.
metastasizes to lung and the prognosis is poor. Sonography
shows a predominantly solid mass with cystic components
representing hemorrhage or necrosis. The imaging findings
are nonspecific and the differential diagnoses include hepa-
toblastoma, infantile hemangioendothelioma, undifferenti-
ated embryonal sarcoma, and infected hydatid cyst.
Rhabdomyosarcoma
Primary rhabdomyosarcoma also has nonspecific clinical
and imaging findings. In one case, sonography showed a
large solid tumor (66).
Secondary Hepatic Neoplasms
METASTASES
The malignant tumors of childhood that most frequently
metastasize to the liver are Wilms tumor, neuroblastoma,
rhabdomyosarcoma, and lymphoma. Neuroblastoma can
affect the liver in either stage IV or IV-S disease. Stage IV
disease is characterized by the presence of distant metas-
tases to skeleton, liver, or nodes. Stage IV-S neuroblastoma
occurs in patients under 1 year of age who have small ipsi-
lateral tumors (not crossing the midline) and metastases to
liver, skin, and bone marrow, but not to cortical bone.
Clinically, patients present with hepatomegaly, jaundice,
abdominal pain or mass, or abnormal hepatic function
tests.
Most metastases in children are hypoechoic with smooth,
well-defined margins. Scattered internal echoes may be noted
in larger lesions, related to hemorrhage (Fig. 7.28). Hypo-
echoic hepatic metastases are nearly always hypovascular.
Hyperechoic metastases can be seen in neuroblastoma
(Fig. 7.29), islet cell carcinoma of the pancreas, carcinoid
tumor, and choriocarcinoma. The hyperechogenicity is the
result of internal hemorrhage, calcifications, or hypervas-
cularity. Echogenic metastases can be hypervascular or
hypovascular on Doppler imaging.
Cystic or anechoic metastases are unusual, but they
have been associated with primitive neuroectodermal
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Hypoechoic metastasis, melanoma. Transverse sonogram
Fig. 7.28
showing a hypoechoic mass with central echogenicity,
related to hemorrhage.
tumors (67), ovarian cancers, and metastatic sarcomas.
They have irregular thick walls, septations, or other solid
components, allowing them to be differentiated from sim-
ple hepatic cysts. The cystic changes occur either because
the primary tumor is intrinsically cystic (ovarian tumors)
or because it is necrotic (sarcomas).
Diffuse parenchymal replacement is usually secondary
to stage IV-S neuroblastoma. Sonography shows wide-
spread heterogeneity (Fig. 7.30). The differential diagnoses
for this imaging appearance include hepatic fibrosis,
A B
Diffuse metastases, neuroblastoma. A: Transverse sonogram in a neonate shows widespread parenchymal heterogeneity. B: Computed
Fig. 7.30
tomography shows multiple hypovascular metastases.
Chapter 7 L I V E R 231
Metastatic neuroblastoma. Longitudinal sonogram shows
Fig. 7.29
two hyperechoic metastases (arrows) in the right hepatic
lobe and the primary right adrenal mass (calipers).
cirrhosis, fatty infiltration, and diffuse infiltrating hepato-
blastoma or hepatocellular carcinoma.
POSTTRANSPLANTATION LYMPHOPROLIFERATIVE DISORDER
Posttransplantation lymphoproliferative disorder and
lymphoma are complications of solid organ transplanta-
tion (68,69). Hepatic involvement has been reported in
up to 70% of patients with abdominal lymphoprolifera-
tive disease. The sonographic findings are single or multi-
ple hypoechoic masses with homogeneous or heteroge-
neous echotexture and well-defined margins (Fig. 7.31).
Other patterns include widespread parenchymal hetero-
geneity due to diffuse tumor infiltration and periportal
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232 P E D I AT R I C S O N O G R A P H Y
A B
Posttransplant lymphoproliferative disease. Eighteen-year-old girl with a heart transplant. A: Transverse sonogram of the right hepatic
Fig. 7.31
lobe demonstrates a well-defined, heterogeneously hypoechoic mass (calipers). RK  right kidney. B: A more cranial scan shows a
smaller, homogeneous hypoechoic lesion (arrow).
hypoechogenicity. Periportal infiltration may result in bil-
iary obstruction.
LYMPHOMA
Lymphomatous involvement of the liver is more often
secondary to non-Hodgkin lymphoma than to Hodgkin
lymphoma. The sonographic findings include well-defined,
homogeneous, anechoic, or hypoechoic nodules and
hepatomegaly (70,71) (Fig. 7.32). Larger lesions may con-
tain septations or have a target appearance characterized
by an echogenic center and peripheral hypoechoic rim
Hepatic lymphoma. Longitudinal sonogram demonstrates
Fig. 7.32
several anechoic lesions in the left hepatic lobe.
(70). Hepatosplenomegaly alone is a nonspecific finding.
Approximately 50% of patients with hepatomegaly have
no histologic evidence of lymphoma. On the other hand,
patients with normal-sized livers can have extensive lym-
phomatous infiltration (71).
LEUKEMIA
Hepatosplenomegaly, due to organ infiltration, occurs in
approximately two thirds of children with acute lym-
phoblastic leukemia and in approximately half of patients
with acute myelogenous leukemia (72,73). Sonography can
show hepatic enlargement and hypoechoic or hyperechoic
lesions. Other findings are splenomegaly, para-aortic lymph
node enlargement, and ascites (74).
Benign Neoplasms
INFANTILE HEMANGIOENDOTHELIOMA
Infantile hemangioendothelioma is the most common benign
hepatic tumor of childhood (3942). It is derived from
endothelial cells and exhibits initial rapid growth followed
by a slow spontaneous involution over several months to
years (75). Approximately 85% of cases are diagnosed in the
first 6 months of life, with about one third presenting in the
first month of life and virtually all by 3 years of age (41,42).
Based on glucose transporter-1 (GLUT-1) immunore-
activity, there are two distinct clinical forms of heman-
gioendothelioma: GLUT-1positive infantile heman-
gioendothelioma and GLUT-1negative hepatic vascular
malformation (76,77). Infantile hemangioendotheliomas
are usually diagnosed in the first few weeks or months
of life. They are asymptomatic and are detected on
screening sonography performed for evaluation of
hepatomegaly or because of cutaneous hemangiomas,
which may accompany visceral lesions. In comparison,
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congenital vascular malformations are commonly sympto-
matic and become apparent at or soon after birth.
Presenting findings include cardiac failure, thrombocytope-
nia with consumptive coagulopathy (Kasabach-Merritt
syndrome), and hemoperitoneum due to spontaneous
tumor rupture (41,42,78,79). Serum -fetoprotein levels
are usually normal but occasionally they are elevated (80).
Pathologically, both tumors contain vascular channels
lined by plump endothelial cells, enclosed within a reticu-
lar network (76,78). Rarely, the channels are lined by
immature, pleomorphic cells. This form has malignant
potential with transformation into angiosarcoma, and
metastases have been described (76,81).
Sonographic Findings
The sonographic findings vary, with smaller lesions
appearing more homogeneous and larger ones having a
more complex appearance, containing calcifications, cystic
spaces and fibrosis. GLUT-1positive infantile heman-
gioendotheliomas usually appear as multiple small, hypoe-
choic nodules (Figs. 7.33 and 7.34). GLUT-1negative
congenital vascular malformations commonly appear as a
large complex mass (Fig. 7.35) (76,8187). Both types are
usually well circumscribed with round or lobular borders.
They may show acoustic enhancement.
Doppler sonography in GLUT-positive and -negative
tumors shows high-frequency peak systolic shifts and
diminished systolic-diastolic flow variation (Fig 7.35B)
(86). Peak Doppler systolic shifts range between 0.8 and
5.5 kHz at 3 MHz insonation. These shifts are nonspecific
and overlap with those of malignant tumors. Color
Doppler shows peripheral or central vascularity (Figs.
7.33B and 7.34B). Due to arteriovenous shunting in the
tumor, the celiac and hepatic arteries are dilated and the
infraceliac aorta is small.
A B
Infantile hemangioendothelioma (GLUT positive). A: Longitudinal sonogram demonstrates multiple hypoechoic lesions in the right
Fig. 7.33
hepatic lobe. B: Color Doppler interrogation shows flow in the periphery of the lesions.
Chapter 7 L I V E R 233
Since hemangioendotheliomas have a natural history of
regression and involution, the initial treatment is medical
management, including digitalis, diuretics, steroids, and
interferon. If these methods fail, embolic or surgical treat-
ment may be required for treatment (88,89).
CAVERNOUS HEMANGIOMA
Cavernous hemangioma is unusual in neonates and
infants, but it can occur in older children and adolescents
(90). Most hemangiomas are small and asymptomatic and
are incidental findings during hepatic sonography. Occa-
sionally, giant hemangiomas cause enough mass effect to
produce hepatomegaly or an enlarging abdomen, and
rarely a hemangioma will hemorrhage or rupture and
cause pain. -Fetoprotein levels are usually normal but
occasionally they are elevated (90).
Pathologically, cavernous hemangiomas contain multi-
ple small, blood-filled spaces that are lined by mature, flat
endothelial cells and separated by fibrous septa. The vas-
cular spaces may contain areas of fibrosis, thrombosis,
hemorrhage, or calcification. Malignant potential is
absent.
The classic sonographic appearance of hemangioma is
that of a hyperechoic, homogeneous mass with well-
defined margins (Fig. 7.36). The hyperechoic appearance is
related to the numerous interfaces caused by the walls of
the sinusoids. Large hemangiomas may have a complex
appearance with central hypoechoic areas related to fibro-
sis, thrombosis, degeneration, or necrosis. Other findings
include a peripheral hypoechoic halo and acoustic
enhancement. Acoustic enhancement is especially evident
in larger lesions.
Hemangiomas are characterized by slow blood flow.
Pulsed Doppler imaging shows a systolic shift of less than
0.7 kHz, reflecting the slow blood flow (91). Color Doppler
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234 P E D I AT R I C S O N O G R A P H Y

A B

Infantile hemangioendothelioma. A: Transverse sonogram

Fig. 7.34
demonstrates two hypoechoic lesions (arrows) with
echogenic borders in the right hepatic lobe and a dilated hepatic vein
(HV). B: Color Doppler interrogation shows peripheral vascularity.
C: Arterial phase computed tomography shows multiple enhancing
C vascular lesions. (Case courtesy of Edward Lee, MD.)

imaging shows peritumoral or intratumoral flow or a mixed
pattern (52). On contrast-enhanced microbubble sonogra-
phy, hemangiomas show peripheral puddling that is brighter
than adjacent liver in the hepatic arterial phase, centripetal
enhancement over time, and sustained enhancement that is
greater than normal liver in the portal venous phase (37).
The differential diagnosis for a hyperechoic mass
includes metastases and focal fatty infiltration. The combi-
nation of clinical history and imaging findings usually
allows a specific diagnosis to be established. If the diagno-
sis remains uncertain, contrast-enhanced CT, MRI, or
scintigraphy with labeled red blood cells may be helpful
for further evaluation.
MESENCHYMAL HAMARTOMA
Mesenchymal hamartoma, also referred to as lymphan-
gioma, bile cell fibroadenoma, hamartoma, and cystic
hamartoma, is a benign tumor that is thought to be a con-
genital abnormality originating in the connective tissue
along the portal tracts (39,41,42). It usually affects chil-
dren 2 to 3 years of age (range, 6 months to 7 years) and
is slightly more common in boys (92). Affected patients
present with a palpable mass or abdominal enlargement
and rarely with congestive heart failure caused by arteri-
ovenous shunting in the tumor. Pedunculated hamartomas
may undergo torsion and present as an acute abdomen
(93). Malignant transformation to an undifferentiated
embryonal sarcoma has been reported, but is rare (58).
On pathologic section, mesenchymal hamartoma is a
large (usually over 8 cm in diameter) encapsulated mass
composed of multiple cystic spaces containing clear fluid,
mucoid, or gelatinous material. The spaces are separated
by fibrous stroma (39,41,42).
Sonographically, mesenchymal hamartoma usually
appears as a well-circumscribed, multilocular mass contain-
ing anechoic spaces separated by echogenic septa (93,94)
(Figs. 7.37 and 7.38). The tumor can appear predominantly
solid if the cystic spaces are small or the fluid content is
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A B

Congenital vascular malformation (GLUT-negative heman-

Fig. 7.35
gioendothelioma). A: Transverse sonogram shows a large
complex mass (calipers) with cystic and solid areas in the left hepatic
lobe. B: Transverse Doppler image of the hepatic artery proper (cursor)
shows arterial flow, which has a high-frequency systolic shift and high
diastolic flow. C: Arterial phase contrast-enhanced computed tomog-
C raphy shows a hypervascular mass.

A B
Cavernous hemangioma. A: An 18-year-old girl. Transverse sonogram shows a hyperechoic mass (calipers) anterior to the hepatic vein
Fig. 7.36
(arrow). B: In another adolescent girl, a longitudinal scan demonstrates a sharply marginated mass (M) in the right hepatic lobe, the
typical appearance of hemangioma.
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Cystic mesenchymal hamartoma. Transverse scan in a

Fig. 7.37
2-year-old boy shows a well-circumscribed, anechoic
mass with multiple thin septations. LIV  right lobe of liver.

A B

Cystic mesenchymal hamartoma. A, B: Two transverse

Fig. 7.38
scans reveal a complex mass (arrows) containing multiple
anechoic cysts surrounded by echogenic parenchyma or septa. C: Fat-
saturated, coronal T2-weighted magnetic resonance image shows high-
signal-intensity, multilocular mass with septations. (Case courtesy of
C Edward Lee, MD.)
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Chapter 7 L I V E R 237

highly proteinaceous or contains debris (Fig. 7.39) (93,95).

A dilated proximal aorta and large hepatic veins may be
observed if there is arteriovenous shunting in the tumor.
Calcification is rare but can be seen in the septa. Cyst rup-
ture has been associated with ascites (96). The solid parts of
the mass can show flow on color Doppler imaging.

FOCAL NODULAR HYPERPLASIA

Focal nodular hyperplasia (FNH) and hepatic adenomas
account for less than 5% of hepatic tumors in children
(39,41,42). Focal nodular hyperplasia is thought to be a
developmental hyperplastic response of normal hepatocytes
to a preexisting vascular malformation (97,98). The tumor
is usually asymptomatic and discovered incidentally on
imaging studies, but patients can present with pain or
hepatomegaly if the tumor is large and produces mass effect.
-Fetoprotein is normal. The prevalence of focal nodular
hyperplasia appears increased in patients with hereditary
hemorrhagic telangiectasia and in patients who have received
chemotherapy for neoplastic diseases (98101). Solid, benign mesenchymal hamartoma. Transverse
Pathologically, focal nodular hyperplasia is a well- Fig. 7.39
sonogram shows a well-circumscribed, homogeneous,
circumscribed, unencapsulated mass, composed of an abnor- echogenic mass (arrows) in the right lobe of the liver. Pathologic exam-
mal arrangement of normal hepatocytes, Kupffer cells, and bile ination showed a multicystic mass containing thick proteinaceous material.
ducts (39,41,42). Other characteristic pathologic features are a
subcapsular location, central fibrous stellate scar, and vascular
network that is arranged in a radial or spoke-wheel pattern. cult to detect, leading to the term stealth lesion (103). The
There is no strong association with preexisting abnormalities. central scar is seen as an echogenic linear or stellate area in
At sonography, focal nodular hyperplasia appears as a the center of the lesion.
solitary, well-circumscribed lesion. It is usually subcapsular Pulsed Doppler imaging shows a pulsatile arterial
and it may be pedunculated. Most lesions are isoechoic or waveform with low or midrange frequency shifts rang-
nearly isoechoic to normal parenchyma and are detected on ing from 1.0 to 4.0 kHz (103). Color Doppler evaluation
gray-scale imaging because they exert mass effect on adja- of the mass can show peripheral flow or flow in the cen-
cent vessels or deform the hepatic contour (97,102,103) tral scar extending to the periphery in a spoke-wheel
(Fig. 7.40). Because of its isoechoic pattern, it can be diffi- pattern (Fig. 7.40B). On contrast-enhanced sonography,

A B
Focal nodular hyperplasia. A: Longitudinal view through the left lobe reveals an echogenic subcapsular mass (calipers) that is nearly
Fig. 7.40
isoechoic to adjacent liver. The central scar (arrow) is barely visible. B: Color Doppler sonogram shows flow in the scar (arrow) and in
several radiating branches (arrowheads).
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238 P E D I AT R I C S O N O G R A P H Y

A B

C D
Hepatic adenoma. Transverse (A) and longitudinal (B) scans show a heterogeneous hyperechoic mass (arrows) relative to normal
Fig. 7.41
parenchyma in the right lobe. PV  portal vein. C: Peripheral (arrows) and central flow are noted on color Doppler interrogation. D: Con-
trast-enhanced computed tomography shows a complex mass containing fat (f) and blood (bl).

the lesion enhances more than liver in the hepatic arte-
rial and venous phases of perfusion (37,104,105).
HEPATIC ADENOMA
Hepatic adenomas in childhood have been associated with
type I glycogen storage disease (von Gierke disease), Fan-
coni anemia, galactosemia, and use of anabolic steroids
(106). Patients may be asymptomatic or they may present
with hepatomegaly or abdominal pain due to spontaneous
tumor infarction, hemorrhage, or rupture. Liver function
studies are usually normal. Pathologically, hepatic adenoma
is a well-defined, encapsulated tumor, composed entirely of
hepatocytes, which often contain lipid and blood products.
Bile ducts and portal tracts are absent (39,41,42).
Similar to focal nodular hyperplasia, hepatic adenomas
tend to be solitary and well circumscribed. On occasion, they
are pedunculated. Their echogenicity varies and they may be
hypoechoic or hyperechoic to adjacent parenchyma. Most
are heterogeneous because of the presence of hemorrhage,
glycogen, or fat (107) (Fig. 7.41). A central scar is absent.
Color Doppler imaging can show peripheral, central, or
combined flow with a random stippled pattern of internal
vascularity (Fig. 7.41C). Doppler frequency shifts range
from 1.0 to 4.0 kHz. Contrast-enhanced sonography
demonstrates homogeneous arterial phase enhancement
with absence of portal venous phase enhancement, whereas
in focal nodular hyperplasia it shows pronounced arterial
and portal venous enhancement (37,108).
NODULAR REGENERATIVE HYPERPLASIA
Nodular regenerative hyperplasia of the liver refers to a
regenerative nodular lesion in a noncirrhotic liver (109,110).
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Chapter 7 L I V E R 239

Nodular regenerative hyperplasia. Transverse image of Hepatic cyst. Longitudinal scan shows the classic findings
Fig. 7.42 Fig. 7.43
the upper abdomen shows two isoechoic nodules (N) in of a cyst (C): sharply defined margins, anechoic matrix,
the left hepatic lobe. imperceptible walls, and enhanced sound transmission (arrow).

It can be a sporadic occurrence, but it also has been associ-
ated with myeloproliferative and lymphoproliferative syn-
dromes, immune-related disorders, and long-term use of
drugs, including steroids and antineoplastic agents. Patients
may be asymptomatic or they may present with hepato-
megaly. The median age of affected children is 8 years (109).
Pathologically, nodular regenerative hyperplasia is character-
ized by a localized proliferation of hepatocytes and their sup-
porting stroma and minimal if any portal fibrosis. The
lesions vary in size from 1 mm to several centimeters.
Sonography shows multiple well-defined nodules that
may be isoechoic, hypoechoic, or hyperechoic to normal
parenchyma (Fig. 7.42) (109,110). The liver size can be
normal, small, or increased (109). Hypervascularity is
noted on color Doppler examination (110).
The classic sonographic criteria of a simple hepatic cyst
are an anechoic lumen, round or oval shape, imperceptible
or thin walls, and acoustic enhancement (Fig. 7.43). Hem-
orrhage or infection can contain internal echoes, a fluid-
debris level, septations, or a thick wall. Rarely, the cysts are
pedunculated and then they may be mistaken for a mesen-
teric, omental, or ovarian cyst prior to surgical exploration.
Multiple cysts occur in association with inherited syn-
dromes, such as autosomal dominant polycystic disease,
von Hippel-Lindau disease, Byler syndrome (familial intra-
hepatic cholestasis), Turner syndrome, and tuberous sclerosis
(Fig. 7.44) (117).

FATTY TUMORS
Fatty tumors are rare and usually incidentally detected on
imaging studies. These include angiomyolipomas, which are
often associated with tuberous sclerosis (111), and adenomas
and lipomas, which are found as isolated lesions. Sonography
shows a hyperechoic mass with varying degrees of acoustic
shadowing (see Fig. 7.41) (111,112). Angiomyolipomas may
also have a target appearance, with a hyperechoic center rep-
resenting the lipomatous elements of the tumor and a hypoe-
choic rim representing the angiomatous components.

Cysts
Simple hepatic cysts are relatively uncommon lesions in chil-
dren (113115). They are thought to arise from intrahepatic
biliary ducts that fail to involute. Simple hepatic cysts are
usually solitary, have an epithelial lining, and contain serous
fluid. They are usually detected incidentally on imaging stud-
ies, but large ones may present as an abdominal mass or Autosomal recessive polycystic disease. Multiple cystic
hepatomegaly or produce abdominal pain secondary to mass Fig. 7.44
lesions, representing dilated ducts, are present through-
effect, superimposed infection, or hemorrhage (113,116). out the liver.
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240 P E D I AT R I C S O N O G R A P H Y

A B
Acute hepatitis. A: Transverse scan shows hypoechoic parenchyma with bright portal triads (starry sky appearance). B: Longitudinal
Fig. 7.45
scan in another patient shows an enlarged lymph node (N) in the hepatic hilum. GB  gallbladder; PV  portal vein.

The differential diagnostic considerations of simple tion is present without architectural disruption. In chronic
cysts include echinococcal disease, abscess, evolving or old active hepatitis, there is extensive inflammation, fibrosis,
hematomas, and inherited syndromes discussed above. The and architectural distortion (122).
clinical history or the patients nationality or travel history, Sonography is not required in patients with clinical evi-
especially in cases of hydatid disease, can help suggest the dence supporting the diagnosis of uncomplicated acute hep-
correct diagnosis. In problem cases, a CT scan or percuta- atitis, but imaging can be useful when there is uncertainty
neous needle aspiration may be needed for diagnosis. about whether the cause of jaundice is clolestatic or
Mesothelial cyst is a very rare hepatic lesion that is obstructive. Sonography is usually normal in mild hepatitis.
lined by mesothelial cells and is a type of mesenteric cyst Common sonographic findings in severe acute hepatitis
(118). Immunohistochemical analysis is needed to estab- include hepatomegaly, decreased parenchymal echogenicity,
lish the diagnosis and differentiate the mesothelial cyst and increased echogenicity of the portal venule walls
from other cysts. (starry sky liver) an enlarged porta hepatis nodes (Fig.
7.45). Other findings are thickening of the gallbladder wall,
a small gallbladder with intraluminal sludge, and peric-
INFECTIONS holecystic fluid (Fig. 7.46) (123,124). The sonographic
Viral Hepatitis
Hepatitis is usually of viral origin and due to hepatitis A,
B, C, D, or E viruses, although a number of systemic
viruses, such as cytomegalovirus, herpes simplex virus,
varicella zoster virus, and Epstein-Barr virus, also can
result in hepatitis (119121). Hepatitis A and E are trans-
mitted by the fecal-oral route, whereas hepatitis B, C, and
D are bloodborne infections. Hepatitis A and E are not
chronic, whereas hepatitis B, C, and D can progress to
chronic infection. Hepatitis A is the most common viral
hepatitis in the United States, followed by hepatitis B and
C. Hepatitis D and E are relatively rare. Noninfectious
causes of hepatitis include drugs, toxins, autoimmune dis-
eases, and sclerosing cholangitis.
Histologically, acute uncomplicated hepatitis is charac-
terized by swollen hepatocytes and periportal infiltration
by lymphocytes. It usually resolves. Fulminant hepatic fail-
ure is characterized by hepatic necrosis and liver failure.
The prognosis depends on the extent of tissue necrosis.
Chronic hepatitis is the persistence of biochemical abnor-
malities beyond 6 months. It is classified as persistent or Acute hepatitis. Longitudinal sonogram demonstrates a
Fig. 7.46
active. In chronic persistent hepatitis, periportal inflamma- thick-wall gallbladder and pericholecystic fluid (arrows).
LWBK505-C07_p214-274.qxd 7/7/10 1:29 PM Page 241 Aptara Inc
findings of acute hepatitis are nonspecific and they may be
seen in infiltrative neoplastic diseases, such as leukemia and
non-Hodgkin lymphoma; in patients with right-sided heart
failure; and in fasting patients secondary to depletion of
glycogen stores (125,126).
In chronic persistent or chronic active hepatitis, the
echogenicity of the hepatic parenchyma increases and the
echotexture becomes coarse or heterogeneous. The con-
spicuity of the portal venous radicles decreases as the
echogenicity of the parenchyma increases. The gallbladder
may be small and contain thick bile, sludge, or stones.
Pyogenic Abscess
Pyogenic liver abscesses result from penetrating injuries;
contiguous spread from adjacent organs such as lung or
bowel; remote sites of infection with organisms reaching
the liver by arterial or portal venous spread; or, less com-
monly, ascending cholangitis (127). The common causative
agent is Staphylococcus aureus in infants and children and
Escherichia coli in neonates. Patients present with fever,
upper abdominal pain or tenderness, hepatomegaly, and
elevated liver function tests.
Pyogenic abscesses can occur in any part of the liver, but
most (80%) are found in the posterior part of the right lobe.
Like abscesses elsewhere in the body, hepatic abscesses tend
to be round or oval, hypoechoic masses with thick, irregu-
lar walls and varying degrees of through-sound transmis-
sion. Internal septations, debris, fluid-fluid levels and a
hypoechoic rim related to edema are also common (Fig.
7.47). Gas-containing lesions are hyperechoic and demon-
strate acoustic shadowing and reverberation artifacts.
The sonographic appearance of hepatic abscess is nonspe-
cific and the differential diagnosis includes hydatid or amebic
infection, chronic hematoma, cystic metastases, and necrotic
tumors. Percutaneous needle aspiration can aid in establish-
A B
Pyogenic hepatic abscess. A: Longitudinal sonogram through the right lobe of the liver demonstrates a heterogeneous mass with thick
Fig. 7.47
walls (arrowheads) and a fluid-debris level (arrow). B: Longitudinal scan in another patient shows a hypoechoic lesion with an
echogenic wall, adjacent hypoechoic rim and posterior sound transmission (open arrow). Blood cultures in both patients grew Staphylococcus
aureus.
Chapter 7 L I V E R 241
ing a diagnosis and also guide aspiration and drainage. Pyo-
genic hepatic abscesses are treated by percutaneous aspiration
or catheter drainage and antibiotic therapy (128,129).
Fungal Abscess
Fungal microabscesses are found almost exclusively in
immunocompromised children. The common causative
agents are Candida albicans and Aspergillus species.
Although large single fungal abscesses may be observed,
fungal infection more commonly causes multiple small
lesions, several millimeters in diameter. The abscesses are
scattered throughout both lobes of the liver and often
involve the spleen and occasionally the kidneys (130).
Most fungal abscesses appear as small, round, hypo-
echoic lesions. Other sonographic patterns include the
wheel within a wheel pattern, the bulls-eye pattern, and
homogeneous hyperechogenicity (130). The wheel within a
wheel pattern is seen early in the course of infection, and
consists of a central hypoechoic area of necrosis, an adja-
cent echogenic ring of inflammatory cells, and an outer
hypoechoic zone of fibrosis. The bulls-eye or target lesion
occurs during the period of granulocyte recovery when the
neutrophil count returns to normal. It is characterized by
a central echogenic nidus and a peripheral hypoechoic
zone (Fig. 7.48). The hyperechoic lesions occur later in the
course of infection. This pattern reflects the presence of
scar tissue with or without calcification.
The imaging appearances of fungal infection are
nonspecific, and they may mimic metastases, pyogenic
abscesses, granulomatous infection, cat-scratch disease, and
lymphoma (131). Patients with fungal abscesses are treated
medically, since size and multiplicity of the abscesses make
percutaneous and surgical drainage difficult or impossible.
Some sterilized lesions may persist and in some instances
may calcify.
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242 P E D I AT R I C S O N O G R A P H Y
Candida microabscesses. Transverse sonogram shows
Fig. 7.48
small hypoechoic lesions (arrows) (1 cm in diameter)
with central echogenic foci (bulls-eye lesions).
Hydatid Disease
Hydatid disease (Echinococcosis) is a parasitic infestation
caused by Echinococcus granulosus and less commonly by
Echinococcus alveolaris. Endemic areas include the Middle
East, the southern United States, and northern Canada. The
infection occurs through ingestion of contaminated food.
The adult tapeworm, Echinococcus, lives in the intestine of
the host, usually the dog, where it lays eggs, which are
excreted in feces and then swallowed by an intermediate
host (usually sheep). The liver is the most commonly
A B
Hydatid disease. A: Transverse sonogram shows a complex mass containing detached membranes, typical of hydatid disease. B: Lon-
Fig. 7.49
gitudinal view at a different level shows multiple masses. The more anterior lesion (arrows) has features resembling those of a simple
cyst (e.g., thin walls and anechoic contents). The other two cysts (arrowheads) are complex and contain debris and septations.
affected organ, although the lungs, spleen, kidneys, central
nervous system, and bone can be involved (132,133).
Patients present with an enlarged liver and abdominal pain.
Large cysts may obstruct the bile ducts, causing jaundice.
The sonographic appearance of E. granulosus infection
includes a unilocular cyst; a complex cyst with multiple
internal daughter cysts; and a complex cyst with septa-
tions, echogenic debris, or floating membranes (Fig. 7.49)
(132135). Daughter cysts appear as numerous small
fluid-filled areas surrounded by thick walls inside a parent
cyst. The demonstration of daughter cysts is considered
pathognomonic of hydatid disease (136). Calcification
may be seen in the walls of the cysts or in the septations.
Hepatic involvement by E. alveolaris usually produces
a large, predominantly solid mass with poorly defined
margins and heterogeneous matrix containing multiple
hyperechoic and hypoechoic areas (135). A less common
pattern is a predominantly cystic mass with echogenic
debris or solid areas. Calcifications and biliary ductal
dilatation may be noted.
The diagnosis of hydatid disease is established by sero-
logic testing. The lesion may be treated medically, surgi-
cally, or with percutaneous aspiration and drainage
(137,138). The response to medical treatment is higher in
those lesions without daughter cysts. Sonographic findings
during medical treatment include a decrease in the size of
the cyst, detachment of the cyst membranes, and increased
echogenicity related to involution of the cyst cavity.
Amebic Abscess
Amebiasis is caused by the parasite Entamoeba histolytica,
which is endemic in tropical and subtropical climates, with
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Amebic abscess. Transverse scan demonstrates an oval,
Fig. 7.50
predominantly hypoechoic mass (arrows) with irregular
margins and central low-level echoes. Posterior acoustic enhance-
ment is noted.
cases also reported in the southwestern United States. The
most frequent site of involvement by amebiasis is the intes-
tine. In the bowel, cysts that have been ingested in con-
taminated water or food dissolve, and the trophozoites
colonize the colon, usually the cecum and ascending colon.
The parasites may then penetrate the colonic mucosa and
reach the liver via the portal system. Hepatic abscess is the
most common extraintestinal complication of amebiasis.
Patients present with hepatomegaly and right upper quad-
rant pain or tenderness.
Amebic abscesses are usually solitary and have a propen-
sity for peripheral locations, particularly the right lobe near
the dome (139). They usually appear as unilocular, round or
oval, hypoechoic masses containing fine low-level echoes
A B
Chronic granulomatous disease related to histoplasmosis. A, B: Two longitudinal sonograms show two calcifications (arrows). The more
Fig. 7.51
central one demonstrates acoustic shadowing.
Chapter 7 L I V E R 243
(Fig. 7.50) (139,140). Occasionally, they have a target
appearance. The margins of the lesions may be smooth or
irregular. Acoustic enhancement is variable. The imaging fea-
tures are nonspecific and similar to those of pyogenic abscess.
Clinical history, hemagglutination titers, surgery, or percuta-
neous aspiration are necessary to establish the diagnosis.
Medical therapy is usually effective, but percutaneous
drainage may be required in some cases. Most treated ame-
bic abscesses resolve completely, but a small subgroup of
treated patients will have persistent cystic lesions that
mimic benign, simple cysts (141).
Ascariasis
Ascaris lumbricoides is a well-known cause of acute
cholangitis and cholecystitis, but it can penetrate and col-
onize the liver parenchyma, forming an abscess (142).
Sonography shows a hypoechoic lesion with ill-defined
margins and central echogenicity. The presence of linear
echogenic structures with central hypoechoic tubes is highly
suggestive of Ascaridae.
Schistosomiasis
Schistosoma reach the liver through the portal vein and
incite a granulomatous reaction leading to occlusion of
portal vein branches and portal hypertension. Sonographic
findings are echogenic portal tracts and hepatomegaly.
Chronic Granulomatous Disease
Chronic granulomatous disease is an Xlinked recessive dis-
order characterized by inability of the leukocytes to lyse
phagocytized bacteria. Patients present with recurrent infec-
tions of lung, bones, lymph nodes, or liver usually due to
Staphylococcus aureus or Escherichia coli. Sonography shows
single or multiple, hypoechoic lesions with or without acoustic
enhancement (143). These lesions may represent abscesses or
granulomas and percutaneous aspiration is required for dif-
ferentiation. With treatment, the lesions either resolve or
become more echogenic due to calcification (Fig. 7.51).
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244 P E D I AT R I C S O N O G R A P H Y
Cat-scratch disease. Longitudinal scan shows multiple
Fig. 7.52
hypoechoic lesions in the right hepatic lobe.
Cat-Scratch Disease
Cat-scratch disease is characterized by a granulomatous
or suppurative reaction to a gram-negative bacillus, Bar-
tonella henselae. It affects children and adolescents who
have been scratched by a domestic cat. Patients present
with fever and unilateral lymph node enlargement proxi-
mal to the site of inoculation. Hepatic involvement occurs
in less than 10% of patients. At sonography, hepatic gran-
ulomata appear as multiple small hypoechoic lesions,
ranging between 3 mm and 2 cm in diameter (Fig. 7.52)
(144). The appearance is nonspecific and the differential
diagnosis includes other infectious diseases, such as pyo-
genic or fungal abscesses, neoplastic diseases including
metastatic disease and lymphoma, and other granuloma-
tous diseases such as tuberculosis and sarcoidosis.
Acquired Immunodeficiency Syndrome
Patients with AIDS are at risk for developing a variety of
infections and neoplasms of the liver and biliary tract.
The common infectious agents are Pneumocystis carinii,
cytomegalovirus, and Mycobacterium avium intracellu-
lare. Sonographic abnormalities include hepatomegaly;
punctate hyperechoic foci related to calcifications (Fig.
7.53); diffuse or patchy echogenicity related to steatosis;
and focal mass lesions (145147). The latter may be neo-
plastic (usually lymphoma) or infectious (e.g., abscess).
Associated biliary tract abnormalities include gallblad-
der dilatation and wall thickening, biliary sludge or gall-
stones, and biliary duct dilatation or stricture (148).
DIFFUSE PARENCHYMAL DISEASES
Causes of diffuse hepatic replacement include fatty infil-
tration, fibrosis, hemochromatosis, cirrhosis, and meta-
bolic and storage diseases.
Acquired immunodeficiency syndrome. Transverse scan
Fig. 7.53
shows multiple punctate echogenic foci, corresponding
to calcifications.
Steatosis
Hepatic steatosis results from an excessive accumulation
of triglycerides within hepatocytes. Histologically, there
are two types of steatosis: microvacuolar and macrovac-
uolar steatosis (149,150). In microvacuolar steatosis, the
hepatocytes contain small fat vacuoles or droplets that do
not displace the nucleus from the center of the cell; in
macrovacuolar steatosis, large vacuoles of fat fill the
hepatocytes, pushing the nucleus against the cell wall.
Microvacuolar steatosis is associated with acute fatty
liver of pregnancy, Reye syndrome, cystic fibrosis, and
massive tetracycline therapy. Patients are acutely ill, pre-
senting with a painful liver, vomiting, jaundice, and
coma. Microvacuolar steatosis is rarely reversible.
Macrovacuolar steatosis is usually asymptomatic and has
been associated with nutritional abnormalities (starva-
tion, obesity, parenteral nutrition, intestinal bypass),
metabolic disorders (diabetes mellitus, hyperlipidemia,
galactosemia, tyrosinemia), drugs (exogenous steroids),
viral infections, cystic fibrosis, and congenital generalized
lipodystrophy. Macrovacuolar steatosis is reversible if the
underlying abnormality can be corrected.
Fatty infiltration can be diffuse or focal. Sonographic
findings of diffuse steatosis include hepatomegaly, increased
parenchymal echogenicity (i.e., referred to as the bright
liver), and increased attenuation of the sound beam, result-
ing in poor visualization of the intrahepatic vessels, poste-
rior part of the liver, and diaphragm (Fig. 7.54) (150153).
The findings vary with the extent of fat deposition. Mild
steatosis is characterized by a minimal diffuse increase in
echogenicity: vessels and diaphragm are still visualized.
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Chapter 7 L I V E R 245

A B
Diffuse fatty infiltration of the liver in patient with cystic fibrosis. A: Transverse sonogram demonstrates increased echogenicity of the
Fig. 7.54
liver compared to the right kidney (K) and nonvisualization of the portal and hepatic veins. The echoes in the posterior part of the liver
are not as bright as those in the anterior portion, indicating sound attenuation. B: More cranial sonogram demonstrates nonvisualization of the right
hemidiaphragm.

Moderate steatosis is characterized by increased echogenic- hypoechoic on sonography. The cause is unknown,
ity and slight impairment of visualization of the vessels and although a decrease in portal venous blood flow leading to
diaphragm. Marked steatosis is seen as markedly increased decreased delivery of triglycerides to hepatocytes is postu-
hepatic echogenicity and poor or nonvisualization of the lated (150). Focal sparing, also termed skip areas,
vessels and diaphragm. The adjacent renal cortex also occurs in the same areas as focal fatty infiltrationalong
appears hypoechoic to the liver. The sensitivity of sonogra- the gallbladder fossa (Fig. 7.56), around the falciform lig-
phy for identifying diffuse steatosis increases with increasing ament, in the porta hepatis, or in a subcapsular location.
severity of fatty infiltration. The likelihood of an abnormal Color Doppler sonography may show an aberrant vein
sonogram is nearly 100% with moderate to severe degrees coursing to or around the area (155).
of fatty infiltration (30% hepatocytes with fat vacuoles)
(154). Compared with biopsy, the overall sensitivity of
sonography for diagnosing fatty infiltration is 89% and the
specificity is 93% (153).
Focal steatosis spares areas of liver parenchyma and
may mimic a mass. Ischemia related to decreased portal
venous blood flow is thought to be the cause of focal fat
accumulation. Common sites of focal steatosis are along
the gallbladder fossa (Fig. 7.55), around the falciform
ligament or the interlobar fissure, in the medial segment
of the left lobe adjacent to the porta hepatis, and in a
subcapsular location (150). The margins of the fatty
areas are geographic or finger-like and well defined (Fig.
7.55). Features that are helpful in separating focal fat
from space-occupying lesions are (a) the typical peripor-
tal or periligamentous location; (b) absence of mass
effect, vascular displacement, or bulging of the hepatic
contour; (c) sharply angulated geographic margins; and
(d) a nonspherical configuration. Steatosis can resolve in
1 to 2 weeks, whereas tumor remains stable or increases
in size.

Focal Fatty Sparing Focal fatty infiltration of the liver. Longitudinal sonogram
Focal fatty sparing refers to normal areas of parenchyma Fig. 7.55
demonstrates an area of subcapsular steatosis (arrow-
in a background of diffuse fatty infiltration. It appears head ) in the anterior segment of the right lobe. GB  gallbladder.
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246 P E D I AT R I C S O N O G R A P H Y

Focal hepatic sparing. Longitudinal view shows a focal

Fig. 7.56 Hepatic fibrosis with autosomal recessive polycystic dis-
hypoechoic area (arrow) in the right hepatic lobe anterior Fig. 7.57
ease. Transverse sonogram shows diffuse parenchymal
to the gallbladder (GB). This characteristic location should suggest the
heterogeneity and dilated ducts.
diagnosis of focal sparing.

Hepatic Fibrosis increased red cell breakdown, usually related to

Hepatic fibrosis may occur in isolation or in association hemolytic anemia. Transfusional iron overload is found
with congenital disorders (156). Congenital conditions in patients who undergo multiple blood transfusions.
associated with hepatic fibrosis include autosomal reces- Iron is deposited in the liver and also in the spleen and
sive polycystic disease and Caroli disease and Meckel- bone marrow.
Gruber, Jejune (asphyxiating thoracic dystrophy), Jou- Hemochromatosis may decrease parenchymal echogenic-
bert, and Ivemark syndromes. Isolated congenital ity (Fig. 7.58), but in most patients, the liver appears normal.
hepatic fibrosis is an inherited autosomal recessive dis-
ease. Patients present with hepatomegaly and signs of
portal hypertension, usually in later childhood or ado-
lescence. Liver function may be normal if cirrhosis is
absent. Histologically, the hepatic lobules are sur-
rounded by dense broad fibrous bands containing dilated
bile ducts. These bands cause compression of portal
venules, leading to portal hypertension. There is no dam-
age to hepatocytes.
Sonographic findings include increased parenchymal
echogenicity in a periportal or diffuse distribution, and
dilated bile ducts (Fig. 7.57). Signs of cirrhosis and por-
tal hypertension may also be observed.

Hemochromatosis
Hemochromatosis refers to the presence of increased iron
storage in the liver. There are three types of hemochro-
matosis: (a) primary or genetic, (b) secondary, and (c)
transfusional iron overload (158). Primary hemochro-
matosis is a human leukocyte antigen (HLA)linked
inherited disorder in which a mucosal defect in the intes- Hemosiderosis. A 16-year-old boy with a history of multi-
tinal wall leads to increased absorption of ingested Fig. 7.58
ple blood transfusions. Longitudinal sonogram demon-
iron, which is deposited in hepatocytes. Secondary or ery- strates decreased echogenicity of the liver relative to the right kidney
thropoietic hemochromatosis is seen in patients with (K). In this age patient, the liver should be hyperechoic to kidney.
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A B
Cirrhosis. A: Longitudinal sonogram shows irregular, nodular margins of the liver (arrows). B: Transverse sonogram in another patient
Fig. 7.59
shows diffuse, coarse hepatic echogenicity.
MRI is the best imaging test to confirm the presence of iron
deposition. However, MRI often is normal in mild hemo-
siderosis and patients will require a biopsy for confirma-
tion of the diagnosis.
Cirrhosis
Cirrhosis is a chronic disease process characterized by
parenchymal destruction, scarring, fibrosis, and nodular
regeneration with consequent disorganization of the lob-
ular and vascular architecture (159). Causes of cirrhosis
in infants and children include chronic hepatitis, biliary
atresia, cystic fibrosis, metabolic disease (Wilson dis-
ease, glycogen storage disease, tyrosinemia, galac-
tosemia, 1-antitrypsin deficiency), prolonged total par-
enteral nutrition, Budd-Chiari syndrome, and drugs.
Patients present with hepatomegaly, jaundice, and
ascites.
Based on the morphologic appearance, cirrhosis has
been classified into three groups: micronodular, macron-
odular, and mixed. In micronodular cirrhosis, the nodules
are of similar size and nearly always less than 3 mm
in diameter. Causes of micronodular disease include
chronic biliary obstruction, hemochromatosis, and
venous outflow obstruction. In macronodular cirrhosis,
the nodules are of varying size, but most are larger than
3 mm in diameter. This pattern is often due to chronic
viral hepatitis.
SONOGRAPHIC FINDINGS
In the early stages of cirrhosis, the liver may appear nor-
mal on sonography. With progression of disease, sono-
graphic findings include (a) a small right hepatic lobe and
medial segment of the left lobe, with compensatory
hypertrophy of the lateral segment of the left lobe and
Chapter 7 L I V E R 247
the caudate lobe; (b) nodular hepatic margins; (c) coars-
ened or heterogeneous parenchyma; (d) increased
parenchymal echogenicity; (e) decreased penetration of
the sound beam; (f) hypoechoic or hyperechoic regener-
ating nodules; and (g) a small or nonvisualized gallblad-
der (Fig. 7.59). Extrahepatic findings of cirrhosis include
ascites, splenomegaly, and collateral vessels when portal
hypertension develops.
While generally not necessary for the recognition of
an abnormality, the most reliable measurements of the
liver relate to the relative size of the caudate lobe
(160162). The caudatetoright lobe ratio is obtained
by dividing the transverse diameter of the caudate lobe by
the transverse diameter of the right lobe. The normal cau-
date to right lobe ratio is 0.37 versus 0.83 in cirrhotic liv-
ers. A ratio exceeding 0.65 is considered suspicious of cir-
rhosis. The volume of the caudate lobe also can be
compared to the right lobe. This measurement is obtained
by multiplying the longitudinal, transverse, and antero-
posterior diameters of the caudate lobe and dividing them
by the transverse diameter of the right lobe. The mean
ratio in patients with cirrhosis is 16.7 versus 3.2 in
healthy individuals. Ratios greater than 5.4 are consid-
ered abnormal.
Doppler findings of cirrhosis without portal hyper-
tension include decreased hepatic vein pulsatility with
absent or reversed flow or a flattened waveform, color
aliasing, and turbulence. The normal increase in the
postprandial hepatic artery resistive index may also be
absent.
Transient elastography is a recent rapid, noninvasive
technique that measures liver stiffness. This technique uses
a probe with a vibrator. Low-amplitude and low-frequency
vibrations are transmitted to the hepatic parenchyma by
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248 P E D I AT R I C S O N O G R A P H Y

the transducer. The vibrations induce elastic shear waves hepatic or splenic infarction, and growth retardation.
that propagate through the hepatic tissue. Pulsed echo Liver fibrosis may occur, but cirrhosis is rare. Sono-
acquisitions are acquired to measure the velocity of the graphic findings are hepatomegaly and increased
shear waves, which are directly related to tissue stiffness. parenchymal echogenicity. Niemann-Pick disease has sim-
The stiffer the tissue, the faster the shear wave moves. ilar findings, except cirrhosis and hepatocellular adenoma
Liver stiffness increases in fibrosis. Limited results suggest can develop.
that elastography can identify moderate or severe cirrhosis Wilson disease is an autosomal recessive abnormality
(164,165). characterized by excessive copper deposition in the liver,
brain, and cornea. Cirrhosis, hepatic adenoma, and hepa-
Metabolic Liver Diseases tocellular carcinoma are complications of long-standing
A number of inborn errors in metabolism can present with disease. Tyrosinemia is an autosomal recessive disorder
liver dysfunction, including cystic fibrosis, disorders of car- due to a defect of fumarylacetoacetase. In neonates, acute
bohydrate metabolism (glycogen storage disease, galac- liver failure is common. In older infants, micronodular or
tosemia, hereditary fructose intolerance), lysosomal stor- macronodular cirrhosis and hepatocellular carcinoma
age disorders (Gaucher disease, Niemann-Pick disease), occur. Sonographic findings include a diffusely enlarged,
Wilson disease, and tyrosinemia (166). heterogeneous, echogenic liver (172).
Cystic fibrosis is characterized by an abnormality in the
cystic fibrosis transmembrane conductance regulator
(CFTR). The role of CFTR is to facilitate water and solute DISORDERS OF HEPATIC VESSELS
movement via chloride secretion and therefore promote bile
flow. The absence of CFTR leads to biliary cirrhosis and Portal Hypertension
portal hypertension. The prevalence of cirrhosis in cystic Portal hypertension is most often the result of increased
fibrosis is between 5% and 15%, with a median patient age intrahepatic resistance to hepatopetal portal venous flow.
at time of diagnosis of approximately 10 years (167,168). Rarely, it is caused by increased portal blood flow due to
Sonographic findings of cystic fibrosis liver disease include an arteriovenous fistula (173). Clinical signs include
increased echogenicity due to steatosis and/or fibrosis and splenomegaly, ascites, prominent abdominal veins (caput
findings of cirrhosis and portal hypertension (169). In a sin- medusae), hematemesis due to esophageal varices, hepatic
gle-center study, patients with a heterogeneous liver had a encephalopathy, and hypersplenism. Obstruction to portal
5.2-fold increased incidence of developing cirrhosis and a venous flow can occur at three levels: (a) prehepatic,
6.1-fold increased incidence of developing portal hyperten- caused by portal or splenic vein thrombosis; (b) intrahe-
sion compared to children with normal liver sonograms patic, secondary to cirrhosis; and (c) posthepatic, second-
(170). ary to hepatic vein occlusion, congestive heart failure, or
Glycogen storage disease, the most common inborn constrictive pericarditis.
error of carbohydrate metabolism, is an autosomal reces-
sive disorder characterized by excessive glycogen deposi-
tion in hepatocytes and proximal renal tubules (166).
Type I (Von Gierke disease) is the most common glyco-
gen storage disease and manifests in the neonatal period
with hepatomegaly, nephromegaly, and hypoglycemia.
Glycogen content in the liver is increased (normal 6%),
but there is no cirrhosis or fibrosis. Sonographic findings
are hepatomegaly and increased echogenicity secondary
to fatty infiltration (171). Hepatic adenoma and hepato-
cellular carcinoma are complications of long-standing
disease. Treatment is dietary management of hypo-
glycemia.
Galactosemia is an autosomal recessive disorder
caused by deficiency of galctose-1-phosphatase uridyl
transferase. It manifests in the neonatal period with liver
failure, jaundice, and hypoglycemia. Histologic changes
include steatosis, hepatic fibrosis, and cirrhosis. Sono-
graphic findings are similar to the glycogen storage disor-
ders with additional findings of cirrhosis and portal
hypertension.
Gaucher disease is the commonest lysosomal storage Portal hypertension. Transverse scan shows a large
disorder (166). It is caused by deficiency of B-glucosidase, Fig. 7.60
portal vein (PV), measuring 2.5 cm in diameter. Also note
resulting in accumulation of glucosylceramide. Clinical ascites (AS) anterior to the liver and heterogeneous hepatic
findings are hepatosplenomegaly, abdominal pain from parenchyma.
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Chapter 7 L I V E R 249

A B
Portal hypertension, altered portal venous flow. A: Transverse Doppler sonogram shows bidirectional portal vein flow. B: Doppler scan
Fig. 7.61
in another patient shows reversed (hepatofugal) portal vein flow. Hepatopetal (forward) arterial flow is seen above the baseline. (Case
courtesy of Brian Coley, MD.)

VASCULAR ABNORMALITIES new ones form to divert blood from the liver to lower-pres-
Portal vein size initially increases in patients with portal sure systemic vessels (hepatofugal flow). There are two
hypertension (Fig. 7.60). The size of the vein is related to main types of collaterals: tributary and developed collater-
the size and number of varices, and as portosystemic col- als (Fig. 7.63). Tributary collaterals are vessels that
laterals develop and blood flow is diverted from the liver,
portal vein diameter decreases. Portal vein dilatation alone
has a low sensitivity but high specificity (95% to 100%) for
diagnosis of portal hypertension. The respiratory-related
variation in the size of the portal vein may be absent or
diminished.
Doppler findings of portal hypertension include decreased
portal venous inflow (sensitivity 83%), diminished portal
vein pulsatility (sensitivity 94%), and bidirectional or
reversed portal venous flow (sensitivity 75%) (Fig. 7.61)
(174180). As portal venous flow decreases, the diameter
and flow velocity of the hepatic artery increases in order to
maintain perfusion to the hepatic parenchyma. This devel-
opment referred to as arterialization of the hepatic blood
supply (178), appears as increased arterial color signal in the
porta hepatis.
Finally, as hepatic vascular resistance increases, disten-
sibility of the hepatic veins diminishes. Hepatic vein pul-
satility is lost and a monophasic flow pattern develops
(Fig. 7.62).

PORTOSYSTEMIC COLLATERALS Portal hypertension, altered hepatic venous flow. Longitu-

When there is increased intrahepatic resistance to portal Fig. 7.62
dinal Doppler sonogram shows nonpulsatile flow in the
venous flow, portosystemic collateral pathways open and left hepatic vein (arrows).
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250 P E D I AT R I C S O N O G R A P H Y

Azygos and hemiazygos Gastrorenal

collateral

Dilated gastro-
esophageal veins
Coronary

Short gastrics

Paraumbilical Splenoretroperitoneal
collateral collateral

Pancreatic veins
Communications at level of Gastrorenal
intra-abdominal organs in contact collateral
with the retroperitoneum.
Superior mesenteric
vein
Inferior mesenteric vein
Vena cava

Normal venous
communications
in intestines
Anastomosis between
superior, middle and
inferior hemorrhoidal
veins

A B
Portal hypertension. Diagram shows the two main types of portosystemic shunts. A: Tributary collaterals of the portal venous system.
Fig. 7.63
Tributary collaterals are vessels that normally communicate with the portal venous system. The most common are the left gastric or
coronary vein, the short gastric veins, and the superior and inferior mesenteric veins. B: Developed collaterals. Developed collaterals arise from
recanalization of preexisting vessels that are not functional tributaries of the portal venous system. The most common are the paraumbilical vein
and splenorenal and splenoretroperitoneal vessels. (Adapted from Freeney PC. Venogrphy. In: Margulis AR, Burhenne JH (eds), Alimentary Tract
Radiology, St. Louis: CV Mosby; 1989:19511993).

normally drain the portal venous system, such as the left
gastric or coronary vein, the short gastric veins, and the
superior and inferior mesenteric veins. They communicate
with the systemic venous system via the retroperitoneal,
iliac, azygous, and hemiazygous veins. Developed collater-
als arise from recanalization of preexisting vessels that lack
a functional communication with the portal venous sys-
tem. These include the paraumbilical vein and splenorenal
and splenoretroperitoneal vessels.
The left gastric (coronary) vein is one of the most
important portosystemic shunts since it is responsible for
the formation of esophageal varices (181,182). The left
gastric vein arises near the portosplenic confluence and
ascends to the gastroesophageal junction. In healthy chil-
dren, the left gastric vein is very small and difficult to visu-
alize by sonography. In cirrhosis, the dilated gastric vein
can be seen posterior to the left lobe of the liver on scans
obtained near the splenic vein and portal vein confluence
(Fig. 7.64).
Gastroesophageal collateral vessels, formed by enlarge-
ment of the left gastric vein and branches of the splenic
vein, appear as tortuous anechoic or hypoechoic structures
near the gastroesophageal junction in close proximity to
the diaphragm (Fig. 7.65). Esophageal varices are seen
near the gastroesophageal junction on scans with the
transducer angled cranially through the left lobe of the
liver.
The recanalized paraumbilical vein connects the left
portal vein to the inferior epigastric veins in the anterior
abdominal wall. On physical examination, the dilated veins
in the abdominal wall form the clinical sign termed the
caput medusae. These abdominal wall veins drain cau-
dally into tributaries of the hypogastric vein and then into
the inferior vena cava. Cranially, the abdominal veins drain
into thoracic veins before entering the superior vena cava.
On transverse sonograms, the dilated paraumbilical vein is
seen as an anechoic, round or oval structure (3 mm in
diameter) running in the falciform ligament or ligamentum
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Chapter 7 L I V E R 251

Enlarged gastric (coronary) vein. Longitudinal scan of the

Fig. 7.64
epigastrium shows dilated and markedly tortuous vessels
(arrows) beneath the left lobe of the liver. (Case courtesy of Angela
Levy, MD.)

teres fissure. Its origin from the left portal vein and its ter-
mination on the undersurface of the anterior abdominal
wall near the umbilicus are best seen on a parasagittal view
(Fig. 7.66). Mean flow velocity is 16 cm/sec (range 7 to
33 cm/sec) (8). In about 15% of healthy individuals with-
out portal hypertension, a remnant of the umbilical vein
may be patent and flow (hepatopetal or hepatofugal) can be
seen in the ligamentum teres fissure by Doppler techniques
(8). However, flow velocity in healthy individuals does not
exceed 5 cm/sec and flow is not visualized anterior to the
liver surface.
The splenorenal collateral pathway shunts blood
from the splenic vein via the splenorenal ligament into
the left renal vein. Splenorenal veins are best identified
between the splenic and renal hila on transverse scans
(Fig. 7.67).
Other recruited pathways include the gastrorenal,
intestinal (mesentericocaval), and hemorrhoidal collater-
als. Gastrorenal collaterals divert blood from the left gas-
tric vein and short gastric veins to the left adrenal vein,
which empties into the renal vein. Intestinal collaterals
shunt blood from the superior mesenteric vein to the inferior

Esophageal varices. Longitudinal color Doppler scan at

Fig. 7.65
the level of the gastroesophageal junction shows tortuous
dilated venous channels (arrowheads). Ao  aorta; L  liver. (Case
courtesy of Brian Coley, MD.)
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252 P E D I AT R I C S O N O G R A P H Y

A B
Recanalized paraumbilical vein. A: Sagittal color Doppler image shows blood flow in the paraumbilical vein (arrows) as it courses from
Fig. 7.66
the portal vein (PV) to the anterior abdominal wall. B: Pulsed Doppler scan shows hepatofugal flow (away from the liver) in the paraum-
bilical vein (arrow). (Panel A courtesy of Brian Coley, MD.)

vena cava through the root of the small bowel mesentery.
The inferior mesenteric vein shunts splanchnic blood to the
inferior hemorrhoidal vein.
The principle of shunting blood into collateral path-
ways is that flow goes from a dilated splanchnic vein
into a dilated systemic vein. Hepatofugal flow in the col-
lateral pathways allows the diagnosis of portal hyper-
tension to be established. Pulsed and color Doppler
imaging show high Doppler shifts and turbulent or bidi-
rectional flow at the junction of the portal and systemic
circulations.
NONVASCULAR COMPLICATIONS
Nonvascular findings of portal hypertension include
splenomegaly, a thick lesser omentum, ascites, and signs of
cirrhosis. Splenomegaly is a nonspecific sign of portal
hypertension. The splenic vein dilates and reversal of flow
may be noted on Doppler imaging (Fig. 7.68).

A B
Splenorenal collaterals. A: Transverse scan shows multiple vessels (arrows) between the splenic hilum and left kidney (K). B: Color
Fig. 7.67
Doppler image shows communication between the splenic vein (SV) and left renal vein (LRV). Kid  left kidney. (Panel B courtesy of
Brian Coley, MD.)
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Chapter 7 L I V E R 253

Splenic varices. Coronal view of the spleen (S) demon-

Fig. 7.68
strates a dilated tortuous splenic vein (arrows).

Increased thickness of the lesser omentum results from
lymphatic congestion and dilatation of omental and coro-
nary veins that course through the omentum (183). The
thickness of the omentum is measured from the origin of
the celiac axis to the inferior surface of the liver on the
sagittal view and should be less than 1.7 times the diame-
ter of the aorta at the same level (Fig. 7.69). Omental
thickness greater than 1.7 times the aortic diameter is an
indicator of portal hypertension (183). Other causes of
omental thickening include obesity, systemic steroid ther-
apy, and lymphadenopathy.
Surgical Portosystemic Shunts
Portosystemic shunts are performed to reduce portal venous
pressure by diverting portal venous blood into the systemic
circulation. The common surgically created portosystemic
shunts are the mesocaval, splenorenal, portacaval, and
mesoatrial shunts. Gray-scale signs of shunt patency are a
decrease in the thickness of the lesser omentum, diminution
or disappearance of the collateral veins, decrease in the
diameter of the portal vein, and increase in the diameter of
the inferior vena cava compared with preoperative sono-
grams. Doppler findings of shunt patency include flow at the
anastomotic site and hepatofugal (reversed) flow in the main
and intrahepatic portal veins (184). Turbulence and aliasing,
reflecting high-velocity flow, are other signs of shunt
patency. Findings of shunt occlusion include thrombus
within the shunt or the portal veins, new or increasing col-
lateral vessel formation, absence of Doppler signal in the
shunt or anastomotic site, and ascites (184).

Thickened lesser omentum. Longitudinal scan. The thick-

Fig. 7.69
ness of the lesser omentum is the distance (white line)
between the anterior wall of the aorta (A) at the level of the celiac axis
(arrow) and the posterior hepatic surface. In this patient, the omental
thickness is greater than 2.7 times the aortic diameter (omentum 
3.5 cm, aorta  1.3 cm), an indicator of portal hypertension.
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254 P E D I AT R I C S O N O G R A P H Y

A B
Normal transjugular intrahepatic portosystemic shunt (TIPS). A: Gray-scale image shows an intrahepatic stent (arrow). AS  ascites.
Fig. 7.70
B: Color Doppler image shows color throughout the stent, indicating patency. Pulsed Doppler interrogation of the shunt at the hepatic
vein end demonstrates mild pulsatility and peak flow velocity of 91 cm/sec.

Transjugular Intrahepatic Portosystemic Shunts
Transjugular intrahepatic portosystemic shunts (TIPS) has
virtually replaced the surgically created portosystemic
shunts for decompressing the portal system, specifically for
decreasing esophageal varices in patients with gastroin-
testinal bleeding. In the TIPS procedure, a catheter is
inserted into the internal jugular vein and then advanced
into the hepatic veins, where a needle is used to create a
tract between an intrahepatic portal vein and hepatic vein.
A stent is then inserted, forming the portosystemic shunt.
The stent is easily recognized on gray-scale sonography
as a tubular structure with echogenic corrugated walls
connecting a portal vein and hepatic vein. Despite the
metallic nature of the stent, ring-down artifacts are not
encountered. A patent shunt fills entirely with color signal
(Fig. 7.70). Other Doppler findings of shunt patency are
antegrade (hepatofugal) flow in the portal vein; nonpul-
satile or minimally pulsatile flow in the stent; and peak
flow velocities of 90 to 130 cm/sec in the stent (185187).
Flow should be toward the shunt.
Shunt complications include stent thrombosis or stenosis
and stenosis of the draining hepatic vein. The absence of flow
in the stent is diagnostic of stent thrombosis (Fig. 7.71)
(185187). The sonographic findings of stent and/or hepatic

Transjugular intrahepatic portosystemic shunt thrombo-

Fig. 7.71
sis. Color Doppler image shows absence of color signal
within the stent. There also is ascites, which had reaccumulated since
shunt placement.
LWBK505-C07_p214-274.qxd 7/7/10 1:29 PM Page 255 Aptara Inc
vein stenosis are a peak shunt velocity less than 90 or greater
than 220 cm/sec; a temporal decrease in shunt velocity of
greater than 40 cm/sec or an increase of greater than
60 cm/sec; a mean portal vein velocity less than 30 cm/sec;
reversed flow in the hepatic vein draining the stent; and a
change in flow direction, from retrograde to antegrade, in
the left or right portal vein branch flow (185187). Sec-
ondary signs of shunt malfunction include reaccumulation of
ascites and reappearance of collateral vessels.
Portal Vein Thrombosis
Portal vein thrombosis can be idiopathic or a result of neo-
plastic invasion or bland thrombosis. Tumor invasion
occurs most often with hepatoblastoma and hepatocellular
carcinoma. Causes of bland portal vein thrombosis include
umbilical vein catheterization, dehydration or shock, sep-
sis, portal phlebitis, hypercoagulable states, chemotherapy,
hereditary thrombophilic disorders, and portal hyperten-
sion (188191). These conditions decrease portal venous
flow velocity, leading to stasis. Affected patients present
with acute or subacute abdominal pain or tenderness and
occasionally with splenomegaly.
ACUTE PORTAL VEIN THROMBOSIS
The classic sonographic findings of acute portal vein
thrombosis are an enlarged vein, echogenic intraluminal
thrombosis, and the absence of flow on color Doppler
examination (Fig. 7.72) (192). A small amount of flow
may be seen around a partially occlusive thrombus. The
acute thrombus is usually more echogenic than the adja-
cent nonclotted portal vein. However, it can be anechoic
and mimic a patent portal vein on gray-scale sonography.
In this instance, Doppler sonography can confirm the
A B
Acute portal vein thrombus. A: Longitudinal sonogram shows low-level echoes (arrows) in the portal vein (PV). B: Color Doppler imag-
Fig. 7.72
ing shows absent flow, confirming thrombus.
Chapter 7 L I V E R 255
absence of flow. The sonographic appearance of tumor and
bland thrombosis is often similar. However, if vessels can
be identified within the thrombus by pulsed or color
Doppler sonography, the diagnosis of tumor can be
strongly suggested. Bland thrombus is avascular. Another
Doppler finding of portal vein thrombosis is a decreased
hepatic artery resistive index (15,193).
The sensitivity, specificity, and negative predictive value
of color Doppler sonography for the diagnosis of portal
vein thrombosis are greater than 90%, with a positive pre-
dictive value of approximately 60% (194). False-positive
diagnoses are the result of low-velocity portal venous flow,
which can be difficult to detect sonographically.
CHRONIC PORTAL VEIN THROMBOSIS
Chronic portal vein thrombosis is characterized by peri-
portal collateral vein formation, which functions to
increase hepatopetal flow. These collateral channels are
referred to as the cavernous transformation of the portal
vein or portal cavernoma. Sonographic findings of cav-
ernous transformation include multiple tortuous vessels in
the portal hepatis and nonvisualization of the main portal
vein. Doppler findings include antegrade or bidirectional
portal venous waveforms in the cavernoma (Fig. 7.73)
(15,195,196) and increased hepatic arterial diameter and
flow.
Other intrahepatic and splanchnic collateral pathways
that develop in patients with portal vein thrombosis include
left gastric vein to perisplenic vein collaterals, hepatic vein
to portal vein collaterals, and pericholecystic vein to portal
vein collaterals (i.e., gallbladder wall varices) (195198).
Secondary findings of chronic portal vein thrombosis
include splenomegaly, a thickened lesser omentum, and
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256 P E D I AT R I C S O N O G R A P H Y

A B
Cavernous transformation of the portal vein. A: Transverse scan demonstrates multiple anechoic structures (arrows) in the porta
Fig. 7.73
hepatis. A normal portal vein cannot be identified. Pulsed Doppler spectrum shows bidirectional portal venous waveforms within the
cavernoma. B: Color Doppler imaging in another patient shows venous flow in the cavernoma (arrows).

spontaneous splenorenal shunts. The sensitivity of sonog- reversed flow in the portal vein. Secondary findings include
raphy for the diagnosis of cavernous transformation is ascites, pleural effusion, and gallbladder wall edema.
nearly 100% (196). Nonvisualization of the hepatic veins is not conclusive
evidence of hepatic vein occlusion because patent veins
Budd-Chiari Syndrome
The Budd-Chiari syndrome refers to the clinical and
pathologic abnormalities seen in the setting of acute
hepatic vein occlusion. It is a cause of postsinusoidal
hypertension. Patients present with acute onset of ascites,
jaundice, right upper quadrant pain, and hepatomegaly.
The obstruction can be at the level of the major hepatic
veins or at the level of the inferior vena cava near the
hepatic vein ostia, with or without secondary hepatic vein
occlusion (199).

OCCLUSION OF MAJOR HEPATIC VEINS

Primary occlusion of the major hepatic veins can be idio-
pathic or due to neoplastic invasion, usually secondary to
hepatoblastoma, hepatocellular carcinoma, or Wilms
tumor. Causes of idiopathic or bland thrombosis include
cirrhosis, hypercoagulable states, trauma, polycythemia
(200), and Gaucher disease (201).
The primary sonographic findings of acute venous
obstruction are hepatomegaly, echogenic intraluminal
thrombus, and absence of hepatic vein flow on Doppler
examination (Fig. 7.74). Other Doppler findings include
homogeneous color enhancement of the caudate lobe with
patchy parenchymal flow in other hepatic segments, loss of Acute Budd-Chiari syndrome. Sagittal sonogram shows a
hepatic vein pulsatility, reversed or turbulent flow in the Fig. 7.74
right hepatic vein (arrows) filled with echogenic throm-
nonoccluded segments of the hepatic veins, and slow or bus. Also note ascites (AS) surrounding the liver.
LWBK505-C07_p214-274.qxd 7/7/10 1:29 PM Page 257 Aptara Inc
Chronic hepatic vein occlusion (BuddChiari syndrome).
Fig. 7.75
A transverse sonogram through the porta hepatis demon-
strates multiple tubular channels (arrows) representing collateral
channels. Normal hepatic veins cannot be identified.
may be difficult to identify if the liver is enlarged or if the
patient has cirrhosis. In addition, false-negative results can
occur when cardiac pulsations are transmitted to the liver,
resulting in artifactual waveforms in the hepatic veins. The
sonographic findings in the chronic stage of the Budd-
Chiari syndrome are an atrophic echogenic segment or
lobe of the liver; small or nonvisualized hepatic veins; com-
pensatory enlargement of the caudate lobe, which serves as
a drainage route for venous blood flow; and collateral ves-
sel formation (Fig. 7.75). Secondary findings include
splenomegaly and portosystemic collateral vessel forma-
tion, related to the complications of cirrhosis and portal
hypertension.
Collateral pathways must develop in patients with
Budd-Chiari syndrome because hepatic vein outflow is
blocked. The common pathways are the intrahepatic
hepatic vein to hepatic vein, the hepatic vein to subcapsu-
lar systemic vein, and the hepatic vein to inferior vena
cava collaterals. Doppler evaluation of the collateral path-
ways shows retrograde flow away from the liver
(202204).
OCCLUSION OF THE INFERIOR VENA CAVA
The causes of inferior vena caval occlusion include a con-
genital membrane or cord, neoplastic invasion, extrinsic
compression by tumor or an enlarged caudate lobe, and
thrombosis from hypercoagulable states (205,206). The
obstruction to caval flow results in hepatic venous con-
gestion and subsequent thrombus formation. The congen-
ital membrane appears as a thin, highly echogenic intralu-
minal band with or without acoustic shadowing (203).
Acute thrombosis appears as an echogenic intraluminal
defect. Doppler findings include absent flow in the
obstructed segment of cava and decreased or reversed flow
in the hepatic veins.
Chapter 7 L I V E R 257
The segment of the cava below the obstruction is usu-
ally dilated. Doppler evaluation of this segment shows
slow or reversed flow, a continuous waveform pattern, and
absence of normal respiratory change.
The treatment of hepatic vein or inferior vena caval
occlusion is anticoagulant therapy; ablation of obstructive
membranes; or, less often, surgical portocaval shunting
(207). Findings of treatment response include recanaliza-
tion of the hepatic veins and regression of portosystemic
collaterals (205).
Hepatic Veno-occlusive Disease
Obstruction of the small sublobular veins, also termed
hepatic veno-occlusive disease, can be idiopathic or it
can be secondary to toxins, radiation, chemotherapy, and
bone marrow transplantation (208211). Hepatotoxins
cause hepatic edema, slowing blood flow within portal and
hepatic venules to the point where hepatic venous stasis
and subsequent thrombosis develop. Chemotherapy and
irradiation produce inflammation of the endothelium of
the small venules and ultimately vessel occlusion. In the
United States, hepatic veno-occlusive disease is most often
associated with chemotherapy and radiation therapy given
prior to bone marrow transplantation.
Obstruction of the sublobular veins can be difficult to
diagnose by imaging studies, since these veins cannot be
directly visualized. However, hepatic veno-occlusive dis-
ease should be suspected if there is slow or reversed por-
tal venous flow, monophasic hepatic vein waveforms,
decreased or reversed diastolic flow in the hepatic artery,
or an increase in the hepatic artery resistive index (Fig.
7.76) (212). Mean hepatic artery resistive index is 0.69 in
normal subjects and 0.81 in veno-occlusive disease (210).
The major hepatic veins and inferior vena cava are patent
and may show normal phasic flow. Other findings include
a thickened gallbladder wall, ascites, and hepatomegaly.
Arteriovenous Malformations
Arteriovenous malformation (AVM) in the pediatric
population is usually a congenital abnormality charac-
terized by multiple blood vessels with direct arteriove-
nous connections and shunting. The capillary bed is
absent. Most are symptomatic and present in infancy
with findings of high-output congestive heart failure.
Other clinical findings include hepatomegaly, gastroin-
testinal bleeding, and signs of portal hypertension. Less
commonly, AVMs are acquired subsequent to penetrat-
ing trauma (stab wounds, biopsy, or surgical trauma).
They can be associated with hereditary hemorrhagic
telangiectasia (telangiectases, arteriovenous fistulas, and
aneurysms of the skin, lung, liver, and central nervous
system) and they can be a cause of portal hypertension
(213219).
An AVM is typically limited to one hepatic lobe or seg-
ment. The types of malformations include portal vein to
hepatic vein, portal vein to inferior vena cava, and hepatic
artery to portal vein.
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258 P E D I AT R I C S O N O G R A P H Y

A B

Veno-occlusive disease following bone marrow trans-

Fig. 7.76
plantation. A: Longitudinal color Doppler scan of the
main portal vein shows retrograde flow. B: Pulsed Doppler interro-
gation of the hepatic veins in another patient shows loss of venous
pulsatility with a monophasic flow pattern. C: Doppler interrogation
in another patient shows high-resistance arterial flow with
C decreased and reversed diastolic flow. Resistive index was 0.87.
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Chapter 7 L I V E R 259

Hepatic artery to portal vein fistula. Transverse image of

Fig. 7.77
the porta hepatis shows an enlarged portal vein (PV) with
arterialized venous waveforms and turbulent flow. Angiography
demonstrated a fistula from the left hepatic artery to the left portal
vein, with retrograde blood flow in the portal vein.

Gray-scale sonography demonstrates enlargement and
tortuosity of the involved vessels. Pulsed and color
Doppler ultrasonography can demonstrate direct commu-
nication between the involved vessels, turbulent blood
flow in the fistula, and reversed flow or pulsatile (biphasic
or triphasic) waveforms in the portal vein, hepatic vein, or
inferior vena cava (Figs. 7.77 to 7.79) (14,213). An arteri-
alized portal venous waveform can be noted in hepatic
artery to portal vein malformations (Fig. 7.77). Treatment
includes coil embolization and surgical banding.

A B
Portal vein to hepatic vein fistula. A: Color Doppler image shows a communication between the right hepatic vein (HV) and portal vein
Fig. 7.78
(PV). B: Pulsed Doppler sonography of the portal vein shows pulsatile, bidirectional flow.
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260 P E D I AT R I C S O N O G R A P H Y

A B

Portal vein to inferior vena cava fistula. A: Transverse

Fig. 7.79
image shows a communication between the main portal
vein (PV) and inferior vena cava (IVC). B: Color Doppler again shows a
large portocaval shunt with the main portal vein (PV) draining into the
inferior vena cava (IVC). The hepatic artery (HA) is also dilated, but it
did not communicate with the portal vein or cava. C: Pulsed Doppler
interrogation of the right portal vein shows a pulsatile waveform typi-
C cal of systemic flow.

Hepatic Infarction Sonographic findings of acute infarction are a wedge-

Because of the dual blood supply, infarction is relatively
rare. Although hepatic infarction may be secondary to
portal venous occlusion, it is more often related to occlu-
sion of the hepatic artery. Factors predisposing to hepatic
infarction in childhood include trauma, intraoperative lig-
ation of the hepatic artery, vasculitis, hypercoagulable
states, and shock. Clinical findings include abdominal
pain and tenderness, fever, and abnormal hepatic function
tests.
shaped, round or oval, hypoechoic area with indistinct
margins and a peripheral distribution (220). Other findings
include acoustic enhancement and hyperechoic foci repre-
senting gas secondary to tissue necrosis. Infarcted tissue
becomes more echogenic with time and may calcify, and the
borders usually become more distinct. Chronic changes
include lobar or segmental atrophy and cystic collections,
termed bile lakes, which are sequelae of biliary ductal
necrosis. Bile lakes generally have little clinical significance.
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Chapter 7 L I V E R 261

A B
Hepatic peliosis. A: Three-month-old girl with a benign renal tumor and incidentally discovered hepatic lesions. Longitudinal sonogram
Fig. 7.80
shows multiple hypoechoic lesions. B: Computed tomography shows multiple enhancing lesions. Differentiation from infantile heman-
gioendothelioma requires tissue sampling.

Peliosis Hepatis PORTAL VENOUS GAS

Peliosis hepatis is a rare condition characterized by sinusoidal
dilatation (221223). It has been associated with hemato-
logic disorders, human immunodeficiency virus (HIV) infec-
tions (specifically B. henselae and Bartonella quintana infec-
tions), and drugs (including corticosteroids, anabolic
steroids, oral contraceptives, azathioprine, 6-thioguanine,
6-mercaptopurine, and methotrexate). Peliosis hepatis may
be asymptomatic and discovered incidentally at autopsy or
imaging studies. However, patients can be symptomatic, pre-
senting with hepatomegaly, ascites, portal hypertension,
acute hepatic failure, or intraperitoneal hemorrhage second-
ary to lesion rupture (221, 222).
Sonographically, the liver is diffusely heterogeneous
and contains multiple hypoechoic or hyperechoic areas
(Fig. 7.80) (221,223). Color Doppler imaging shows perin-
odular or intranodular flow (221,224,225).
Air in the portal vein occurs in neonates with necrotizing
enterocolitis and in older children with infarcted bowel. The
diagnosis is based on the real-time sonographic demonstra-
tion of multiple high-amplitude echoes moving within the
lumen of the portal vein and its branches in the direction of
blood flow (Fig. 7.81). Doppler imaging shows sharp bidi-
rectional spikes superimposed on the normal monophasic
portal vein waveform at irregular intervals (227). Acoustic
shadowing and reverberation artifacts may be seen. Gas also
may be noted around the wall of the gallbladder.

Passive Venous Congestion

Passive venous congestion is usually the result of right-
sided heart failure and less often a complication of con-
strictive pericarditis. Acute venous congestion causes
increased hepatic venous pressures, resulting in decreased
antegrade arterial and portal venous blood flow. Patients
present with tender hepatomegaly, abnormal liver function
tests, or both findings.
Gray-scale findings include hepatomegaly and dilated
hepatic veins. Doppler sonography of the hepatic veins
shows a small antegrade systolic waveform (rather than the
normal large antegrade systolic waveform), reversed sys-
tolic flow, or a low-velocity monophasic waveform.
Doppler findings in the portal veins include increased pul-
satility related to increased right heart pressure with tricus-
pid insufficiency, retrograde flow, and vena cavalike Portal vein air in a neonate with necrotizing enterocolitis.
biphasic waveforms (226). Secondary findings include peri- Fig. 7.81
Transverse scan shows numerous punctate echogenicities
portal edema, cardiomegaly, pleural effusions, and ascites. in the anterior part of the liver, some of which have acoustic shadowing.
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262 P E D I AT R I C S O N O G R A P H Y
RADIATION EFFECTS
The liver is usually not directly irradiated for therapeutic pur-
poses, but it can be incidentally included in radiation ports
designed to encompass tumors in adjacent organs or bony
structures. Clinically and pathologically, the effects of radia-
tion are classified into acute and chronic stages. The acute
phase has its onset 2 to 6 weeks after the completion of radi-
ation therapy. Patients present with acute hepatic enlarge-
ment, jaundice, and ascites. Histologically, there is a spectrum
of changes varying from mild panlobar congestion to severe
congestion and hemorrhagic necrosis. In the chronic stage,
the irradiated liver is small, contracted, and fibrotic (228).
Sonographically, acute radiation-induced hepatic injury
produces a sharply demarcated area of decreased echogenic-
ity, reflecting edema and hepatic congestion. The sharp,
straight line of demarcation between the normal and abnor-
mal liver corresponds to the predetermined radiation port in
each patient (229). Sonographic findings in the chronic stage
include a decreased hepatic volume and findings of cirrhosis.
HEPATIC TRAUMA
The liver is the most commonly injured abdominal organ in
children with blunt abdominal trauma (230,231). Blunt
trauma is usually due to motor vehicle accidents, but other
causes include bicycle, skateboard, all-terrain vehicle, or
motorcycle accidents, falls, and assaults. The right hepatic
lobe is injured more often than the left and the posterior seg-
ment of the right lobe is injured more often than the anterior
segment. Caudate lobe injuries are rare and almost always
occur with right or left lobe injuries (232). In newborns, causes
of hepatic injury include birth trauma and umbilical catheter-
ization (233). An elevated -fetoprotein level has been
reported in a newborn with intrahepatic hematoma (233).
In the hemodynamically stable patient, CT scans are
the initial study to assess the extent of hepatic injury and
A B
Hematoma. A: Acute hematoma. Transverse image in a neonate with a traumatic delivery shows a poorly defined, echogenic lesion
Fig. 7.82
(arrows) in the posterior segment of the right lobe, consistent with acute blood products. B: Subacute hematoma. Longitudinal sono-
gram in another patient shows a well-defined, oval, predominantly hypoechoic lesion (calipers) with echogenic components anteriorly.
determine whether nonoperative management or laparo-
tomy is appropriate (234,235). Sonography, using the
four-quadrant abdominal scanning technique, referred to
as focused abdominal sonography for trauma (FAST), can
be useful in detecting hemoperitoneum in acutely injured
patients and in the follow up evaluation of patients who
are managed conservatively (236238). Sonography has a
limited sensitivity in the initial evaluation of acute
parenchymal injury, although some recent studies have
shown that contrast-enhanced sonography may improve
detection of intrahepatic lesions (239).
Acute Injuries
The spectrum of hepatic injuries includes subcapsular
and parenchymal hematomas, lacerations and fractures and
vascular injuries. Subcapsular hematomas result in lenticu-
lar-shaped fluid collections that flatten or indent the under-
lying hepatic parenchyma. Most are found along the antero-
lateral margin of the right hepatic lobe. Intrahepatic
hematomas are round or oval lesions that may be either well
circumscribed or poorly marginated (Fig. 7.82). Hepatic lac-
erations result in linear or branching parenchymal defects
(Fig. 7.83) that may be superficial or deep. Hepatic fractures
are deep parenchymal lacerations that extend through two
visceral surfaces and result in avulsed segmental or lobar
fragments. Injuries to the hepatic veins or inferior vena cava
are life-threatening lesions with a high mortality, because
they can result in exsanguination. Hemoperitoneum often
accompanies hepatic injuries. It may be small, confined to
the right subphrenic and subhepatic spaces, or more exten-
sive, accumulating in the paracolic gutter and the pelvic cul-
de-sac. Gas may be identified within a parenchymal lesion
1 to 2 days after blunt abdominal trauma, secondary to tis-
sue ischemia and necrosis (240).
The echogenicity of the blood varies with the age of the
injury (241). Fresh hemorrhage usually appears hyperechoic
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Chapter 7 L I V E R 263

A B

C
Laceration. A, B: Two transverse sonograms show a well defined, hypoechoic linear lesion (arrow, cursors) in the right lobe. C: CT scan
Fig. 7.83
7 days earlier at time of original injury shows a laceration through the right hepatic lobe.

relative to surrounding liver due to the presence of fibrin
and clot formation (see Fig. 7.82A). Within 2 to 3 days, the
hematoma/laceration becomes more hypoechoic and even-
tually it becomes cystic as the blood undergoes liquefaction
with resorption of hemoglobin (Fig. 7.82B) (233,242).
Follow-up imaging in conservatively treated patients
usually demonstrates a substantial decrease in the hemo-
peritoneum in a week and often a decrease in the size of the
parenchymal injury. Failure to demonstrate decreased size
of the hemoperitoneum within 1 week and/or increased
hemoperitoneum is worrisome for continuing bleeding.
Umbilical vein catheterization is a cause of hepatic
injury in the neonate. Sonographic findings include
superimposition of the umbilical vein catheter over the
liver but not in a vessel; portal vein air; intrahepatic, sub-
capsular, or perihepatic fluid collections (hematomas);
and ascites (Fig. 7.84) (243,244). These hematomas
usually resolve after removal of the umbilical venous
catheter.
Complications
Late complications of hepatic trauma are biloma and
pseudoaneurysm (245247). Bilomas are walled-off collec-
tions of bile. They appear as homogeneous, thin-walled,
anechoic collections in the liver or the peritoneal cavity.
Most resolve spontaneously. Pseudoaneurysms result when
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264 P E D I AT R I C S O N O G R A P H Y
A B
Catheter erosion of the umbilical vein. A: Transverse scan shows a small hematoma (arrows) anterior to the liver (L) and ascites. B: A
Fig. 7.84
more cranial transverse scan shows the umbilical venous catheter (open arrow) coursing through the hepatic parenchyma. Also note
air in the portal venous system, characterized by hyperechoic foci (white arrows) with acoustic shadowing.
lacerations cross the hepatic artery or its branches. They
appear as hypoechoic masses with acoustic enhancement.
They may contain echogenic debris representing fibrin or
areas of clotted blood. Pulsed or color flow Doppler imaging
can confirm arterial flow in a pseudoaneurysm. However,
flow can be absent if the lumen is thrombosed. Focal fatty
infiltration, presumably related to local vascular injury, and
calcifications are other late sequelae of hepatic trauma.
LIVER TRANSPLANTATION
Preoperative Evaluation
Liver transplantation is the only treatment for end-stage
liver disease. Three main types of transplantation proce-
dures are used in children: a whole cadaveric allograft, a
split cadaveric allograft, and a living related donor allograft
(248,249). Due to the limited number of available cadaveric
donor livers and the large number of patients awaiting
transplantation, the living related donor option has become
particularly important. The split cadaveric allograft consists
of dividing the donor liver. In this technique, the left lateral
segment is transplanted into a small child and the right lobe
and remainder of the left lobe are transplanted into a large
child, adolescent, or adult. In living related donor trans-
plantation in smaller children, the recipient liver is replaced
with the left lateral segment of the left lobe or with the
whole left lobe. In larger children and adults, the recipient
liver is replaced with the right lobe of a living donor.
Surgical Anatomy
In the cadaveric transplantation, the portal vein, inferior
vena cava, common hepatic artery, and common bile duct
of the donor are anastomosed to the recipient vessels. The
donor bile duct is anastomosed to the recipient common
duct, or if the duct is too small, it is anastomosed to a loop
of small bowel. In the living related donor transplantation,
the left hepatic artery, left portal vein, and left and middle
hepatic veins are anastomosed to the recipient vessels. The
recipient vena cava is preserved. Biliary drainage is via a
Roux-en-Y hepaticojejunostomy.
Imaging Guidelines
Preoperative sonography is used to assess the anatomy, size,
and patency of the portal vein and the direction of portal
vein flow; hepatic arterial anatomy; the presence of collateral
vessels; and inferior vena caval size and patency (248). Pre-
operative sonography may detect other clinically important
anomalies, especially in patients with biliary atresia. These
anomalies include partial or complete malrotation of the
bowel, polysplenia, and vascular anomalies, such as absence
of the inferior or superior vena cava or the hepatic artery.
Postoperative imaging is performed to detect trans-
plant-related complications (248,250253). The complica-
tions are similar in cadaveric and living-related donor graft-
ing and include vascular stenosis or thrombosis, biliary leak
or stricture, bilomas, abscesses, and posttransplant lym-
phoproliferative disorder (see previous discussion).
Normal Posttransplantation Liver
The normal liver allograft has a homogeneous or minimally
heterogeneous echotexture. The hepatic artery shows a
rapid systolic upstroke with a systolic acceleration time
(time from end-diastole to first systolic peak) of less than
0.1 seconds, continuous flow throughout diastole, and a
resistive index of 0.5 to 0.7 (253255). The main portal
vein shows antegrade flow with mild pulsatility due to res-
piration. The hepatic vein shows a typical phasic waveform
reflecting changes in blood flow during the cardiac cycle.
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Hematoma at allograft resection site. Transverse image
Fig. 7.85
obtained 2 days after partial liver transplantation demon-
strates a fluid collection, representing hematoma (arrows) at the mar-
gin of the liver. ST  fluid-filled stomach.
A hypoechoic rim around the portal vein or its
branches is another common observation (251). This usu-
ally corresponds to lymphedema caused by surgical dis-
ruption of lymphatic vessels. However, a periportal hypo-
echoic collar has been reported with acute rejection and
hepatic necrosis (256).
In the immediate postoperative period, fluid collections
and hematomas are common in the perihepatic and sub-
hepatic spaces and also at the parenchymal resection site in
patients with reduced-size liver transplantation (i.e., single
lobe or segment transplant) (Fig. 7.85) (248,257259). The
fluid usually resolves spontaneously without complication.
Postoperative Vascular Complications
HEPATIC ARTERY COMPLICATIONS
Although the hepatic artery has a small role in maintaining
the viability of the normotopic liver, the transplant liver
including the donor bile duct is highly dependent on the
hepatic artery for its perfusion. Since arterial occlusion
leads to hepatic necrosis and death, the sonographic detec-
tion of hepatic artery thrombosis is usually an indication
for immediate retransplantation.
Hepatic artery thrombosis occurs in up to 40% of allo-
grafts, usually in the first 2 postoperative months
(248,251,253,255). It most commonly involves the anasto-
motic site. Doppler sonography shows no arterial flow in
the porta hepatis or in the hepatic parenchyma. After
thrombosis occurs, collateral arteries can develop, usually
from the superior mesenteric artery, and intrahepatic
arterial flow may be identified (254,255). The arterial wave-
forms in collateral arteries show a tardus parvus pattern and
a resistive index less than 0.5. The sensitivity of Doppler
sonography for diagnosis of hepatic artery thrombosis is as
high as 90% (248,254,255,260). A false-negative diagnosis
Chapter 7 L I V E R 265
Hepatic artery stenosis. Spectral Doppler image of the
Fig. 7.86
intrahepatic artery shows a tardus parvus waveform
(delayed early systolic acceleration and diminished amplitude and
rounding of the systolic peak). Also note elevated diastolic flow.
can result if there is collateral vessel formation (261). A
false-positive diagnosis occurs in low-flow states caused by
severe hepatic edema or systemic hypotension (262).
Hepatic artery stenosis occurs in up to 15% of liver
transplantations, usually at the anastomotic site, although
it may also be found more distally (248,255). The gray-
scale finding of arterial stenosis is vessel narrowing. How-
ever, the site of narrowing is often difficult to identify, and
the diagnosis is made on the basis of Doppler imaging. The
Doppler signs of arterial stenosis include (a) peak systolic
velocity at or just beyond the point of stenosis that is three
to four times greater than the velocity in the prestenotic
hepatic artery, (b) prolonged systolic acceleration time
(0.08 seconds), (c) turbulence at the stenotic site, (d) a
resistive index less than 0.5, and (e) an intrahepatic tardus
parvus waveform with elevated diastolic flow (Fig. 7.86)
(248,254,255). The sensitivity of Doppler sonography for
diagnosis of arterial stenosis is 80% to 90%. Anastomotic
stenosis may be treated with balloon angioplasty.
PORTAL VEIN COMPLICATIONS
Portal vein thrombosis occurs in 3% to 10% of pediatric
liver transplants, usually at the anastomotic site between
the donor and recipient portal vein segments (248,263). It
is more frequent in reduced-size liver transplantation than
in whole liver transplantation. Gray-scale sonography
shows an echogenic thrombus within the lumen of the
involved portal vein. Doppler sonography demonstrates
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266 P E D I AT R I C S O N O G R A P H Y

A B
Portal vein stenosis. A: Gray-scale image of the portal vein after segmental liver transplantation shows narrowing (arrow) at the anas-
Fig. 7.87
tomotic site between the donor and recipient portal veins and poststenotic dilatation (open arrow). Pulsed Doppler waveform shows
turbulent flow with aliasing in the stenotic segment. Poststenotic flow velocity was 2 meters/sec. B: Color Doppler image shows the narrowed ves-
sel (black arrows), aliasing (mixed red-yellow signal) at the stenotic site, and poststenotic dilatation of the portal vein (open arrow). (Case courtesy
of Brian Coley, MD.)

absent flow in the portal vein and collateral vessels. Occa-
sionally, reversed flow is seen in the intrahepatic branches,
related to development of arterioportal shunts.
Portal vein stenosis occurs in less than 5% of patients.
Gray-scale findings of portal vein stenosis are a discrete nar-
rowed segment with greater than 50% reduction in the size
of the lumen at the stenotic site relative to the prestenotic area
(148,255,263,264). Doppler imaging shows (a) a systolic
velocity at the stenotic site that is three to four times greater
than that in the prestenotic segment, (b) poststenotic jet with
a velocity between 1 and 3 meters/sec, and (c) turbulence
(263,265). Color Doppler sonography shows focal color
aliasing (turbulence) at the vascular anastomosis (Fig. 7.87).
HEPATIC VEIN COMPLICATIONS
Hepatic vein complications can occur at the surgical anas-
tomosis or they can be secondary to extension of inferior
vena cava thrombus or stenosis (255). In hepatic vein
thrombosis, gray-scale sonography shows echogenic
thrombus in one or more hepatic veins. Doppler imaging
shows absent flow. In hepatic vein stenosis, gray-scale
imaging is usually normal. Doppler interrogation shows a
velocity in the stenotic segment that is four times that in
the main hepatic vein trunk proximal to the stenosis and
absent or diminished intrahepatic flow with a monophasic
waveform (266,267).

INFERIOR VENA CAVA COMPLICATIONS OTHER VASCULAR COMPLICATIONS

Inferior vena cava thrombosis occurs in less than 1% of
patients, usually at the anastomotic site between the supe-
rior and inferior cava. Sonographic findings include
echogenic intraluminal thrombus and decreased or absent
flow on Doppler imaging (248).
The gray-scale finding of stenosis is focal narrowing of
the inferior vena cava at or near the anastomosis. Doppler
sonography shows (a) high-velocity flow at the stenotic site
that is three to four times that in the prestenotic segment, (b)
turbulence and aliasing at the stenotic site, (c) monophasic
waveform in the inferior vena cava, and (d) reversed or
monophasic flow in the hepatic veins (Fig. 7.88) (248).
Hepatic artery pseudoaneurysms and arteriovenous fistu-
las may develop at the anastomotic site or as a complica-
tion of biopsy or angioplasty. Gray-scale findings of
pseudoaneurysm are an anechoic mass with turbulent
swirling flow on color Doppler imaging. Findings of arte-
riovenous fistula are an anechoic mass with high-velocity,
turbulent arterial flow (Fig. 7.89).
Parenchymal Complications
Parenchymal abnormalities include infarction, abscess,
hematoma, biloma, seroma, and rejection. Infarction
occurs in about 10% of transplant recipients. Sonography
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A B
Inferior vena cava/hepatic vein stenosis in a young adult. A: Sagittal pulsed Doppler image of the middle hepatic vein shows a
Fig. 7.88
monophasic wave pattern. B: Doppler image of the inferior vena cava at the anastomosis shows a monophasic waveform.
Arteriovenous fistula. A longitudinal sonogram through
Fig. 7.89
the left lobe of the liver shows a hypoechoic mass
(arrows). Doppler waveforms show turbulent arterial flow.
Chapter 7 L I V E R 267
shows a hypoechoic area with heterogeneous or homoge-
neous echotexture and absent flow on Doppler imaging.
The appearance is nonspecific and differentiation among
infarct and abscess, hematoma, biloma, or seroma may
require percutaneous needle aspiration. Prior to aspiration,
the fluid collection should be evaluated by Doppler sonog-
raphy to determine that it does not represent a pseudo-
aneurysm.
Allograft rejection is a clinical diagnosis proven by
biopsy. The gray-scale finding of acute rejection is
parenchymal heterogeneity. Doppler findings include
monophasic rather than triphasic hepatic vein waveform
and increased arterial resistance (268271). Gray-scale
and Doppler findings are neither sensitive nor specific for
the diagnosis of rejection and their role is detection of
other causes of hepatic graft dysfunction.
Biliary Complications
Stricture and bile leakage occur in approximately 20% of
liver transplantations (272,273). They usually are at the
anastomotic site and occur in the first 3 months of trans-
plantation, although they may develop months or years
after surgery. Nonanastomotic bile leaks and strictures are
less common and may occur anywhere in the biliary tree.
The rate or type of complication does not differ between
whole organ and reduced size transplants. Factors predis-
posing to biliary complications are the surgical technique
used for biliary reconstruction and prolonged ischemia
time (248).
The sonographic findings of biliary stricture are nar-
rowing of the common bile duct and intrahepatic ductal
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268 P E D I AT R I C S O N O G R A P H Y
A B
Bile duct stricture 1 month after hepatic transplant. A: Longitudinal image shows dilated intrahepatic ducts. B: Ductal dilatation resolved
Fig. 7.90
following stent placement (arrow).
dilatation (Fig. 7.90) (268,272,273). Treatment includes
percutaneous dilatation, stent placement (Fig. 7.90B), and
reoperation.
Bile leakage usually occurs at the anastomotic site near
the T-tube insertion and appears as a subhepatic fluid col-
lection. Small leaks may close spontaneously. Larger ones
may require placement of a stent or surgical revision of the
anastomosis.
Miscellaneous Complications
Portal venous gas has been reported in transplant recipients
(274). Sonographic findings include multiple high-amplitude
echoes moving within the lumen of the portal vein in the
direction of blood flow. These high-amplitude echoes are
intermittently visible at irregular intervals. Portal venous gas
does not necessarily signify a catastrophic event. It may be a
transient finding without clinical significance.
Extrahepatic transplant-related complications include
right adrenal hemorrhage, pancreatitis, and lymphoprolif-
erative disorder. Right adrenal hemorrhage is due to
clamping of the adrenal vein during performance of the
inferior vena caval anastomosis (275). Sonography demon-
strates an echogenic or complex suprarenal mass. Pancre-
atitis may be associated with traumatic injury during sur-
gery or immunosuppressive drugs.
REFERENCES
1. Pobiel RS, Bisset GS III. Pictorial essay: imaging of liver tumors
in the infant and child. Pediatr Radiol 1995;25:495506.
2. Siegel M. Pediatric liver imaging. Semin Liver Dis 2001;21:
251269.
3. Bismuth H. Surgical anatomy and anatomical surgery of the
liver. World J Surg 1982;6:39.
4. Breuer CK, Vacanti JP. Surgical liver disease. In: Oldham KT,
Colombani PM, Foglia RP, eds. Surgery of infants and children:
scientific principles and practice. Philadelphia, PA: Lippincott
Williams & Wilkins, 2005:14591473.
5. Gazelle GS, Haaga JR. Hepatic neoplasms: surgically relevant seg-
mental anatomy and imaging techniques. AJR Am J Roentgenol
1992;158:10151018.
6. Smith D, Downey D, Spouge A, et al. Sonographic demonstration
of Couinauds liver segments. J Ultrasound Med 1998;17:375381.
7. Soyer P. Segmental anatomy of the liver: utility of a nomenclature
accepted worldwide. AJR Am J Roentgenol 1993;161:572573.
8. Wachsberg RH, Obolevich AT. Blood flow characteristics of
vessels in the ligamentum teres fissure at color Doppler sonog-
raphy: findings in healthy volunteers and in patients with por-
tal hypertension. AJR Am J Roentgenol 1995;164:14031405.
9. Patriquin HB, Perreault G, Grignon A, et al. Normal portal
venous diameter in children. Pediatr Radiol 1990;20:451453.
10. Loberant N, Barak M, Gaitini D, et al. Closure of the ductus
venosus in neonates: findings on real-time gray-scale, color-flow
Doppler, and duplex Doppler sonography. AJR Am J
Roentgenol 1992;159:10831085.
11. Loberant N, Herskovits M, Barak M, et al. Closure of the duc-
tus venosus in premature infants: findings on real-time gray-
scale, color-flow Doppler, and duplex Doppler sonography. AJR
Am J Roentgenol 1999;172:227229.
12. Rizzo AJ, Haller JO, Mulvihill DM, et al. Calcification of the
ductus venosus: a cause of right upper quadrant calcification in
the newborn. Radiology 1989;173:8990.
13. Vade A, Lim-Dunham J, Iqbal N. Imaging of the ductus veno-
sus in neonates: from patency to closure. J Ultrasound Med
2001;20:681687.
14. Gallego C, Miralles M, Marin C, et al. Congenital hepatic
shunts. Radiographics 2004;24:755772.
15. Corness JA, McHugh K, Roebuck DJ, et al. The portal vein in
children: radiological review of congenital anomalies and
acquired abnormalities. Pediatr Radiol 2006;36:8796, quiz
170171.
16. Fraser-Hill MA, Atri M, Bret PM, et al. Intrahepatic portal
venous system: variations demonstrated with duplex and color
Doppler US. Radiology 1990;177:523526.
LWBK505-C07_p214-274.qxd 7/7/10 1:29 PM Page 269 Aptara Inc
17. Becker CD, Cooperberg PL. Sonography of the hepatic vascu-
lar system. AJR Am J Roentgenol 1988;150:9991005.
18. Abu-Yousef MM. Normal and respiratory variations of the
hepatic and portal venous duplex Doppler waveforms with
simultaneous electrocardiographic correlation. J Ultrasound
Med 1992;11:263268.
19. Kao SCS, Bell EF, Brown BP, et al. Duplex Doppler sonography
of changes in portal vein flow in healthy term newborn infants
after feeding. J Ultrasound Med 1996;15:121125.
20. Abu-Yousef MM, Milam SG, Farner RM. Pulsatile portal vein
flow: a sign of tricuspid regurgitation on duplex Doppler
sonography. AJR Am J Roentgenol 1990;155:785788.
21. Hosoki T, Arisawa J, Marukawa T, et al. Portal blood flow in
congestive heart failure: pulsed duplex sonographic findings.
Radiology 1990;174:733736.
22. Scheinfeld MH, Bilali A, Koenigsberg M. Understanding the
spectral Doppler waveform of the hepatic veins in health and
disease. Radiographics 2009;29:20812098.
23. Jequier S, Jequier JC, Gong J, et al. Doppler waveform of
hepatic veins in healthy children. AJR Am J Roentgenol 2000;
175:8590.
24. Joynt LK, Platt JF, Rubin JM, et al. Hepatic artery resistance
before and after standard meal in subjects with diseased and
healthy livers. Radiology 1995;196:489492.
25. Lafortune M, Dauzat M, Pomier-Layrargues G, et al. Hepatic
artery: effect of a meal in healthy persons and transplant recip-
ients. Radiology 1993;187:391394.
26. Donoso L, Martinez-Noguera A, Zidan A, et al. Papillary
process of the caudate lobe of the liver: sonographic appear-
ance. Radiology 1989;173:631633.
27. Konus OL, Ozdemir A, Akkaya A, et al. Normal liver, spleen and
kidney dimensions in neonates, infants, and children: evaluation
with sonography. AJR Am J Roentgenol 1998;171:16931698.
28. Belton RL, Van Zandt TF. Congenital absence of the left lobe of
the liver: a radiographic diagnosis. Radiology 1983;147:
184187.
29. Champetier J, Yver R, Letoublon C, et al. A general review of
anomalies of hepatic morphology and their clinical implica-
tions. Anat Clin 1985;7:285299.
30. Radin DR, Colletti PM, Ralls PW, et al. Agenesis of the right
hepatic lobe of the liver. Radiology 1987;164:639642.
31. Lim JH, Ko YT, Han MC, et al. The inferior hepatic fissure: sono-
graphic appearance. AJR Am J Roentgenol 1987;149:495497.
32. Grunz J, Luisiri A, Cradock T. Torsion of a hepatic lobe in the
neonate-ultrasound findings. Pediatr Radiol 1992;22:192193.
33. Koplewitz BZ, Manson DE, Ein SH. Post traumatic torsion of
accessory lobe of the liver and gallbladder. Pediatr Radiol
1999;29:799802.
34. Siegel MJ. Liver and biliary tract. In: Siegel MJ, ed. Pediatric
body CT. 2nd ed. Philadelphia, PA: Lippincott Williams &
Wilkins, 2008:177216.
35. Siegel MJ, Chung EM, Conran RM. Pediatric liver: focal
masses. Magn Reson Imaging Clin N Am 2008;16:437452.
36. Sato M, Ishida H, Konno K, et al. Liver tumors in children and
young patients: sonographic and color Doppler findings.
Abdom Imaging 2000;25:596601.
37. Brannigan M, Burns PN, Wilson SR. Blood flow patterns in
focal liver lesions at microbubble-enhanced US. Radiographics
2004;24:921935.
38. Riccabona M, Uggowitzer M, Klein E, et al. Echo-enhanced
color Doppler sonography in children and adolescents. J Ultra-
sound Med 2000;19:789796.
39. Ishak KG, Goodman Z, Stocker JT. Tumors of the liver and
intrahepatic bile ducts. In: Atlas of tumor pathology. 3rd ed.
Washington, DC: Armed Forces Institute of Pathology, 1999.
40. Mueller BU, Lopez-Terrada D, Finegold MJ. Tumors of the
liver. In: Pizzo PA, Poplack DG, eds. Principles and practice of
pediatric oncology. 5th ed. Philadelphia, PA: Lippincott
Williams & Wilkins, 2006:887904.
Chapter 7 L I V E R 269
41. Stocker J, Conran R, Selby D. Tumor and pseudotumors of the
liver. In: Stocker J, Askin F, eds. Pathology of solid tumors in
children. London, UK: Chapman & Hakk, 1998:83110.
42. Stocker JT, Husain AN, Dehner LP, et al. The liver, gallbladder,
and biliary tract. In: Stocker JT, Dehner LP, eds. Pediatric
pathology. Philadelphia, PA: Lippincott Williams & Wilkins,
2001:705795.
43. Chen JC, Chen CC, Chen WJ, et al. Hepatocellular carcinoma
in children: clinical review and comparison with adult cases.
J Pediatr Surg 1998;33:13501354.
44. Franco LM, Krishnamurthy V, Bali D, et al. Hepatocellular
carcinoma in glycogen storage disease type Ia: a case series.
J Inherit Metab Dis 2005;28:153162.
45. Ni Y-H, Chang M-H, Hsu H-Y, et al. Hepatocellular carcinoma
in childhood: clinical manifestations and prognosis. Cancer
1991;68:17371741.
46. Wernecke K, Vassallo P, Bick U, et al. The distinction between
benign and malignant liver tumors on sonography: value of a
hypoechoic halo. AJR Am J Roentgenol 1992;159:10051009.
47. Dachman AH, Pakter RL, Ros PR, et al. Hepatoblastoma: radi-
ologic-pathologic correlation in 50 cases. Radiology 1987;164:
1519.
48. Bates SM, Koller MS, Ramos IM, et al. Hepatoblastoma: detec-
tion of tumor vascularity with duplex Doppler US. Radiology
1990;176:505507.
49. Reinhold C, Hammers L, Taylor CR, et al. Characterization of
focal hepatic lesions with duplex sonography: findings in 198
patients. AJR Am J Roentgenol 1995;164:11311135.
50. Van Campenhout I, Patriquin H. Malignant microvasculature
in abdominal tumors in children: detection with Doppler US.
Radiology 1992;183:445448.
51. Nino-Murcia M, Ralls PW, Jeffrey RB Jr, et al. Color flow
Doppler characterization of focal hepatic lesions. AJR Am J
Roentgenol 1992;159:11951197.
52. Numata K, Tanaka K, Mitsui K, et al. Flow characteristics of
hepatic tumors at color Doppler sonography: correlation with
arteriographic findings. AJR Am J Roentgenol 1993;160:515521.
53. Letourneau JG, Steely JW, Crass JR, et al. Upper abdomen: CT
findings following partial hepatectomy. Radiology 1988;166:
139141.
54. Dubois J, Garel L, Russo P, et al. Pediatric case of the day.
Fibrolamellar hepatocellular carcinoma. Radiographics 1993;
13:691692.
55. Ichikawa T, Federle MP, Grazioli L, et al. Fibrolamellar hepa-
tocellular carcinoma: imaging and pathologic findings in 31
recent cases. Radiology 1999;213:352361.
56. McLarney JK, Rucker PT, Bender GN, et al. Fibrolamellar car-
cinoma of the liver: radiologic-pathologic correlation. Radi-
ographics 1999;19:453471.
57. Smith MT, Blatt ER, Jedlicka P, et al. Best cases from the AFIP:
fibrolamellar hepatocellular carcinoma. Radiographics 2008;28:
609613.
58. Wei ZG, Tang LF, Chen ZM, et al. Childhood undifferentiated
embryonal liver sarcoma: clinical features and immunohisto-
chemistry analysis. J Pediatr Surg 2008;43:19121919.
59. Buetow PC, Buck JL, Pantongrag-Brown L, et al. Undifferenti-
ated (embryonal) sarcoma of the liver: pathologic basis of imag-
ing findings in 28 cases. Radiology 1997;203:779783.
60. Crider MH, Hoggard E, Manivel JC. Best cases from the AFIP.
Undifferentiated embryonal sarcoma of the liver. Radiographics
2009;29:16651668.
61. Ros PR, Olmsted WW, Dachman AH, et al. Undifferentiated
(embryonal) sarcoma of the liver: radiologic-pathologic corre-
lation. Radiology 1986;160:141145.
62. Awan S, Davenport M, Portmann B, et al. Angiosarcoma of the
liver in children. J Pediatr Surg 1996;31:17291732.
63. Buetow PC, Buck JL, Ros PR, et al. Malignant vascular tumors
of the liver: radiologic-pathologic correlation. Radiographics
1994;14:153166.
LWBK505-C07_p214-274.qxd 7/7/10 1:29 PM Page 270 Aptara Inc
270 P E D I AT R I C S O N O G R A P H Y
64. Gebel M. Malignant focal liver diseases. In: Gebel M, ed. Ultra-
sound in gastroenterology and heptaology. Blackwell Publish-
ing, 2000:8389.
65. Surendrababu NRS, Rao A, Samuel R. Primary hepatic
leiomyosarcoma in an infant. Pediatr Radiol 2006;36:366.
66. Huang FC, Eng HL, Chen CL, et al. Primary pleomorphic rhab-
domyosarcoma of the liver: a case report. Hepatogastroenterol-
ogy 2003;50:7376.
67. Shah BK, McHugh K. Cystic liver metastases from extracranial
primitive neuroectodermal tumour: a case report. Pediatr
Radiol 2000;30:834836.
68. Pickhardt PJ, Siegel MJ. Abdominal manifestations of post-
transplantation lymphoproliferative disorder. AJR Am J
Roentgenol 1998;171:10071013.
69. Pickhardt PJ, Siegel MJ, Hayashi RJ, et al. State of the art. Post-
transplantation lymphoproliferative disorder in children: clini-
cal, histopathologic and imaging features. Radiology 2000;217:
1625.
70. Castroagudin JF, Molina E, Abdulkader I, et al. Sonographic
features of liver involvement by lymphoma. J Ultrasound Med
2007;26:791796.
71. Soyer P, Beers BV, Teillet-Thiebaud F, et al. Hodgkins and non-
Hodgkins hepatic lymphoma: sonographic findings. Abdom
Imaging 1993;18:339343.
72. Margolin JF, Steuber CP, Poplack DG. Acute lymphoblastic
leukemia. In: Pizzo PA, Poplack DG, eds. Principles and prac-
tice of pediatric oncology. 5th ed. Philadelphia, PA: Lippincott
Williams & Wilkins, 2006:538590.
73. Golub TR, Areci RJ. Acute myelogenous leukemia. In: Pizzo
PA, Poplack DG, eds. Principles and practice of pediatric oncol-
ogy. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins,
2006:591644.
74. Amemiya S, Akahane M, Takita J, et al. Imaging findings of
upper abdominal involvement by acute megakaryoblastic
leukaemia. Pediatr Radiol. 2008;38:457461.
75. Peddu P, Huang D, Kane PA, et al. Vanishing liver tumours.
Clin Radiol 2008;63:329339.
76. Dimashkieh HH, Bove KE. GLUT1 endothelial reactivity dis-
tinguishes hepatic infantile hemangioma from congenital
hepatic vascular malformation with associated capillary prolif-
eration. Hum Pathol 2004;35:200209.
77. Hernandez F, Navarro M, Encinas JL, et al. The role of GLUT1
immunostaining in the diagnosis and classification of liver vas-
cular tumors in children. J Pediatr Surg 2005;40:801804.
78. Kassarjian A, Zurakowski D, Dubois J, et al. Infantile hepatic
hemangiomas: clinical and imaging findings and their correla-
tion with therapy. AJR Am J Roentgenol 2004;182:785795.
79. Prokurat A, Kluge P, Chrupek M, et al. Hemangioma of the
liver in children: proliferating vascular tumor or congenital vas-
cular malformation. Med Pediatr Oncol 2002;39:524529.
80. Sari N, Yalcin B, Akyuz C, et al. Infantile hepatic hemangioen-
dothelioma with elevated serum alpha-fetoprotein. Pediatr
Hematol Oncol 2006;23:639647.
81. Regier TS, Ramji FG. Pediatric hepatic hemangioma. Radi-
ographics 2004;24:17191724.
82. Burrows PE, Dubois J, Kassarjian A. Pediatric hepatic vascular
anomalies. Pediatr Radiol 2001;31:535545.
83. Donaldson JS. Hemangioendothelioma of the liver. In: Siegel
BA, Proto AV, eds. Pediatric disease. Fourth series. Test and syl-
labus. Reston, VA: American College of Radiology, 1993:
436462.
84. Herman TE, Siegel MJ, Herman TE, et al. Special imaging case-
book. Infantile hepatic hemangioendothelioma. J Perinatol 2000;
20:447449.
85. Klein MA, Slovis TL, Chang CH, et al. Sonographic and
Doppler features of infantile hepatic hemangiomas with patho-
logic correlation. J Ultrasound Med 1990;9:619624.
86. Paltiel HJ, Patriquin HB, Keller MS, et al. Infantile hepatic
hemangioma: Doppler US. Radiology 1992;182:735742.
87. Roos JE, Pfiffner R, Stallmach T, et al. Infantile hemangioen-
dothelioma. Radiographics 2002;23:16491655.
88. Daller JA, Bueno J, Gutierrez J, et al. Hepatic hemangioen-
dothelioma: clinical experience and management strategy.
J Pediatr Surg 1999;34:98106.
89. Fellows KE, Hoffer FA, Markowitz RI, et al. Multiple collater-
als to hepatic infantile hemangioendotheliomas and arteriove-
nous malformations: effect on embolization. Radiology 1991;
181:813818.
90. Reiger TS, Ramji RG. Pediatric hepatic hemangioma. Radi-
ographics 2004;24:17191724.
91. Taylor KJW, Ramos I, Morse SS, et al. Focal liver masses:
differential diagnosis with pulsed Doppler US. Radiology 1987;
164:643647.
92. Kim SH, Kim WS, Cheon JE, et al. Radiological spectrum of
hepatic mesenchymal hamartoma in children. Korean J Radiol
2007;8:498505.
93. Vazquez-Lima I, Vazquez MG, Fernandez R, et al. Torsed
pedunculated hepatic hemartoma. Pediatr Radiol 2009;39:
6265.
94. Gow KW, Lee L, Pruthi S, et al. Mesenchymal hamartoma of
the liver. J Pediatr Surg 2009;44:468470.
95. Mulrooney DA, Carpenter B, Georgieff M, et al. Hepatic mes-
enchymal hamartoma in a neonate: a case report and review of
the literature. J Pediatr Hematol Oncol 2001;23:316317.
96. George JC, Cohen MD, Tarver RD, et al. Ruptured cystic mes-
enchymal hamartoma: an unusual cause of neonatal ascites.
Pediatr Radiol 1994;24:304305.
97. Buetow PC, Pantongrag-Brown L, Buck JL, et al. Focal nodular
hyperplasia of the liver: radiologic-pathologic correlation.
Radiographics 1996;16:369388.
98. Kondo F. Focal nodular hyperplasia of the liver: controversy
over etiology. J Gastroenterol Hepatol 2000;15:12291231.
99. Buscarini E, Danesino C, Plauchu H, et al. High prevalence of
hepatic focal nodular hyperplasia in subjects with hereditary
hemorrhagic telangiectasia. Ultrasound Med Biol 2004;30:
10891097.
100. Marabelle A, Campagne D, Dechelotte P, et al. Focal nodular
hyperplasia of the liver in patients previously treated for pedi-
atric neoplastic diseases. J Pediatr Hematol Oncol 2008;30:
546549.
101. Sorge I, Bierbach U, Finke R, et al. Multiple malignant and
benign lesions in the liver in a child with adrenocortical carci-
noma. Pediatr Radiol 2008;38:588559.
102. Cheon J-E, Kim WS, Kim I-O, et al. Radiologic features of focal
nodular hyperplasia of the liver in children. Pediatr Radiol
1998;28:878883.
103. Golli M, Mathieu M, Anglade M-C, et al. Focal nodular hyper-
plasia of the liver: value of color Doppler US in association with
MR imaging. Radiology 1989;187:113117.
104. Kim MJ, Lim HK, Kim SH, et al. Evaluation of hepatic focal
nodular hyperplasia with contrast-enhanced gray scale harmonic
sonography: initial experience. J Ultrasound Med 2004;23:
297305.
105. Yen YH, Wang JH, Lu SN, et al. Contrast-enhanced ultrasono-
graphic spoke-wheel sign in hepatic focal nodular hyperplasia.
Eur J Radiol 2006;60:439444.
106. Di Rocco M, Calevo MG, Taro M, et al. Hepatocellular ade-
noma and metabolic balance in patients with type Ia glycogen
storage disease. Mol Genet Metab 2008;93:398402.
107. Golli M, Tran Van Nhie J, Mathie D, et al. Hepatocellular ade-
noma: color Doppler US and pathologic correlations. Radiol-
ogy 1994;190:741774.
108. Dietrich CF, Schuessler G, Trojan J, et al. Differentiation of
focal nodular hyperplasia and hepatocellular adenoma by con-
trast-enhanced ultrasound. Br J Radiol 2005;78:704707.
109. Trenschel GM, Schubert A, Dries V, et al. Nodular regenerative
hyperplasia of the liver: case report of a 13-year-old girl and
review of the literature. Pediatr Radiol 2000;30:6468.
LWBK505-C07_p214-274.qxd 7/7/10 1:29 PM Page 271 Aptara Inc
110. Chu WC, Roebuck DJ. Nodular regenerative hyperplasia of the
liver simulating metastases following treatment for bilateral
Wilms tumor. Med Pediatr Oncol 2003;41:8587.
111. Robinson JD, Grand EG, Haller JO, et al. Hepatic angiomy-
olipomas in tuberous sclerosis. Report of two cases. J Ultra-
sound Med 1989;8:575578.
112. Fobbe F, Hamm B, Schwarting R. Angiomyolipoma of the liver:
CT, MR, and ultrasound imaging. J Comput Assist Tomogr
1988;12:658659.
113. Quillin SP, McAlister WM. Congenital solitary nonparasitic cyst
of the liver in a newborn. Pediatr Radiol 1992;22:543544.
114. Rogers TN, Woodley H, Ramsden W, et al. Solitary liver cysts in
children: not always so simple. J Pediatr Surg 2007;42: 333339.
115. Everson GT, Taylor MR, Doctor RB. Polycystic disease of the
liver. Hepatology 2004;40:774782.
116. Avni EF, Rypens F, Donner C, et al. Hepatic cysts and hypere-
chogenicities: perinatal assessment and unifying theory on their
origin. Pediatr Radiol 1994;24:569572.
117. Herman TE, Siegel MJ. Central dot sign on CT of liver cysts. J
Comput Assist Tomogr 1990;14:10191021.
118. Komori K, Hoshino K, Shirai J, et al. Mesothelial cyst of the
liver in a neonate. Pediatr Surg Int 2008;24:463465.
119. Haber B. Viral hepatitis. In: Pediatric gastroenterology. The
requisites in pediatrics. Philadelphia, PA: Mosby Elsevier,
2008:289304.
120. Jonas MM, Perez-Atayde AR. Liver disease in infancy and
childhood. In: Schiffs diseases of the liver. 10th ed. Philadel-
phia, PA: Lippincott Williams & Wilkins, 2007:13051347.
121. Schiff ER. Viral hepatitis. In: Schiffs diseases of the liver. 10th ed.
Philadelphia, PA: Lippincott Williams & Wilkins, 2007:707728.
122. De Groote J, Desmet VJ, Gedigk P, et al. A classification of
chronic hepatitis. Lancet 1994;2:626628.
123. Sharma MP, Dasarathy S. Gallbladder abnormalities in acute
viral hepatitis: a prospective ultrasound evaluation. J Clin Gas-
troenterol 1991;13:697700.
124. Toppet V, Souayah H, Delplace O, et al. Lymph node enlarge-
ment as a sign of acute hepatitis A in children. Pediatr Radiol
1990;20:249252.
125. Abu-Judeh HH. The starry sky liver with right-sided heart
failure. AJR Am J Roentgenol 2002;178:78.
126. Cazier PR, Sponaugle DW. Starry sky liver with fasting: varia-
tions in glycogen stores. J Ultrasound Med 1996;15:405407.
127. Chusid MJ. Pyogenic hepatic abscess in infancy and childhood.
Pediatrics 1978;62:554559.
128. Bari S, Sheikh KA, Malik AA, et al. Percutaneous aspiration
versus open drainage of liver abscess in children. Pediatr Surg
Int 2007;23:6974.
129. Lee SH, Tomlinson C, Temple M, et al. Imaging-guided percu-
taneous needle aspiration or catheter drainage of neonatal liver
abscesses: 14-year experience. AJR Am J Roentgenol 2008;190:
616622.
130. Pastakia B, Shawker TH, Thaler M, et al. Hepatosplenic can-
didiasis: wheels within wheels. Radiology 1988;166:417421.
131. Rappaport DC, Cumming WA, Ros PR. Disseminated hepatic
and splenic lesions in cat-scratch disease: imaging features. AJR
Am J Roentgenol 1991;156:12271228.
132. Pedrosa I, Saiz A, Arrazola J, et al. Hydatid disease: radiologic
and pathologic features and complications. Radiographics
2000;20:795817.
133. Yuksel M, Demirpolat G, Sever A, et al. Hydatid disease involv-
ing some rare locations in the body: a pictorial essay. Korean J
Radiol 2007;8:531540.
134. Czermak BV, Unsinn KM, Gotwald T, et al. Echinococcus multi-
locularis revisited. AJR Am J Roentgenol 2001;176:1207 1212.
135. Czermak BV, Akhan O, Hiemetzberger R, et al. Echinococcosis
of the liver. Abdom Imaging 2008;33:133143.
136. Esfahani F, Rooholamini SA, Vessal K. Ultrasonography of
hepatic hydatid cysts: new diagnostic signs. J Ultrasound Med
1988;7:443450.
Chapter 7 L I V E R 271
137. Goktay AY, Secil M, Gulcu A, et al. Percutaneous treatment of
hydatid liver cysts in children as a primary treatment: long-term
results. J Vasc Interv Radiol 2005;16:831839.
138. Khuroo MS, Zargar SA, Mahajan R. Echinococcus granulosus
cysts in the liver: management with percutaneous drainage.
Radiology 1991;180:141145.
139. Berry M, Bazaz R, Bhargava S. Amebic liver abscess: sono-
graphic diagnosis and management. J Clin Ultrasound 1986;14:
239242.
140. Oleszcuk-Raszke K, Cremin BJ, Fisher RM, et al. Ultrasonic
features of pyogenic and amoebic hepatic abscesses. Pediatr
Radiol 1989;19:230233.
141. Blessmann J, Khoa ND, Van An L, et al. Ultrasound patterns
and frequency of focal liver lesions after successful treatment of
amoebic liver abscess. Trop Med Int Health 2006;11:504508.
142. Bari S, Sheikh KA, Ashraf M, et al. Ascaris liver abscess in chil-
dren. J Gastroenterol 2007;42:236240.
143. Garel LA, Pariente DM, Nezelof C, et al. Liver involvement in
chronic granulomatous disease: the role of ultrasound in diag-
nosis and treatment. Radiology 1984;153:117121.
144. Hopkins KL, Simoneaus SF, Patrick LE, et al. Imaging manifes-
tations of cat-scratch disease. AJR Am J Roentgenol 1996;166:
435438.
145. Grumbach K, Coleman BG, Gal AA, et al. Hepatic and biliary tract
abnormalities in patients with AIDS. Sonographic-pathologic cor-
relation. J Ultrasound Med 1989;8:247254.
146. Cappell MS. Hepatobiliary manifestations of the acquired
immune deficiency syndrome. Am J Gastroenterol 1991;86:
15.
147. Towers MJ, Withers CE, Hamilton PA, et al. Visceral calcifica-
tion in patients with AIDS may not always be due to Pneumo-
cystis carinii. AJR Am J Roentgenol 1991;156:745747.
148. Rushin JA, Sivit CJ, Rakusan TA, et al. AIDS-related cholangi-
tis in children: sonographic findings. AJR Am J Roentgenol
1992;159:626627.
149. Gholson CF, Bacon BR. Metabolic and systemic diseases. In:
Gitnick G, LaBrecque DR, Moody FG, eds. Diseases of the
liver and biliary tract. Mosby-Year Book, Inc., 1992:489 523.
150. Valls C, Iannacconne R, Alba E, et al. Fat in the liver: diagno-
sis and characterization. Eur Radiol 2006;16:22922308.
151. Haber HP. Cystic fibrosis in children and young adults: findings
on routine abdominal sonography. AJR Am J Roentgenol 2007;
189:8999.
152. Quillin SP, Siegel MJ, Rothbaum R. Hepatobiliary sonography
in cystic fibrosis. Pediatr Radiol 1993;23:533535.
153. Joseph AEA, Saverymuttu SH, Al-Sam S, et al. Comparison of
liver histology with ultrasonography in assessing diffuse
parenchymal liver disease. Clin Radiol 1991;43:2631.
154. Palmentieri B, de Sio I, La Mura V, et al. The role of bright liver
echo pattern on ultrasound B-mode examination in the diagno-
sis of liver steatosis. Dig Liver Dis 2006;38:485489.
155. Liu L-P, Dong B-W, Yu X-L, et al. Analysis of focal spared areas
in fatty liver using color Doppler imaging and contrast-
enhanced microvessel display sonography. J Ultrasound Med
2008;27:387394.
156. Loomie KM, Ryan MJ. Congenital hepatic fibrosis. In: Pedi-
atric gastroenterology. The requisites in pediatrics. Philadel-
phia, PA: Mosby Elsevier, 2008:153160.
157. Akhan O, Karaosmanoglu AD, Ergen B. Imaging findings in
congenital hepatic fibrosis Eur J Radiol 2007;61:1824.
158. Gerety BM. Hemochromatosis. In: Freeny PC, Stevenson GW,
eds. Alimentary tract radiology. St. Louis, MO: CV Mosby,
1994:15601665.
159. Shepherd R. Complications and management of chronic liver
disease. In: Kelly DA, ed. Diseases of the liver and biliary sys-
tem. 2nd ed. Oxford, UK: Blackwell Publishing, 2004: 259281.
160. Giorgio A, Amoroso P, Lettieri G, et al. Cirrhosis: value of cau-
date to right lobe ratio in diagnosis with US. Radiology 1986:
161:443445.
LWBK505-C07_p214-274.qxd 7/7/10 1:29 PM Page 272 Aptara Inc
272 P E D I AT R I C S O N O G R A P H Y
161. Goyal AK, Pokharana DS, Sharma SK. Ultrasonic diagnosis in
cirrhosis: reference to quantitative measurements of hepatic
dimensions. Gastrointest Radiol 1990;15:3234.
162. Hess CF, Schmiedl U, Koelbel G, et al. Diagnosis of liver cir-
rhosis with US: receiver-operating characteristic analysis of
multidimensional caudate lobe indexes. Radiology 1989;171:
349351.
163. Ferrell H, Male R, Cardiel M, et al. Cirrhosis: diagnosis by liver
surface analysis with high frequency ultrasound. Gastrointest
Radiol 1992;17:7478.
164. de Ledinghen V, Le Bail B, Rebouissoux L, et al. Liver stiffness
measurement in children using FibroScan: feasibility study and
comparison with Fibrotest, aspartate transaminase to platelets
ratio index, and liver biopsy. J Pediatr Gastroenterol Nutr
2007;45:443450.
165. Lamireau T, Franchi S, Fabre M, et al. A dedicated Fibroscan
probe to evaluate liver fibrosis in children: feasibility and per-
formance for the diagnosis of cirrhosis. Hepatology 2007;46:
277A.
166. Chakpapani A, Green A. Metabolic liver disease in the infant
and older child. In: Kelly DA, ed. Diseases of the liver and bil-
iary system. 2nd ed. Oxford, UK: Blackwell Publishing,
2004:211242.
167. Colombo C, Russo MC, Zazzeron L, et al. Liver disease in cys-
tic fibrosis. J Pediatr Gastroenterol Nutr 2006;43(suppl 1):
S49S55.
168. Lindblad A, Glaumann H, Strandvik B. Natural history of liver
disease in cystic fibrosis. Hepatology 1999;30(5):11511158.
169. Patriquin H, Lenaerts C, Smith L, et al. Liver disease in children
with cystic fibrosis: US-biochemical comparison in 195
patients. Radiology 1999;211:229232.
170. Lenaerts C, Lapierre C, Patriquin H, et al. Surveillance for cys-
tic fibrosis-associated hepatobiliary disease: early ultrasound
changes and predisposing factors. J Pediatr 2003;143:343350.
171. Lee P, Mather S, Owens C, et al. Hepatic ultrasound findings in
the glycogen storage diseases. Br J Radiol 1994;67:10621066.
172. Gallant JM, Barnewolt CE, Buonomo C. Pediatric case of the
day. Hepatorenal tyrosinemia. Radiographics 1996;16:
12211224.
173. Hupertz V, Winans C. Portal hypertension. In: Wyllie R, Hyams
JS, eds. Pediatric gastrointestinal and liver disease. 3rd ed.
Netherlands: Saunders Elsevier, 2006:951965.
174. Mori H, Hayashi K, Fukuda T, et al. Intrahepatic portosystemic
venous shunt: occurrence in patients with and without liver cir-
rhosis. AJR Am J Roentgenol 1987;149:711714.
175. Rabinowitz SS, Norton KI, Benkov KJ, et al. Sonographic eval-
uation of portal hypertension in children. J Pediatr Gastroen-
terol Nutr 1990;10:395401.
176. Tuney D, Aribal ME, Ertem D, et al. Diagnosis of liver cirrho-
sis in children based on colour Doppler ultrasonography with
histopathologic correlation. Pediatr Radiol 1998;28:859864.
177. Westra SJ, Zaninovic AC, Vargas J, et al. The value of portal
vein pulsatility on duplex sonograms as a sign of portal hyper-
tension in children with liver disease. AJR Am J Roentgenol
1995;165:167172.
178. Sellier N, Adamsbaum C, Checoury A, et al. Sonographic
hepatic arterialisation in newborns receiving parenteral nutri-
tion. Pediatr Radiol 1988;18:471473.
179. Bolondi L, Li Bassi S, Gaiani S, et al. Liver cirrhosis: changes in
Doppler wave form of hepatic veins. Radiology 1991;178:
513516.
180. Colli A, Cocciolo M, Riva C, et al. Abnormalities of Doppler
waveform of the hepatic veins in patients with chronic liver dis-
ease: correlation with histologic findings. AJR Am J Roentgenol
1994;162:833837.
181. Wachsberg RH, Simmons MZ. Coronary vein diameter and
flow direction in patients with portal hypertension: evaluation
with duplex sonography and correlation with variceal bleeding.
AJR Am J Roentgenol 1994;162:637641.
182. Grant EG, Tessler FN, Gomes AS, et al. Color Doppler imaging of
portosystemic shunts. AJR Am J Roentgenol 1990;154: 393397.
183. Patriquin H, Tessier G, Grignon A, et al. Lesser omental thick-
ness in normal children: baseline for detection of portal hyper-
tension. AJR Am J Roentgenol 1985;145:693696.
184. Lafortune M, Patriquin H, Pomier G, et al. Hemodynamic
changes in portal circulation after portosystemic shunts: use of
duplex sonography in 43 patients. AJR Am J Roentgenol 1987;
149:701706.
185. Kanterman RY, Darcy MD, Middleton WD, et al. Doppler
sonography findings associated with transjugular intrahepatic
portosystemic shunt malfunction. AJR Am J Roentgenol 1997;
168:467472.
186. Surratt RS, Middleton WD, Darcy MD, et al. Morphologic and
hemodynamic findings at sonography before and after creation
of a transjugular intrahepatic portosystemic shunt. AJR Am J
Roentgenol 1993;160:627630.
187. Foshager MC, Ferral H, Finlay DE, et al. Color Doppler sonog-
raphy of transjugular intrahepatic portosystemic shunts (TIPS).
AJR Am J Roentgenol 1994;163:105111.
188. Schwartz DS, Gettner PA, Konstantino MM, et al. Umbilical
venous catheterization and the risk of portal vein thrombosis.
J Pediatr 1997;131:760762.
189. Brisse H, Orbach D, Lassau N, et al. Portal vein thrombosis dur-
ing antineoplastic chemotherapy in children: report of five cases
and review of the literature. Eur J Cancer 2004;40:26592666.
190. Kim JH, Lee YS, Kim SH, et al. Does umbilical vein catheteri-
zation lead to portal venous thrombosis? Prospective US evalu-
ation in 100 neonates. Radiology 2001;219:645650.
191. Pinto RB, Silveira TR, Bandinelli E, et al. Portal vein thrombo-
sis in children and adolescents: the low prevalence of hereditary
thrombophilic disorders. J Pediatr Surg 2004;39:13561361.
192. Parvey HR, Raval B, Sandler CM. Portal vein thrombosis:
imaging findings. AJR Am J Roentgenol 1994;162:7781.
193. Platt JE, Rubin JM, Ellis JH. Hepatic artery resistance changes
in portal vein thrombosis. Radiology 1995;196:9598.
194. Tessler RN, Gehring BJ, Gomes AS, et al. Diagnosis of portal
vein thrombosis: value of color Doppler imaging. AJR Am J
Roentgenol 1991;157:193196.
195. De Gaetano AM, Lafortune M, Patriquin H, et al. Cavernous
transformation of the portal vein: patterns of intrahepatic and
splanchnic collateral circulation detected with Doppler sonog-
raphy. AJR Am J Roentgenol 1995;165:11511155.
196. Frider B, Marn AM, Goldberg A. Ultrasonographic diagnosis
of portal vein cavernous transformation in children. J Ultra-
sound Med 1989;8:445449.
197. Chawla Y, Dilawari JB, Katariya S. Gallbladder varices in por-
tal vein thrombosis. AJR Am J Roentgenol 1994;162:643645.
198. West MS, Garra BS, Horii SC, et al. Gallbladder varices: imag-
ing findings in patients with portal hypertension. Radiology
1991;179:179182.
199. Barakat M. Unusual hepatic-portal-systemic shunting demon-
strated by Doppler sonography in children with congenital hepatic
vein ostial occlusion. J Clin Ultrasound 2004;32:172178.
200. Cario H, Pahl HL, Schwarz K, et al. Familial polycythemia vera
with Budd-Chiari syndrome in childhood. Br J Haematol
2003;123:346352.
201. Haliloglu M, Hoffer FA, Haight AE, et al. Budd-Chiari syn-
drome caused by Gauchers disease. Pediatr Radiol 1999;29:
908910.
202. Bolondi L, Gaiani S, Li Bassi S, et al. Diagnosis of Budd-Chiari
syndrome by pulsed Doppler ultrasound. Gastroenterology
1991;100:13241331.
203. Chawla Y, Kumar S, Dhiman RK, et al. Duplex Doppler sonog-
raphy in patients with Budd-Chiari syndrome. Gastroenterol
Hepatol 1999;9:904907.
204. Ralls PW, Johnson MB, Radin DR, et al. Budd-Chiari syn-
drome: detection with color Doppler sonography. AJR Am J
Roentgenol 1992;159:113116.
LWBK505-C07_p214-274.qxd 7/7/10 1:29 PM Page 273 Aptara Inc
205. Gentil-Kocher S, Bernard O, Brunelle F, et al. Budd-Chiari syn-
drome in children: report of 22 cases. J Pediatr 1988;113:
3033.
206. Lee DH, Ko YT, Yoon Y, et al. Sonography and color Doppler
imaging of Budd-Chiari syndrome of membranous obstruction
of the inferior vena cava. J Ultrasound Med 1994;13:159163.
207. Millener P, Grant EG, Rose S, et al. Color Doppler imaging
findings in patients with Budd-Chiari syndrome: correlation
with venographic findings. AJR Am J Roentgenol 1993;161:
307312.
208. Campbell MS, Rosen MA, Faust TW. Vascular diseases of the
liver. In: Schiff ER, Sorrell MF, Maddrey WC, eds. Schiffs dis-
eases of the liver. 10th ed. Philadelphia, PA: Lippincott Williams
& Wilkins, 2007:11711184.
209. Benya EC, Sivit CH, Quinones RR. Abdominal complications
after bone marrow transplantation in children: sonographic
and CT findings. AJR Am J Roentgenol 1993;161:10231027.
210. Day DL, Carpenter BLM. Abdominal complications in pedi-
atric bone marrow transplantation recipients. Radiographics
1993;13:11011112.
211. Herbetko J, Grigg AP, Buckley AR, et al. Venoocclusive liver
disease after bone marrow transplantation: findings at duplex
sonography. AJR Am J Roentgenol 1992;158:10011005.
212. Ghersin E, Brook OR, Gaitini D, et al. Color Doppler demon-
stration of segmental portal flow reversal: an early sign of
hepatic veno-occlusive disease in an infant. J Ultrasound Med
2003;22:11031106.
213. Aarts R, Ijland MM, de Blaauw I, et al. Severe gastrointestinal
tract bleeding in a two-month-old infant due to congenital
intrahepatic arterioportal fistula. Eur J Radiol 2006;59:2528.
214. Bodner G, Peer S, Karner M, et al. Nontumorous vascular mal-
formations in the liver: color Doppler ultrasonographic find-
ings. J Ultrasound Med 2002;21:187197.
215. da Costa e Silva EJ, de Albuquerque SC. Congenital hepatic
shunt. Pediatr Radiol 2009;39:1125.
216. Marchand V, Uflacker R, Baker SS, et al. Congenital hepatic
arterioportal fistula in a 3-year-old child. J Pediatr Gastroen-
terol Nutr 1999;28:435441.
217. Part JH, Cha SH, Han JK, et al. Intrahepatic portosystemic
venous shunt. AJR Am J Roentgenol 1990;155:527528.
218. Ralls PW, Johnson MB, Radin R, et al. Hereditary hemorrhagic
telangiectasia: findings in the liver with color Doppler sonogra-
phy. AJR Am J Roentgenol 1992;159:5961.
219. Saxena AK, Sodhi KS, Arora J, et al. Congenital intrahepatic
portosystemic venous shunt in an infant with Down syndrome.
AJR Am J Roentgenol 2004;183:17831784.
220. Lev-Toaff AS, Friedman AC, Cohen LM, et al. Hepatic infarcts:
new observations by CT and sonography. AJR Am J Roentgenol
1987;149:8790.
221. Iannaccone R, Federle MP, Brancatelli G, et al. Peliosis hepatis:
spectrum of imaging finding. AJR Am J Roentgenol 2006;187:
W43W52.
222. Jacquemin E, Pariente D, Fabre M, et al. Peliosis hepatis with
initial presentation as acute hepatic failure and intraperitoneal
hemorrhage in children. J Hepatol 1999;30:11461150.
223. Samyn M, Hadzic N, Davenport M, et al. Peliosis hepatis in
childhood: case report and review of the literature. J Pediatr
Gastroenterol Nutr 2004;39:431434.
224. Kleinig P, Davies RP, Maddern G, et al. Peliosis hepatis: central
fast surge ultrasound enhancement and multislice CT
appearances. Clin Radiol 2003;58:995998.
225. Steinke K, Terraciano L, Wiesner W. Unusual cross-sectional imag-
ing findings in hepatic peliosis. Eur Radiol 2003;13:19161919.
226. Gore RM, Mathieu DG, White M, et al. Passive hepatic conges-
tion: cross-sectional imaging features. AJR Am J Roentgenol
1994;162:7175.
227. LaFortune MD, Trinh BC, Burns PN, et al. Air in the portal
vein: sonographic and Doppler manifestations. Radiology
1991;180:667670.
Chapter 7 L I V E R 273
228. Tefft M, Mitus A, Das L, et al. Irradiation of the liver in children:
review of experience in the acute and chronic phases, and in the
intact normal and partially resected. AJR Am J Roentgenol
1970;108:365385.
229. Garra BS, Shawker TH, Chang R, et al. The ultrasound appear-
ance of radiationinduced hepatic injury. J Ultrasound Med
1988;7:605609.
230. Cooper A, Barlow B, DiScala C, et al. Mortality and truncal
injury: the pediatric perspective. J Pediatr Surg 1994;29:3338.
231. Taylor GA. Imaging of pediatric blunt abdominal trauma: what
have we learned in the past decade? Radiology 1995;195:
600601.
232. Stalker HP, Kaufman RA, Towbin R. Patterns of liver injury in
childhood: CT analysis. AJR Am J Roentgenol 1986;147:
11991205.
233. Lam CY, Chan KF, Fan TW, et al. Intrahepatic hematoma:
hepatic lesion in a newborn with high alpha-fetoprotein level.
Pediatr Radiol 2005;35:11391141.
234. Siegel MJ. The child with abdominal trauma. In: Hilton SVW,
Edwards DK, eds. Practical pediatric radiology. 3rd ed.
Philadelphia, PA: W.B. Saunders Co.,
235. Siegel MJ. Thoracoabdominal trauma. In: Siegel MJ, ed. Pedi-
atric body CT. Philadelphia, PA: Lippincott Williams &
Wilkins, 2008:429457.
236. Benya EC, Lim-Dunham JE, Landrum O, et al. Abdominal
sonography in examination of children with blunt abdominal
trauma. AJR Am J Roentgenol 2000;174:16131616.
237. Kennedy C, Kempf J. FAST exams in pediatric abdominal
trauma. Acad Emerg Med 2002;9:519.
238. Mizzi A, Shabani A, Watt A. The role of follow-up imaging in
paediatric blunt abdominal trauma. Clin Radiol 2002;57:
908912.
239. Valentino M, Serra C, Pavlica P, et al. Blunt abdominal trauma:
diagnostic performance of contrast-enhanced US in children
initial experience. Radiology 2008;246:903909.
240. Abramson SJ, Berdon WE, Kaufman RA, et al. Hepatic
parenchymal and subcapsular gas after hepatic laceration caused
by blunt abdominal trauma. AJR Am J Roentgenol 1989;153:
10311032.
241. Share JC, Pursely D, Teele RL. Unsuspected hepatic injury in
the neonate-diagnosis by ultrasonography. Pediatr Radiol
1990;20:320322.
242. Mouratidis B, Antonio G. Sonographic diagnosis of subcapsu-
lar liver hematoma mimicking tumor in a neonate. J Clin Ultra-
sound 2000;28:5357.
243. Coley BD, Sequin J, Cordero L, et al. Neonatal total parenteral
nutrition ascites from liver erosion by umbilical vein catheters.
Pediatr Radiol 1998;28:923927.
244. Lim-durham JE, Bade A, Capitano HN, et al. Characteristic
sonographic findings of hepatic erosion by umbilical vein
catheters. J Ultrasound Med 2007;26:661666.
245. Gross M, Lynch F, Canty T, et al. Management of pediatric liver
injuries: a 13-year experience at a pediatric trauma center.
J Pediatr Surg 1999;34:811817.
246. MacGillivray DC, Valentine RJ. Nonoperative management of
blunt pediatric liver injurylate complications: case report.
J Trauma 1989;29:251254.
247. Sidhu MK, Shaw DWW, Daly CP, et al. Post-traumatic
hepatic pseudoaneurysms in children. Pediatr Radiol 1999;29:
4652.
248. Berrocal T, Parron M, Alvarez-Luque A, et al. Pediatric liver
transplantation: a pictorial essay of early and late complica-
tions. Radiographics 2006;26:11871209.
249. Tanaka K, Uemoto S, Tokunaga Y, et al. Living related liver
transplantation in children. Am J Surg 1994;168:4148.
250. Unsinn KM, Freund MC, Ellemunter H, et al. Spectrum of
imaging findings after pediatric liver transplantation: part I,
posttransplantation anatomy. AJR Am J Roentgenol 2003;181:
11331138.
LWBK505-C07_p214-274.qxd 7/7/10 1:29 PM Page 274 Aptara Inc
274 P E D I AT R I C S O N O G R A P H Y
251. Westra SJ, Zaninovic AC, Hall TR, et al. Imaging in pediatric
liver transplantation. Radiographics 1993;13:10811099.
252. Unsinn KM, Freund MC, Ellemunter H, et al. Spectrum of imag-
ing findings after pediatric liver transplantation: part 2, post-
transplantation complications. AJR Am J Roentgenol 2003;181:
11391144.
253. Broniszczak D, Szymczak M, Kaminski A, et al. Vascular com-
plications after pediatric liver transplantation from the living
donors. Transplant Proc 2006;38:14561458.
254. Dodd GD, Memel DS, Zajko AB, et al. Hepatic artery stenosis
and thrombosis in transplant recipients: Doppler diagnosis with
resistive index and systolic acceleration time. Radiology
1994;192:657661.
255. Glockner JF, Forauer AR. Vascular or ischemic complications
after liver transplantation. AJR Am J Roentgenol 1999;173:
10551059.
256. Meyer JI, Khalil R, Remer EM. Periportal low attenuation due
to hepatic necrosis in a patient after liver transplant. AJR Am J
Roentgenol 1996;167:9899.
257. Andronikou S, Millar AJ, Kader E, et al. Anatomical consider-
ations in the imaging of reduced-size liver transplantation in
children. Pediatr Radiol 2002;32:793797.
258. Ben-Ami TE, Martich V, Yousefzadeh DK, et al. Anatomic fea-
tures of reduced-size liver transplant: postsurgical imaging
characteristics. Radiology 1993;187:165170.
259. Kamel IR, Kruskal JB, Raptopoulos V. Imaging for right lobe
living donor liver transplantation. Semin Liver Dis 2001;21:
271282.
260. Dravid VS, Shapiro MJ, Needleman L, et al. Arterial abnor-
malities following orthotopic liver transplantation: arterio-
graphic findings and correlation with Doppler sonographic
findings. AJR Am J Roentgenol 1994;163:585589.
261. Hall TR, McDiarmid SV, Grant EG, et al. False-negative duplex
Doppler studies in children with hepatic artery thrombosis after
liver transplantation. AJR Am J Roentgenol 1990;154: 573575.
262. Rollins NK, Timmons C, Superina RA, et al. Hepatic artery
thrombosis in children with liver transplants: false-positive
findings at Doppler sonography and arteriography in four
patients. AJR Am J Roentgenol 1993;160:291294.
263. Lee J, Ben-Ami T, Yousefzadeh D, et al. Extrahepatic portal
vein stenosis in recipients of living-donor allografts: Doppler
sonography. AJR Am J Roentgenol 1996;167:8590.
264. Suzuki L, de Oliveira IR, Widman A, et al. Real-time and
Doppler US after pediatric segmental liver transplantation. Por-
tal vein stenosis. Pediatr Radiol 2008;38:403408.
265. Chong WK, Beland JC, Weeks SM. Sonographic evaluation of
venous obstruction in liver transplants. AJR Am J Roentgenol
2007;188:W515W521.
266. Ko E, Kim TK, Kim PN, et al. Hepatic vein stenosis after living
donor liver transplantation: evaluation with Doppler US. Radi-
ology 2003;229:806810.
267. Suzuki L, de Oliveira IR, Widman A, et al. Real-time and
Doppler US after pediatric segmental liver transplantation: II.
Hepatic vein stenosis. Pediatr Radiol 2008;38:409414.
268. Nghuen HV, Tran K, Winter TC, et al. Imaging of complications
in liver transplantation. Radiographics 1996;16:825840.
269. Jequier S, Jequier JC, Hanquinet S, et al. Orthotopic liver trans-
plants in children: change in hepatic venous Doppler wave pat-
tern as an indicator of acute rejection. Radiology 2003;226:
105112.
270. Longley DG, Skolnick ML, Sheahan DG. Acute allograft
rejection in liver transplant recipients: lack of correlation with
loss of hepatic artery diastolic flow. Radiology 1988;169:
417420.
271. Marder DM, DeMarino GB, Sumkin JH, et al. Liver transplant
rejection: value of the resistive index in Doppler US of hepatic
arteries. Radiology 1989;173:127129.
272. Pariente D, Bihet MH, Tammam S, et al. Biliary complications
after transplantation in children: role of imaging modalities.
Pediatr Radiol 1991;21:175178.
273. Peclet MH, Ryckman FC, Pedersen SH, et al. The spectrum of
bile duct complications in pediatric liver transplantation.
J Pediatr Surg 1994;29:214220.
274. Chezmar JL, Nelson RC, Bernardino ME. Portal venous gas
after hepatic transplantation: sonographic detection and clini-
cal significance. AJR Am J Roentgenol 1989;153:12031205.
275. Bowen A, Keslar PJ, Newman B, et al. Adrenal hemorrhage
after liver transplantation. Radiology 1990;176:8588.
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Gallbladder and Biliary Tract
Gallbladder Gallbladder Torsion
Normal Anatomy Hyperplastic Cholecystoses
Scanning Technique Other Polypoid Masses
Normal Sonographic Anatomy Miscellaneous Diseases
Normal Variants and Congenital Anomalies
Bile Ducts
Sonographic Signs of Gallbladder Disease
Scanning Techniques
Cholelithiasis
Normal Anatomy
Fetal Gallstones
Cholestatic Diseases: Overview
Sludge
Biliary Atresia and Neonatal Hepatitis
Cholecystitis
Intrahepatic Cholestatic Syndromes
Hydrops
Choledochal Cyst
onography is the imaging study of choice for the eval-
S uation of suspected diseases of the gallbladder and bil-
iary tract. This chapter reviews the normal anatomy of
the gallbladder and biliary tract, the clinical and sono-
graphic features of the common and uncommon disorders
affecting these structures, and pitfalls in diagnoses.
GALLBLADDER
Normal Anatomy
The gallbladder is a pear-shaped structure lying at the infe-
rior margin of the liver in the interlobar fissure between the
right and left hepatic lobes. The middle hepatic vein
courses in the same anatomic plane and can help to iden-
tify the gallbladder fossa. The segments of the gallbladder
include the fundus, body, and neck (Fig. 8.1). The fundus
is the bulbous distal end of the gallbladder. It is positioned
anterior, lateral, and caudad with respect to the body and
neck and often projects beyond the caudal margin of the
liver parenchyma. The body and neck have a posterome-
dial orientation and are directed toward the porta hepatis
and to the left of the fundus. The neck of the gallbladder
is the narrow proximal end that is continuous with the cys-
tic duct. The cystic duct joins with the common hepatic
duct to form the common bile duct.
Scanning Technique
The gallbladder usually is examined with a 5.0- or 7.5-MHz
transducer, but in large or obese patients a 3.5-MHz probe
may be needed. In cooperative patients, the gallbladder
should be examined during suspended respiration. The
examination is obtained with the patient supine in the left
lateral decubitus and left posterior oblique positions. Occa-
sionally, an erect position or even prone position can help to
confirm the presence or absence of calculi. Transverse and
CHAPTER
MARILYN J. SIEGEL
8
Caroli Disease
Spontaneous Perforation of the
Extrahepatic Bile Ducts
Inspissated Bile Syndrome
Inflammatory Diseases of the
Bile Ducts
Biliary Tract Obstruction
Choledocholithiasis
Cystic Duct Stones
Biliary Duct Neoplasms
Biliary Duct Strictures
long-axis scans are acquired through the neck, body, and
fundus of the gallbladder.
Consumption of food, particularly fatty food, stimu-
lates contraction of the gallbladder. This results in an arti-
factually thick-walled gallbladder, which can impair visu-
alization of luminal abnormalities. Therefore, examination
of the gallbladder should be performed after the patient
has fasted for 4 to 6 hours.
Normal Sonographic Anatomy
On transverse scans, the gallbladder appears as a round or
oval structure posterior to or partly within the interlobar
fissure. On longitudinal scans, it has an oval or pear shape
(Fig. 8.2). The hyperechoic interlobar fissure courses
between the gallbladder caudally and the right portal vein
cranially. The wall of the gallbladder is thin, hyperechoic,
and smooth. The upper limit of wall thickness in the fast-
ing state is 3 mm (1).
The cystic duct in children is usually not seen unless it
is dilated, and then usually only the distal part of the duct
near its insertion into the common bile duct will be seen.
The duct is best examined in the long-axis plane with the
patient in the supine or left posterior oblique position.
Feeding of a fatty meal can be useful to assess patency
of the cystic duct. In healthy individuals, maximum emp-
tying of the gallbladder occurs between 45 and 60 min-
utes after the fatty meal, and the mean volume decreases
by approximately 60%. Contraction of the gallbladder
after a fatty meal supports the diagnosis of a patent cystic
duct.
GALLBLADDER SIZE AND WALL THICKNESS
Normal measurements for gallbladder size have been
reported in fasting individuals. The most commonly
reported measurements are the width and length. Since
275
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276 P E D I AT R I C S O N O G R A P H Y

Normal gallbladder anatomy. The gallbladder has three

Fig. 8.1
segments: fundus, body, and neck. The cystic duct drains
the gallbladder and joins the common hepatic duct to form the
common bile duct.

A B

Normal sonographic anatomy. A: Transverse sonogram in a

Fig. 8.2
left posterior oblique position. The gallbladder is a round
anechoic structure with a thin echogenic wall. B: Longitudinal scan in a
left posterior oblique position shows an oval-shaped gallbladder.
C: Color Doppler sonogram in another patient shows flow in the neck
C (arrow) of the gallbladder (GB).
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Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 277

there is considerable variation in the range of normal mea-
surements, the practical usefulness of gallbladder size in the
diagnosis of disease is limited. In most cases, measurements
are not required for recognition of an abnormality.
In neonates and young infants (younger than 1 year old),
the length of the gallbladder is 1.5 to 3 cm and the width is
less than 1 cm (1). In children 2 to 16 years of age, the length
is 3.0 to 8.0 cm and the width is less than 3.5 cm (1) Gall-
bladder volume can be calculated using the formula for an
ellipsoid (height  width  length / 0.5) (1). In neonates, the
approximate volume is 1.6 cm. Volume measurements have
been used to determine the postprandial ejection fraction.
DOPPLER IMAGING
Color Doppler imaging can show flow in the neck of the
gallbladder (2). This normal finding is seen more easily
when the gallbladder is contracted (Fig. 8.2C) (3).
Normal Variants and Congenital Anomalies
Anatomic variants are potential pitfalls in the diagnosis of
gallbladder disease. Recognition of these clinically insignifi-
cant variations is important lest they are mistaken for pathol-
ogy.
Folds secondary to kinking or folding of the gallblad-
der are commonly identified at sonography (4). The two
most common folds are the junctional fold at the junction
of the body and neck of the gallbladder and the phrygian
cap (Fig. 8.3). The phrygian cap is produced by folding of
the gallbladder fundus. Folds produce an acoustic shadow
and thus may be mistaken for stones if not recognized. The
diagnosis of a fold can be confirmed by scanning the
patient in multiple planes.
Congenital anomalies of the gallbladder include agene-
sis, ectopia, duplication, and septate gallbladder. Agenesis of
the gallbladder is a rare anomaly, with a reported incidence

A B

Gallbladder folds. A: Long-axis sonogram in the supine

Fig. 8.3
position. The junctional fold between the body and neck of
the gallbladder appears as a short linear echo (arrow). B: Left lateral
decubitus position. In this position, the gallbladder is unfolded and the
fold is no longer seen. PV  portal vein. Folds can be mistaken for cal-
culi or polyps, but scanning in multiple planes should minimize errors
in diagnosis. C: Phrygian cap. The gallbladder fundus is folded upon
C itself, creating the appearance of a septum (arrow).
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278 P E D I AT R I C S O N O G R A P H Y
of 0.01% to 0.04% (5). The diagnosis can be suggested
when the gallbladder fossa between the two lobes of the
liver is visualized and it does not contain a gallbladder
despite optimal fasting of the patient. Agenesis is associated
with biliary atresia.
The common ectopic locations of the gallbladder are
retrohepatic (posterior to the right or left hepatic lobes),
intrahepatic, and suprahepatic (between the liver and
the diaphragm) (6). Less common locations include the
lower abdomen, retroperitoneum, anterior abdominal
wall, lesser peritoneal sac, and falciform ligament (6).
A duplicated gallbladder has a partition that divides
the lumen longitudinally into two fluid-filled compart-
ments (79) (Fig. 8.4). Each compartment has a separate
cystic duct. Less commonly, the gallbladder is bilobed with
A B
C rupture of the right hepatic duct.
a single cystic duct. Triple and quadruple gallbladders have
also been described. Complications of gallbladder duplica-
tions include stone formation, cholecystitis, fistulas, tor-
sion, and carcinoma (8).
The septate gallbladder contains thin septations, which
divide the lumen into two or more compartments. Innu-
merable septations, which traverse the lumen in multiple
planes, create a honeycomb appearance (Fig. 8.5) (4,1012).
Stone formation and choledochal cyst are associated with
multiseptated gallbladder (11).
Abnormalities of fixation are rare anomalies. The gall-
bladder may be completely peritonealized and attached
only by a narrow pedicle formed by the cystic duct and
artery. It thus hangs freely in the abdominal cavity and is
prone to torsion.
Duplicated gallbladder. Longitudinal (A) and transverse
Fig. 8.4
(B) scans show two noncommunicating anechoic struc-
tures (labeled as 1 and 2), proven by scintigraphy to be a duplicated
gallbladder. C: Transverse sonogram in another patient shows two
fluid-filled gallbladders (1 and 2). The echogenic mass (arrows) adja-
cent to the more medial gallbladder represents an abscess due to
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A B
Septated gallbladders. Longitudinal sonograms in two different patients. A: Bilobed gallbladder. The gallbladder contains a single septa-
Fig. 8.5
tion (arrow). B: Multiseptated gallbladder (arrows) containing innumerable thin septations, creating a honeycomb appearance.
Sonographic Signs of Gallbladder Disease
ABNORMALITIES OF SIZE
The gallbladder is considered to be abnormally small if the
diameter is less than 1 cm in infants and less than 2 cm in
older children despite adequate fasting. The causes of a
small or contracted gallbladder include the postprandial
state, congenital hypoplasia, acute viral hepatitis, cystic
fibrosis, and chronic cholecystitis. Microgallbladders
occur in up to 30% of patients with cystic fibrosis (Fig. 8.6)
(13,14). Conversely, a large gallbladder has been associated
Microgallbladder in cystic fibrosis. Transverse scan shows
Fig. 8.6
a small, thick-walled gallbladder (arrow) with multiple cal-
culi (arrowhead). The adjacent liver (L) is fatty, impairing sound trans-
mission.
Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 279
with prolonged fasting and cystic or common bile duct
stenosis or occlusion.
NONVISUALIZATION OF THE GALLBLADDER
In fasting infants and children, nonvisualization of the
gallbladder is often due to biliary atresia. Occasionally, it
is due to agenesis or ectopia, physiologic contraction after
a feeding, or sludge. The sludge-filled gallbladder is diffi-
cult to recognize because it has an echogenicity similar to
that of the liver.
GALLBLADDER WALL THICKENING
The normal gallbladder wall measures 3 mm or less in
thickness in fasting patients. Gallbladder wall thickening is
a nonspecific finding that can be caused by a variety of con-
ditions including acute and chronic cholecystitis, hepatic
dysfunction (viral hepatitis, cirrhosis), hypoalbuminemia,
pancreatitis, congestive heart failure, bone marrow trans-
plantation, sepsis, metachromatic leukodystrophy, acquired
immunodeficiency syndrome (AIDS) cholangiopathy, and
physiologic contraction after a meal (Fig. 8.7) (1518).
Diffuse wall thickening can have several sonographic
appearances: a uniformly echogenic pattern, a diffusely
hypoechoic pattern, and alternating hypoechoic and
hyperechoic bands (striated pattern) (19). A rim of fluid
may surround the thickened wall. Focal wall thickening is
not as common as diffuse wall thickening and may be sec-
ondary to cholecystitis or adenomyomatosis.
Cholelithiasis
The incidence of gallstones in the pediatric population
ranges between 1.9% and 4% (20,21). Approximately
10% of gallstones occur in infants under 6 months of age,
20% in patients 6 months to 10 years of age, and 70% in
adolescents (22).
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280 P E D I AT R I C S O N O G R A P H Y

A B

Diffuse gallbladder wall thickening. A: Patient with right

Fig. 8.7
heart failure. Longitudinal scan shows circumferential,
echogenic wall thickening and surrounding hypoechoic pericholecys-
tic fluid (arrows). B: Hepatitis. Transverse sonogram shows diffuse
echogenic wall thickening (arrows). C: Postprandial scan. Longitudinal
image 1 hour after the patient ingested food shows a small gallbladder
(arrow) with striated wall thickening. The pseudothickening is due to
C physiologic contraction.

Neonatal cholelithiasis has been associated with con-
genital anomalies of the biliary tract, total parenteral
nutrition, furosemide therapy, phototherapy, dehydration,
infection, hemolytic anemias, and short-gut syndrome.
Neonates who undergo parenteral nutrition are especially
at risk for cholelithiasis, because the parenteral nutrition
produces bile stasis.
The common causes of cholelithiasis in older children
and adolescents are cystic fibrosis, malabsorption, total
parenteral nutrition, liver disease, Crohn disease, bowel
resection, and hemolytic anemia (22,23). Less commonly,
gallstones are associated with the use of drugs, such as
cephalosporin and cyclosporine, and metachromatic
leukodystrophy. Metachromatic leukodystrophy, or sul-
fatide lipidosis, is an autosomal recessive disorder of
sphingolipid metabolism. Cholelithiasis is thought to result
from gallbladder hypomotility secondary to sulfatide
accumulation in the wall of the gallbladder. In general,
about 85% of pediatric patients have underlying diseases
that predispose to calculus formation. Calculus formation
is idiopathic in the remaining patients.
The classic symptoms of gallstone disease in older chil-
dren are right upper quadrant pain and vomiting. Younger
children tend to present with nonspecific symptoms, such
as jaundice or irritability (23). The complications of gall-
stone disease include cholecystitis, choledocholithiasis,
cholangitis, gallbladder perforation, and pancreatitis,
although these are exceedingly rare in the pediatric age
group (20,21). Pancreatitis is reported in approximately
10% of children with gallstone disease and is probably the
most common complication (20).
Gallstones in children are usually black pigment
(50%), cholesterol (21%), or calcium carbonate (24%)
stones (24). Black pigment stones are associated with
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Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 281

hemolysis, parenteral nutrition, and cirrhosis. Cholesterol
stones are associated with obesity. Calcium carbonate
stones are common in premature neonates and patients
who undergo abdominal surgery (24). Pigment stones
account for a higher percentage of stones in prepubertal
children, whereas cholesterol stones are relatively more
common in adolescents (23). Unless symptomatic, gall-
stones may not require surgical intervention and they may
resolve without treatment.
SONOGRAPHIC FINDINGS
The sonographic appearance of a gallstone is an
echogenic intraluminal structure that causes distal
acoustic shadowing and moves with changes in patient
position (Fig. 8.8). The shadowing produced by gallblad-
der stones is clean, implying that it has distinct mar-
gins and lacks internal echoes or reverberations. Clean
shadowing results because the sound wave is absorbed
within the stone rather than being reflected (Fig. 8.8). Fis-
sured stones containing air can produce ring-down arti-
facts with internal reverberation echoes. Cholesterol
stones can produce very short ring-down artifacts, called
comet-tail artifacts (25). (See Chapter 2 for more detailed
discussion on artifacts.)
Calculi typically layer in the dependent portion of the
gallbladder lumen (see Fig. 8.8) because their specific grav-
ity exceeds that of bile. However, stones that contain a
high cholesterol content or gas, and thus have a specific
gravity less than that of normal bile, float in the bile rather
than being dependent. On occasion, stones are immobile
because they are impacted in the neck of the gallbladder or
they are adherent to the wall of the gallbladder.
The sensitivity of sonography for detecting gallstones is
greater than 95%. The demonstration of posterior acoustic
shadowing is important for the diagnosis because it corre-
lates with cholelithiasis in virtually all patients, whereas
nonshadowing echogenic foci may represent stone disease,
polyps, or other masses.
PITFALLS AND ARTIFACTS IN DIAGNOSIS OF GALLSTONES
False-negative Diagnoses
The definitive diagnosis of gallstones is based on identifi-
cation of a clean acoustic shadow. The production of an
acoustic shadow is dependent on the position of the stone
within the sound beam, the size of the stone, and the sur-
face characteristics of the stone (smooth or rough). Shad-
owing does not relate to the calcium content of the stone.
Shadowing occurs because the calculus blocks enough
of the sound beam to prevent sound transmission beyond
it. If the stone is at the center or focal zone of the transducer
(i.e., the narrowest part of the beam), the sound beam is
absorbed and an acoustic shadow is produced. If the beam
strikes the edge of the stone, the sound is reflected, produc-
ing comet-tail or reverberation artifacts rather than shad-
owing. It is easier to elicit an acoustic shadow with a
higher-frequency transducer or with a focused transducer,
both of which narrow the beam width, than with a low-
frequency transducer.
The smaller the stone, the more difficult it is to demon-
strate acoustic shadowing. Despite optimal techniques,
small (3 mm) stones may not shadow but will still appear
echogenic (Fig. 8.9). Scanning the patient in the right or left
decubitus and upright positions may allow the stones to
roll within the gallbladder and layer on top of one another.

A B
Cholelithiasis. A: Longitudinal sonogram in a lateral decubitus position shows a large echogenic focus (arrow) in the gallbladder neck,
Fig. 8.8
which produces clean acoustic shadowing (open arrow). B: Longitudinal scan in another patient shows multiple shadowing echogenic
foci. The calculi layer in the dependent portion of the gallbladder. Arrows indicate acoustic shadows.
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282 P E D I AT R I C S O N O G R A P H Y

A B
Nonshadowing stones. A: Longitudinal sonogram. The gallbladder (arrows) is distended and contains multiple tiny echogenic foci
Fig. 8.9
(3 mm diameter), which do not shadow. B: Repositioning the patient allows the stones to layer on top of one another and create an
acoustic shadow (open arrows).

The result is an aggregate of small stones that behaves
acoustically as a larger stone in its ability to produce poste-
rior shadowing (Fig. 8.9). A calculus with a rough surface
will absorb more sound than one with a flat, smooth sur-
face. Fortunately, most calculi have rough surfaces.
When the gallbladder is packed with stones, it can be
more difficult to identify. A highly echogenic linear reflec-
tion with distal acoustic shadowing is seen in the gallblad-
der fossa (Fig. 8.10). The shadow that is cast prevents visu-
alization of the intraluminal bile, more deeply positioned
stones, and posterior wall of the gallbladder. The demon-
stration of a wall echo shadow (WES) or double-arc shadow
sign, consisting of two parallel curved hyperechoic lines
separated by a thin hypoechoic space and distal acoustic
shadowing, confirms the diagnosis of gallstones (Fig. 8.10).
The first hyperechoic line represents the wall of the gall-
bladder or the gallbladder wall interface; the second hyper-
echoic line represents bright echoes from the gallstones, and
the hypoechoic space in between represents either bile
between the wall of the gallbladder and the gallstones or a

A B
Wall echo shadow (WES) sign. A: The WES sign of a gallbladder filled with stones is characterized by two parallel, curved echogenic
Fig. 8.10
lines separated by a thin anechoic space. The first or anterior echogenic line (arrow) represents the wall of the gallbladder or the inter-
face between the gallbladder wall and the liver. The anechoic space is bile between the gallbladder wall and stones or a hypoechoic part of the
wall. The posterior or deeper echogenic line (arrowhead) represents bright echoes from the stones, which cast a large acoustic shadow. B: Re-
scanning the patient in another position causes the stones to layer, allowing recognition of the gallbladder lumen (arrows).
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Air in the gallbladder. Air in the gallbladder wall causes
Fig. 8.11
ring-down artifact with bright reverberation echoes (dirty
acoustic shadowing) (arrows). The gallbladder lumen and posterior
wall are not well seen.
hypoechoic portion of the gallbladder wall. Rotating the
patient into another position may allow the stones to reset-
tle in a dependent part of the gallbladder, allowing visuali-
zation of the gallbladder lumen.
False-positive Diagnoses
Artifactual echoes in the lumen of the gallbladder are pro-
duced when structures adjacent to the gallbladder are aver-
aged into the lumen. These echoes can be mistaken for cal-
culi or sludge. Artifactual echoes are not constant and
change with changes in transducer or patient position.
A B
Tumefactive biliary sludge. Longitudinal left lateral decubitus (A) and transverse supine (B) scans of a 2-month-old girl on hyperali-
Fig. 8.12
mentation show a mobile echogenic polypoid mass (sludge ball) (arrow) with through-transmission, but no acoustic shadowing, in the
dependent part of the gallbladder.
Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 283
Likewise, echogenic folds or infolding of the gallbladder
can be mistaken for gallstones.
Air in the gallbladder wall or lumen can mimic gall-
stones. When air is present, bright ring-down artifacts with
reverberation echoes will be observed and the posterior
wall will not be seen (Fig. 8.11).
Aggregated or tumefactive sludge (i.e., sludge ball) is a
cause of a mobile nonshadowing echogenic mass, which
can mimic a gallstone (Fig. 8.12). However, sludge balls
change in appearance or disappear on serial sonograms,
whereas gallstones remain stable in size or increase. Hemo-
bilia is a rare cause of an echogenic nonlayering mass
within the gallbladder.
Fetal Gallstones
Fetal gallstones have been reported in the third trimester of
pregnancy (2628). Sonography demonstrates echogenic
foci, which may or may not demonstrate acoustic shadow-
ing, in the lumen of the fetal gallbladder. Postnatal sonog-
raphy has shown that many of these echogenic foci resolve
spontaneously in the first year of life, supporting conser-
vative therapy.
Sludge
Biliary sludge refers to the presence of particulate matter
in the bile. This occurs when solutes in bile precipitate.
Calcium bilirubinate granules and cholesterol crystals are
the most common causes of sludge. Bile stasis following a
prolonged fasting, hyperalimentation, and extrahepatic
bile duct obstruction are major factors in sludge forma-
tion. Sickle cell disease and other hemolytic diseases also
predispose to biliary sludge. A palpable enlarged gallblad-
der may be the first sign of sludge formation in the infant.
The sonographic appearance of sludge is that of non-
shadowing, low- to medium-amplitude echoes that layer in
the most dependent part of the gallbladder and show
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284 P E D I AT R I C S O N O G R A P H Y

A B
Biliary sludge. Transverse supine (A) and longitudinal left lateral decubitus (B) sonograms demonstrate low-level echoes (arrows) lay-
Fig. 8.13
ering in the dependent part of the gallbladder. There is no acoustic shadowing from the sludge, but there is acoustic enhancement
behind the gallbladder.

acoustic enhancement (Fig. 8.13). Because of its viscous
nature, the fluid-fluid level formed by the sludge moves
slowly with changes in patient position. If the sludge
completely fills the gallbladder, it may be difficult to dis-
tinguish from liver because of a similar echogenicity. This
appearance has been termed hepatization of the gall-
bladder (Fig. 8.14). The sludge-filled gallbladder can be
recognized by recognizing the normal gallbladder wall
(29). The wall is avascular because there are no inflamma-
tory changes.
On occasion, the particular material in sludge does not
form a fluid-fluid level, but instead it coalesces and
appears as a mobile nonshadowing echogenic mass,
referred to as a sludge ball or tumefactive biliary sludge
(see Fig. 8.12 and earlier discussion). Sludge balls are
echogenic, but they are not associated with posterior
acoustic shadowing. These lesions are transient and dis-
appear spontaneously. The mobility of the sludge and dis-
solution on serial sonograms differentiate sludge balls
from polypoid tumors.
PITFALLS AND ARTIFACTS IN DIAGNOSIS OF SLUDGE
Low-level echoes in the gallbladder lumen are not always due
to particulate matter. When soft tissue structures adjacent to
the gallbladder are averaged into the anechoic, fluid-filled
lumen, they cause low-level echoes, called side-lobe artifacts,
which mimic sludge (Fig. 8.15). Repositioning the patient so
that the gallbladder falls away from the adjacent gas-filled
bowel loops, changing transducer angulation, and reducing
gain and power can differentiate between true sludge and
pseudosludge. Unlike true sludge, artifactual echoes will not
layer with changes in patient position and may disappear. In
addition, the anterior surface of pseudosludge can be
curved, whereas true sludge has a flat surface.
Other causes of echogenic intraluminal bile include
hemobilia, pus, inflammatory debris, and milk of calcium.

A B
Gallbladder hepatization. A: Longitudinal sonogram demonstrates a massively dilated hydropic gallbladder (arrows) filled with sludge.
Fig. 8.14
The echogenicity of the sludge is close to that of normal liver (L). B: Color Doppler sonography shows absence of hyperemia.
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Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 285

A B
Pseudosludge due to side-lobe artifacts (artifacts which arise from sound beams that are peripheral to the main sound beam). A: An
Fig. 8.15
air-filled loop of bowel adjacent to the gallbladder creates artifactual echoes (arrows) in the gallbladder fundus. B: In another patient,
adjacent left lobe of the liver produces echoes (arrow) within the gallbladder lumen. Pseudosludge will not layer with changes in patient position.

Causes of hemobilia include blunt hepatic trauma, pene- Cholecystitis

trating injuries, most commonly liver biopsy, bleeding
dyscrasias, and vascular abnormalities. Acute hemobilia is
echogenic. Subacute blood appears as a heterogeneous or
hypoechoic nonshadowing mobile mass, reflecting the pres-
ence of clot formation and retraction.
Milk of calcium bile is an uncommon condition char-
acterized by tenacious bile containing high calcium con-
tent, usually calcium carbonate. It has been associated
with chronic cholecystitis and partial or complete obstruc-
tion of the cystic duct, usually by a calculus in the neck of
the gallbladder. Sonographic findings include an anechoic
supernatant and an echogenic dependent fluid layer caus-
ing acoustic shadowing.
ACUTE CALCULOUS CHOLECYSTITIS
Acute cholecystitis is significantly less common in children
than in adults. Most cases of acute cholecystitis in child-
hood result from cystic duct obstruction secondary to cal-
culi (20). Clinical findings include right upper quadrant or
epigastric pain, right upper quadrant tenderness, jaundice,
fever, and leukocytosis (20).
The common sonographic findings of acute calculus
cholecystitis include cholelithiasis, an enlarged gallbladder, a
thickened gallbladder wall (thickness 3 mm), localized ten-
derness (sonographic Murphy sign), sludge, and perichole-
cystic fluid (Figs. 8.16 and 8.17). Each of these features in

A B
Acute calculous cholecystitis in an adolescent girl with a positive Murphy sign. Longitudinal (A) and transverse (B) scans demonstrate
Fig. 8.16
gallbladder distention, wall thickening (arrows), and a gallstone. Wall thickness (calipers)  9 mm.
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286 P E D I AT R I C S O N O G R A P H Y
Acute cholecystitis. Transverse scan demonstrates a
Fig. 8.17
thickened wall (arrows) with a circumferential hypo-
echoic halo, representing pericholecystic fluid (i.e., edema).
isolation is nonspecific, but the combination of sonographic
signs in the appropriate clinical setting has a sensitivity of
greater than 90% for the diagnosis of acute cholecystitis.
The most sensitive criteria for diagnosing acute cholecystitis
are gallbladder tenderness in association with calculi.
Color Doppler imaging in patients with acute cholecys-
titis may show flow in the gallbladder wall, usually in the
fundal (distal) segment (2,30) (Fig. 8.18). In healthy adult
individuals, flow is more likely to be observed near the
neck of the gallbladder (2).
Acute cholecystitis. Color Doppler sonogram shows
Fig. 8.18
increased flow in the wall of the gallbladder, predomi-
nantly in the fundus, and sludge in the lumen.
Emphysematous cholecystitis. Longitudinal sonogram
Fig. 8.19
shows linear hyperechogenicity, representing gas
(arrows), in the nondependent wall of the gallbladder, with distal rever-
beration artifacts (open arrow). GB  gallbladder lumen.
Complications
Rare complications include emphysema, gangrene, and per-
foration. Emphysematous cholecystitis is produced by gas-
forming bacteria. The sonographic appearance is that of
hyperechoic foci, representing bubbles of gas, in the nonde-
pendent portion of the gallbladder lumen or within the wall
of the gallbladder (Fig. 8.19). Dirty acoustic shadowing and
reverberation (ring-down) artifacts are noted distal to the
gas bubbles (31). Gas also can be seen in the biliary tree. The
finding of pericholecystic or intraluminal hyperechogenici-
ties due to air is not specific for acute cholecystitis and also
can be seen in necrotizing enterocolitis (32). The clinical his-
tory should allow differentiation of these two conditions.
The diagnosis of gangrenous cholecystitis is based on
the presence of echogenic intraluminal membranes parallel-
ing the wall of the gallbladder, irregular or asymmetric wall
thickening, and pericholecystic fluid (33,34). The wall
thickening is heterogeneous and characterized by either
multiple striations (alternating hypoechoic and echogenic
lines) or irregular mass-like protrusions projecting into the
gallbladder lumen (Fig. 8.20). A sonographic Murphy sign
is often absent presumably due to infarction and necrosis of
nerve fibers supplying the gallbladder (35). Color Doppler
imaging shows hypervascular pericholecystic fat (33).
Gallbladder perforation most commonly occurs in the
fundus of the gallbladder and is a complication of prolonged
inflammation and gangrenous cholecystitis. Perforated chole-
cystitis results in the formation of a pericholecystic abscess or
less commonly bile peritonitis or a cholecystenteric fistula
(36). The sonographic finding of pericholecystic abscess is
a localized, thick-walled, pericholecystic fluid collection
(Fig. 8.21). Other findings of perforation are a thickened,
hypoechoic gallbladder wall, cholelithiasis (Fig. 8.21), small
gallbladder size, and interruption of the gallbladder wall at
the site of perforation (the hole sign) (37).
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Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 287

Gangrenous cholecystitis. Longitudinal scan shows a dis-
Fig. 8.20
tended gallbladder with striated wall thickening (arrows). Wall
thickness (calipers)  10 mm. There are also multiple shadowing calculi.
Perforated cholecystitis with abscess formation. Longitu-
Fig. 8.21
dinal scan shows an echogenic calculus (arrowheads) in
the neck of the gallbladder and a localized, thick-walled, perichole-
cystic fluid collection (arrow), shown to be an abscess at surgery.

CHRONIC CHOLECYSTITIS
Chronic cholecystitis in childhood results from chronic irri-
tation of the gallbladder secondary to gallstones, cystic
fibrosis or recurrent attacks of acute cholecystitis. Sono-
graphic findings include a contracted gallbladder, sludge,
gallstones, and focal or diffuse thickening of the gallblad-
der wall. A sonographic Murphy sign and hyperemia are
absent. Occasionally, the wall of the gallbladder calcifies,
producing a porcelain gallbladder.
ACALCULOUS CHOLECYSTITIS
Acalculous cholecystitis has been associated with recent
surgery, burns, sepsis, and debilitation (38,39). In these
patients, prolonged bile stasis results in increased viscosity
of the bile and subsequently cystic duct obstruction. Inflam-
mation results when organisms in the obstructed gallblad-
der invade the mucosa and gallbladder wall. The clinical
findings are fever, right upper quadrant pain, and vomiting.
The sonographic criteria of acalculous cholecystitis are
similar to those of acute calculus cholecystitis except that
calculi are absent. Imaging findings include gallbladder
distention, intraluminal sludge, wall thickening (3 mm),
pericholecystic fluid, and inflammatory change in the peri-
cholecystic fat (Fig. 8.22). The response to cholecystokinin

A B
Acalculous cholecystitis. A: Longitudinal sonogram in a neonate patient with jaundice shows a debris-filled gallbladder (GB) with a
Fig. 8.22
thickened wall (arrows) and some pericholecystic fluid (arrowhead). B: Color Doppler image demonstrates hyperemia of the gallblad-
der wall and the pericholecystic fat.
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288 P E D I AT R I C S O N O G R A P H Y
is usually poor and gallbladder contractility is minimal or
absent (40). Color Doppler sonography shows increased
flow in the gallbladder wall and pericholecystic soft tissues
(Fig. 8.22B).
Hydrops
Hydrops is a disorder characterized by massive distention
of the gallbladder in the absence of inflammation (20). The
causes of hydrops include fasting or dehydration leading to
bile stasis and functional obstruction of the cystic duct;
extrinsic compression of the common bile duct by inflamed
portal nodes; and vasculitis with secondary ischemia. The
bile trapped within the obstructed gallbladder is eventually
absorbed and replaced with serous fluid secreted by the
gallbladder mucosa.
Neonatal hydrops occurs in the clinical setting of sep-
sis, hyperalimentation, inspissated bile syndrome, shock,
and congestive heart failure. In older infants and children,
hydrops has been associated with Kawasaki disease
(mucocutaneous lymph node syndrome), leptospirosis,
ascariasis, typhoid fever, familial Mediterranean fever, sep-
sis, and total parenteral nutrition (41). Hydrops may be
asymptomatic or it may manifest as a right upper quadrant
mass or pain. Patients are afebrile, which helps to separate
hydrops from acute cholecystitis.
Sonography shows a markedly enlarged gallbladder
(3 cm in length in infants younger than 1 year of age
and 7 cm in older children) with normal wall thickness
(Fig. 8.23). The gallbladder may have a biconvex appear-
ance on longitudinal scans, rather than the normal ovoid
configuration. Sludge may or may not be present. The
intrahepatic and extrahepatic ductal structures are normal.
Rehydration and resolution of the associated disease
almost always result in spontaneous decompression of the
Hydrops of the gallbladder. Longitudinal sonogram in a
Fig. 8.23
neonate shows a markedly dilated gallbladder. The wall
thickness is normal. The gallbladder length (calipers) is 4.0 cm.
gallbladder (22). Perforation is a rare complication of
hydrops associated with Kawasaki disease.
Gallbladder Torsion
Torsion or volvulus of the gallbladder is rare and is the
result of increased mobility of the gallbladder related to a
long suspensory mesentery. Affected patients present with
symptoms similar to those of acute cholecystitis. The
sonographic findings are a massively distended, thick-
walled gallbladder lying in a horizontal position and
a spiral appearance of the cystic artery and the cystic
duct (42).
Hyperplastic Cholecystoses
Adenomyomatosis and cholesterolosis are rare noninflam-
matory abnormalities of the gallbladder in childhood
(43,44). These conditions have also been termed hyper-
plastic cholecystosis since they are characterized by
hyperplasia of the gallbladder wall.
Pathologically, adenomyomatosis is characterized by
hyperplasia of the luminal epithelium, thickening of
the muscularis, and diverticular formations, termed
Rokitansky-Aschoff sinuses. The sonographic find-
ings include diffuse or focal wall thickening and intra-
mural diverticula. Diverticula that contain bile appear
as tiny anechoic spaces within the thickened gallbladder
wall, while diverticula that contain sludge or cholesterol
crystals or calculi appear as small hyperechoic foci with
or without acoustic shadowing or comet-tail artifacts
(Fig. 8.24) (43,44).
Cholesterolosis is characterized by abnormal accumu-
lations of triglycerides and cholesterol esters or precursors
in the mucosa and submucosa of the gallbladder, resulting
Adenomyomatosis. Longitudinal sonogram shows a thick-
Fig. 8.24
walled gallbladder with small echogenic intramural nod-
ules representing Rokitansky-Aschoff sinuses (arrows). One of the
mural diverticula is associated with a comet-tail artifact (open arrow).
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Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 289

Cholesterolosis. Longitudinal lateral decubitus sonogram

Fig. 8.25
demonstrates multiple echogenic, nonshadowing intralu- Inflammatory polyp. Longitudinal image demonstrates a
minal masses (arrowheads). By comparison, in adenomyomatosis the Fig. 8.26
nonshadowing polypoid mass (arrow) attached to the
masses are sessile and in the wall. gallbladder wall.

in formation of cholesterol polyps. At ultrasonography,
cholesterol polyps appear as small, nonmobile, nonshad-
owing echogenic masses protruding from the wall into the
gallbladder lumen (Fig. 8.25).
Other Polypoid Masses
Other polypoid masses of the gallbladder include adenomas,
papillomas, hamartomas, inflammatory polyps, fibroepithelial
polyps (4549) (Figs. 8.26 and 8.27), mucus retention cysts,
heterotopic pancreatic and gastric tissue, and adenocarci-
noma. These conditions are even rarer than adenomyomato-
sis and cholesterolosis. These lesions appear as hyperechoic
masses that may be pedunculated or sessile. Very large masses
can fill the gallbladder lumen (Fig. 8.27). Thickening of the
gallbladder wall adjacent to a mass should raise the possibility
of malignancy.
Miscellaneous Diseases
GALLBLADDER VARICES
Gallbladder varices are an unusual manifestation of portal
hypertension and represent portosystemic shunts between
the cystic vein and the systemic anterior abdominal wall

A B
Fibroepithelial polyp. A: The gallbladder lumen contains a large (5  4 cm) echogenic mass (arrows). PV  portal vein. B: Color Doppler
Fig. 8.27
image shows flow within the mass. The gallbladder wall is thin and avascular (arrows).
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290 P E D I AT R I C S O N O G R A P H Y

A B
Gallbladder varices in a child with cavernous transformation of the portal vein. Longitudinal gray-scale (A) and color Doppler (B) images
Fig. 8.28
of the gallbladder (GB) show wall thickening with anechoic channels (arrows), shown to be vessels with Doppler imaging.

veins or portal vein branches within the liver (50,51). The
sonographic findings are a thickened gallbladder wall con-
taining anechoic channels corresponding to dilated veins
(Fig. 8.28). Color and pulsed Doppler sonography confirm
the diagnosis of varices by showing vessels with portal
venous waveforms in the gallbladder wall.
TRAUMA
Traumatic injury to the gallbladder occurs in 2% to 3% of
patients with blunt abdominal trauma (52). Gallbladder
injuries may be classified as contusion, laceration, perfora-
tion, or complete avulsion. Sonographic findings include peri-
cholecystic fluid collections, intraluminal blood, thickened
gallbladder wall, a collapsed gallbladder in a fasting patient,
and discontinuity of the gallbladder wall (Fig. 8.29) (52).
BILE DUCTS
Scanning Techniques
Sonography of the bile ducts is usually performed with a
5.0- or 7.5-MHz transducer. In large or obese patients, a
3.5-MHz probe may be needed. In cooperative patients, the

Traumatic gallbladder perforation. Transverse sonogram

Fig. 8.29
shows a collapsed gallbladder with a thickened wall.
There is a full-thickness tear (arrow) on the medial wall of the fundus.
(Reprinted from Akay HO, Senturk S, Cigdem MK, et al. Isolated trau-
matic gallbladder rupture: US findings and the role of repeat US in
diagnosis. Pediatr Radiol 2008;38:691693, with permission.)
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Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 291

A B
Sonographic demonstration, normal common bile duct. A: Transverse sonogram of the porta hepatis showing the common bile duct
Fig. 8.30
(arrow) lying anterior and to the right of the main portal vein (V) and hepatic artery (arrowhead). B: Longitudinal view. The common duct
(arrows) is anterior to the portal vein (V). The right hepatic artery (arrowhead) is a rounded anechoic structure posterior to the common duct and
anterior to the portal vein. The distal segment of the common bile duct (arrow) enters the pancreas (P).

examination should be done during suspended respiration.
Both sagittal and transverse scans are obtained. The proxi-
mal portion of the common bile duct (level of the porta
hepatis) is examined with the patient in the supine and left
posterior oblique or left decubitus positions. The distal part
of the duct is scanned with the patient in the supine and
right posterior oblique positions. Scanning the patient in
the erect position may improve visualization of the distal
common bile duct, because it allows air in the gastric
antrum and duodenum to rise and fluid to empty into the
distal antrum and duodenum. The dependent fluid in the
gastric antrum then serves as an acoustic window.
Normal Anatomy
The biliary tree is composed of the intrahepatic ducts, the
common hepatic duct, and the common bile duct. The
intrahepatic ducts are located adjacent to the portal veins
and hepatic arteries and form the portal triad (see Fig. 8.1)
(53,54). They course from the periphery of the liver to the
hepatic hilum, where they join to form the main left and
right hepatic ducts. Because of their small size, normal
intrahepatic bile ducts and the cystic duct are not routinely
seen at sonography.
The main right and left hepatic ducts join to form the
common hepatic duct. The common hepatic duct is defined
as that portion of the extrahepatic bile duct caudal to the
confluence of the hepatic ducts and proximal to the inser-
tion of the cystic duct. It usually lies anterior to and to the
right of the main portal vein and the hepatic artery. In
approximately 15% of individuals the common duct is
posterior to the right hepatic artery.
The common bile duct is that portion of the extrahe-
patic bile duct that extends from the junction of the cystic
duct and common hepatic duct to the level of the ampulla
of Vater, where it joins the main pancreatic duct. It courses
caudally in the hepatoduodenal ligament along with the
hepatic artery and portal vein to the level of the pancreatic
head (Fig. 8.30). In approximately 60% to 70% of individ-
uals, the common bile duct and the pancreatic duct unite to
drain through a common orifice in the ampulla of Vater. In
the remainder of individuals, the ducts enter the duodenum
separately. The papilla of Vater appears as a blind-ending
cylindrical or oval structure projecting into the duodenal
lumen at the distal end of the common bile duct (55).
SONOGRAPHIC MEASUREMENTS
The diameter of the common duct is measured on the sagit-
tal scan. The upper limits of the common duct should not
exceed 1 mm in neonates, 2 mm in infants up to 1 year of
age, 4 mm in children 1 to 10 years of age, and 6 mm in
adolescents and young adults (56). The distal portion of the
common duct is usually larger than the proximal portion.
Ductal size may increase by 1 mm or more during deep
inspiration and the Valsalva maneuver (57). An increase in
ductal diameter also occurs after cholecystectomy.
SPECIAL TECHNIQUES
Rescanning after ingestion of a fatty meal can be helpful in
diagnosing ductal obstruction. In response to a fatty meal,
nonobstructed ducts either remain unchanged or decrease
in caliber (58). In ductal obstruction, the common bile
duct often increases in size (2 mm).
Cholestatic Diseases: Overview
Jaundice is the most common indication for imaging the
biliary tract and gallbladder. The list of potential causes of
jaundice is extensive, but there are several disorders that
account for the majority of cases of cholestasis in the
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292 P E D I AT R I C S O N O G R A P H Y
pediatric population. These are reviewed in the following
discussion. The hepatocellular causes of jaundice have
been discussed in Chapter 7.
In the neonate, biliary atresia, the neonatal hepatitis
syndrome, and choledochal cyst are the common causes
of jaundice, accounting for about 70% to 80% cases of
neonatal cholestasis (5961). Other biliary abnormalities
include bile duct paucity (Alagille syndrome) (62),
inspissated bile syndrome, and spontaneous perforation
of the extrahepatic bile duct (22,60). In older children,
jaundice is most often due to hepatocellular disease,
such as hepatitis and cirrhosis, and less often due to bil-
iary tract inflammation (cholangitis) or obstruction. The
causes of obstructive jaundice include choledochal cyst;
neoplasms, particularly rhabdomyosarcoma, lymphoma,
or neuroblastoma; cholelithiasis; and, rarely, stricture
(22,63).
The combination of liver function tests and pertinent
historical and physical findings generally suffices to differ-
entiate between obstructive and nonobstructive causes of
jaundice. Imaging studies, such as sonography, are used to
confirm or alter the clinical impression. Besides demon-
strating the presence of obstruction, these studies can
show the level and cause of obstruction. If the extrahep-
atic ducts are visualized by sonography and are normal in
caliber and there is no evidence of intraductal dilatation,
further radiologic evaluation is rarely needed. Computed
tomography (CT) and magnetic resonance imaging (MRI)
play a role in patients in whom the results of sonography
are equivocal or nondiagnostic or when more anatomic
detail is needed for surgical planning (64,65). Hepatobil-
iary scintigraphy is used primarily to confirm suspected
diagnoses of choledochal cysts, biliary atresia, and neona-
tal hepatitis.
Biliary Atresia and Neonatal Hepatitis
Biliary atresia and the neonatal hepatitis syndrome are the
common causes of conjugated hyperbilirubinemia. Biliary
atresia affects about 1 in 16,000 live newborns (66). The
cause is unclear, but it is believed to be caused by in utero
vascular or inflammatory insult resulting in failure of
the remodeling process at the hepatic hilum with persist-
ence of fetal bile ducts (59,66). Histologically, there is
destruction of the extrahepatic bile ducts, with scarring,
obliteration, and concomitant damage to intrahepatic bile
ducts.
The neonatal hepatitis syndrome is the term given to
nonspecific hepatic inflammation that develops secondary
to several different causes, including infection (cyto-
megalovirus, herpes simplex, toxoplasmosis, protozoa,
syphilis), metabolic defects (1antitrypsin deficiency,
galactosemia, glycogen storage disease, tyrosinosis), and
Alagille syndrome. The cause is thought to be an in utero
inflammatory process (67). Both biliary atresia and the
neonatal hepatitis syndrome usually present at 3 to 4
weeks of life with cholestasis and jaundice. Hepatic func-
tion tests in both conditions show elevated serum transam-
inase and bilirubin levels.
Approximately 10% to 20% of patients with biliary
atresia have other anomalies. These include choledochal
cyst, polysplenia, preduodenal portal vein, azygous contin-
uation of the inferior vena cava, diaphragmatic hernia,
situs inversus, hydronephrosis, and congenital heart
defects (59,60,68,69).
Distinguishing between neonatal hepatitis and biliary
atresia is important, because neonatal hepatitis is man-
aged medically, whereas biliary atresia requires early sur-
gical intervention to prevent biliary cirrhosis. Surgical
treatment varies with the level of obstruction. When the
obstruction is in the distal common bile duct (15% of
patients), a direct anastomosis between the patent por-
tion of the extrahepatic bile duct and intestine (Roux-
en-Y) is performed. When the atresia extends into the
ducts in the porta hepatis, the surgery of choice is a Kasai
hepatoportoenterostomy, in which a segment of small
bowel is attached to the portal region to permit bile to
empty from persistent small patent ductules (59,60,70).
The success rate of the Kasai procedure in preserving liver
function is 90% in infants under 2 months of age, 50%
in infants between 2 and 3 months of age, and less than
20% in infants older than 3 months of age (59,60). Liver
transplantation may be required in older infants and
children.
SONOGRAPHIC FINDINGS
The liver size and parenchymal echogenicity may be nor-
mal or increased in both biliary atresia and neonatal hep-
atitis. The intrahepatic ducts are usually not seen in either
condition. In biliary atresia, a remnant of the extrahepatic
bile duct remnant may be noted in the porta hepatis
(7176). This appears as an avascular, echogenic, triangu-
lar or tubular structure anterior to the portal vein (Fig.
8.31). This finding has been termed the triangular cord
and correlates with fibrous tissue in the porta hepatis at
histologic examination. The sign is relatively reliable for
the diagnosis of biliary atresia and has specificity as high
as 100% and sensitivity of approximately 62% to 85%
(7577).
Doppler findings of biliary atresia include an enlarged
main hepatic artery and subcapsular flow (i.e., arterial
flow extending to the hepatic surface) (77,78). The mean
diameter of the hepatic artery in patients with biliary
atresia is 2.1 mm (standard deviation [SD]  0.7 mm)
versus 1.5 mm (SD  0.4 mm) in neonates with other
causes of neonatal cholestasis. The finding of peripheral
arterial flow has a sensitivity and specificity of approxi-
mately 100% and 85%, respectively, in the diagnosis of
atresia (77). False-positive causes of subcapsular flow
include hepatitis and total parenteral nutritioninduced
cholestasis.
In neonatal hepatitis, the gallbladder may be large, nor-
mal, or small (Fig. 8.32). In biliary atresia, the gallbladder is
usually small or absent (Fig. 8.31), although in about 10%
of infants it is normal sized (1.5 cm in diameter). A normal
gallbladder is more likely to be seen when the atresia is dis-
tal to the insertion of the cystic duct. A change in gallbladder
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A B

C D
Biliary atresia. A: Transverse scan shows normal hepatic parenchymal echogenicity and a small gallbladder (arrow). The common bile duct
Fig. 8.31
was not visualized. B: Triangular cord sign. Longitudinal sonogram through the porta hepatis shows an echogenic cord (arrowheads) ante-
rior to the portal vein (PV), corresponding to fibrosis along the course of the common hepatic/bile duct. C: Color Doppler image shows the avascular
fibrous cord (arrowheads) anterior to the portal vein (PV). D: Color Doppler shows the arterial flow (arrows) extending to the hepatic surface. An arterial
waveform was seen in the enlarged vessel.

Neonatal hepatitis. Longitudinal sonogram shows normal

Fig. 8.32
hepatic parenchymal echogenicity and a normal-sized
gallbladder (arrows).
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294 P E D I AT R I C S O N O G R A P H Y

size after a milk feeding suggests that the common hepatic

and common bile duct are patent and favors the diagnosis of
neonatal hepatitis. Gallbladder contractility is unlikely in
patients with biliary atresia, occurring in less than 10% of
cases, since the biliary tree is obstructed (79).
Ultrasonography alone does not suffice to separate
biliary atresia and neonatal hepatitis, and it serves mainly
to rule out other causes of cholestasis, such as chole-
dochal cyst. The combined use of sonography and
scintigraphy with hepatobiliary agents (99mT c-iminodi-
aceticacid [IDA] analogs) can correctly separate the two
disorders.

POSTOPERATIVE FINDINGS
Intrahepatic cysts have been reported in patients with
biliary atresia after portoenterostomy (80). The fibrous
changes in the intralobular spaces and the inflammatory
process around the bile ducts are postulated to be
causes of the cyst formation. Patients with biliary atre-
sia and cysts have a higher risk of developing cholangi-
tis (79).
Intrahepatic Cholestatic Syndromes
Intrahepatic cholestasis is another cause of neonatal jaun-
dice. This is a heterogeneous subset of cholestatic diseases,
characterized by intrahepatic cholestasis with or without
bile duct hypoplasia or paucity. These syndromes may be
sporadic, but there are familial forms (most commonly
Alagille and Byler syndromes). Differentiation of the vari-
ous cholestatic conditions usually is based on the combi-
nation of clinical, laboratory, and histologic findings rather
than on imaging findings.
ALAGILLE SYNDROME
Alagille syndrome (also known as arteriohepatic dysplasia
or syndromic paucity of the intrahepatic bile ducts) is the
most common of the familial intrahepatic cholestatic syn-
dromes (60,62,66). Pathologically, there is a paucity of
interlobular bile ducts. It is a hereditary disorder, usually
an autosomal dominant trait with variable penetrance,
although cases may be sporadic. Some patients with Alag-
ille syndrome have a deletion in the short arm of chromo-
some 20, specifically in the Jagged 1 gene. Patients present
with jaundice in the newborn period. They also have con-
genital anomalies, involving the heart (most commonly
peripheral pulmonic stenosis), skeleton (butterfly vertebrae
and hemivertebra), eye, and kidneys, and abnormal facies
(frontal bossing, deep-set eyes, bulbous tip of the nose, and
pointed chin), which helps to distinguish Alagille syn-
drome from biliary atresia and neonatal hepatitis syn-
drome. Imaging findings are similar to those described for
neonatal hepatitis.
BYLER DISEASE
Byler disease (also known as progressive familial intra-
hepatic fibrosis) is a familial intrahepatic cholestatic
syndrome. Histologically, there is periportal fibrosis,
micronodular cirrhosis, and periductal cysts, commonly
Byler disease. Longitudinal scan shows a cystic area with
Fig. 8.33
a dot (arrow) representing a portal vein surrounded by
fluid.
found in the liver hilum. Symptoms, including jaun-
dice, pruritus, and hepatomegaly, usually appear by the
end of the first year of life. Although some patients
survive into adulthood, many die in the second decade
of life.
The sonographic findings of Byler disease are multiple
saccular cystic lesions, some of which contain echogenic
foci (the central dot sign) (Fig. 8.33). The dot represents
portal veins surrounded by fluid (81). Unlike Caroli dis-
ease (see later discussion), the cysts in Byler disease do not
communicate with the bile ducts.
Choledochal Cyst
Choledochal cyst is a congenital dilatation of the common
bile duct associated with biliary obstruction (66). The
diagnosis is made in 30% of patients in the first year of
life, in 50% between 1 and 10 years of age, and in 20%
in the second decade or later (82). The classic clinical
presentation is jaundice, abdominal pain, and mass,
although this triad is present in only 20% to 50% of
patients (82). The precise cause is unknown, but it may be
the result of an anomalous junction of the pancreatic and
distal common bile duct, which allows reflux of pancre-
atic enzymes into the biliary tree. The resultant cholangi-
tis weakens the bile duct wall, leading to the cyst forma-
tion (82,83).
Four types of choledochal cyst have been described
(Fig. 8.34) (82,84). The type I cyst, accounting for 80% to
90% of cases, is subdivided into type IA, cystic dilatation
of the common duct; type IB, focal segmental common
duct dilatation; and type IC, fusiform dilatation of the
common bile duct. The type II cyst, accounting for about
2% of cases, is a true diverticulum arising from the com-
mon duct. The type III cyst, accounting for 1% to 5% of
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IA
II
Classification scheme of chole-
Fig. 8.34
dochal cysts. See text for dis-
cussion. (Reproduced from Savader SJ,
Benenati JF, Venbrux AC, et al. Choledochal
cysts: classification and cholangiographic
appearance. AJR 1991;156:327331, with
permission). IVA
cases, also called choledochocele, involves only the
intraduodenal portion of the common bile duct. The type
IV cyst is subdivided into type IVA, multiple intrahepatic
and extrahepatic cysts, and type IVB, multiple extrahe-
patic cysts. Caroli disease, historically referred to a type V
choledochal cyst, is characterized by multiple intrahepatic
cysts. It is no longer considered a true choledochal cyst
and is now classified as a separate disorder. Choledochal
cysts in neonates and young infants may coexist with bil-
iary atresia.
Sonography shows a well-defined, fluid-filled mass in
the porta hepatis that is in continuity with the extrahe-
patic bile duct and is separate from the gallbladder
(Fig. 8.35) (82,85). Large cysts may contain biliary sludge.
Intrahepatic biliary duct dilatation is present in about half
of affected patients and is limited to the central portions
of the left and right main hepatic ducts (Fig. 8.35). Gen-
eralized intrahepatic ductal dilatation, typical of acquired
obstruction, is absent. The choledochocele differs from
the other choledochal cysts and appears as a fluid-filled
mass that protrudes into the wall of the duodenum. Of
Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 295
IB IC
III
IVB
note, choledochal cysts tend to be smaller and ductal
dilatation is absent when there is concomitant biliary
atresia (68,69).
Complications associated with choledochal cysts
include stone formation in the cyst, gallbladder, or pancre-
atic duct; ascending cholangitis; intrahepatic abscess; bil-
iary cirrhosis; pancreatitis; and neoplasia (82). Adenocar-
cinoma is the most common associated neoplasia. The risk
of malignancy increases with increasing patient age. Large
choledochal cysts may cause duodenal obstruction (87).
The definitive treatment is surgical removal with biliary
drainage via a Roux-en-Y loop (hepaticojejunostomy).
Caroli Disease
Caroli disease, also known as congenital cystic dilation of
the intrahepatic biliary tract, has two forms. One form is
characterized by saccular dilation of the intrahepatic bile
ducts, calculus formation and cholangitis, and the absence
of cirrhosis and portal hypertension. Patients may present
with pain, fever, and jaundice. The second form is associated
with congenital hepatic fibrosis and portal hypertension.
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296 P E D I AT R I C S O N O G R A P H Y
A B
C (R) hepatic ducts.
Stone formation and cholangitis are absent or occur late in
the patients course. Patients may present with portal hyper-
tension.
Both forms of Caroli disease are associated with renal
cystic disease, including cysts in the medulla and cortex
and at the corticomedullary junction (88). Patients with
Caroli disease, like those with choledochal cysts, have an
increased risk of developing cholangiocarcinoma.
Sonography shows multiple dilated tubular and cystic
structures, typical of biliary radicals. These can extend to the
periphery of the liver. The dilated ducts may contain intralu-
minal protrusions arising from the wall, echogenic bands or
bridges, and small fibrovascular bundles that produce an
echogenic dot in the nondependent part of the dilated duct,
called the central dot sign (Fig. 8.36) (89). Color Doppler
examination can show arterial flow in the vascular radicles
(90). The extrahepatic bile ducts can be normal, narrowed,
or associated with a choledochal cyst. Renal findings include
enlarged kidneys, cortical or medullary cysts, and highly
Choledochal cyst. A: Transverse sonogram demonstrates
Fig. 8.35
fusiform dilatation of the common hepatic duct (CHD),
which is separate from the gallbladder (GB), and a dilated left hepatic
duct (HD). B: Longitudinal scan shows the dilated common bile (CD)
extending to the pancreatic head (P). C: Intraoperative cholangiogram
showing a dilated common bile duct (CD) and dilated left (L) and right
echogenic medullary pyramids. Findings of portal hyperten-
sion may be present in patients with hepatic fibrosis. Demon-
stration of continuity of the intrahepatic cysts with the bile
ducts is important to exclude autosomal dominant renal cys-
tic disease, polycystic liver disease, and simple liver cysts.
Spontaneous Perforation of the Extrahepatic Bile Ducts
Spontaneous perforation of the extrahepatic bile ducts is
a cause of neonatal jaundice and ascites. The pathogene-
sis is uncertain, but it has been suggested that the wall of
the common bile duct is weakened either by dilatation due
to stenosis, stricture, cholelithiasis, or inspissated bile, or
by a localized congenital weakness. If biliary pressure
increases, as a result of obstruction of the distal common
bile duct, the weakened wall may dilate and rupture. The
result of perforation is either bile ascites or a loculated
bile collection (i.e., biloma), which can subsequently rup-
ture into the peritoneal cavity. The most frequent site of
perforation is the junction of the cystic and common bile
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Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 297

A B

Caroli disease. A: Transverse sonogram demonstrates

Fig. 8.36
multiple dilated biliary ducts in the right lobe posteriorly.
PV  portal vein. B: High-resolution sonogram shows the central dot
sign (arrows) representing fibrovascular bundles. C: Computed tomog-
raphy scan demonstrates multiple dilated ducts, some of which con-
C verge posteriorly, creating more saccular areas.

ducts. Rarely, the perforation involves the common
hepatic duct, gallbladder, or junction of the cystic duct
and gallbladder (91).
Affected infants present in the first 3 months of life
with ascites, mild jaundice, failure to thrive, and abdomi-
nal distension. The serum bilirubin level is elevated, while
other liver function tests are normal. This feature is help-
ful in differentiating perforation from neonatal hepatitis
and biliary atresia, which have similar clinical findings but
abnormal liver function tests (91).
Sonography demonstrates a nondilated biliary tree and
generalized ascites or a loculated fluid collection in the porta
hepatis (Fig. 8.37) (91). Echogenic debris or fine septations
may be present within the ascitic fluid. Gallbladder, distal
common duct or extraluminal calculi also may be noted.
The biliary tree is not dilated because it is not obstructed.
Surgical placement of a drainage tube in the area of
perforation usually results in spontaneous closure. Suture
repair of the common duct and placement of a transhe-
patic stent are rarely required.
Inspissated Bile Syndrome
The inspissated bile syndrome (also known as bile plug
syndrome) refers to extrahepatic bile duct obstruction by
biliary sludge. There are no underlying anatomic abnor-
malities of the liver. This condition predominantly affects
full-term infants. Causes of bile inspissation include
hemolysis, total parenteral nutrition, various intestinal
diseases (Hirschsprung disease, intestinal atresias, and
stenoses), and cystic fibrosis. Sonography shows dilated
intrahepatic and/or extrahepatic bile ducts that contain
highly echogenic bile without acoustic shadowing (Fig.
8.38). Sludge also may be seen within the gallbladder lumen.
Blunt abdominal trauma, surgical procedures, and
hepatic biopsies can cause bleeding into the ducts. The
appearance is similar to that of inspissated bile.
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A B

Spontaneous perforation of the common bile duct.

Fig. 8.37
A: Transverse sonogram through the upper abdomen
shows a calculus (arrow) in the gallbladder neck. B: More caudad, a
loculated fluid (F) collection and an extraluminal calculus (arrow) are
noted in the porta hepatis. C: Intraoperative cholangiogram confirms
perforation (arrow) of the common bile duct at its junction with the
C cystic duct.

Inspissated bile. Longitudinal image shows echogenic,

Fig. 8.38
nonshadowing bile (arrows) in a dilated common hepatic
and common bile duct.
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Sclerosing cholangitis. Transverse scan shows a dilated
Fig. 8.39
common hepatic duct (calipers  8 mm diameter) and
dilated, thick-walled intrahepatic ducts with areas of segmental
narrowing.
Inflammatory Diseases of the Bile Ducts
SCLEROSING CHOLANGITIS
Sclerosing cholangitis is a chronic cholestatic disorder char-
acterized by obliterative fibrosis of the extrahepatic and
intrahepatic bile ducts leading to biliary cirrhosis (92). The
disease usually affects adolescents and adults rather than
younger children. It has been associated with chronic
inflammatory bowel disease, Langerhans cell histiocytosis,
and immunodeficiency disorders (66,92). Histologic exam-
ination shows multiple segmental strictures, diverticula
A B
Acquired immunodeficiency syndromerelated cholangitis. A: Longitudinal sonogram shows a thick-walled gallbladder with perichole-
Fig. 8.40
cystic fluid (arrows). B: Transverse sonogram demonstrates intrahepatic ductal dilatation with focal narrowing.
Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 299
formation between areas of stricture, and mural thickening
of the bile ducts. Clinical manifestations include jaundice
and right upper quadrant pain. Liver function tests show a
cholestatic profile.
Sonographic findings include dilated, thick-walled
intrahepatic ducts that are focally narrowed secondary to
stricture formation (Fig. 8.39). Other findings include
cholelithiasis, intraductal stones, and a thick-walled gall-
bladder. In long-standing disease, sonography may show
findings of cirrhosis and portal hypertension.
ACQUIRED IMMUNODEFICIENCY SYNDROMERELATED CHOLANGITIS
Biliary tract abnormalities in patients with AIDS are acal-
culous cholecystitis and cholangitis. The inflammatory
changes may be caused by the immune deficiency itself or
secondary to infection by opportunistic organisms, such as
cytomegalovirus, Cryptosporidium, or Mycobacterium
avium-intracellulare. The sonographic findings in AIDS-
related cholangitis are similar to those of sclerosing cholan-
gitis and include dilated, thick-walled intrahepatic ducts
with segmental narrowing and a thick-walled, dilated gall-
bladder (19,93) (Fig. 8.40). An additional finding of AIDS-
related cholangitis is a hyperechoic nodule in the distal end
of the common bile duct, caused by edema of the papilla of
Vater (94).
Biliary Tract Obstruction
The sonographic diagnosis of biliary obstruction is based on
the demonstration of dilated intrahepatic or extrahepatic
bile ducts. Dilated intrahepatic biliary radicles appear as
multiple, anechoic branching structures that enlarge as they
approach the porta hepatis. The intrahepatic ducts are con-
sidered dilated if their diameter exceeds 2 mm or is more
than 40% of the diameter of the adjacent portal vein. The
use of Doppler techniques allows a more confident diagno-
sis of intrahepatic ductal dilatation (Fig. 8.41).
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300 P E D I AT R I C S O N O G R A P H Y
Dilated intrahepatic ducts. Transverse color Doppler image
Fig. 8.41
allows differentiation of vessels and dilated ducts (calipers).
The causes of obstructive jaundice are neoplasm, particu-
larly rhabdomyosarcoma; enlarged nodes in the porta hepatis;
acute pancreatitis; biliary calculi; and, less commonly,
stricture. The appearance of the transition point from a dilated
to narrowed or obliterated duct may help in making a specific
diagnosis. An abrupt change in caliber from a markedly dilated
common duct to one that is obliterated suggests a neoplasm or
stricture, whereas gradual smooth tapering of a mildly or
moderately dilated common bile duct into the pancreatic head
is more characteristic of pancreatitis. Other features of
malignant lesions are masses in the porta hepatis or pancreas,
a dilated gallbladder, and invasion of adjacent vessels or other
retroperitoneal structures. A common bile duct calculus
often produces gradual tapering of the common bile duct
with an abrupt termination at the level of the calculus.
A B
Choledocholithiasis. A: Longitudinal sonogram through the gallbladder demonstrates stones (arrows) with acoustic shadowing. B: Lon-
Fig. 8.42
gitudinal scan at head of the pancreas shows multiple small stones (arrows) in a dilated distal common bile duct (diameter  7 mm).
SPECIALIZED TECHNIQUES FOR IMAGING OBSTRUCTION
Valsalva Maneuver
Sonography at the end of the Valsalva maneuver may help
differentiate between obstructed and nonobstructed bile
ducts (95). The diameter of the common duct at the level of
the main portal vein is measured during quiet respiration and
the Valsalva maneuver. Normal and nonobstructed ducts
demonstrate a positive response to the Valsalva maneuver
(i.e., a decrease in ductal diameter 1 mm). In extrahepatic
biliary obstruction, the duct does not change in size. The sen-
sitivity and specificity of this sonographic finding in predict-
ing extrahepatic biliary obstruction exceed 90%.
Postprandial Sonography
Sonography after a fatty meal is another technique to
improve the accuracy of diagnosing biliary obstruction.
Normal ducts either remain stable or decrease in size. In
ductal obstruction, the common bile duct usually increases
in size (2 mm). The optimal time to assess the response
to fat stimulation is 45 to 60 minutes after the meal.
SONOGRAPHIC ACCURACY
False-negative examinations (i.e., normal bile duct size
with biliary obstruction) can occur in early complete, par-
tial, or intermittent obstruction. A cause of a false-negative
response to a fatty meal or the Valsalva maneuver is
fibrotic or rigid duct that is unable to change caliber. False-
positive examinations (dilated bile ducts without biliary
obstruction) may occur following cholecystectomy.
Choledocholithiasis
Stones in the common bile duct usually originate in the
gallbladder and migrate distally. The calculi can obstruct
anywhere in the biliary duct, but most cause obstruction at
the level of the pancreatic head (Fig. 8.42). Patients usually
present with abdominal pain or, less commonly, with pan-
creatitis or cholangitis. The sonographic diagnosis is based
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Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 301

PITFALLS IN DIAGNOSIS (PSEUDOCALCULI)

Air in bowel adjacent to the duct may mimic a common
duct stone. This artifact can be recognized by scanning the
patients in different positions and also by carefully follow-
ing the course of the duct. Gas-filled bowel will move or
show peristalsis.
The right hepatic artery can indent the proximal com-
mon bile duct, producing an echo, which can be mistaken
for an intraductal calculus. The absence of associated
P acoustic shadowing as well as scanning in different planes
should demonstrate that the origin of the echo is from the
wall of the hepatic artery. Prominent folds secondary to
ductal tortuosity may cause distal shadowing and may
mimic intraductal stones.

Cystic Duct Stones

Choledocholithiasis. Longitudinal sonogram shows a
Fig. 8.43
dilated common bile duct (calipers), measuring 8 mm, and
a small impacted calculus (arrow) in the distal duct. The stone has the
same echogenicity as the pancreatic head (P), making identification of
its margins difficult. The acoustic shadow is the clue to the diagnosis.
on demonstration of a stone in the bile duct. A distal
impacted calculus can be difficult to detect because of adja-
cent or overlying bowel gas (Fig. 8.43) and because the cal-
culus is surrounded by the echogenic pancreatic head.
Scanning with the patient in an oblique or erect position
may improve detection of a distal duct stone. Identifying
acoustic shadowing also can aid in stone detection.
The demonstration of stones within the cystic duct is
difficult because of the small caliber of the duct. How-
ever, stones or sludge may be visible when the duct is
dilated.
Mirizzi syndrome is a rare cause of extrahepatic biliary
obstruction in children. It is secondary to an impacted cys-
tic duct stone, which causes extrinsic compression or
inflammatory stricture of the common duct, resulting in
obstructive jaundice. The usual sites of impaction are the
proximal cystic duct near the neck of the gallbladder and
the distal cystic duct near its insertion into the common
duct. Sonographic findings include calculi in the gallbladder
neck or in the cystic duct, dilated intrahepatic ducts includ-
ing the common hepatic duct, and a normal-sized common
bile duct below the level of the cystic duct stone (Fig. 8.44).
Biliary Duct Neoplasms
Rhabdomyosarcoma of the biliary tract is rare, but it is the
most common neoplasm of the biliary tract in children.

A B
Cystic duct stone. A: Longitudinal sonogram shows a large echogenic calculus (calipers) in the cystic duct. A smaller calculus (arrow)
Fig. 8.44
is noted in the common bile duct, which is dilated. B: Intraoperative cholangiogram shows the stone in the cystic duct (arrow).
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302 P E D I AT R I C S O N O G R A P H Y
Rhabdomyosarcoma. Transverse scan demonstrates an
Fig. 8.45
echogenic mass (arrows) in the porta hepatis and intra-
ductal biliary dilatation (arrowheads).
Rhabdomyosarcomas usually arise in the porta hepatis.
The tumor has two age peaks of occurrence, with the first
occurring between 2 and 6 years of age and the second
between 14 and 18 years of age. Affected patients present
with obstructive jaundice (96). Rhabdomyosarcoma
spreads by direct extension to contiguous structures or by
hematogenous or lymphatic dissemination to lymph nodes,
lungs, bone, bone marrow, or liver. The sonographic find-
ings of biliary tract rhabdomyosarcoma are intrahepatic
and extrahepatic ductal dilatation and a mass in the porta
hepatis (Fig. 8.45).
Granular cell tumor is a rare benign tumor that can
occur anywhere along the biliary tree. It tends to affect
young African American girls (97,98). The tumor appears
as an echogenic intraductal mass. The intrahepatic and
extrahepatic bile ducts proximal to the tumor and the gall-
bladder are dilated. The differential diagnosis includes rhab-
domyosarcoma. Tissue sampling is required for diagnosis.
PITFALLS IN DIAGNOSIS
Sludge within the common duct appears echogenic and
thus may mimic intraductal tumor. The diagnosis of sludge
is usually possible based on the clinical history, absence of
a demonstrable mass, and resolution of the sludge on serial
sonograms.
Biliary Duct Strictures
Biliary stricture is an uncommon cause of ductal obstruc-
tion, but the diagnosis needs to be considered in patients
with biliary obstruction in whom no other obstructing
lesion can be visualized. An abrupt transition from a
dilated duct to one of normal caliber is a finding suggestive
of stricture.
REFERENCES
1. Wolson AH. Ultrasound measurements of the gallbladder. In:
Goldberg BB, Kurtz AB, eds. Atlas of ultrasound measure-
ments. Chicago, IL: Year Book Publishers, Inc., 1990:108112.
2. Jeffrey RB, Nino-Murcia M, Ralls PW, et al. Color Doppler
sonography of the cystic artery: comparison of normal controls
and patients with acute cholecystitis. J Ultrasound Med
1995;14:3336.
3. Tessler FN, Tublin ME. Blood flow in healthy gallbladder walls on
color and power Doppler sonography: effect of wall thickness and
gallbladder volume. AJR Am J Roentgenol 1999;173:12471249.
4. Meilstrup JW, Hopper KD, Thieme GA. Imaging of gallbladder
variants. AJR Am J Roentgenol 1991;157:12051208.
5. Jackson RJ, McClellan D. Agenesis of the gallbladder. Am Surg
1989;55:3640.
6. Pradeep VM, Ramachandran K, Sasidharan K. Anomalous posi-
tion of the gallbladder: ultrasonographic and scintigraphic demon-
stration in four cases. J Clin Ultrasound 1992;20:593597.
7. Diaz MJ, Fowler W, Hantow BJ. Congenital gallbladder dupli-
cation: preoperative diagnosis by ultrasonography. Gastrointest
Radiol 1991;16:198200.
8. Huang BK, Chess MA. Cholecystitis of a duplicated gallbladder
complicated by a cholecystoenteric fistula. Pediatr Radiol 2009;
39:385388.
9. Starinsky R, Strauss S, Vinograd I, et al. Duplicated gallbladder
in a child: sonographic appearance. J Clin Ultrasound 1991;19:
575577.
10. Adear H, Barki Y. Multiseptate gallbladder in a child: inciden-
tal diagnosis on sonography. Pediatr Radiol 1990;20:192.
11. Pery M, Kaftori JK, Maran H, et al. Ultrasonographic appear-
ance of multiseptate gallbladder: report of a case with coexist-
ing choledochal cyst. J Clin Ultrasound 1985;13:570573.
12. Strauss S, Starinsky R, Alon Z. Partial multiseptate gallbladder:
sonographic appearance. J Ultrasound Med 1993;4:201203.
13. Akata D, Akhan O, Ozcelik U, et al. Hepatobiliary manifesta-
tions of cystic fibrosis in children: correlation of CT and US
findings. Eur J Radiol 2002;41:2633.
14. Mueler-Abt PR, Frawley KJ, Greer RM, et al. Comparison of
ultrasound and biopsy in children with cystic fibrosis related
liver disease. J Cystic Fibros 2007;7:215221.
15. Dickey KW, Barth RA, Stewart JA. Recurrent transient
gallbladder wall thickening associated with interleukin-2
chemotherapy. J Clin Ultrasound 1993;21:5861.
16. Kim TS, Kim I-O, Kim WS, et al. Involvement of the gallblad-
der in childhood metachromatic leukodystrophy: ultrasono-
graphic findings. J Ultrasound Med 1996;15:821825.
17. Chung CJ, Sivit CJ, Rakusan TA, et al. Hepatobiliary abnor-
malities on sonography in children with HIV infection. J Ultra-
sound Med 1994;13:205210.
18. Vriesman AC, Engelbrecht MR, Smithuis R, et al. Diffuse gall-
bladder wall thickening: differential diagnosis. AJR Am J
Roentgenol 2007;188:495501.
19. Teefey SA, Baron RL, Bigler SA. Sonography of the gallbladder:
significance of striated (layered) thickening of the gallbladder
wall. AJR Am J Roentgenol 1991;156:945947.
20. Gilger MA. Diseases of the gallbladder. In: Wyllie R, Hyams JS,
eds. Pediatric gastrointestinal disease. 3rd ed. Philadelphia, PA:
Saunders Elsevier, 2006:9891001.
21. Suchy FJ, McEvoy CF. Biliary tract disease in children. Pediatr
Gastorenterol 1996;43:7598.
22. Gubernick JA, Rosenberg HK, Ilaslan H, et al. US approach to
jaundice in infants and children. Radiographics 2000;20:173195.
23. Boctor D. Cholelithiasis. In: Liacouras CA, Piccoli DA, eds.
Pediatric gastroenterology. Requisites in pediatrics. Philaldel-
phia, PA: Mosby Elsevier, 2008:243252.
24. Stringer MD, Soloway RD, Taylor DR, et al. Calcium carbon-
ate gallstones in children. J Pediatr Surg 2007;42:16771682.
LWBK505-C08_p275-304.qxd 7/7/10 1:30 PM Page 303 Aptara Inc
25. Shapiro RS, Winsberg F. Comet-tail artifact from cholesterol
crystal: observations in the postlithotripsy gallbladder and an
in-vitro model. Radiology 1990;177:153156.
26. Brown DL, Teele RL, Doubilet PM, et al. Echogenic material in
the fetal gallbladder: sonographic and clinical observations.
Radiology 1992;182:7376.
27. Devonald KJ, Ellwood DA, Colditz PB. The variable appear-
ances of fetal gallstones. J Ultrasound Med 1992;11:579585.
28. Suchet IB, Labatte MF, Dyck CS, et al. Fetal cholelithiasis: a
case report and review of the literature. J Clin Ultrasound
1993;21:198202.
29. Hammond DI. Unusual causes of sonographic nonvisualization
or nonrecognition of the gallbladder: a review. J Clin Ultra-
sound 1988;16:7785.
30. Paulson EK, Kliewer MA, Hertzberg BS, et al. Diagnosis of
acute cholecystitis with color Doppler sonography: significance
of arterial flow in thickened gallbladder wall. AJR Am J
Roentgenol 1994;162:11051108.
31. Konno K, Ishida H, Naganuma H, et al. Emphysematous chole-
cystitis: sonographic findings. Abdom Imaging 2002;27:191195.
32. Avni EF, Rypen F, Cohen E, et al. Pericholecystic hypere-
chogenicities in necrotizing enterocolitis: a specific sonographic
sign. Pediatr Radiol 1991;21:179181.
33. McDonnell CH III, Jeffrey RB Jr, Vierra MA. Inflamed peric-
holecystic fat: color Doppler flow imaging and clinical features.
Radiology 1994;193:547550.
34. Teefey SA, Baron RL, Radke HM, et al. Gangrenous cholecysti-
tis: new observations on sonography. J Ultrasound Med 1991;10:
603606.
35. Simeone JF, Brink JA, Mueller PR, et al. The sonographic diag-
nosis of acute gangrenous cholecystitis: importance of the Mur-
phy sign. AJR Am J Roentgenol 1989;152:289290.
36. Sood BP, Kalra N, Gupta S, et al. Role of sonography in the diagno-
sis of gallbladder perforation. J Clin Ultrasound 2002;30:270274.
37. Chau W-K, Wong K-B, Chan S-C, et al. Ultrasonic hole sign:
a reliable sign of perforation of the gallbladder? J Clin Ultra-
sound 1992;20:294299.
38. Tsakayannis DE, Kozakewich PW, Lillehei CW. Acalculous
cholecystitis in children. J Pediatr Surg 1996;31:127131.
39. Ryu JK, Ryu KH, Kim KH. Clinical features of acute acalculous
cholecystitis. J Clin Ultrasound 2003;36:166169.
40. Raduns K, McGahan JP, Beal S. Cholecystokinin sonography:
lack of utility in diagnosis of acute acalculous cholecystitis. Radi-
ology 1990;175:463466.
41. Suddelson EA, Reid B, Woolley MM, et al. Hydrops of the gall-
bladder associated with Kawasaki syndrome. J Pediatr Surg
1987;22:956959.
42. Levard G, Weil D, Barret D, et al. Torsion of the gallbladder in
children. J Pediatr Surg 1994;29:569570.
43. Alberti D, Callea F, Camoni G, et al. Adenomyomatosis of the
gallbladder in childhood. J Pediatr Surg 1998;33:14111412.
44. Yoshimitsu K, Honda H, Aibe H, et al. Radiologic diagnosis of
adenomyomatosis of the gallbladder: comparative study among
MRI, helical CT and transabdominal US. J Comput Assist
Tomogr 2001;25:843850.
45. Barzilai M, Lerner A. Gallbladder polyps in children: a rare
condition. Pediatr Radiol 1997;27:5456.
46. Beck PL, Shaffer EA, Gall DG, et al. The natural history and
significance of ultrasonographically defined polypoid lesions of
the gallbladder in children. J Pedatri Surg 2007;42:19071912.
47. Hallgrimsson P, Skaane P. Hypoechoic solitary inflammatory
polyp of the gallbladder. J Clin Ultrasound 1988;16:603604.
48. Levy AD, Murakata LA, Abbott RM, et al. From the archives of the
AFIP. Benign tumors and tumorlike lesions of the gallbladder and
extrahepatic bile ducts: radiologic-pathologic correlation. Armed
Forces Institute of Pathology. Radiographics 2002;22:376413.
49. Stringer MD, Ceylan J, Ward K, et al. Gallbladder polyps in
children-classification and management. J Pediatr Surg 2003;38:
16801684.
Chapter 8 G A L L B L A D D E R A N D B I L I A R Y T R A C T 303
50. Chawla Y, Dilawari JB, Katariya S. Gallbladder varices in por-
tal vein thrombosis. AJR Am J Roentgenol 1994;162:643645.
51. Yamada RM, Hessel G. Ultrasonographic assessment of the
gallbladder in 21 children with portal vein thrombosis. Pediatr
Radiol 2005;35:290294.
52. Akay HO, Senturk S, Cigdem MK, et al. Isolated traumatic
gallbladder rupture: US findings and the role of repeat US in
diagnosis. Pediatr Radiol 2008;38:691693.
53. Bret PM, de Stempel JV, Atri M, et al. Intrahepatic bile duct and
portal vein anatomy revisited. Radiology 1988;169:405407.
54. Lim JH, Ryu KN, Ko YT, et al. Anatomic relationship of intra-
hepatic bile ducts to portal veins. J Ultrasound Med 1990;9:
137143.
55. Lim JH. Papilla of Vater: normal sonographic appearance.
J Ultrasound Med 1996;15:3335.
56. Hernanz-Schulman M, Ambrosino MM, Freeman PC, et al.
Common bile duct in children: sonographic dimensions. Radi-
ology 1982;145:437.
57. Wachsberg RH. Respiratory variation of extrahepatic bile
duct diameter during ultrasonography. J Ultrasound Med
1994;13:617.
58. Willson SA, Gosink BB, VanSonnenberg E. Unchanged size of a
dilated common bile duct after a fatty meal: results and signifi-
cance. Radiology 1986;160:2931.
59. Balistreri WF, Grand R, Hoofnagle JH, et al. Biliary atresia: cur-
rent concepts and research directions. Summary of a sympo-
sium. Hepatology 1996;23:16821690.
60. Jonas MM, Perz-Atayde AR. Liver diseases in infancy and
childhood. In: Schiff ER, Sorrell MF, Maddrey WC, eds. Dis-
eases of the liver. 10th ed. Philadelphia, PA: Lippincott
Williams & Wilkins, 2007:13051347.
61. Siegel MJ. Jaundice in infants and children. Ultrasound Clin
North Am 2006;1:431441.
62. Alagille D, Estrada A, Hadchouel M, et al. Syndromic paucity
of interlobular bile ducts (Alagille syndrome or arteriohepatic
dysplasia): review of 80 cases. J Pediatr 1987;110:195200.
63. Brunelle F. Choledocholithiasis in children. Semin Ultrasound
CT MR 1987;8:118125.
64. Anupindi SA, Victoria T. Magnetic resonance cholangiopancre-
atography: techniques and applications. Magn Reson Imaging
Clin N Am 2008;16:453466.
65. Siegel MJ. Liver and biliary tract. In: Siegel MJ, ed. Pediatric
body CT. 2nd ed. Philadelphia, PA: Lippincott Williams &
Wilkins; 2008:177216.
66. Mieli-Vergani G, Hadzic N. Biliary atresia and neonatal disor-
ders of the bile ducts. In: Wyllie R, Hyams JS, eds. Pediatric gas-
trointestinal and liver disease. 3rd ed. Philadelphia, PA: Saun-
ders Elsevier, 2006:869881.
67. Ng VL. Neonatal hepatitis. In: Wyllie R, Hyams JS, eds. Pediatric
gastrointestinal and liver disease. 3rd ed. Philadelphia, PA:
Saunders Elsevier, 2006:851868.
68. Kim WS, Kim IO, Yeon KM, et al. Choledochal cyst with or
without biliary atresia in neonates and young infants: US dif-
ferentiation. Radiology 1998;209:465469.
69. Torrisi JM, Haller JO, Velcek FT. Choledochal cyst and biliary
atresia in the neonate: imaging findings in five cases. AJR Am
J Roentgenol 1990;155:12731276.
70. Carceller A, Blanchard H, Alvarez F, et al. Past and future of
biliary atresia. J Pediatr Surg 2000;35:717720.
71. Choi S-O, Park W-H, Lee H-J, et al. Triangular cord: a sono-
graphic finding applicable in the diagnosis of biliary atresia.
J Pediatr Surg 1996;31:363366.
72. Humphrey TM, Stringer MD. Biliary atresia: US diagnosis.
Radiology 2007;244:845851.
73. Kendrick APT, Phua KB, Subramaniam R, et al. Making the
diagnosis of biliary atresia using the triangular cord sign and
gallbladder length. Pediatr Radiol 2000;30:6973.
74. Kanegawa K, Akasaka Y, Kitamura E, et al. Sonographic diagno-
sis of biliary atresia in pediatric patients using the triangular
LWBK505-C08_p275-304.qxd 7/7/10 1:30 PM Page 304 Aptara Inc
304 P E D I AT R I C S O N O G R A P H Y
cord sign versus gallbladder length and contraction. AJR Am
J Roentgenol 2003;181:13871390.
75. Park W-H, Choi S-O, Lee H-J, et al. A new diagnostic approach
to biliary atresia with emphasis on the ultrasonographic trian-
gular cord sign: comparison of ultrasonography, hepatobiliary
scintigraphy, and liver needle biopsy in the evaluation of infan-
tile cholestasis. J Pediatr Surg 1997;32:15551559.
76. Park W-H, Choi S-O, Lee H-J. The ultrasonographic triangu-
lar cord couples with gallbladder images in the diagnostic pre-
diction of biliary atresia from infantile intrahepatic cholestasis.
J Pedatr Surg 1999;34:17061710.
77. Lee MS, Kim M-J, Lee M-J, et al. Biliary atresia: color Doppler
US findings in neonates and infants. Radiology 2009;252:
282289.
78. Kim WS, Cheon J-C, Youn BJ, et al. Hepatic arterial diameter
measured with US: adjunct for US diagnosis of biliary atresia.
Radiology 2007;245:549555.
79. Ikeda S, Sera Y, Ohshiro H, et al. Gallbladder contraction in
biliary atresia: a pitfall of ultrasound diagnosis. Pediatr Radiol
1998;28:451453.
80. Takahashi A, Tsuchida Y, Suzuki N, et al. Incidence of intrahe-
patic biliary cysts in biliary atresia after hepatic portoenterostomy
and associated histopathologic findings in the liver and porta
hepatis at diagnosis. J Pediatr Surg 1999;34:13641368.
81. Herman TE, Siegel MJ. Central dot sign on CT of liver cysts.
J Comput Assist Tomogr 1990;14:10191021.
82. Kim OH, Chung HJ, Choi BG. Imaging of the choledochal cyst.
Radiographics 1995;15:6988.
83. Babbitt DP, Starshak RJ, Clemett AR. Choledochal cyst: a con-
cept of etiology. AJR Am J Roentgenol 1973;119:5762.
84. Savader SJ, Benenati JF, Venbrux AC, et al. Choledochal cysts:
classification and cholangiographic appearance. AJR Am
J Roentgenol 1991;156:327331.
85. Yu J, Turner MA, Fulcher AS, et al. Congenital anomalies and
normal variants of the pancreaticobiliary tract and the pancreas
in adults: part 1, biliary tract. AJR Am J Roentgenol 2006;187:
15361543.
86. Arenas-Jiminez JJ, Gomez-Fernandez-Montes J, Mas-estelles J,
et al. Large choledochocele: difficulties in radiologic diagnosis.
Pediatr Radiol 1999;29:807810.
87. Komuro H, Makino S-I, Tahara K. Choledochal cyst associated
with duodenal obstruction. J Pediatr Surg 2000;35:12591262.
88. Fulcher AS, Turner MA, Sanyal AJ. Case 38: Caroli disease and
renal tubular ectasia. Radiology 2001;220:720723.
89. Lall NU, Hogan MJ. Caroli disease and the central dot sign.
Pediatr Radiol 2009;39:754.
90. Lee M-G, Cho KS, Auh YH, et al. Hepatic arterial color Doppler
signals in Carolis disease. Clin Imaging 1992;16:234238.
91. Haller JO, Conden VR, Berdon WE, et al. Spontaneous perfora-
tion of the common bile duct in children. Radiology 1989;172:
621624.
92. Debray D, Pariente D, Urvoas E, et al. Sclerosing cholangitis in
children. J Pediatr 1994;124:4956.
93. Grumbach K, Coleman BG, Gal AA, et al. Hepatic and biliary
tract abnormalities in patients with AIDS. Sonographic-
pathologic correlation. J Ultrasound Med 1989;8:247254.
94. Da Silva F, Boudghene F, Lecomte I, et al. Sonography in AIDS-
related cholangitis: prevalence and cause of an echogenic nod-
ule in the distal end of the common bile duct. AJR Am J
Roentgenol 1993;160:12051207.
95. Quinn RJ, Meredith C, Slade L. The effect of the Valsalva
maneuver on the diameter of the common hepatic duct in
extrahepatic biliary obstruction. J Ultrasound Med 1992;11:
143145.
96. Wexler LH, Meyer WH, Helman LJ. Rhabdomyosarcoma and
the undifferentiated sarcomas. In: Pizzo PA, Poplack DG, eds.
Principles and practice of pediatric oncology. 5th ed. Philadel-
phia, PA: Lippincott Williams & Wilkins, 2006:9711001.
97. Foulner D. Case report: granular cell tumour of the biliary
tree-the sonographic appearance. Clin Radiol 1994;49:
503504.
98. Reynolds EM, Tsivis PA, Long JA. Granular cell tumor of
the biliary tree in a pediatric patient. J Pediatr Surg 2000;35:
652654.
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Spleen and Peritoneal Cavity
Spleen Malignant Tumors
Sonographic Technique Splenic Infection
Gross Anatomy and Function Splenic Involvement in Pancreatitis
Sonographic Anatomy Splenic Infarction
Anatomic Variants Splenic Vein Thrombosis
Congenital Anomalies Storage Diseases
Splenomegaly Splenic Trauma
Acute Splenic Sequestration
Peritoneal Cavity
Splenic Cysts
Sonographic Technique
Benign Splenic Masses
Normal Anatomy
SPLEEN
The spleen is rarely the site of primary disease, but it is
often secondarily involved by infectious, inflammatory,
and neoplastic conditions originating at other sites.
Sonography provides an easy means of screening for
splenic abnormalities, and it is often the initial imaging
examination performed to evaluate suspected splenic
pathology (1).
Sonographic Technique
The spleen is evaluated with the patient in the supine
position. The right lateral decubitus position can be help-
ful if there is gaseous distention of the stomach or colon
obscuring visualization of the spleen with the patient
supine. Imaging is performed in longitudinal and trans-
verse planes. A 5.0- or 7.5-MHz transducer is adequate
in infants and small children, while a 3-MHz transducer
may be necessary in older children and adolescents. A
higher-resolution linear array transducer can be useful
for evaluation of superficial lesions.
Gross Anatomy and Function
The spleen is an intraperitoneal organ composed of lym-
phoid tissue, red blood cells, and reticuloendothelial cells.
It is the largest unit of lymphatic tissue in the body and
serves two functions: participating in the immune response
and filtering blood.
The spleen is located in the left upper quadrant of the
abdomen, lying between the fundus of the stomach and
the diaphragm. It is invested by a fibroelastic cover,
which gives off numerous fibrous trabeculae. The splenic
pulp is composed of two main tissues: the white pulp and
red pulp. The white pulp is a sheath of lymphatic tissue
that surrounds arteries and contains lymphatic follicles
and reticuloendothelial cells. The red pulp contains
CHAPTER
MARILYN J. SIEGEL
9
Peritoneal Fluid
Ascites
Specific Fluid Collections
Mesenteric Cysts
Benign Peritoneal Tumors
Malignant Masses
Infection
Segmental Omental Infarction
Mesenteric Lymphadenopathy
Trauma
Pneumoperitoneum
blood-filled sinuses (or sinusoids) and mononuclear
phagocytic cells. It is the site where abnormal or senes-
cent red blood cells are filtered prior to removal from the
circulation. Although an active site of red blood cell pro-
duction in the fetus, the spleen is hematopoietically inac-
tive in the child and adult. Hematopoiesis can resume
postnatally in disorders such as thalassemia major and
osteopetrosis.
Sonographic Anatomy
The normal spleen has an inverted comma shape, with
a convex superolateral surface conforming to the shape
of the left hemidiaphragm, and a concave inferior sur-
face conforming to the shape of the left kidney. Other
border-forming structures include the stomach, located
anterior and medial to the spleen, and the tail of the pan-
creas, located medial to the splenic hilum.
On gray-scale images acquired with a lower-resolution
transducer (5.0 to 7.5 MHz), the spleen appears homoge-
neous with an echogenicity that is greater than that of the
kidney and equal to or slightly greater that that of the liver
(Fig. 9.1). With a high-resolution transducer (12 MHz or
greater), discrete nodules may be noted in the parenchyma,
likely representing white pulp lymphoid follicles (2). The
splenic vein and artery follow a fairly straight course
toward the splenic hilum, running transversely behind the
body and tail of the pancreas. They can be seen entering
the hilum on color Doppler interrogation before branching
in the parenchyma (Fig. 9.1C).
The spleen is almost entirely surrounded by peri-
toneum and is held in position by the gastrosplenic and
splenorenal ligaments (Fig. 9.2). These ligaments allow
some mobility of the spleen, but they prevent any substan-
tial displacement. The normal ligaments are not seen sono-
graphically.
305
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A
B

Normal spleen. Longitudinal (A) and transverse gray-scale

Fig. 9.1
(B) views through the left upper quadrant. The spleen (S) is
hyperechoic relative to the normal left kidney (LK). C: Color Doppler
image shows flow in vessels entering the hilum, which then branch
C into the parenchyma.

Diagram of splenic ligaments. GS  gastrosplenic liga-

Fig. 9.2
ment; S  spleen; SR  splenorenal ligament.
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Table 9.1 Normal Splenic Lengths by Age and Sex
Age and Sex
03 mo
F 4.4
M 4.6
36 mo
F 5.2
M 5.8
612 mo
F 6.3
M 6.4
12 y
F 6.3
M 6.8
24 y
F 7.5
M 7.6
46 y
F 8.0
M 8.1
68 y
F 8.2
M 8.9
810 y
F 8.7
M 9.0
1012 y
F 9.1
M 9.8
1214 y
F 9.8
M 10.2
1417 y
F 10.3
M 10.7
Adapted from Megremis SD et al. Spleen length in childhood with US: normal values
based on age, sex and somoatometric parameters. Radiology 2004;231:129134.
Splenic size can be evaluated by measuring length or
volume. Splenic length and volume increase proportionally
with increasing patient age and body size (3,4). Measure-
ment of splenic length is easier to perform than that of
splenic volume, and is thus more frequently utilized in clin-
ical practice. Splenic length is measured in the coronal
plane at the level of the splenic hilum. The upper limits of
normal for splenic length based on patient age are shown
in Table 9.1 (3). Although measurements are available,
visual inspection usually suffices to determine if the spleen
is larger than expected. Extension of the spleen below the
inferior margin of the left kidney or the right hepatic lobe,
medial extension anterior to the aorta, and loss of concav-
ity of the medial surface are signs of splenic enlargement.
Anatomic Variants
VARIATIONS IN POSITION
The spleen is sufficiently soft and pliable that left upper
quadrant masses can cause displacement or deformity of its
Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 307
shape. Likewise, it can move into a more caudal location
when adjacent organs, particularly the left kidney, are surgi-
cally removed or congenitally absent. Congenital diaphrag-
Mean (mm) (SD)
matic eventration or hernia can lead to an intrathoracic
location.
0.57
0.84 SPLENIC LOBULATIONS AND CLEFTS
Occasionally, a lobule of splenic tissue extends medially
0.47 from the inferior portion of the spleen and may be seen
0.65 anterior to the left upper renal pole. Awareness of this vari-
ation is important so that it is not mistaken for an adrenal
0.68
or renal mass. Splenic clefts are common and usually occur
0.78
on the lateral or superior diaphragmatic portion of the
0.69 spleen. They are easily distinguished from a laceration by
0.72 their well-defined margins and absence of perisplenic
hematoma.
0.83
1.07 PSEUDOPERISPLENIC MASS
In some individuals, the left lobe of the liver extends to the
0.74 left lateral abdominal wall, wrapping around the spleen
1.01 and mimicking a perisplenic mass or fluid collection (5)
(see Fig. 7.19, Chapter 7, Gastrointestinal Tract). The
0.99
demonstration of portal triads within the left hepatic lobe,
0.91
continuity of the left hepatic lobe with remaining hepatic
0.92 parenchyma, or movement of the left hepatic lobe over the
1.02 spleen with respiratory motion allows a diagnosis of exten-
sion of a normal left hepatic lobe.
1.09
1.05 Congenital Anomalies
WANDERING SPLEEN AND SPLENIC TORSION
1.02
Wandering spleen refers to a spleen that does not have nor-
0.81
mal fixed ligamentous attachments (gastrosplenic and
0.69 splenorenal ligaments) (6). The ligamentous attachments in
0.90 this condition are elongated, resulting in a highly mobile
spleen that may change position within the abdomen. The
mobile spleen typically rotates centrally or inferiorly. Chil-
dren with wandering spleens may be asymptomatic and
present with a palpable mass on physical examination.
However, they can present with intermittent abdominal
pain if the spleen undergoes intermittent torsion and spon-
taneous detorsion, or they may present with an acute sur-
gical abdomen if splenic torsion with infarction has
occurred (610). Symptomatic children are usually between
3 months and 10 years of age, with most patients being
under 1 year of age.
The sonographic findings are absence of the spleen in
the normal location and a mass elsewhere in the
abdomen with a size, shape, and echotexture similar to
normal spleen (810). The hilum of the spleen is directed
anteriorly. Findings of splenic enlargement, parenchymal
heterogeneity (Fig. 9.3), a twisted splenic pedicle, a
whorled appearance of the pancreatic tail, and ascites
indicate torsion (1113). With infarction, Doppler imag-
ing shows absence of flow within the spleen and in the
splenic artery at the hilum (9,14,15). On serial imaging,
the spleen will demonstrate anechoic areas as it under-
goes liquefaction necrosis and gradually diminishes in
size.
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308 P E D I AT R I C S O N O G R A P H Y
Splenic infarction secondary to torsion of a wandering
Fig. 9.3
spleen. Longitudinal sonogram demonstrates an enlarged
spleen (S) with a heterogeneous echotexture and hypoechoic areas
representing liquefaction necrosis. The spleen is in the mid abdomen.
Complications of splenic infarction include abscess for-
mation, peritonitis, bowel obstruction, pancreatitis, and
necrosis of the pancreatic tail (11,16). Chronic torsion
with venous congestion has been associated with the devel-
opment of gastric varices, splenomegaly, and hyper-
splenism (17). Treatment for uncomplicated wandering
spleen is splenopexy; splenectomy is usually performed for
splenic infarction (9).
ACCESSORY SPLEENS
Accessory spleens are a common anatomic variant and are
secondary to failure of fusion of some of the embryonic
buds of splenic tissue in the dorsal mesogastrium (10).
They have been noted in approximately 15% of autopsy
series in children (18). Most accessory spleens are located
near the splenic hilum, but they may be found along the
course of the splenic vessels or in the pancreatic tail
(10,19). Because of the close relationship of the developing
spleen with the mesonephros and left gonadal anlage, they
can be found in the scrotum or attached to the left ovary,
a condition termed splenogonadal fusion. Although they
are generally single, approximately 10% of patients have
two splenules.
Generally, accessory spleens remain small and are inci-
dental findings of no clinical significance. However, acces-
sory splenic tissue can undergo compensatory hypertro-
phy in patients who have had prior splenectomies for
hematologic diseases (e.g., idiopathic thrombocytopenic
purpura and hemolytic anemia). In these patients, the
accessory splenic tissue can hypertrophy, resulting in
recurrent hypersplenism (20). Hypertrophied accessory
spleens can reach a size of 5 cm or more. Rarely, accessory
spleens can twist on their pedicle, presenting as an acute
abdomen (21).
At sonography, accessory spleens appear as round or
oval, solid structures, usually 2 to 3 cm in diameter, with an
Accessory spleen. Longitudinal view shows a small ovoid
Fig. 9.4
nodule (arrow) at the splenic hilum. The echogenicity is
equal to that of adjacent splenic (S) parenchyma. LK  left kidney.
echogenicity similar to that of the normal spleen (Fig. 9.4).
A feeding artery or draining vein can be seen on Doppler
imaging. Sonographic findings of associated torsion include
a thick-walled, hypoechoic mass and a whorled or twisted
appearance of the vascular pedicle (20,22).
SPLENOSIS
Splenosis is the result of splenic rupture secondary to
trauma or surgery with subsequent autotransplantation
of splenic tissue. The peritoneal cavity is the most com-
mon site of splenosis, but splenic tissue can be found
elsewhere in the abdomen or chest. At sonography, the
splenic nodules in splenosis are round masses that are
indistinguishable from accessory spleens (23). A history
of splenic trauma or splenectomy also supports spleno-
sis, while absence of these clinical attributes favors an
accessory spleen (23). Additionally, the masses in spleno-
sis are distributed throughout the peritoneum and the
retroperitoneum, while accessory spleens are usually
found in the left side of the abdomen near the splenic
hilum.
POLYSPLENIA AND ASPLENIA
Polysplenia and asplenia are part of the spectrum of
anomalies known as heterotaxy or cardiosplenic syn-
dromes. Cardiosplenic syndromes are associated with
cardiac and pulmonary abnormalities along with visceral
heterotaxy.
Polysplenia
Polysplenia is characterized by multiple splenic nodules,
which can be located in the right or left upper quadrants.
Associated abdominal anomalies include interruption of
the inferior vena cava with azygous continuation, short
pancreas, abnormal rotation of the bowel, and renal age-
nesis or hypoplasia (10,2426). Thoracic anomalies
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Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 309

Polysplenia. Transverse sonogram shows multiple echogenic

Fig. 9.5
spleens (S) in the right upper quadrant.

include bilateral left lungs (two lobes and hyparterial Asplenia

bronchus), partial anomalous pulmonary venous return,
bilateral superior vena cava, and cardiac anomalies,
including atrial and ventricular septal defects, transposi-
tion of the great vessels, and pulmonary stenosis or atre-
sia (24).
Sonography shows multiple small, echogenic nodules,
most commonly in the right upper quadrant, but they may
be bilateral (Fig. 9.5) (10). The spleens usually are of
equal size, but there can be one or two large spleens along
with multiple small splenules. Other findings include an
interrupted inferior vena cava; short pancreas, in which
the body and tail are small or absent (Fig. 9.6), and abnor-
mal rotation of the bowel, usually nonrotation or reverse
rotation.
Asplenia is characterized by absence of splenic tissue.
Associated abdominal anomalies include total or partial
sinus inversus, transverse liver, microgastria, intestinal
malrotation, and renal anomalies. Thoracic anomalies
include bilateral morphologic right lungs (trilobed lungs)
and complex cyanotic heart lesions, including single ven-
tricle, atrioventricular canal, transposition of the great ves-
sels, and total anomalous pulmonary venous drainage
(10,24,27,28). The diagnosis of asplenia is important
because affected children are at increased risk for sepsis
and require prophylactic antibiotic therapy.
The sonographic findings of asplenia are an absent
spleen and associated anomalies discussed above (Fig. 9.7).
The left lobe of the liver typically crosses the midline (i.e.,

A B
Polysplenia with short pancreas. A: Transverse sonogram of the left upper quadrant shows a round pancreatic head (arrows). The body
Fig. 9.6
and tail are absent. L  liver. B: Longitudinal scan of the right upper quadrant shows two spleens (S) anterior to the right kidney (RK).
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310 P E D I AT R I C S O N O G R A P H Y
A B
C nal series shows a right-sided stomach and dextrocardia.
transverse liver), extending into the splenic fossa. It is
important not to mistake this extension for the spleen.
SITUS INVERSUS
Situs inversus refers to mirror-image positioning of the vis-
cera and vascular structures. The spleen is located in the
right upper quadrant and has a normal echogenicity.
Splenomegaly
The common disorders associated with splenomegaly in
children are infectious processes, often Epstein-Barr virus
Asplenia. A: Transverse sonogram shows a transverse
Fig. 9.7
liver (L) that extends into the left upper quadrant, filling the
empty splenic fossa. B: The stomach (ST) is in the right upper quad-
rant posterior to the right lobe of the liver (L). C: Upper gastrointesti-
infection and cat-scratch disease; the hemoglobinopathies;
and hematologic malignancies, such as leukemia and lym-
phoma. Other causes of splenic enlargement include portal
hypertension, portal vein thrombosis, storage disorders
such as Gaucher disease and Niemann-Pick disease, and
sequestration of hematologic elements secondary to extra-
corporeal oxygenation (ECMO), presumably related to
splenic pooling of red blood cells that are damaged during
ECMO.
Massive splenomegaly is obvious on sonography, as
the markedly enlarged spleen becomes substantially larger
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Splenomegaly. Longitudinal sonogram through the left
Fig. 9.8
upper quadrant of a patient with lymphoma demonstrates
an enlarged spleen (S) that extends below the inferior margin of the
left kidney (LK).
than the left kidney; measurements generally are not
required for diagnosis (Fig. 9.8). Measurement of splenic
length can be helpful when splenic enlargement is mild. As
noted earlier, age-specific maximal values for normal
splenic lengths have been established (Table 9.1) (3,4).
Although splenomegaly is a nonspecific finding, there
are often other findings that can suggest a specific diagno-
sis. Hepatic heterogeneity, irregular or nodular hepatic con-
tours, an enlarged left lobe, and a dilated portal vein should
suggest the diagnosis of cirrhosis. Hypoechoic lesions can
be seen with infections, including cat-scratch disease and
systemic candidiasis; lymphoma; metastatic disease; and
splenic infarction. Findings of portosystemic collateral ves-
sels can establish the diagnosis of portal hypertension as the
cause of splenomegaly (Fig. 9.9). Retroperitoneal and
mesenteric lymph node enlargement and splenomegaly are
findings suspicious for lymphoma.
Acute Splenic Sequestration
Acute sequestration is an occasional presentation of
homozygous sickle cell anemia. This condition is charac-
terized by rapid massive splenic enlargement, due to
pooling of blood in the sinusoids, with a sudden decrease
in the hematocrit level (1,9). At sonography, the spleen
is enlarged and heterogeneous with areas of increased
and decreased echogenicity related to hemorrhage and
infarction.
Splenic Cysts
Splenic cysts can be congenital, infectious, or posttrau-
matic in origin. Patients may be asymptomatic or present
with epigastric fullness, a palpable left upper quadrant
mass, or chronic, low-grade pain due to compression of
Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 311
Splenomegaly in a patient with portal hypertension. The
Fig. 9.9
varices (arrows) in the splenic hilum indicate that portal
hypertension is the cause of splenic enlargement. S  spleen.
adjacent organs. Acute pain can occur because of infection
or rupture of the cyst (2933). In North America, most
splenic cysts are congenital or posttraumatic. However,
worldwide, parasitic infection usually due to echinococcal
infection is probably the most common cause of splenic
cysts (30).
Congenital cysts, also referred to as epidermoid or
true cysts, are lined by epithelium and surrounded by a
fibrous wall. They usually are solitary and unilocular
and rarely contain calcifications. The fluid within the
cyst can be clear or turbid and may contain protein,
blood, fat, or cholesterol crystals. Posttraumatic cysts
lack an epithelial lining and are considered false cysts or
pseudocysts.
The characteristic sonographic appearance of a splenic
cyst is a well-circumscribed, spherical, hypoechoic or ane-
choic lesion with a smooth wall and through-sound trans-
mission (Fig. 9.10) (33). A rim of splenic tissue usually is
visible around part of the cyst, helping to confirm its
intrasplenic origin (10). Flow is absent on color Doppler
sonography. A complex mass with internal echoes, septa-
tions (Fig. 9.11), or fluid-fluid levels or a homogeneously
echogenic mass can be observed when the cysts contain
cholesterol crystals or breakdown products of hemoglo-
bin. The diagnosis of echinococcal cyst should be sus-
pected if daughter cysts are present within a large cystic
lesion or if cystic lesions are observed in other organs
(29). Rim calcification may be noted in posttraumatic and
parasitic cysts (29,33). Cyst rupture should be suspected if
the cyst has a discontinuous margin and there is free
peritoneal fluid.
The differential diagnostic considerations of a cystic
splenic lesion include abscess, hematoma cystic neoplasm
(lymphangioma and hemangioma), cystic or necrotic metas-
tases, intrasplenic pancreatic pseudocyst, and cerebrospinal
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A B

C D
Splenic cyst. Transverse (A) and longitudinal (B) images in a 5-year-old girl with a palpable left upper quadrant mass shows a round,
Fig. 9.10
sharply marginated, anechoic cyst (C). C: Color Doppler sonogram shows no internal flow. Flow is noted in hilar vessels. D: Computed
tomography scan demonstrates a water attenuation mass. An epidermoid cyst was removed at surgery.

Complex splenic cyst. Transverse sonogram demonstrates

Fig. 9.11
a well-defined fluid-filled cyst with internal septations
(arrows). The lesion is surrounded by a rim of normal splenic
parenchyma (S). Pathologic examination showed a splenic pseudo-
cyst, likely secondary to trauma.
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fluid pseudocyst. The latter is a complication of ven-
triculoperitoneal shunting (34). When clinical or labora-
tory data are inconclusive for a specific diagnosis,
fine-needle aspiration of the cyst contents under sono-
graphic guidance can be helpful for both diagnosis and
drainage.
Benign Splenic Masses
Most splenic tumors in childhood are benign and include
hemangioma, lymphangioma, and hamartoma. Patients
generally are asymptomatic and the lesions are discovered
incidentally, either as a palpable mass on physical exami-
nation or as an incidental finding on an imaging examina-
tion performed for other indications. Large lesions may
produce pain due to compression of adjacent organs, hem-
orrhage, or rupture.
In many cases, the sonographic appearances of the var-
ious masses overlap and clinical correlation, other imaging
studies such as computed tomography (CT) or magnetic
resonance imaging (MRI), or tissue sampling may be
required for diagnosis.
HEMANGIOMA
Hemangiomas are the most common primary splenic neo-
plasm (35,36). They are composed of vascular channels
lined by a single endothelial layer and filled with red blood
cells. Splenic hemangiomas may be seen as an isolated lesion
or as part of a syndrome, including Klippel-Trenaunay-
Weber (capillary port wine stains, venous varicosities,
and soft tissue and bone overgrowth of an extremity)
and Beckwith-Wiedemann syndrome (hemihypertrophy,
macroglossia, and anterior abdominal wall defects) (37,38).
Complications associated with hemangiomas include rup-
A B
Splenic hemangioma. A: Longitudinal sonogram shows a well-defined echogenic mass (arrows) surrounded by normal parenchyma.
Fig. 9.12
B: Longitudinal scan in another patient shows two echogenic hemangiomas (arrows).
Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 313
ture, hypersplenism, and Kasabach-Merritt syndrome
(thrombocytopenia, anemia, and coagulopathy) (35).
The imaging appearance of hemangioma in the spleen
is similar to that in the liver. The lesions are usually well
marginated, homogeneous, and hyperechoic to normal
splenic parenchyma (Fig. 9.12) (35,36,39). However, some
hemangiomas can be hypoechoic and large lesions can be
complex with cystic and solid components. Peripheral or
central calcifications with acoustic shadowing may be
present (36,40). Color signal with arterial waveforms can
be noted on Doppler imaging. Doppler examination, with
and without compression of the lesion by the transducer,
shows that the color signal disappears during compression
and reappears immediately after compression has been
released (41).
LITTORAL CELL ANGIOMA
Littoral cell angioma is a rare vascular neoplasm that is
usually benign but occasionally can have some malignant
features (35,42). It arises in the lining (littoral) cells of the
splenic red pulp sinuses. Histologic examination shows
multiple nodules containing branching vascular channels
lined by endothelial cells. The malignant form has atypi-
cal cells and shows invasion of surrounding organs.
Sonographic findings include splenomegaly and
multiple lesions of varying size, which may be isoechoic,
hypoechoic, or hyperechoic to normal splenic parenchyma
(Fig. 9.13) (35,42,43). Flow may be seen in the lesions on
color Doppler imaging (Fig. 9.13C).
PELIOSIS
Peliosis is a rare condition characterized by multiple
blood-filled spaces without an endothelial lining. It is
associated with human immunodeficiency virus (HIV)
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314 P E D I AT R I C S O N O G R A P H Y

A B

C D
Littoral cell angioma. A, B: Two longitudinal images show heterogeneous splenic echotexture with multiple hypoechoic masses. C: Flow
Fig. 9.13
is noted within the lesions on color Doppler imaging. D: Fat-suppressed T2-weighted image shows multiple high-signal-intensity masses
in the spleen.

infection, disseminated tuberculosis, hematologic malig-

nancies, and use of anabolic steroids (1,35). On sonogra-
phy, peliosis usually appears as multiple small hypoechoic
lesions. These small lesions can coalesce to form a larger
multiloculated mass with septations (35).

LYMPHANGIOMA
Lymphangiomas are congenital malformations of the lym-
phatic system composed of endothelial-lined spaces filled
with lymph and separated by fibrous bands (35). They
may be solitary or multiple (35).
Sonographically, lymphangioma usually appears as a
multilocular cyst containing hypoechoic or anechoic
locules and echogenic septations (Fig. 9.14) (35,44). Less
commonly, it is unilocular. Internal echoes can be seen if
the cyst fluid is hemorrhagic or highly proteinaceous
(Fig. 9.15). Calcifications can be present in the walls or
the septations. The lesion is relatively avascular on Doppler Splenic lymphangioma. Transverse sonogram demon-
sonography, although vessels, representing arteries and Fig. 9.14
strates a multilocular anechoic mass (arrows) with a single
veins, can be identified within the septa. septation (open arrow) in the lower pole of the spleen. LK  left kidney.
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Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 315

A B
Splenic lymphangiomas. Transverse (A) and longitudinal (B) sonograms show multiple echogenic lesions in the splenic parenchyma.
Fig. 9.15
Also noted is a small amount of chylous ascites (A). The lesions contained chylous fluid at pathologic examination.

HAMARTOMA INFLAMMATORY PSEUDOTUMOR

Splenic hamartomas are benign, solid lesions consisting of
an admixture of normal lymphoid tissue and disorganized
congested splenic sinuses (red pulp). They have been asso-
ciated with Beckwith-Wiedemann syndrome and tuberous
sclerosis (35,45). They are typically solitary, but multiple
lesions can occur.
Sonographically, hamartomas usually appear as well-
circumscribed, hypoechoic masses (Fig. 9.16) (35,46).
Occasionally, they appear isoechoic or hyperechoic to
normal spleen or complex with cystic changes. The tumor
is vascular on Doppler imaging (Fig. 9.17) (47,48).
Inflammatory pseudotumors are rare, benign lesions com-
posed of fibroblastic stroma and polymorphous inflam-
matory cells, including plasma cells, lymphocytes, neu-
trophils, and eosinophils (49). The cause is unknown, but
it is speculated that they represent a reparative process of
an inflammatory lesion. At sonography, they appear as
well-circumscribed homogeneous or heterogeneous,
hypoechoic masses (49,50). Calcification may be identi-
fied in the matrix of the lesion or within the wall (Fig.
9.18) (49). Increased flow may be noted on color Doppler
imaging.

Splenic hamartoma. Longitudinal sonogram shows a

Fig. 9.16
hypoechoic mass (calipers) in the lower pole of the spleen.
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A B
Hamartoma. A: Transverse scan show a well-marginated, hypoechoic mass (calipers) in the splenic parenchyma. B: Power Doppler
Fig. 9.17
sonogram shows increased flow in the lesion. (Reprinted from Abbott RM, Levy AD, Aguilerea NS, et al. Primary vascular neoplasms of
the spleen: radiologic-pathologic correlation. Radiographics 2004;24:11371163, with permission.)

A B

Inflammatory pseudotumor. A: Longitudinal gray-scale

Fig. 9.18
image shows a well-defined, hypoechoic mass (arrows)
with slightly heterogeneous echotexture in the upper pole of the
spleen. B: Color Doppler shows increased vascularity. C: Computed
C tomography scan shows heterogeneous enhancement.
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Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 317

A B
Lymphoma. A: Transverse image of the spleen in a patient with Hodgkin lymphoma demonstrates multiple hypoechoic masses (calipers)
Fig. 9.19
in the splenic parenchyma. B: Color Doppler image shows flow in the parenchyma around the lesions, but no flow within the lesions.

Malignant Tumors ANGIOSARCOMA

LYMPHOMA
Lymphoma is the most common malignant splenic neo-
plasm. Splenic involvement occurs in both Hodgkin disease
and non-Hodgkin lymphoma. The affected spleen may or
may not be enlarged, and conversely mild to moderate
splenomegaly may be present in patients in whom no tumor
is identified in the excised spleen. When splenomegaly is
marked, however, the likelihood of involvement by lym-
phoma is high.
The sonographic appearance of lymphoma ranges from
splenic enlargement alone to solitary or multiple masses.
The masses are typically hypoechoic or anechoic and lack
acoustic enhancement (Fig. 9.19) (40,51). They are avas-
cular on Doppler imaging. Associated lymphadenopathy
may be noted in the splenic hilum, mesentery, and retro-
peritoneum.
Angiosarcoma is a very rare malignant splenic tumor com-
posed of disorganized anastomosing vascular channels
lined by endothelial cells with large irregular nuclei and a
high mitotic rate (35,52). Early and widespread metastases
to the liver, lung, bone, and lymph nodes are frequent. The
sonographic appearance is that of a solid or complex mass
(52). Flow may be seen in the solid echogenic parts of the
tumor on Doppler imaging.
METASTATIC DISEASE
Splenic metastases are rarely diagnosed antemortem,
although in postmortem studies, metastatic disease is not

LEUKEMIA
Splenic involvement by leukemia can occur during active
stages of the disease or during remission. On pathologic
section, leukemia primarily involves the red pulp and, in
contrast to lymphoma, discrete nodules are infrequent
(35). Splenomegaly is usually the only imaging finding.
Splenic echogenicity may be normal (i.e., greater than the
kidney) or decreased (equal to or decreased compared with
the kidney). The splenic parenchyma is generally homoge-
nous and focal masses are rarely identified (Fig. 9.20).
Splenic size decreases during treatment and echogenicity
returns to normal.

LANGERHANS CELL HISTIOCYTOSIS Leukemic infiltration. Longitudinal sonogram shows

Langerhans cell histiocytosis may cause splenomegaly or, Fig. 9.20
extension of the spleen (S) below the interior margin of
less commonly, multiple hypoechoic nodules within the the left kidney (LK), indicating splenomegaly. The spleen is isoechoic
spleen (1). relative to the kidney.
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318 P E D I AT R I C S O N O G R A P H Y

Pyogenic abscess. Transverse sonogram demonstrates a

Fig. 9.21
well-defined, round hypoechoic mass (M) with internal
debris (arrowheads) in the splenic parenchyma. Staphylococcus
aureus grew on blood culture.

infrequent. Metastatic lesions are usually small; the spleen
may or may not be enlarged. The lesions are predomi-
nantly hypoechoic to normal parenchyma, but they may
be isoechoic or hyperechoic. They can be homogeneous or
complex, containing cystic and solid components.
the upper extremity or neck. Approximately 5% to 10%
develop disseminated disease involving the spleen and
liver. Sonographically, splenic lesions are multiple, small,
and hypoechoic (Fig. 9.22). Calcifications can be seen in
treated lesions (53).

Splenic Infection FUNGAL ABSCESS

The spleen may be involved by a variety of pyogenic, fun- Fungal abscesses are most often due to Candida albicans
gal, amebic, and opportunistic infections. Patients with infection and occur primarily in immunosuppressed
splenic infection present with fever; abdominal, left shoul- patients, usually those with acute leukemia, lymphoma, or
der, chest, or flank pain; and splenomegaly.

PYOGENIC ABSCESS
Pyogenic abscess usually is a result of hematogenous seed-
ing of infection and less often the result of direct spread
from adjacent organs (usually kidney or pancreas). The
common causative organisms in pyogenic infections are
Staphylococcus aureus, Streptococcus, and gram-negative
organisms, such as Salmonella.
The sonographic appearance of a pyogenic splenic
abscess is similar to that of abscesses in other solid organs,
appearing as a hypoechoic, complex mass with internal
echoes, fluid-fluid levels, or septations (Fig. 9.21). The
margins may be irregular or smooth. Foci of increased
echogenicity with distal acoustic shadowing and/or ring-
down artifact is seen if gas is present within the abscess
cavity. This is specific for the diagnosis of abscess, but it is
not a common finding.
Cat-scratch disease is another cause of bacterial
abscess. It affects children who have been scratched by a
domestic cat and is caused by a gram-negative bacillus,
Bartonella henselae, which incites a granulomatous or sup-
purative reaction. Patients present with painful lym- Cat-scratch disease. Transverse sonogram of the spleen
Fig. 9.22
phadenopathy at the inoculation site, which is typically in demonstrates multiple tiny hypoechoic foci (arrowheads).
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Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 319

A B
Candidiasis. A: Longitudinal sonogram shows several small hypoechoic lesions (arrowheads) in the splenic parenchyma. One lesion
Fig. 9.23
has central echogenicity, creating a bulls-eye appearance (arrow). B: Longitudinal sonogram of an enlarged spleen in another patient
shows multiple tiny hypoechoic lesions.

chronic granulomatous disease. Other fungi resulting in
splenic abscess include Aspergillus and Cryptococcus. The
sonographic patterns of fungal abscesses include (a) a
wheel within a wheel appearance (hypoechoic center sur-
rounded by alternating hyperechoic and hypoechoic rings),
(b) bulls-eye lesion (central echogenic area surrounded by
a hypoechoic rim) (Fig. 9.23), (c) uniformly hypoechoic
lesions, and (d) echogenic foci with acoustic shadowing
(54). The lesions are usually multiple and less than 2 cm in
diameter. Calcifications may be noted after treatment.
ACQUIRED IMMUNODEFICIENCY SYNDROME
Patients with acquired immunodeficiency syndrome (AIDS)
are at increased risk for developing multifocal abscesses.
The common infecting organisms include Pneumocystis
carinii, cytomegalovirus, C. albicans, Mycobacterium
tuberculosis, and Mycobacterium avium-intracellulare
infection (MAI). Sonographic findings are indistinguishable
from those seen in fungal infection and cat-scratch disease
and range from splenomegaly to multiple, small lesions.
Disseminated Pneumocystis can appear as tiny highly
reflective foci in the liver, spleen, kidneys, pancreas, and
mesenteric lymph nodes (55). Splenic abscesses may calcify
following therapy (56). Calcifications also can be seen in
the liver, kidneys and pancreas, and lymph nodes.
Splenic Involvement in Pancreatitis
Although rare, pancreatitis can extend to involve the
spleen because of the close anatomic relationship of the
spleen and splenic vessels to the pancreatic tail. The most
common abnormalities are perisplenic fluid collection,
splenic vein thrombosis (Fig. 9.24), splenic infarction,

A B
Pancreatitis, splenic vein thrombosis. A: Transverse color Doppler image in a young adult male at the expected level of the confluence
Fig. 9.24
of splenic and superior mesenteric veins shows flow in the superior mesenteric vein (arrow) but not in the splenic vein, which was
thrombosed. B: Transverse image through the stomach (ST) shows multiple collateral vessels in the anterior gastric wall.
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320 P E D I AT R I C S O N O G R A P H Y

and subcapsular hemorrhage. Splenic abscess and
pseudoaneurysm formation also have been reported (57).
Pseudocysts arising in the tail of the pancreas adjacent to
the splenic hilum can occasionally extend into the splenic
parenchyma. Gastric, esophageal, and colonic varices can
be seen with splenic vein thrombosis (Fig. 9.24B).
Splenic Infarction
Splenic infarction results from occlusion of the splenic
artery or its branches. In children, hemoglobinopathies,
such as sickle cell disease or sickle thalassemia, are the pri-
mary causes of splenic infarction. Less common causes of
infarction include emboli from a cardiovascular source,
splenic torsion (see above), portal hypertension, and infil-
trative disorders such as Gaucher disease, amyloidosis,
leukemia, and lymphoma. Small infarcts may be asympto-
matic. Large infarcts can cause left upper quadrant or
abdominal pain and fever.
The sonographic appearance of splenic infarction
varies depending on the age of the infarct. An acute infarct
appears as a wedge-shaped hypoechoic lesion in the
periphery of the spleen (Fig. 9.25) (58). The apex of the
lesion is directed toward the splenic hilum and the base
parallels the subcapsular splenic surface. Occasionally, lin-
ear echoes can be noted within the infarcted tissue, repre-
senting intravascular gas (Fig. 9.26). Doppler sonography
reveals absent flow in the areas of infarction (58). How-
ever, arterial signal can be noted if there is superimposed
infection. The gray-scale sonographic appearance of an
acute splenic infarct is nonspecific and indistinguishable
from abscess, hematoma, or tumor.
As the infarct ages, the affected splenic tissue increases
in echogenicity and atrophies. Eventually, the splenic con-
tour retracts secondary to scarring and fibrosis. Chronic
infarction in patients with homozygous sickle cell anemia
often results in a globally small, densely calcified spleen
(Fig. 9.27).
Splenic Vein Thrombosis
Splenic vein thrombosis is most commonly the result of
pancreatitis. The sonographic findings include splenomegaly,
an intraluminal filling defect in the splenic vein, or non-
visualization of the vein (see Fig. 9.24). Splenic vein
thrombosis may result in gastric, esophageal, and colonic
varices.

B
A

Acute splenic infarcts. A: Longitudinal sonogram shows a

Fig. 9.25
peripheral, wedge-shaped, hypoechoic infarct (arrows) in
inferior part of the spleen. B: Longitudinal sonogram in a patient with
sickle cell disease and acute left upper quadrant pain shows a hetero-
geneous spleen with peripheral hypoechogenicity (arrows). C: Color
Doppler image shows perfusion only in the central portion of the
C spleen, not in the peripheral infarcts.
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Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 321

A B
Acute infarction. A: Longitudinal gray-scale sonogram shows multiple linear echoes in the splenic parenchyma (S), representing
Fig. 9.26
intravascular gas. B: Color Doppler sonogram shows absent flow in the splenic (S) hilum. The splenic parenchyma is hypoechoic to
the left kidney (LK).

Sonography in children with Gaucher disease shows a

Storage Diseases
GAUCHER DISEASE
Gaucher disease is an autosomal recessive disorder caused
by deficiency of the lysosomal enzyme glucocerebrosidase,
resulting in accumulation of glucocerebrosides within
macrophages (59). There are two major forms of Gaucher dis-
ease. The less frequent infantile or neuropathic form leads to
progressive central nervous system involvement and death in
the first years of life. The more common nonneuropathic form
presents with hepatosplenomegaly and bone infarctions.
markedly enlarged spleen that may have a homogenous
echotexture or heterogeneous echotexture with hypoe-
choic foci (Fig. 9.28). The latter areas represent clusters of
Gaucher cells, occasionally with areas of fibrosis (59,60).
Rarely, focal lesions are hyperechoic (6062). Following
treatment, these lesions may resolve completely without
sequelae or they can calcify, likely related to infarction
(61). Other storage diseases include Niemann-Pick disease
and the mucopolysaccharidoses, which may have appear-
ances similar to Gaucher disease.

A B
Chronic splenic infarction in a patient with sickle cell anemia. A: Longitudinal sonogram demonstrates a small, intensely echogenic
Fig. 9.27
spleen (arrow) superior to the left kidney. B: Unenhanced computed tomography scan shows a small calcified spleen (S).
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322 P E D I AT R I C S O N O G R A P H Y

Gaucher disease. Multiple hypoechoic lesions are noted in
Fig. 9.28
the splenic parenchyma. (Reprinted from Chippington A,
McHugh K, Vellodi A. Splenic nodules in paediatric Gaucher disease
treated by enzyme replacement therapy. Pediatr Radiol 2008;38:657660,
with permission.)
Splenic laceration. Longitudinal scan shows a complex
Fig. 9.30
injury with several branches (arrows). Increased
echogenicity, representing hematoma (H), is noted posterior to the
fracture line.

SARCOIDOSIS abdominal trauma. However, in stable patients with mini-

Sarcoidosis is a multisystem granulomatous disease of
unknown origin. Abdominal disease has been reported in ado-
lescent patients (63). Imaging findings include splenomegaly
and multiple nodules. Abdominal lymphadenopathy and
hepatomegaly may also be noted.
Splenic Trauma
CT is usually the primary diagnostic imaging to evaluate
hemodynamically stable patients with substantial blunt
mal blunt injury to the left upper quadrant, sonography
can be used to diagnose hematomas, lacerations, and
hemoperitoneum (6468).
Intraparenchymal hematomas appear as rounded or
oval lesions (Fig. 9.29). Splenic lacerations usually involve
the lateral border of the spleen and may be linear (simple)
or branching (complex) (Fig. 9.30). Splenic fractures tra-
verse the entire thickness of the splenic parenchyma. Sub-
capsular hematomas are typically crescent-shaped (Fig.
9.31). Large subcapsular hematomas may flatten the

A B
Acute splenic hematomas. A: Transverse sonogram following blunt trauma demonstrates a round, echogenic, intraparenchymal
Fig. 9.29
hematoma (H) and a linear laceration (arrows). B: Longitudinal sonogram in another patient shows a round, echogenic hematoma
(arrows). LK  left kidney.
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Subcapsular splenic hematoma, subacute injury. Trans-
Fig. 9.31
verse image shows crescentic, hypoechoic fluid (f) col-
lections adjacent to the splenic (S) capsule. ST  stomach.
normally convex lateral splenic margin (Fig. 9.31). Other
findings of splenic trauma include splenomegaly and a left
pleural effusion.
Splenic parenchymal injury has a variable echogenicity
depending on the age of the blood. Acute hematomas, less
than 24 hours old, appear echogenic. The hematoma
becomes increasingly hypoechoic over time as hemoglobin
is resorbed and the clot undergoes lysis.
The use of color Doppler sonography can increase
lesion conspicuity by demonstrating focal avascular
regions in the splenic parenchyma. The presence of
perisplenic fluid or poorly defined or irregular splenic
margins also supports the diagnosis of splenic injury.
Splenic injuries may heal completely with no residual
defect or they may leave a scar or cyst at the site of the
injury. The sonographic finding of scarring is surface
irregularity.
PERITONEAL CAVITY
Primary abnormalities of the peritoneal cavity are rare in
children. However, the peritoneal cavity and its special-
ized folds, the mesentery and omentum, are often
involved in infectious, neoplastic, and traumatic condi-
tions that originate at other sites in the abdomen or
pelvis.
Sonographic Technique
The peritoneal cavity is evaluated with the patient in the
supine position using a standard-frequency transducer that
Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 323
is appropriate for the patients body habitus. The field of
view should include the entire depth of the peritoneal cav-
ity. After the initial survey is complete, a higher-frequency
transducer may be used to further interrogate selected
areas of interest.
Normal Anatomy
The peritoneum is a serous membrane, lined by
mesothelial cells, that extends from the abdomen to the
pelvis. It consists of parietal and visceral peritoneum.
The parietal peritoneum lines the abdominal wall, while
the visceral peritoneum covers solid and hollow viscera.
The peritoneal cavity lies between these two layers. It
contains a series of communicating spaces that are not
usually seen at imaging unless they are distended with
fluid.
LIGAMENTS AND MESENTERIES
The ligaments, which are folds of peritoneum, provide
support for structures within the peritoneal cavity. A lig-
ament that connects the small bowel or parts of the
colon to the posterior abdominal wall is referred to as a
mesentery. A ligament that joins the stomach to other
structures is called an omentum (69). The ligaments,
omentum, and mesenteries can act as pathways for the
spread of pathologic processes within the peritoneal
cavity.
The small bowel mesentery encloses the jejunum,
ileum, and transverse and sigmoid colons, serving as an
outer covering and connecting these segments to the pos-
terior abdominal wall. The root of the small bowel
mesentery extends from the duodenojejunal flexure in the
left upper quadrant to the ileocecal junction in the right
lower quadrant of the abdomen. It contains the superior
mesenteric artery and its branches, the superior mesen-
teric vein and its tributaries, a varying number of lymph
nodes, and fat.
The mesenteries of the transverse and sigmoid colon
are called the transverse and sigmoid mesocolon. The
transverse mesocolon joins the second part of the duode-
num and head of the pancreas to the transverse colon
(70). It contains the middle colic artery and vein. The
sigmoid mesocolon extends from the descending colon
into the pelvis, containing sigmoidal and hemorrhoidal
vessels.
The lesser omentum (also knows as the gastrohepatic
ligament) connects the lesser curvature of the stomach to
the liver. The greater omentum (also known as the gastro-
colic ligament) connects the greater curvature to the trans-
verse colon (Fig. 9.32).
The mesentery encloses the liver and gives rise to its
fibrous capsule and ligaments. There is a bare area in the
posterior part of the right lobe of the liver that is devoid of
peritoneal covering (Fig. 9.32) (71). The liver in this bare
area is attached to the diaphragm by the coronary liga-
ments. The spleen has a peritoneal covering that is limited
medially at the hilum, also resulting in a bare area (71).
As a result of these bare areas, fluid originating from
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324 P E D I AT R I C S O N O G R A P H Y

traumatic, infectious, or inflammatory processes in these

organs can track into the peritoneal cavity or retroperi-
toneum.
There are several other important ligaments in the
upper abdomen: the falciform, hepatoduodenal, duode-
nocolic, gastrosplenic, and splenorenal ligaments. The
falciform ligament connects the liver to the anterior
abdominal wall. The anatomic distribution of the other
ligaments is self-evident by the name of the particular
ligament.

PERITONEAL COMPARTMENTS
The transverse mesocolon divides the peritoneal cavity
into two unequal parts: supramesocolic and inframesocolic
compartments (6971).

Sagittal diagram of greater omentum (G), lesser omentum
Fig. 9.32
(L), and bare area of the liver (arrows). ST  stomach.
Supramesocolic Compartment
The supramesocolic compartment is arbitrarily divided into
left and right peritoneal spaces by the abdominal mesenter-
ies (Fig. 9.33). The left peritoneal space is further subdivided
into four compartments: the anterior and posterior perihe-
patic spaces and the anterior and posterior subphrenic
spaces. The anterior perihepatic space lies anterior to the
liver and is limited medially by the falciform ligament. The
left posterior perihepatic space extends along the undersur-
face of the lateral segment of the left hepatic lobe and is lim-
ited medially by the gastrohepatic ligament. The left anterior

A B
Peritoneal spaces of the upper abdomen. The left peritoneal spaces are indicated by heavy black lines, and the right peritoneal
Fig. 9.33
spaces by vertical hatching. A, B: Four divisions of the left peritoneal space are present. Anterior to the liver, and limited by the fal-
ciform ligament medially, is the left anterior perihepatic space (1). Posterior to the visceral hepatic surface is the left posterior perihepatic space
(2). The anterior subphrenic space (3) lies between the gastric fundus and diaphragm, while the posterior subphrenic (perisplenic) space (4) sur-
rounds the spleen (S). The right peritoneal space consists of the perihepatic space and the lesser sac. The perihepatic space (5) is limited
anteromedially by the falciform ligament and posteromedially by the hepatic bare area. The lesser sac has two components: the superior recess
(6) and inferior recess (7). e  esophagus; L  liver. (From Heiken JP, Menias CO, Elsayes K. Abdominal wall and peritoneal cavity. In: Lee KTL,
Sagel SS, Stanley RJ, et al., eds. Computed body tomography with MRI correlation. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins,
2006:11011153, with permission.)
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Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 325

subphrenic space courses between the gastric fundus and the

diaphragm, while the posterior subphrenic (or perisplenic)
space surrounds the spleen. Below the spleen, the posterior
subphrenic space is separated from the remainder of the
peritoneal cavity by the phrenocolic ligament.
The right peritoneal space has two major divisions:
the right perihepatic space and the lesser sac (Fig. 9.33)
(6971). These two spaces communicate via the epiploic
foramen (foramen of Winslow). The right perihepatic
space consists of a subphrenic and a subhepatic space.
The subphrenic space courses along the anterior and lat-
eral surfaces of the liver, limited on the left by the falci-
form ligament. The subhepatic space continues beneath
the visceral surface of the right lobe, extending medially
and then anterior to the right kidney. The posterior recess
of the perihepatic space is known as the Morison
pouch, which is the most dependent part of the subhe-
patic space. The lesser sac contains two major compart-
ments: a smaller, medial compartment on the right (also
known as the superior recess), which surrounds the
medial surface of the caudate lobe; and a larger lateral
compartment on the left (the inferior recess), which lies
between the stomach and the visceral surfaces of the
spleen and the pancreas.
Spread of peritoneal fluid. Natural flow of intraperitoneal
Inframesocolic Compartment Fig. 9.34
fluid is directed along pathways determined by peri-
The inframesocolic compartment is divided by the toneal reflections and recesses. Fluid within the inframesocolic com-
obliquely oriented small bowel mesentery into a smaller partment preferentially flows into the pelvis, where it accumulates in
right infracolic space and a larger left infracolic space the posterior cul-de-sac and the lateral perivesical fossae. Fluid in
(71). The right infracolic space is limited laterally by the the right infracolic space flows along the recesses of the small
ascending colon and inferiorly by the junction of the bowel mesentery before pooling at the junction of the mesentery
with the cecum. Fluid in the left infracolic space pools in the sigmoid
small bowel mesentery with the cecum. The left infra-
mesocolon before overflowing into the pelvis. Once in the pelvis,
colic space is bordered laterally by the descending colon fluid can flow via the right or left paracolic gutters into the upper
and inferiorly by the sigmoid colon and its peritoneal abdomen. A.C.  ascending colon; D.C.  descending colon; S.B.
reflections. The pouch of Douglas, located posterior to mesentery  small bowel mesentery; Tr mesocolon, transverse
the bladder and anterior to the rectosigmoid colon, is the mesocolon. (Adapted from Heiken JP, Menias CO, Elsayes K. Abdom-
most dependent recess in the greater peritoneal cavity. inal wall and peritoneal cavity. In: Lee KTL, Sagel SS, Stanley RJ, et
al., eds. Computed body tomography with MRI correlation. 4th ed.
Peritoneal Fluid Philadelphia, PA: Lippincott Williams & Wilkins, 2006:11011153, with
permission.)
PATHWAYS OF FLUID SPREAD
The natural flow of peritoneal fluid is along pathways
determined by the mesentery and peritoneal reflections
(Fig. 9.34) (71). Abscesses and metastases tend to grow in left paracolic gutter is slower and weaker than along the
areas where fluid pools, which is in the most dependent right paracolic gutter, and the cephalad extension of fluid is
recesses. The most dependent portion of the peritoneal usually limited by the phrenocolic ligament (6971).
cavity is the pelvis. Therefore, most fluid accumulates in
the cul-de-sac or pouch of Douglas and lateral paravesical Ascites
recesses (Fig. 9.34). Ascites is the accumulation of fluid within the peritoneal
Once in the pelvis, fluid can flow via the right or left cavity, resulting from either increased fluid production or
paracolic gutters into the upper abdomen. Flow into the impaired drainage. The causes of ascites include hypoalbu-
supramesocolic compartment occurs preferentially by way minemia, third-spacing (shift of fluid into the peritoneal
of the right paracolic gutter into the right subhepatic space, cavity, usually secondary to shock), congestive heart fail-
particularly the posterior compartment or Morison pouch. ure, cirrhosis, peritonitis, and malignancy. Sonography is a
From the right subhepatic space, fluid may extend to the sensitive method for localizing peritoneal fluid. Uncompli-
right subphrenic space. Direct spread of fluid across the cated ascites is anechoic or hypoechoic (Fig. 9.35). Internal
midline to the left subphrenic space is prevented by the fal- echoes can indicate the presence of blood, exudate, chyle,
ciform and coronary ligaments of the liver. Flow along the or neoplastic cells.
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326 P E D I AT R I C S O N O G R A P H Y

Peritoneal fluid. Transverse view of the pelvis shows large

Fig. 9.35
amount of anechoic ascites in the cul-de-sac (C) and lat-
eral paravesical spaces (PV). BL  bladder.

Ascites. Transverse view through the lower abdomen

When there is a small amount of peritoneal fluid, it
may be localized to just one or two spaces, such as Mori-
son pouch, the cul-de-sac, the pouch of Douglas, or lat-
eral paravesical spaces (Fig. 9.35). Moderate to large
collections of fluid can extend throughout the peritoneal
recesses (Fig. 9.36). When a large amount of ascites is
present, the small bowel loops are displaced centrally
within the abdomen and fluid accumulates adjacent to
Fig. 9.37
demonstrates a large amount of fluid with freely floating
bowel (B) loops.
and between bowel loops (Fig. 9.37). The leaves of the
small bowel mesentery also become more prominent and
may be recognized as a series of linear echogenic struc-
tures radiating toward the center of the abdomen.

A B
Peritoneal spaces of the upper abdomen. Sonographic demonstration. A: Transverse scan shows peritoneal fluid in the anterior (a) and
Fig. 9.36
posterior (p) perihepatic spaces. L  liver. B: Coronal scan of the left upper abdomen reveals fluid in the anterior (*) perisplenic space.
S  spleen.
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Loculated ascites. Longitudinal sonogram of the right
Fig. 9.38
flank shows a septated fluid collection in the pericolic
gutter.
Scanning the patient in different positions can help
establish if the fluid is free flowing or loculated. Free fluid
has imperceptible margins, confirms to the shape of peri-
toneal spaces and surrounding organs, and usually does
not exert mass effect. Loculated fluid has discrete margins
and can show mass effect, displacing and compressing
adjacent structures. Internal septations also may be noted
(Fig. 9.38). Loculated ascites can mimic a duplication
cyst, urachal cyst, lymphocele, biloma, hematoma,
abscess, and cerebrospinal fluid pseudocyst. Correlation
with clinical history is needed and percutaneous needle
aspiration may be necessary to make a diagnosis.
Specific Fluid Collections
BILOMA
Intraperitoneal bile accumulation (biloma) is usually a result
of traumatic or surgical injury to the biliary tree. The bile
incites an inflammatory reaction, resulting in formation of
adhesions that wall off the fluid collection. Bilomas appear
as round or oval fluid collections, usually in the right upper
quadrant, although they are not limited to this area.
URINE ASCITES
Urine ascites can be the result of urinary tract obstruction
or a traumatic or surgical injury to the kidney, ureter, or
bladder. The ascitic fluid usually is retroperitoneal, but it
can be intraperitoneal if there has been traumatic or oper-
ative disruption of the boundaries between the retroperi-
toneum and peritoneal cavity. The appearance of urine
ascites is similar to that of uncomplicated ascites.
CEREBROSPINAL FLUID PSEUDOCYST
Intra-abdominal cerebrospinal fluid (CSF) is an
expected consequence of ventriculoperitoneal shunt
Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 327
drainage. The fluid is usually distributed throughout
the peritoneal cavity. Loculated collections (termed
CSF pseudocysts) result when adhesions develop
around the shunt catheter. These adhesions limit the
distribution of CSF in the peritoneal cavity, interfering
with its absorption. At sonography, the CSF pseudocyst
appears as a well-circumscribed anechoic mass (Fig.
9.39). The catheter is typically noted within or adjacent
to the fluid collection, appearing as a linear echogenic
structure (Fig. 9.39B), which may have distal acoustic
shadowing.
PERITONEAL INCLUSION CYST
Functioning ovaries produce fluid that is absorbed by the
peritoneum. Pelvic inflammatory disease can lead to for-
mation of adhesions, walling off the fluid and creating a
cystic mass termed a peritoneal inclusion cyst. Sono-
graphic findings include a cystic mass, which may be
unilocular or multilocular and contains a normal ovary
(see Fig. 13.16, Chapter 13, Female Pelvis) (7274).
Mesenteric Cysts
Mesenteric cysts (also called abdominal lymphangiomas)
result from failure of developing lymphatic tissue to estab-
lish a normal communication with the remainder of the
lymphatic system (7578). Pathologically, the cysts are
thin-walled, multilocular lesions, containing either chy-
lous or serous fluid (7578). They may arise within the
small bowel mesentery, omentum, mesocolon, or
retroperitoneum, but most cysts are located in the small
bowel mesentery. Patients usually come to medical atten-
tion because of a palpable abdominal mass, but they can
present with acute abdominal pain if the cyst undergoes
torsion, rupture, or hemorrhage.
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328 P E D I AT R I C S O N O G R A P H Y

A B
Cerebrospinal fluid (CSF) pseudocyst. A: Longitudinal sonogram of the pelvis shows a loculated anechoic fluid (F) collection. BL  blad-
Fig. 9.39
der. B: A more cephalad sonogram shows echogenic shunt tubing with its tip (arrowhead) in the fluid collection. The cyst was drained
surgically and yielded CSF.

The typical sonographic appearance is that of a thin- Benign Peritoneal Tumors

walled, multiseptated, anechoic mass (Fig. 9.40), although
occasionally the cysts are unilocular (Fig. 9.41). Debris or
septations may be present if the fluid contents are highly
proteinaceous or hemorrhagic, and occasionally a fat-fluid
layer is present. Calcifications are rare. Peritoneal fluid
may be noted if there is cyst rupture. The mesenteric cyst
is avascular on color Doppler imaging.
A variety of lesions can mimic mesenteric cysts. These
include ovarian cyst, CSF pseudocyst, enteric duplication
cyst, and extrapancreatic pseudocyst.
HEMANGIOMA
Hemangiomas are vascular tumors lined by proliferating
endothelial cells and filled with red blood cells. Most are
found in cutaneous or subcutaneous tissues, but visceral
locations, including the mesentery and omentum, have
been described (79). They commonly develop within the
first few months of life and undergo rapid proliferation and
then rapid involution and regression. Sonography can
show a lobulated or nodular mass that may be hypoechoic,

A B
Mesenteric cyst. A: Longitudinal scan through the midabdomen demonstrates a large anechoic mass with multiple echogenic septa-
Fig. 9.40
tions. B: Power Doppler image demonstrates an avascular mass.
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Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 329

Mesenteric cyst. Transverse sonogram through the left

Fig. 9.41
upper quadrant shows a unilocular cystic mass (M) with
low-level internal echoes. Histologic examination showed a mesen-
teric cyst with proteinaceous debris.

hyperechoic, or of mixed echogenicity relative to adjacent representing matted nodes (Fig. 9.43) (80,81). The nodes
soft tissues (Fig. 9.42). Color Doppler findings are a hyper- are usually homogenous and hypoechoic relative to sur-
vascular mass with a high systolic velocity and a low resis- rounding tissues. Marked vascularity may be seen on color
tive index (79). Doppler imaging.

CASTLEMAN DISEASE INFLAMMATORY PSEUDOTUMOR

Castleman tumor, or angiomatous lymphoid hamartoma,
is a rare condition of unknown cause characterized by
mass-like proliferation of lymphoid tissue (80,81). It most
commonly involves the mediastinum, but it can arise in the
mesentery. Intra-abdominal disease may involve the
mesentery, retroperitoneum, or both locations and may be
localized or widespread.
The sonographic appearance varies from discretely
enlarged mesenteric lymph nodes to a conglomerate mass,
Inflammatory pseudotumor, also termed inflammatory
myofibroblastic tumor, is a benign mesenteric mass occur-
ring predominantly in adolescents or young adults (8284).
Pathologically, the lesion contains spindle cells, mature
plasma cells, and lymphocytes. Patients usually present
with fever and an abdominal mass; other findings include
malaise, weight loss, anemia, thrombocytosis, and poly-
clonal hypergammaglobulinemia. Sonographic findings are
nonspecific and the lesion can appear as an infiltrative mass

A B
Hemangioma. A: Sagittal sonogram of the left flank shows a multinodular echogenic mass anterior to the left kidney (LK). B: Contrast-
Fig. 9.42
enhanced computed tomography scan during the arterial phase demonstrates heterogeneous enhancement of the lesion (arrows).
(Reprinted from Chateil J-F, Feuga CS, Perel Y, et al. Capillary haemangioma of the greater omentum in a 5-month-old female infant: a case report.
Pediatr Radiol 2000;30:837839, with permission.)
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330 P E D I AT R I C S O N O G R A P H Y
or as well-defined peritoneal masses with homogeneous or
heterogeneous echotexture (82,83). Increased vascularity
may be noted on color Doppler sonography (83).
DESMOID TUMOR
The mesenteric desmoid tumor, also known as mesenteric
fibromatosis, is a locally aggressive process with a propen-
sity to invade and recur, but not metastasize. Pathologi-
cally, it is an unencapsulated mass containing fibroblasts in
a collagenous and/or myxoid stroma (85). It can occur
sporadically, but is also common in patients with Gardner
syndrome, an autosomal dominant disorder characterized
by diffuse adenomatous colonic polyps, especially those
patients who have undergone prior surgery. Clinical find-
ings include abdominal pain, a palpable mass, small bowel
obstruction, bowel perforation, and/or gastrointestinal
bleeding. The sonographic appearance is that of a solid
mesenteric mass displacing adjacent visceral structures. It
may be well circumscribed or have irregular margins
A B
Cystic peritoneal mesothelioma. A: Sagittal sonogram through the right side of the abdomen demonstrates a multilocular mass with sep-
Fig. 9.44
tations and some internal echoes (arrowheads). B: Longitudinal scan in another patient shows a multiseptated cystic mass.
Castleman disease. Transverse scan through the right
Fig. 9.43
lower quadrant demonstrates an oval-shaped, hypo-
echoic mesenteric mass (M). Surgical exploration showed proliferat-
ing lymphoid tissue in the small bowel mesentery.
extending into the mesenteric fat. The echotexture may be
homogeneous or heterogeneous (85,86).
CYSTIC PERITONEAL MESOTHELIOMA
Cystic peritoneal mesothelioma is a rare neoplasm that
originates in the serous lining of the peritoneal cavity
(77,87). Pathologically, it is composed of thin-walled
cysts, filled with watery fluid and lined by mesothelial
cells (77). It does not have malignant potential and it
does not metastasize, but it commonly recurs locally. The
clinical presentation is chronic or intermittent abdomi-
nal pain.
At sonography, it appears as a multiseptated, cystic
mass that may exert mass effect on adjacent structures but
does not show signs of infiltration (Fig. 9.44). The cysts
range from several millimeters to several centimeters in
diameter. The tumor can contain internal echoes related
to infection or hemorrhage. The imaging appearance is
similar to that of lymphangioma.
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Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 331

FATTY TUMORS
Lipoma
Benign lipomas may arise within the mesentery or in the
peritoneal lining (88). Small lipomas can be incidental
findings on imaging studies. Large lipomas can present as
abdominal masses or cause abdominal pain secondary to
compression of adjacent structures or complications such
as small bowel volvulus with the lipoma acting as a lead
point for torsion of the mesentery (8991). The sono-
graphic appearance is that of an intensely echogenic mass,
reflecting the predominant fat content.

Lipoblastoma
Lipoblastoma is a benign tumor that occurs almost exclu-
sively in infants and young children younger than 5 years of
age (88,9294). Pathologically, it contains variably differen-
tiated adipocytes, primitive mesenchymal cells, myxoid
matrix, and fibrous trabeculae (88). The tumor lacks a cap-
sule and can show an infiltrative growth pattern. Sonography
shows an echogenic mass, corresponding to fat, with more
Lymphoma. Longitudinal sonogram through the right
highly reflective septations representing fibrous trabeculae. Fig. 9.46
lower quadrant shows two enlarged, homogeneous,
The tumor margins may be well defined or infiltrative, with
hypoechoic nodes (arrows).
tumor growing along fascial planes and invading muscle (Fig.
9.45) (88,9294). Liposarcomas also contain soft tissue ele-
ments in addition to fatty tissue, but they are exceedingly rare
mately 50% of children with non-Hodgkin lymphoma and
in young children (88). Definitive differentiation between
in about 5% of children with Hodgkin lymphoma at the
lipoblastoma and liposarcomas requires tissue sampling.
time of presentation (95). At sonography, lymphomatous
Diffuse infiltrating lipomatosis is another cause of
involvement of the mesentery can appear as multiple, dis-
increased mesenteric fat. It represents overgrowth of nor-
cretely enlarged lymph nodes (Fig. 9.46) or as large con-
mal mesenteric fat. It is usually idiopathic, but it can be
glomerate masses displacing bowel loops and obscuring
seen in association with steroid therapy. Imaging studies
margins of adjacent structures (Fig. 9.47). Lymphomatous
show diffuse accumulation of normal, highly echogenic fat.
nodes are predominantly anechoic or hypoechoic to sur-
Malignant Masses rounding organs and soft tissues (Figs. 9.46 and 9.47).
They can be avascular or show central or peripheral flow
LYMPHOMA
Lymphoma is the most common malignant neoplasm of
the mesentery. Mesenteric involvement is seen in approxi-

Peritoneal lipoblastomatosis. Transverse sonogram shows a Lymphoma. Longitudinal color Doppler sonogram shows a
Fig. 9.45 Fig. 9.47
large, echogenic mass with multiple highly reflective septa large, predominantly hypoechoic, heterogeneous mass in
filling the abdomen and obscuring adjacent tissue planes. S  spine. the left mid abdomen. The tumor is essentially avascular.
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332 P E D I AT R I C S O N O G R A P H Y

A B

Lymphoma, calcifications. Longitudinal (A) and transverse

Fig. 9.48
(B) sonograms show a lobulated mesenteric mass with
central calcification (arrows). C: Computed tomography scan demon-
C strates a soft tissue mesenteric mass with ring calcification.

on color Doppler imaging (Fig. 9.47). Calcifications may
be seen in the mesenteric masses prior to or after radiation
or combined radiation treatment and chemotherapy (Fig.
9.48).
Small mesenteric lymph nodes are a nonspecific find-
ing. Other causes of mesenteric lymph node enlargement
include primary mesenteric adenitis (see later discus-
sion), acute appendicitis, inflammatory diseases such
as Crohn disease, tuberculosis, histoplasmosis, and
AIDS.
OTHER MALIGNANT TUMORS
Primary malignant intraperitoneal neoplasms in children
include the small, round blue cell tumors, such as rhab-
domyosarcoma, neuroblastoma, and extraskeletal Ewing
sarcoma; ectomesenchymoma (characterized by the pres-
ence of both neuroectodermal and mesenchymal tissues)
mesothelioma; desmoplastic round cell tumor; gastroin-
testinal stromal tumor; and extragonadal germ cell tumors
(9699).
The sonographic findings of malignant peritoneal
tumors range from one or more lobulated complex soft tis-
sue masses to diffuse irregular thickening of the mesentery
and omentum without discrete masses (Fig. 9.49). The
masses extend along the mesentery, displacing the small
bowel. Ancillary findings include intra-abdominal and
pelvic adenopathy, bowel dilatation due to partial obstruc-
tion, hepatic metastases, and ascites.
METASTATIC DISEASE
Metastases are a rare cause of a peritoneal mass in children.
Primary tumors that metastasize to mesentery and omentum
are lymphoma, ovary, pancreas, and colon. Sonographic find-
ings of peritoneal carcinomatosis include discrete hypoechoic
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Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 333

A B
Rhabdomyosarcoma. A: Transverse sonogram shows a large, echogenic mass filling the anterior abdomen. The scattered hyperechoic
Fig. 9.49
areas correspond to calcifications. B: Computed tomography scan demonstrates a partially calcified, soft tissue mass in the mesentery
and omentum.

or hyperechoic masses (Fig. 9.50) and rind-like thickening of
the peritoneum or omentum (omental caking).
Infection
ABSCESS
Intraperitoneal abscesses in children are usually caused by
appendicitis or Crohn disease, but they can follow pelvic
or abdominal surgery or trauma, or be a result of pelvic
inflammatory disease. Affected patients present with fever,
leukocytosis, and abdominal pain, although patients with
chronic walled-off abscesses may have fewer clinical signs
or symptoms. The subhepatic and subphrenic spaces and
the pelvis are common locations for abscess formation.
At sonography, abscesses are hypoechoic, contain low-
level echoes, and are surrounded by an echogenic rim
(Fig. 9.51). They can contain septations, fluid-debris levels
(Fig. 9.52), or gas bubbles. Gas appears as tiny, intensely
echogenic foci with posterior reverberation or ring-down
artifacts. Color Doppler sonography can show flow in the
wall of the abscess (Fig. 9.51B).

A B
Peritoneal carcinomatosis. A: Transverse sonogram demonstrates multiple, round, echogenic lymph nodes (arrows) in the omentum.
Fig. 9.50
B: Computed tomography scan shows diffuse soft tissue infiltration of the mesentery and omentum. Neoplastic nodes often have a
round configuration rather than the normal ovoid shape.
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334 P E D I AT R I C S O N O G R A P H Y

A B
Peritoneal abscess. A: Transverse sonogram of the right lower quadrant in a patient with perforated appendicitis demonstrates a hypo-
Fig. 9.51
echoic mass (arrows) with echogenic debris. B: Color Doppler sonogram shows peripheral flow. BL  bladder.

The anatomic areas of the peritoneum best suited for
sonographic evaluation of suspected abscess are the right
upper quadrant, left upper quadrant, and pelvis, because
the liver, spleen, and urinary bladder, respectively, serve as
acoustic windows. Sonography is more limited in the
midabdomen, particularly in postoperative patients,
because of extensive bowel gas due to paralytic ileus and
open wounds, drainage tubes, and dressings, which inter-
fere with sound transmission and limit visibility. In the lat-
ter instances, CT is often the examination of choice to
delineate the extent of abscess and to guide treatment.
PERITONITIS
Peritonitis is an inflammation of the peritoneal lining. Pri-
mary peritonitis occurs in patients who have impaired
immunologic defenses. Secondary peritonitis is usually a

Peritoneal abscess. Transverse sonogram of the pelvis in

Fig. 9.52
a patient with perforated appendicitis demonstrates a
hypoechoic mass with a fluid-debris level (arrows). BL  bladder.
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Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 335

A B
Segmental omental infarction. A: Transverse sonogram shows an ovoid echogenic mass (M) beneath the right rectus muscles (arrows).
Fig. 9.53
B: Computed tomography scan demonstrates a fatty mass (arrow) with soft tissue stranding in the anterolateral aspect of the omentum.

complication of appendicitis or abdominal surgery. Nonin-
fectious peritonitis, usually due to pancreatitis, is less com-
mon than infectious peritonitis.
The sonographic findings of peritonitis include free or
loculated ascitic fluid, sometimes containing echogenic
debris, or septations; thickened bowel walls; and thick-
ened, hyperechoic peritoneum, mesentery, and/or omen-
tum. (See Fig. 10.64 Chapter 10, Gastrointestinal Tract).
has been implicated in some cases. Sonography shows
right-sided mesenteric lymph node enlargement (long axis
of 10 mm and short axis of 5 mm), most commonly in
the ileocecal area. The nodes are ovoid shaped, homoge-
neous, and isoechoic or hypoechoic relative to surrounding
soft tissues (Fig. 9.54). They demonstrate echogenic cen-
tral hila, which can show flow on color Doppler imaging
(107).

Segmental Omental Infarction Trauma

Segmental infarction of the omentum is a rare cause of Peritoneal fluid seen after trauma may represent blood,
acute abdominal pain in children (100102). Most omen- urine, third-space fluid losses, or bowel contents (108,109).
tal infarction is idiopathic, although it can be associated Hemoperitoneum initially pools near the site of bleeding
with prior surgery, trauma, or omental torsion. It is most
common on the right side, thought to be related to an
embryologic variant in the blood supply of the right-sided
omentum, predisposing it to venous thrombosis and
infarction. Segmental infarction commonly involves the
anterolateral aspect of the omentum, although it can
involve any part of the omentum.
The typical sonographic appearance of segmental
infarction is an ovoid or cake-like echogenic mass in the
anterior aspect of the peritoneal cavity just beneath the
rectus muscles and anterolateral to the colon (Fig. 9.53)
(100102). The mass is hyperechoic to surrounding peri-
toneal fat and solid viscera. The echotexture may be
homogeneous or heterogeneous. The focally infarcted
omentum often displaces adjacent structures and is not
compressible when pressure is applied with the transducer.
Varying degrees of vascularity can be noted on color
Doppler imaging.

Mesenteric Lymphadenopathy
Primary mesenteric adenitis is an occasional cause of acute
lower abdominal pain mimicking appendicitis (103106).
The cause is usually unknown, but Yersinia enterocolitica
Mesenteric lymphadenitis. Transverse sonogram through
Fig. 9.54
the right lower quadrant shows several enlarged, oval-
shaped hypoechoic lymph nodes (arrows).
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336 P E D I AT R I C S O N O G R A P H Y
and then flows into more dependent recesses of the peri-
toneal cavity. The amount of hemoperitoneum seen at
sonography is not a measure of ongoing hemorrhage. It
represents the cumulative amount of bleeding occurring
between the time of injury and when sonography was per-
formed. Acute hemoperitoneum can appear hyperechoic or
isoechoic to solid organs. Subacute and chronic hematoma
appears hypoechoic relative to adjacent organs.
Peritoneal hemorrhage usually shows substantial clear-
ing or resolution by 1 week after the injury. Hemoperi-
toneum that remains unchanged for 3 to 7 days after injury
or increases in volume should raise concern for ongoing
intraperitoneal bleeding.
Pneumoperitoneum
Pneumoperitoneum can be an incidental finding during
evaluation of trauma or abdominal pain. It is most often
seen just below the parietal peritoneum, appearing as a
highly echogenic peritoneal line with posterior reverbera-
tion or ring-down artifact. In patients with ascites, the
sonographic finding of pneumoperitoneum is the presence
of tiny mobile echogenic foci within the ascitic fluid. Scan-
ning the patients in supine, erect, and oblique positions can
help confirm the diagnosis of pneumoperitoneum, since air
will shift to the nondependent position.
REFERENCES
1. Paterson A, Frush DP, Donnelly LF, et al. A pattern-oriented
approach to splenic imaging in infants and children. Radi-
ographics 1999;19:14651585.
2. Doria AS, Daneman A, Moineddin R, et al. High-frequency
sonographic patterns of the spleen in children. Radiology
2006;240:821827.
3. Megremis SD, Vlachonikolis IG, Tsilimigaki AM. Spleen length
in childhood with US: normal values based on age, sex and
somatometric parameters. Radiology 2004;231:129134.
4. Rosenberg HK, Markowitz RI, Kolberg H, et al. Normal
splenic size in infants and children: sonographic measurements.
AJR Am J Roentgenol 1991;157:119121.
5. Li DKB, Cooperberg PL, Graham MF, et al. Pseudo perisplenic
fluid collection: a clue to normal liver and spleen echogenic
texture. J. Ultrasound Med 1986;5:397400.
6. Sadler TW. Digestive system. In: Langmans medical embryol-
ogy. 11th ed. Philadelphia: Lippincott Williams & Wilkins,
2010:209234.
7. Buehner M. Wandering spleen. Surg Gynecol Obstet 1992;175:
373387.
8. Dodds WJ, Taylor AJ, Erickson SJ, et al. Radiologic imaging of
splenic anomalies. AJR Am J Roentgenol 1990;155:805810.
9. Emery KH. Splenic emergencies. Radiol Clin North Am 1997;
35:831843.
10. Freeman JL, Jafri SZ, Roberts JL, et al. CT of congenital and
acquired abnormalities of the spleen. Radiographics 1993;13:
597610.
11. Herman TE, Siegel MJ. CT of acute splenic torsion in children with
wandering spleen. AJR Am J Roentgenol 1991;156:151153.
12. Seo T, Ito T, Watanabe Y, et al. Torsion of an accessory spleen
presenting as an acute abdomen with an inflammatory mass
US, CT, and MRI findings. Pediatr Radiol 1994;24:532534.
13. Kessler A, Miller E, Keidar S, et al. Mass at the splenic hilum.
A clue to torsion of a wandering spleen located in a normal left
upper quadrant. J Ultrasound Med 2003;22:527530.
14. Danaci M, Belet U, Yalin T, et al. Torsion in a wandering
spleen. J Clin Ultrasound 2000;28:246248.
15. Bhasin A, Gulati MS, Kashyap R. Value of power Doppler
sonography in the evaluation of torsion in a wandering spleen.
J Clin Ultrasound 2001;29:6061.
16. Murray KE, Morgan A, Chrisite DL. Pancreatitis caused by a
wandering spleen. J Pediatr Gastroenterol Nutr 1994;18:
486489.
17. Warshauer DM. Spleen. In: Lee KTL, Sagel SS, Stanley RJ, et
al., eds. Computed body tomography with MRI correlation.
4th ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2006:
9731006.
18. Erkalis AJ, Filler RM. Splenectomy in childhood: a review of
1413 cases. J Pediatr Surg 1972;7:382388.
19. Waldham BM. Incidence and location of accessory spleens. N
Engl J Med 1981;304:1111.
20. Ambriz P, Munoz R, Quintanar E, et al. Accessory spleen com-
promising response to splenectomy for idiopathic thrombocy-
topenia purpura. Radiology 1985;155:793796.
21. Grinbaum R, Zamir O, Fields S, et al. Torsion of an accessory
spleen. Abdom Imaging 2006;31:110112.
22. Perez Fontan FJ, Soler R, Santos M, et al. Accessory spleen tor-
sion: US, CT and MR findings. Eur Radiol 2001;11:509512.
23. Maillard J-C, Menu Y, Scherrer A, et al. Intraperitoneal spleno-
sis: diagnosis by ultrasound and computed tomography. Gas-
trointest Radiol 1989;14:179180.
24. Applegate KE, Goske MJ, Pierce G, et al. Situs revisited: imag-
ing of the heterotaxy syndrome. Radiographics 1999;19:
837852.
25. Hadar H, Gadoth P, Herskovitz P, et al. Short pancreas in poly-
splenia syndrome. Acta Radiol 1991;32:299301.
26. Herman TE, Siegel MJ. Polysplenia syndrome with congenital
short pancreas. AJR Am J Roentgenol 1991;156:799800.
27. Mishalany H, Mahnovski V, Woolley M. Congenital asplenia
and anomalies of the gastrointestinal tract. Surgery 1982;91:
3841.
28. Rose V, Izukawa T, Moes CAF. Syndromes of asplenia and
polysplenia. A review of cardiac and non-cardiac malformation
in 60 cases with special reference to diagnosis and prognosis. Br
Heart J 1975;37:840852.
29. Dachman AH, Ros PF, Murari PJ, et al. Nonparasitic splenic
cysts: a report of 52 cases with radiologic-pathologic correla-
tion. AJR Am J Roentgenol 1986;147:537542.
30. Franquet T, Montes M, Lecumberri FJ, et al. Hydatid disease of
the spleen: imaging findings in nine patients. AJR Am J
Roentgenol 1990;154:525528.
31. Malhotra A, Jones LT. Epidermoid cyst of the spleen. Pediatr
Radiol 2008;38:714.
32. Ragozzino MW, Singletary J, Patrick R. Familial splenic epider-
moid cyst. AJR Am J Roentgenol 1990;155:12331234.
33. Urrutia M, Mergo PJ, Ros LH, et al. Cystic masses of the spleen: radi-
ologic-pathologic correlation. Radiographics 1996;16:107129.
34. Mata J, Alegret X, Llauger J. Splenic pseudocyst as a complica-
tion of ventriculoperitoneal shunt: CT features. J Comput
Assist Tomogr 1986;10:341342.
35. Abbott RM, Levy AD, Aguilerea NS, et al. Primary vascular
neoplasms of the spleen: radiologic-pathologic correlation.
Radiographics 2004;24:11371163.
36. Ros PR, Moser RP Jr, Dachman AH, et al. Hemangioma of the
spleen: radiologic-pathologic correlation in ten cases. Radiol-
ogy 1987;162:7377.
37. Herman TE, McAlister PWH, Dehner LP, et al. Beckwith-
Wiedemann syndrome and splenic hemangioma: report of a
case. Pediatr Radiol 1997;27:350352.
38. Pakter RL, Fishman EK, Nussbaum A, et al. CT findings in
splenic hemangiomas in the Klippel-Trenaunay-Weber syn-
drome. J Comput Assist Tomogr 1987;11:8891.
39. Panuel M, Ternier F, Michel G, et al. Splenic hemangioma-
report of three pediatric cases with pathologic correlation. Pedi-
atr Radiol 1992;22:213216.
LWBK505-C09_p305-338.qxd 7/7/10 1:31 PM Page 337 Aptara Inc
40. Georg C, Schwerk WB, Goerg K. Sonography of focal lesions of
the spleen. AJR Am J Roentgenol 1991;156:949953.
41. Niizawa M, Ishida H, Morikawa P, et al. Color Doppler sonog-
raphy in a case of splenic hemangioma: value of compressing
the tumor. AJR Am J Roentgenol 1991;157:965966.
42. Ertan G, Tekes A, Mitchell S, et al. Pediatric littoral cell angioma
of the spleen: multimodality imaging including diffusion-
weighted imaging. Pediatr Radiol 2009;39(10):11051109.
43. Goldfield M, Cohen I, Loberant N, et al. Littoral cell angioma
of the spleen: appearance on sonography and CT. J Clin Ultra-
sound 2002;30:510513.
44. Wadsworth DT, Newman B, Abramson SJ, et al. Splenic lym-
phangiomatosis in children. Radiology 1997;202:173176.
45. Kassarjian A, Patenaude YG, Bernard C, et al. Symptomatic
splenic hamartoma with renal, cutaneous and hematological
abnormalities. Pediatr Radiol 2001;31:111114.
46. Thompson SE, Walsh EA, Cramer BC, et al. Radiological fea-
tures of a symptomatic splenic hamartoma. Pediatr Radiol
1996;26:657660.
47. Gerog C, Schwerk WB. Color Doppler imaging of focal splenic
masses. Eur J Radiol 1994;18:214219.
48. Tang S, Shimizu T, Kikuchi Y, et al. Color Doppler sonographic
findings in splenic hamartoma. J Clin Ultrasound 2000;28:
249253.
49. Franquet T, Montes M, Aizcorbe M, et al. Inflammatory
pseudotumor of the spleen: ultrasound and computed tomo-
graphic findings. Gastrointest Radiol 1989;14:181183.
50. Herman TE, Shackelford GD, Ternberg JL, et al. Inflammatory
myofibroblastic tumor of the spleen: report of a case in an ado-
lescent. Pediatr Radiol 1994;24:280282.
51. Georg C, Schwerk WB, Georg K, et al. Sonographic patterns of
the affected spleen in malignant lymphoma. J Clin Ultrasound
1990;18:569574.
52. Thompson WM, Levy AD, Aguilera NS, et al. Angiosarcoma of
the spleen: imaging characteristics in 12 patients. Radiology
2005;235:106115.
53. Cox F, Perlman S, Sathyanarayana J. Splenic abscesses in cat
scratch disease: sonographic diagnosis and follow-up. J Clin
Ultrasound 1989;17:511514.
54. Pastakia B, Shawker TH, Thaler M, et al. Hepatosplenic can-
didiasis: wheels within wheels. Radiology 1988;166:417421.
55. Spouge AR, Wilson SR, Gopinath N, et al. Extrapulmonary
Pneumocystis carinii in a patient with AIDS; sonographic find-
ings. AJR Am J Roentgenol 1990;155:7678.
56. Towers MJ, Withers CE, Hamilton PA, et al. Visceral calcifica-
tion in patients with AIDS may not always be due to Pneumo-
cystis carinii. AJR Am J Roentgenol 1991;156:745747.
57. Fishman EK, Soyer P, Bliss DF, et al. Splenic involvement in
pancreatitis: spectrum of CT findings. AJR Am J Roentgenol
1995;174:631635.
58. Georg C, Schwerk WB. Splenic infarction: sonographic pat-
terns, diagnosis, follow-up, and complications. Radiology
1990;174:803807.
59. Beutler E. Gauchers disease. N Engl J Med 1991;325:13541360.
60. Patlas M, Hadas-Halpern I, Abrahamov A, et al. Spectrum of
abdominal sonographic findings in 103 pediatric patients with
Gaucher disease. Eur Radiol 2002;12:397400.
61. Chippington A, McHugh K, Vellodi A. Splenic nodules in pae-
diatric Gaucher disease treated by enzyme replacement therapy.
Pediatr Radiol 2008;38:657660.
62. Stevens PG, Kumari-Subaiya SS, Kahn LB. Splenic involvement
in Gauchers disease: sonographic findings. J Clin Ultrasound
1989;15:397400.
63. Keesling CA, Frush DP, OHara SM, et al. Clinical and imaging
manifestations of pediatric sarcoidosis. Acad Radiol 1998;5:
122132.
64. Benya EC, Lim-Dunham JE, Landrum O, et al. Abdominal
sonography in examination of children with blunt abdominal
trauma. AJR Am J Roentgenol 2000;174:16131616.
Chapter 9 S P L E E N A N D P E R I T O N E A L C A V I T Y 337
65. Brown MA, Casola G, Sirlin CB, et al. Blunt abdominal trauma:
screening US in 2,693 patients. Radiology 2001;218:352358.
66. Coley BD, Mutabagani KH, Martin LC, et al. Focused abdom-
inal sonography for trauma (FAST) in children with blunt
abdominal trauma. J Trauma 2000;48:902906.
67. Kennedy C, Kempf J. FAST exams in pediatric abdominal
trauma. Acad Emerg Med 2002;9:519.
68. McGahan JP, Richards J, Gillen M. The focused abdominal
sonography for trauma scan: pearls and pitfalls. J Ultrasound
Med 2002;21:789800.
69. Heiken JP, Menias CO, Elsayes K. Abdominal wall and peri-
toneal cavity. In: Lee KTL, Sagel SS, Stanley RJ, et al., eds. Com-
puted body tomography with MRI correlation. 4th ed. Philadel-
phia, PA: Lippincott Williams & Wilkins, 2006:11011153.
70. DeMeo JH, Fulcher AS, Austin RF. Anatomic CT demonstration
of the peritoneal spaces, ligaments, and mesenteries: normal and
pathologic processes. Radiographics 1995;15:755770.
71. Meyers MA, ed. Dynamic radiology of the abdomen. Normal
and pathologic anatomy. New York: Springer Verlag, 1994.
72. Hoffer FA, Kozakewich H, Colodny A, et al. Peritoneal inclu-
sion cysts: ovarian fluid in peritoneal adhesions. Radiology
1988;169:189191.
73. Jain KA. Imaging of peritoneal inclusion cysts. AJR Am J
Roentgenol 2000;174:15591563.
74. Kim JS, Lee HJ, Woo SK, et al. Peritoneal inclusion cysts and
their relationship to the ovaries: evaluation with sonography.
Radiology 1997;204:481484.
75. Konen O, Tahaus V, Dlugh E, et al. Childhood abdominal cys-
tic lymphangioma. Pediatr Radiol 2002;32:8894.
76. Levy AD, Cantisani V, Miettinen M. Abdominal lymphan-
giomas: imaging features with pathologic correlation. AJR Am
J Roentgenol 2004;182:14851491.
77. Stoupis C, Ros PR, Abbitt PL, et al. Bubbles in the belly: imag-
ing of cystic mesenteric or omental masses. Radiographics
1994;14:729737.
78. Wootton-Gorges SL, Thoams KB, Harned RK, et al. Giant cys-
tic abdominal masses in children. Pediatr Radiol 2005;35:
12771288.
79. Chateil J-F, Feuga CS, Perel Y, et al. Capillary haemangioma of
the greater omentum in a 5-month-old female infant: a case
report. Pediatr Radiol 2000;30:837839.
80. Barki Y, Shadked G, Levy I. Metastatic Castleman disease:
sonographic diagnosis. J Clin Ultrasound 1992;20:486488.
81. Garber SJ, Shaw DG. Case report: the ultrasound and com-
puted tomography appearance of mesenteric Castleman dis-
ease. Clin Radiol 1991;43:429430.
82. Day DL, Sane S, Dehner LP. Inflammatory pseudotumor of the
mesentery and small intestine. Pediatr Radiol 1986;16:
210215.
83. Narla LD, Newman B, Spottswood SS, et al. Inflammatory
pseudotumor. Radiographics 2003;23:719729.
84. Uysal S, Tuncbilek I, Unlubay D, et al. Inflammatory pseudotu-
mor of the sigmoid colon mesentery: US and CT findings. Eur
Radiol 2005;15:633635.
85. Levy AD, Rimola J, Mehrotra AK, et al. Benign fibrous tumors
and tumorlike lesions of the mesentery: radiologic-pathologic
correlation. Radiographics 2006;26:245264.
86. Maconi G, Cristaldi M, Vago L, et al. Clinical, ultrasono-
graphic and tomographic features on the natural evolution of
primary mesenteric fibromatosis: a case report. Hepatogas-
troenterology 1998;45:16631666.
87. ONeil JD, Ros PR, Storm BL, et al. Cystic mesothelioma of the
peritoneum. Radiology 1989;170:333336.
88. Moholkar S, Sebire NJ, Roebuch DJ. Radiological-pathological
correlation in lipoblastoma and lipoblastomatosis. Pediatr
Radiol 2006;36:851856.
89. Cherian A, Singh AJ, Broderick N, et al. Small bowel volvulus
due to giant mesenteric lipoma. Pediatr Surg Int 2004;20:
869871.
LWBK505-C09_p305-338.qxd 7/7/10 1:31 PM Page 338 Aptara Inc
338 P E D I AT R I C S O N O G R A P H Y
90. Ozell SK, Apak S, Ozercan IH, et al. Giant mesenteric lipoma
as a rare cause of ileus in a children: report of a case. Surg
Today 2004;34:470472.
91. Wolko JD, Rosenfeld DL, Lazar MJ, et al Torsion of a giant
mesenteric lipoma. Pediatr Radiol 2003;33:3436.
92. Prando A, Wallace S, Marins JLC. Sonographic features of
benign intraperitoneal lipomatous tumors in children-report of
4 cases. Pediatr Radiol 1990;20:571574.
93. Al-Salem AH, Al-Nazer M. Mesenteric lipoblastoma in a 2-
year-old child. Pediatr Surg Int 2003;19:115117.
94. Mo Y-H, Peng S S-F, Li Y-W, et al. Mesenteric lipoblastoma:
case report. Pediatr Radiol 2003;33:3740.
95. Toma P, Granata C, Rossi A, et al. Multimodality imaging of
Hodgkin disease and non-Hodgkin lymphomas in children.
Radiographics 2007;27:13351354.
96. Crombleholme TM, Harris BH, Jacir NN, et al. The desmo-
plastic round cell tumor: a new solid tumor of childhood. J
Pediatr Surg 1993;28:10231025.
97. Fraire AE, Cooper S, Greenberg SD, et al. Mesothelioma of
childhood. Cancer 1988;62:838847.
98. Kim OH, Lee KY. Malignant fibrous histiocytoma of primary
omental origin in an infant. Pediatr Radiol 1994;24:285287.
99. Lev MH, Blickman JG. Extragonadal yolk sac tumor: sono-
graphic and CT findings. AJR Am J Roentgenol 1993;160:
370371.
100. Myers MT, Grisoni E, Sivit CJ. Omental infarction in a 9 year
old girl. Emerg Radiol 1997;2:112114.
101. Grattan-Smith JD, Blews DE, Brand T. Omental infarction in
pediatric patients: sonographic and CT findings. AJR Am J
Roentgenol 2002;178:15371539.
102. Puylaert JBCM. Right-sided segmental infarction of the omentum:
clinical, US and CT findings. Radiology 1992;185:169172.
103. Puylaert JB, van der Zant FM. Mesenteric lymphadenitis or
appendicitis? AJR Am J Roentgenol 1995;165:490.
104. Sivit CJ, Newman KD, Chandra RS. Visualization of enlarged
mesenteric lymph nodes at US examination: clinical signifi-
cance. Pediatr Radiol 1993;23:471475.
105. Swischuk LE, John SD. Mesenteric adenitisacute ileitis: a
constellation of findings definable with ultrasound. Emerg
Radiol 1998;5:210218.
106. Vayner N, Coret A, Plliack G, et al. Mesenteric lymphadenopa-
thy in children examined by US for chronic and/or recurrent
abdominal pain. Pediatr Radiol 2003;33:864867.
107. Quillin SP, Siegel MJ. Color Doppler US of children with acute
lower abdominal pain. Radiographics 1993;13: 12811293.
108. Sivit CJ. Significance of peritoneal fluid identified at US exami-
nation in children with acute abdominal pain. J Ultrasound
Med 1993;12:743745.
109. Sivit CJ, Taylor GA, Bulas DI, et al. Blunt trauma in children:
significance of peritoneal fluid. Radiology 1991;178:185188.
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Gastrointestinal Tract
Esophagus Small Bowel
Technique and Normal Anatomy Technique and Normal Anatomy
Gastroesophageal Reflux Small Bowel Obstruction
Small Bowel Wall Thickening
Stomach
Benign Small Bowel Masses
Technique and Normal Anatomy
Malignant Masses
Congenital Anomalies
Acquired Obstruction Mesenteric Adenitis
Gastric Wall Thickening
Appendix
Benign Masses
Appendicitis
Malignant Masses
Bezoars Meckel Diverticulum
he introduction of the graded-compression technique
T along with continued improvement in gray-scale and
Doppler technology has increased the role of sonogra-
phy in the evaluation of gastrointestinal tract disorders in
children (1). Although fluoroscopic contrast examinations
and endoscopy remain the primary means of evaluating
mucosal and luminal abnormalities, they provide limited
information about bowel wall and extrinsic abnormalities.
Sonography can provide useful information regarding the
gastrointestinal tract, mesentery, and other surrounding
structures. In some conditions, including pyloric stenosis,
intussusception, and acute appendicitis, it has become the
primary imaging study for diagnosis.
Knowledge of the sonographic appearance of the nor-
mal gastrointestinal tract is important in order to recog-
nize abnormalities. A discussion of the methods of exam-
ining each segment of the gastrointestinal tract and the
appearance of normal structures and gastrointestinal tract
pathology is offered in this chapter.
ESOPHAGUS
Technique and Normal Anatomy
Sonographic evaluation of the esophagus is limited to the
distal most segment and gastro-esophageal junction.
These segments are best imaged through a subcostal or
subxiphoid approach, using the liver as an acoustic win-
dow. The examination is performed with the patient
supine or in the right lateral decubitus position. Initially a
curvilinear 5.0 to 7.0 MHz transducer is used. If wall
thickening is detected, a detailed evaluation is performed
with a linear or curved high-frequency (7.513 MHz)
transducer. The transducer is positioned in the midline or
slightly to the left of midline at the level of the diaphragm
CHAPTER
MARILYN J. SIEGEL
10
Colon
Technique
Normal Anatomy
Anorectal Malformations
Necrotizing Enterocolitis
Colonic Wall Diseases
Cystic Fibrosis
Benign Masses
Malignant Masses
Foreign Body Localization
and images are acquired in transverse and longitudinal
planes.
On the longitudinal view, the esophagus appears as a
tubular structure with a thin hypoechoic wall, which rep-
resents the muscularis. Small amounts of fluid and gas may
be identified within the esophageal lumen (Fig. 10.1). On
transverse views, the gastroesophageal junction has a
bulls-eye or target appearance.
Gastroesophageal Reflux
Gastroesophageal reflux is a common condition in children
characterized by the retrograde flow of gastric contents into
the esophagus. Clinical findings include vomiting, dyspha-
gia, hematemesis, failure to thrive, recurrent pneumonias,
wheezing, and apnea. Although barium esophagography
and continuous pH monitoring have been the primary
methods to evaluate gastroesophageal reflux, sonography
has also been used to diagnose this condition, especially in
infants (25). Reflux also may be detected on sonograms
performed for other indications, such as pyloric stenosis,
and thus, the sonographic features need to be recognized.
The sonographic assessment of reflux involves real-
time imaging, which is performed after the infant is given
an amount of fluid equivalent to a normal feeding. The
transducer is positioned in the subxiphoid region, and
images of the distal esophagus, gastroesophageal junction,
and cardia of the stomach are obtained in longitudinal and
transverse planes. The sonographic appearance of gastroe-
sophageal reflux varies depending on the relative amounts
of fluid and gas. Refluxed fluid alone is anechoic or hypoe-
choic. When mixed with air, the refluxed gastric fluid con-
tains echogenic foci representing gas bubbles (Fig. 10.2).
Another sign of reflux is a short intra-abdominal esopha-
gus or gastroesophageal junction (Fig. 10.2) (6). The mean
339
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340 P E D I AT R I C S O N O G R A P H Y

A B
Normal gastroesophageal junction two-month-old boy. A: Longitudinal scan to the left of midline shows the intra-abdominal part of the
Fig. 10.1
esophagus (white arrows) and gastroesophageal junction (curved arrow) posterior to the left lobe of the liver (L). The wall (white arrows)
is hypoechoic. A small amount of air (black arrow), which is echogenic, is present in the lumen. Abdominal esophageal length (white line) measured
from the level of the diaphragm to the fundus of the stomach is 25 mm, which is normal for a neonate. S  stomach. B: Transverse scan shows the
hypoechoic wall (white arrows) surrounding the air-filled lumen (black arrow), the so called bulls eye or target appearance. L  liver.

Gastroesophageal reflux, 2-month-old boy. Longitudinal

Fig. 10.2
scan shows refluxed gastric contents, containing hypoe-
choic fluid and echogenic air (black arrow), in a dilated esophagus
(white arrows). A shortened abdominal esophageal length (white line
from level of diaphragm to gastric fundus), measuring less than 20 mm,
is another sign of reflux. L  liver; S  stomach.
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Chapter 10 G A S T R O I N T E S T I N A L T R A C T 341

length of the abdominal esophagus is 22 mm, 25 mm and
27 mm in healthy neonates less than 1 month, 16 months
and 612 months of age, respectively, versus 17 mm,
21 mm, and 24 mm in a similar aged population with
reflux. Doppler imaging can show color signal in the
refluxed fluid (7,8). The sensitivity of gray-scale and color
Doppler sonography for the diagnosis of reflux is approx-
imately 95% (3,6,7).
The sonographic assessment of gastroesophageal
reflux can be technically difficult. If the child is crying or
moving, it can be quite challenging to maintain a good
acoustic window for continuous viewing of the esophagus.
Therefore, this examination has not enjoyed widespread
popularity.
STOMACH
Technique and Normal Anatomy
The stomach is best viewed when the lumen is adequately
distended with fluid. The body of the stomach, antrum,
and pyloric region are examined with the patient in a right
lateral decubitus position using the right lobe of the liver
as an acoustic window. The gastric fundus can be imaged
using the left lobe of the liver or spleen as an acoustic win-
dow. Imaging is performed in transverse and longitudinal
planes. Images in the transverse plane display the gastric
antrum in long axis, while images in the longitudinal plane
provide a cross-sectional view of the antropyloric region.
On the short-axis view, the gastric antrum has a target
or bulls-eye appearance. The inner anechoic center repre-
sents fluid in the gastric lumen; the adjacent echogenic
layer is the submucosa; and the outer hypoechoic rim is the
muscularis propria (Fig. 10.3A). On long-axis scans, the
antrum is a tubular structure (Fig. 10.3B). The normal
thickness of the wall is 3 mm or less, measured from the
inner border of the echogenic submucosa to the outer bor-
der of the hypoechoic muscularis (911). The hypoechoic
muscle layer alone should measure 2 mm or less in diame-
ter. Measurements of muscle wall thickness should be
obtained with the antrum distended by fluid to avoid con-
fusing a contracted antrum with an abnormally thickened
muscle (9).
Sonography has also been used to quantify gastric emp-
tying. Assessment of emptying is performed following the
administration of predetermined amounts of gastric fluid.
The technique is time consuming and technically difficult
and therefore, as with gastroesophageal reflux disease, it is
unlikely that sonography will ever have widespread use for
the evaluation of gastric emptying.
Congenital Anomalies
MICROGASTRIA
Microgastria is a rare anomaly characterized by a small,
underdeveloped stomach. Associated malformations are
common, including polysplenia and asplenia, colonic
aganglionosis, midgut malrotation, and skeletal abnormal-
ities. Sonographic findings are a small, tubular, midline
stomach and dilated esophagus. When fluid filled, the
small, midline stomach can be seen by sonography (12).
PYLORIC ATRESIA
Pyloric atresia is a rare congenital anomaly that can be iso-
lated or associated with esophageal atresia. Affected patients
present in the first or second day of life with symptoms of
vomiting. Sonography demonstrates a distended stomach
and a collapsed duodenum distal to the obstruction.

A B
Normal antrum. A: Cross-sectional sonogram through the distal stomach shows hypoechoic muscle (calipers) surrounding echogenic
Fig. 10.3
mucosa and gastric contents, creating a target or bulls-eye appearance. Muscular layer measures 2 mm in thickness. L  liver.
B: Long-axis scan of the distal stomach shows a fluid-filled antral lumen (f), surrounded by echogenic mucosa (white arrow) and a hypoechoic mus-
cle layer (black arrow). Open arrow indicates the antral-duodenal junction. B  gastric body; D  duodenal bulb.
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342 P E D I AT R I C S O N O G R A P H Y
Acquired Obstruction
HYPERTROPHIC PYLORIC STENOSIS
Hypertrophic pyloric stenosis (HPS) is a disorder charac-
terized by hypertrophy of the circular muscle of the
pylorus, resulting in narrowing of the pyloric channel and
gastric outlet obstruction. The incidence of HPS is approx-
imately 3 in 1000, with boys affected four to five times
more than girls. There is also a familial predisposition.
Approximately 20% of sons and 7% of daughters of
female index cases develop the disease, while 5% of sons
and 2% of daughters of male index cases are affected. Typ-
ically, affected patients present between 2 and 6 weeks of
age with nonbilious vomiting, which often becomes pro-
jectile. Rarely, symptoms are present in the first week of
life or as late as 5 months of age (13). The clinical diagno-
sis can be made when an olive-shaped mass is palpated in
the epigastrium (14). Gastric hyperperistalsis also may be
visible through the abdominal wall.
Ultrasonography is the diagnostic study of choice to
confirm the diagnosis of HPS (9,11,15,16). Longitudinal
and transverse images are acquired (Fig. 10.4) with the
infant in the right posterior oblique position, which allows
fluid in the gastric fundus to flow into the antropyloric
area, distending this region. The stomach should not be
emptied prior to the examination, because this makes iden-
tification of the antropyloric area difficult (9). If the
antrum does not contain adequate fluid, a glucose solution
or water can be given orally or via a nasogastric tube.
Sonographic Findings
On short-axis views, the hypertrophic muscle has a
target or bulls-eye appearance, reflecting thickened
A B
Fig. 10.4 Diagram of scanning plane for (A) transverse view and (B) longitudinal view of the pylorus.
hypoechoic muscle surrounding echogenic mucosa.
Long-axis view shows the thickened pyloric muscle and
elongated pyloric channel (Fig. 10.5) (9,11,15,16).
Ancillary signs of HPS include the antral nipple sign,
referring to the presence of prolapsed pyloric channel
mucosa into the gastric antrum (Fig. 10.6); the double-
track sign, reflecting the presence of hypoechoic stripes
of fluid in the crevices of the mucosa (Fig. 10.6); exag-
gerated peristaltic waves in the gastric antrum; gastric
dilatation; absent or minimal gastric emptying; and
esophageal reflux (15,17,18). The thickened pyloric
muscle is hypervascular on Doppler interrogation (Fig.
10.7) (19).
The sonographic hallmark of HPS is the thickened
pyloric muscle, defined as wall thickness equal to or
greater than 3 mm, and an elongated pyloric channel,
defined as a length equal to or greater than 17 mm (11,
16,17). Wall thickness measurements between 2.0 and
2.9 mm are nonspecific and can be seen with gastritis or
pylorospasm as well as with HPS. Premature infants are
especially likely to have borderline muscle thickness
(16,20,21). In these infants, the pyloric channel length,
the thickness of the pyloric muscle relative to the rest of
the stomach, and findings of poor gastric emptying and
hyperperistalsis can be useful in confirming the diagno-
sis of pyloric stenosis (21,22).
Potential causes of errors in the sonographic diagnosis
of HPS are overdistention of the stomach and a tangential
rather than a truly midline longitudinal view (9). Overdis-
tension of the stomach causes the pylorus to be displaced
posteriorly, which makes its identification and measure-
ment of thickness more difficult (false-negative diagnosis)
(Fig. 10.8). An off-midline or tangential image can lead
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Chapter 10 G A S T R O I N T E S T I N A L T R A C T 343

A B
Pyloric stenosis. A: Long-axis sonogram shows the thickened pyloric muscle (1) and the elongated pyloric canal (2). Wall thickness
Fig. 10.5
measured 4 mm, and the canal measured 25 mm. B: Cross-sectional view shows a thickened hypoechoic pyloric muscle (arrows) sur-
rounding the central channel, which is filled with compressed echogenic mucosa (m).

to an erroneous diagnosis of a thickened muscle (false-
positive diagnosis) (9).
Measurements of pyloric muscle volume for the diag-
nosis of HPS have been reported, but they have not
gained wide acceptance, since they are technically diffi-
cult to perform (23). Measurements of residual gastric
aspirate have also been proposed as a method for diag-
nosing HPS. Infants with projectile vomiting and 10 mL
or more of residual aspirate in the stomach are more
likely to have HPS, while those with aspirates less than
10 mL are more likely to have gastroesophageal reflux
(24,25).

Pyloric stenosis, antral nipple and double-track signs.

Fig. 10.6
Redundant pyloric mucosa protrudes into the distended
fluid-filled gastric lumen (arrow), producing the antral nipple sign.
Small amounts of hypoechoic fluid in the crevices of the echogenic
mucosal folds (arrowheads) create the double-track sign. Calipers
indicate thickened pyloric muscle. B  gastric body.
Pyloric stenosis. Color Doppler sonography shows
Fig. 10.7
increased flow in a thickened pyloric muscle. (From
Hernanz-Schulman M. Vomiting in the infant. In: Bluth EI, Benson CB,
Ralls PW, et al., eds. Ultrasound: a practical approach to clinical prob-
lems. 2nd ed. New York: Thieme, 2007: 489400, with permission.)
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344 P E D I AT R I C S O N O G R A P H Y

A B
Pyloric stenosis, pitfall in diagnosis. A: Long-axis sonogram. The stomach (St) is overdistended with air and fluid displacing the pylorus
Fig. 10.8
(calipers) posteriorly. The posterior wall of the pyloric channel is difficult to delineate. B: Long-axis view with the stomach less distended
allows better visualization of the elongated pyloric channel (arrows) and thickened pyloric muscle (M). Again notice the nipple and double-track signs.

There is an increased incidence of renal anomalies in
patients with HPS, including ureteropelvic junction
obstruction, primary megaureter, duplex kidneys, renal age-
nesis or ectopia, nephroblastomatosis, and horseshoe kid-
ney (26). HPS also has been associated with prostaglandin-
induced foveolar hyperplasia (27) and portal venous gas,
which seems to be clinically benign (28).
The treatment for HPS is pyloromyotomy (i.e., Ram-
stedt procedure), in which the hypertrophic muscle is split
longitudinally without violating the mucosa. The pyloric
muscle thickness may remain abnormal up to 12 weeks
following successful pyloromyotomy (29,30).
PYLOROSPASM
Pylorospasm, also known as antral dyskinesia, is a disor-
der characterized by transient spasm of the antrum and
pyloric channel. It is a common cause of delayed gastric
emptying and nonbilious vomiting in infants. Sonographic
findings are antral narrowing, delayed gastric emptying
with intermittent flow of fluid from the stomach into the

A B
Pylorospasm. A: Long-axis sonogram demonstrates a contracted antrum (arrows) with a normal wall thickness (3 mm). The pyloric
Fig. 10.9
channel (curved arrow) is normal. D  air-filled transverse duodenum; f  fluid-filled stomach. B: Long-axis scan a minute later shows
a fluid-filled antrum (A) and duodenal bulb (D). Open arrow indicates normal pyloric channel.
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duodenum, and a normal pyloric muscle thickness and
channel length (Fig. 10.9) (9,31,32).
PROSTAGLANDIN E
Prostaglandin E, which is given to maintain patency of the
ductus arteriosus in newborns with cyanotic heart disease,
can result in hyperplasia of the gastric mucosa, which can
produce gastric outlet obstruction. The appearance is sim-
ilar to that of pylorospasm.
ANTRAL MEMBRANES
Antral membranes are located 1 to 2 cm proximal to the
pylorus. They are usually incomplete with a central or
eccentric aperture. If the opening is large and nonobstruct-
ing, the membrane is discovered incidentally on an upper
gastrointestinal series. If the aperture is small, the patient
may present with symptoms of vomiting. Sonographically,
the membrane appears as a linear echodense band extend-
ing across the fluid-filled gastric antrum. Other findings
include gastric dilatation proximal to the membrane and
delayed gastric emptying (33).
Gastric Wall Thickening
GASTRITIS AND ULCER DISEASE
Infection with Helicobacter pylori is the most common
cause of gastritis in children. Affected patients present
with abdominal pain, nausea, and vomiting. Sonographic
findings include antral wall thickening (Fig. 10.10),
echogenic gastric mucosa, delayed gastric emptying, and
an ulcer crater. The wall thickening usually is circumfer-
ential, but rarely it can be focal and asymmetric. A gas-
filled ulcer crater appears as a hyperechoic focus with
ring-down artifact in an area of gastric wall thickening.
Gastritis due to peptic ulcer disease. Transverse sono-
Fig. 10.10
gram shows uniformly thickened antral wall (white line),
measuring 17 mm in diameter.
Chapter 10 G A S T R O I N T E S T I N A L T R A C T 345
In severe disease, the ulcer crater may extend beyond the
wall or perforate.
The major complications of peptic ulcer disease include
obstruction and perforation. Sonographic findings of gastric
perforation include a hypoechoic, complex, or echogenic
fluid collection at the site of the perforation (34), ascites,
abscess formation, and pneumoperitoneum (35,36). Pneu-
moperitoneum appears as an echogenic line with a posterior
reverberation artifact between the anterior abdominal wall
and the anterior hepatic surface. Free air changes position
when the patients position is changed.
MENETRIER DISEASE
Menetrier disease, also called transient protein-losing gas-
tropathy, is characterized by giant hypertrophy of the gas-
tric mucosa. Approximately 5% of all cases of Menetrier
disease occur in childhood, usually affecting children in the
second decade of life. Clinical findings include edema of
the extremities and eyelids, ascites, pleural effusions, and
abdominal pain.
The sonographic features of Menetrier disease include
irregular, thickened, echogenic mucosa and large, tortuous
hypoechoic rugae, especially in the fundus and the body of
the stomach. The gastric wall (muscularis layer) also may
be thickened and hypoechoic (Fig. 10.11) (37,38).
CHRONIC GRANULOMATOUS DISEASE
Chronic granulomatous disease of childhood is a sex-linked
recessive disorder of phagocyte lysozymes, resulting in a
defect in the bactericidal activity of the polymorphonuclear
leukocytes. It primarily affects boys. Affected patients
present with lymphadenopathy, hepatosplenomegaly,
pneumonia, and/or abdominal pain. The antrum is the
most commonly involved part of the gastrointestinal tract.
Menetrier disease. Transverse sonogram shows thick-
Fig. 10.11
ened, hypoechoic gastric wall (arrows). A  aorta; C 
inferior vena cava.
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346 P E D I AT R I C S O N O G R A P H Y
Chronic granulomatous disease. Long-axis sonogram of
Fig. 10.12
the distal stomach showing circumferentially thickened
antral wall (calipers) surrounding a fluid-filled antrum (A).
Occasionally, the fundus is affected. Pathologically,
inflammatory and granulomatous changes are found in
all layers of the bowel wall. Sonography shows circum-
ferential antral narrowing and wall thickening (Fig.
10.12).
EOSINOPHILIC GASTROENTERITIS
Eosinophilic gastroenteritis is characterized by recurrent
episodes of nonbilious vomiting, malabsorption, abdomi-
nal pain associated with an elevated peripheral eosinophil
count, and eosinophilic infiltration of the gastrointestinal
tract. The underlying cause is unknown, although it has
been speculated that intolerance to dietary proteins may be
responsible.
The sonographic finding is gastric and small bowel wall
thickening. In infants, eosinophilic gastroenteritis can
present as pyloric muscle thickening and channel elonga-
tion, mimicking pyloric stenosis (39,40).
Benign Masses
DUPLICATION CYSTS
A duplication cyst is a spherical or tubular structure that
is lined by gastrointestinal epithelium and contains
smooth muscle in its wall. Enteric duplication cysts may
occur anywhere along the gastrointestinal tract and are
usually directly attached to bowel. They share a common
blood supply with the involved intestinal segment. Gas-
tric duplications account for slightly less than 5% of all
gastrointestinal tract duplications (41). They are charac-
teristically located along the greater curvature or antrum
and do not communicate with the stomach. Clinical fea-
tures include an abdominal mass, abdominal pain, and
gastrointestinal hemorrhage. The latter finding results
from ulceration of gastric mucosa within the duplication
cyst.
Gastric duplication. Transverse sonogram of the left
Fig. 10.13
upper quadrant shows a unilocular anechoic cyst with an
inner echogenic layer (arrowheads) representing mucosal lining and an
outer hypoechoic rim representing muscular wall (arrows). L  liver.
The sonographic findings of gastric duplication are a
unilocular cystic mass with an inner echogenic layer, repre-
senting mucosa, and an outer hypoechoic rim, representing
muscular wall (Fig. 10.13). Each of these layers is approx-
imately 1 to 2 mm in thickness. The internal echogenicity
can increase if the cyst contents are hemorrhagic or pro-
teinaceous (4143). Identification of a mucosal lining
allows differentiation from other abdominal cysts. How-
ever, it may not always be possible to demonstrate both lay-
ers of the bowel wall. The mucosal layer can be destroyed
as a result of ulceration by gastric enzymes.
TERATOMA
Teratomas contain cells from all three germ lines: ecto-
derm, endoderm, and mesoderm. Gastric teratoma com-
prises less than 1% of all childhood teratomas (44,45).
They usually arise from the region of the greater curva-
ture; grow exogastrically; contain an admixture of fluid,
fat, and calcification; and are almost always benign. Sono-
graphically, they appear as complex masses containing
cystic and echogenic components. The cystic areas repre-
sent sebum, which is liquid at body temperature. The
echogenic areas can represent calcification, bone, and/or
fat (Fig. 10.14) (4446).
INFLAMMATORY PSEUDOTUMOR
Inflammatory pseudotumor, also known as plasma cell
granuloma or fibroxanthoma, is an inflammatory mass,
rather than a true neoplasm. Histologically, it contains
mature plasma cells and lymphocytes. The tumor usually
arises along the greater curvature (47). At sonography,
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Chapter 10 G A S T R O I N T E S T I N A L T R A C T 347

A B
Gastric teratoma. A: Transverse sonogram through the upper abdomen at the level of the liver (L) and right kidney (RK) shows a com-
Fig. 10.14
plex mass (arrows) with cystic and solid components. B: Axial computed tomography scan shows a cystic mass (arrows) with an
admixture of calcifications, fat, and fluid displacing the stomach (St) anteriorly. The tumor arose from the greater curvature of the stomach.

inflammatory pseudotumor appears either as a poorly
defined mass with mixed echogenicity secondary to hem-
orrhage and necrosis or as diffuse gastric wall thickening.
Enlarged lymph nodes may also be observed. The tumor is
aggressive and tends to recur if incompletely resected.
FOCAL FOVEOLAR HYPERPLASIA
Focal foveolar hyperplasia is a rare cause of a gastric mass.
The normal gastric fovea are pits in the mucosa into which
the deep gastric glands empty. When these pits become
obstructed or inflamed, they appear as polypoid masses.
Affected patients can present with signs and symptoms of
obstruction or with hematemesis. The sonographic appear-
ance of focal foveolar hyperplasia is an echogenic polypoid
mass that is mucosal in location (Fig. 10.15) (48).
MISCELLANEOUS BENIGN GASTRIC MASSES
Other gastric masses include myofibromatosis, polyps,
hematoma, leiomyoma, neurofibroma, hemangioma, car-
cinoid, and lipoma (4951). These lesions can appear as
polypoid, mucosal masses (Fig. 10.16) or as focal gastric
wall thickening. Sonography does not allow differentiation

Focal foveolar hypoplasia. Cross-sectional scan of the Gastric polyps. Long-axis sonogram through the distal
Fig. 10.15 Fig. 10.16
antrum shows thickened echogenic polypoid mucosa stomach of a 4-year-old boy demonstrates two polyps
(arrowhead). (arrowheads), confirmed at endoscopy.
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348 P E D I AT R I C S O N O G R A P H Y
of these lesions and a specific diagnosis requires correla-
tion with clinical history and often tissue sampling.
Malignant Masses
LYMPHOMA
Lymphoma is the most common malignant neoplasm of
the gastrointestinal tract in childhood. Most lymphomas
are the non-Hodgkin subtype. Clinical findings include a
palpable mass and abdominal pain. The sonographic find-
ings are gastric wall thickening and/or a bulky polypoid
mass with intramural and extramural extension (52). Lym-
phoma is usually hypoechoic compared to the normal
gastric wall. Additional findings include splenomegaly and
mesenteric or retroperitoneal lymph node enlargement.
GASTROINTESTINAL STROMAL TUMORS
Gastrointestinal stromal tumors (GISTs) arise in the mus-
cularis propria and show mural, extramural, and intramu-
ral extension. Pediatric GISTs account for less than 2% of
all GISTs. In children, they have a propensity to occur in
girls, presenting as solitary or multifocal tumors. The
mean age at presentation is 12.6 years. They may or may
not demonstrate immunoreactivity with CD117 (KIT,
tyrosine kinase growth factor receptor) (53,54). The clini-
cal presentation includes abdominal pain or discomfort,
hematemesis, melena, and anemia from gastrointestinal
bleeding. The most common location of GISTs in children
is the antrum and body of the stomach.
Sonographic findings include a predominantly
echogenic, heterogeneous mass located in the antrum or
body of the stomach (Fig. 10.17). Nodular and cystic
areas, the latter related to either hemorrhage or necrosis,
are common (5457). Air-fluid and fluid-fluid levels also
have been described (57).
A B
Gastrointestinal stromal tumors (GISTs). A: Eight-year-old girl with epigastric pain. Transverse scan of the upper abdomen shows an
Fig. 10.17
echogenic solid mass (M) arising exophytically from the stomach (St). B: Fourteen-year-old girl with an epigastic mass. Longitudinal
sonogram of the upper abdomen shows a predominantly solid mass (arrows) with anechoic cystic components. The lesions arose from the gastric
antrum. (Panel A courtesy of Edward Lee, MD.)
MISCELLANEOUS MALIGNANT TUMORS
Leiomyosarcoma and carcinoma are additional rare neo-
plasms that can involve the stomach. These tumors can
appear as a polypoid mass or as focal wall thickening,
mimicking lymphoma and benign masses.
Bezoars
A bezoar is a gastric mass composed of ingested foreign
material, usually hair (trichobezoar) or vegetable matter
(phytobezoar). Trichobezoars (hair) are more frequent
lesions in childhood than phytobezoars (vegetable matter).
Bezoars form in the stomach and can extend into the small
bowel, where they can obstruct the lumen. Clinical find-
ings include an epigastric mass, vomiting, early satiety, and
weight loss.
Sonographic findings of a trichobezoar are a complex
mass with mobile echogenic contents. A characteristic fea-
ture of a trichobezoar is a hyperechoic curvilinear band
that courses along the anterior wall of the bezoar and has
marked acoustic shadowing (Fig. 10.18) (58). The hypere-
choic arc-like band is related to the presence of air trapped
in hair fibers or food. Phytobezoars have features similar
to trichobezoars, except that acoustic shadowing is absent.
Lactobezoar is an uncommon type of phytobezoar and
is attributed to the use of powdered milk mixed with an
inadequate amount of water. Sonography shows a well-
defined, heterogeneous, hyperechoic mass with no demon-
strable acoustic shadowing (59).
SMALL BOWEL
Technique and Normal Anatomy
The four abdominal quadrants should be scanned. Initially
a linear or curvilinear 5.0 to 7.0 MHz transducer is used.
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Chapter 10 G A S T R O I N T E S T I N A L T R A C T 349

A B
Gastric bezoar. A: Longitudinal sonogram demonstrates a hyperechoic, curvilinear band (arrows) in the anterior aspect of the bezoar
Fig. 10.18
with marked acoustic shadowing. Histologically, the band contained large amounts of hair, accounting for the echogenicity. B: Com-
puted tomography demonstrates a heterogeneous mass (M) containing soft tissue (hair) and air in the body of the stomach.

Graded compression is applied in order to displace inter- 3 mm is the hallmark of bowel disease. Color Doppler
posing gas and increase conspicuity of abnormal bowel imaging is used to evaluate intestinal inflammation (60).
loops. If wall thickening is detected, a detailed evaluation Normal bowel wall shows almost no color on Doppler
with both gray-scale and color Doppler is performed with a imaging. The average number of visible vessels in normal
linear or curved high-frequency (7.5 to 12 MHz) transducer. bowel wall is 1 to 2 per square centimeter. Color Doppler
In patients with acute abdominal pain no preparation is imaging can show increased vessel density in the bowel wall
required. In patients without acute symptoms at least 4 to when there is active inflammation (61).
5 hrs of fasting can be helpful to minimize excessive gas in
the intestinal lumen. Harmonic imaging can be useful to
increase identification of the bowel layers.
The duodenal bulb is best identified with the patient in
the right lateral decubitus position and the probe placed in
the right upper abdomen or central epigastric region (see Fig.
10.3). In this position, movement of fluid from the duodenal
bulb into the descending and transverse portion of the duo-
denum may also be readily noted. The fourth portion of the
duodenum usually is not recognizable by sonography.
Differentiation of small bowel from colon is possible
based on location (small bowel is central and large bowel is
peripheral), anatomy (valvulae conniventes are present in
the small bowel) and peristalsis (usually present in small
bowel and absent or minimally present in large bowel).
The valvulae conniventes appear as intraluminal linear
echogenic structures, 3 to 5 mm apart. The jejunum has
relatively long folds. The ileum has fewer and shorter folds.
With high-resolution sonography, it is possible to see
five separate layers of the duodenum and small bowel: 1)
the echogenic superficial mucosa, 2) the hypoechoic deep
mucosa, 3) the echogenic submucosa, 4) the hypoechoic
muscularis propria, and 5) the echogenic serosal surface
(Fig. 10.19). These are best seen when the bowel lumen is
fluid-filled. When the bowel is air filled, only one or two Stratified bowel wall, gut signature. 1: Echogenic superfi-
layers may be identified (Fig. 10.20). Fig. 10.19
cial mucosa. 2: Hypoechoic deep (muscularis) mucosa. 3:
The average thickness of normal duodenal and small Echogenic submucosa. 4: Hypoechoic muscularis propria. 5: Echogenic
bowel wall is 2 to 3 mm. Wall thickening greater than serosa. (Case courtesy of Kassa Darge, MD.)
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350 P E D I AT R I C S O N O G R A P H Y
Small Bowel Obstruction
Sonography has a limited role in the detection of mechan-
ical bowel obstruction. Abdominal radiography is typically
the initial study of choice for the evaluation of suspected
bowel obstruction. If the radiographs show a complete
obstruction, additional imaging is not required. Sonogra-
phy may be helpful when there is a distended gasless
abdomen on plain radiography by showing the presence of
an unsuspected mass, ascites, or dilated fluid-filled bowel
lops suggesting obstruction (62).
DUODENAL ATRESIA, STENOSIS, AND DIAPHRAGMS
Congenital duodenal obstruction occurs in 1 in 3400 births.
Duodenal atresia is the most common cause of congenital
duodenal obstruction in the neonate. Less common causes of
congenital duodenal obstruction are duodenal membrane,
duodenal stenosis, and annular pancreas. Duodenal atresia
and stenosis are believed to be related to failure of recanal-
ization of the duodenal lumen during fetal development. The
Normal bowel. Transverse sonogram
Fig. 10.20
shows air-filled descending colon (C)
just beneath the abdominal wall. Two layers of the
bowel wall can be identified: the echogenic submu-
cosa (arrowhead) and the surrounding hypoechoic
muscularis (white arrow). (Case courtesy of Kassa
Darge, MD.)
level of obstruction is invariably at or just below the level of
the papilla of Vater. Approximately one half of all patients
with duodenal atresia have Down syndrome. Other associ-
ated anomalies include other gastrointestinal tract atresias,
renal anomalies, and congenital heart disease. Neonates with
congenital duodenal obstruction typically present with bil-
ious vomiting within the first 24 hours of life.
The classic radiographic findings of duodenal atresia
and high-grade stenosis are marked dilatation of the stom-
ach and duodenum, producing the double bubble sign.
This appearance obviates further imaging evaluation. The
one form of duodenal atresia in which sonography is valu-
able is the type in which there is esophageal atresia without
an associated tracheoesophageal fistula. Under these cir-
cumstances, the diagnosis can be difficult to accomplish
with conventional radiography since the abdomen is gas-
less. Because the distal esophagus, stomach, and duodenum
are filled with fluid, they provide an excellent sonographic
window. Sonography can easily show the massively dilated,
fluid-filled stomach and proximal duodenum (Fig. 10.21).
Duodenal atresia with associated
Fig. 10.21
esophageal atresia. Transverse scan
through the upper abdomen demonstrates a dilated
duodenal bulb (D) and stomach (S). Duodenal wall
thickness is normal.
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Chapter 10 G A S T R O I N T E S T I N A L T R A C T 351

A B
Duodenal membrane. A: Transverse scan of the upper abdomen shows a dilated descending duodenum (D) with an echogenic mem-
Fig. 10.22
brane (arrow). RK  right kidney. B: Image from an upper gastrointestinal series shows contrast agent in a dilated stomach and prox-
imal duodenum (D). A small amount of contrast material is noted in the proximal jejunum.

A duodenal membrane or web is an intraluminal
diaphragm that arises near the ampulla of Vater. The
diaphragm may be complete or partial, depending on the
presence or absence of an aperture. If the diaphragm is
complete, the patient presents with bilious vomiting and a
double-bubble sign on plain radiographs, indistinguishable
from that seen in duodenal atresia. If the web is incomplete,
abdominal radiography may be normal. The sonographic
appearance of a duodenal web is an echogenic curvilinear
band in the dilated proximal duodenum (Fig. 10.22) (62).
mately 10% to 20% of patients with cystic fibrosis present
in the neonatal period with meconium ileus. The clinical
findings are similar to those of ileal atresia.
Sonographic findings of meconium ileus include highly
echogenic bowel contents, dilated bowel loops, and decreased
peristalsis, reflecting obstruction by the thick, tenacious
meconium (Fig. 10.23) (63). The intraluminal echogenicity

JEJUNAL AND ILEAL ATRESIA OR STENOSIS

Atresia and stenosis are causes of intestinal obstruction in the
neonate. Atresia is more common than stenosis. Both are
thought to result from an in utero ischemic event. Patients
present in the first 24 hours of life with vomiting, abdominal
distension, and failure to pass meconium. Associated anom-
alies include midgut malrotation, gastroschisis, duodenal
atresia, and tracheal-esophageal fistula.
Sonography is not indicated in newborns with small
bowel atresia, unless the clinical findings are atypical, per-
haps suggesting an abdominal mass. The sonographic find-
ings of jejunal and ileal atresia are multiple, dilated, fluid-
and air-filled loops of small bowel (63). Peristalsis may be
normal or increased. Ascites may also be noted.

MECONIUM ILEUS
Meconium ileus is a congenital bowel obstruction that
results from inspissation of abnormally thick and tena-
cious meconium in the distal small bowel. It is almost
always a manifestation of cystic fibrosis, and approxi-
Meconium ileus. Longitudinal sonogram of the right flank
Fig. 10.23
shows dilated small bowel (arrows) containing highly
echogenic masses of meconium.
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352 P E D I AT R I C S O N O G R A P H Y

Meconium peritonitis. Transverse sonogram demon-

Fig. 10.24
strates multiple highly echogenic areas (arrows), some
with acoustic shadowing, on the surface of the liver.

may be helpful in distinguishing meconium ileus from distal
bowel atresia, which typically does not have highly reflective
bowel contents.
MECONIUM PERITONITIS AND PSEUDOCYST
Meconium peritonitis is the result of antenatal perfora-
tion of bowel and extrusion of sterile meconium, which
produces a nonbacterial chemical peritonitis with resul-
tant dystrophic calcification. It is associated with bowel
atresia and meconium ileus. Up to one half of all cases of
meconium ileus are complicated by meconium peritonitis
(63). Calcifications can develop as early as 12 hours after
the in utero perforation. Sonographic findings of meco-
nium peritonitis include highly echogenic foci (i.e., calci-
fications) with varying degrees of acoustic shadowing on
the peritoneal surface (Fig. 10.24) and diffuse peritoneal
and mesenteric echogenicity, termed a snowstorm appear-
ance (64,65). Echogenic ascites may also be noted
(64,65).
Meconium pseudocyst is a cyst-like mass that results
when the extruded meconium becomes walled off by
fibrous adhesions. The mass can contain only meconium or
a combination of meconium and trapped bowel loops. Cal-
cifications within the wall are frequent. The sonographic
appearance is a well-defined mass with echogenic contents
owing to a combination of air and meconium (Fig. 10.25).
Wall calcifications appear as highly echogenic peripheral
foci with acoustic shadowing. Intraluminal air produces
high-amplitude echoes, occasionally associated with distal
shadowing or a ring-down artifact.
MIDGUT MALROTATION
Malrotation refers to a spectrum of rotational abnormali-
ties including failure of rotation (colon to the left, small

A B
Meconium pseudocyst. Transverse (A) and longitudinal (B) sonograms through the midabdomen show a large cystic mass (C) con-
Fig. 10.25
taining echoes, representing air and meconium, in the anterior abdomen. The walls are highly echogenic (arrows) related to the pres-
ence of calcification. L  liver; RK  right kidney; SP  spine.
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Diagram showing mesenteric vascular rela-
Fig. 10.26
tionships. A: Normal mesenteric vascular rela-
tionship with the superior mesenteric vein to the right of the
artery. B: Reversal of the normal mesenteric vascular rela-
tionship with the superior mesenteric vein to the left of the
artery. C: Ventral position of superior mesenteric vein rela-
tive to the artery. AO  aorta; SMA  superior mesenteric
artery; SMV  superior mesenteric vein.
bowel to the right), reverse nonrotation (small bowel to the
left, colon to the right), reverse rotation (duodenum ante-
rior and colon posterior to the superior mesenteric artery,
small bowel to the right, cecum malpositioned), and incom-
plete rotation (a range of abnormalities between nonrota-
tion and normal rotation). In malrotation, the attachment
of the bowel is abnormally short, resulting in a narrowed
mesenteric pedicle and an abnormally positioned ligament
of Treitz (66). This anomaly may be associated with other
anomalies including omphalocele, gastroschisis, diaphrag-
matic hernia, and duodenal atresia or web.
Symptoms in patients with malrotation are a result of
a proximal bowel obstruction from extrinsic peritoneal
bands (Ladd bands) crossing the third portion of the duo-
denum, midgut volvulus, or a combination of the abnor-
malities. Patients with malrotation usually present in the
first month of life with vomiting, which is nearly always
bilious, but they may present in later life or remain asymp-
tomatic throughout their lifetime.
The upper gastrointestinal examination is the imaging
study of choice to diagnose malrotation. Ultrasonography
is not needed for the diagnosis, but the findings need to be
recognized because they may be encountered on examina-
tions performed for other clinical indications. The sono-
graphic diagnosis of midgut malrotation is predicated
Normal mesenteric vascular relationship. Transverse
Fig. 10.27
view through the upper abdomen demonstrating the
superior mesenteric vein (V) lying to the right of the superior mesen-
teric artery (A). Ao  aorta; C  inferior vena cava.
Chapter 10 G A S T R O I N T E S T I N A L T R A C T 353
A B C
on identifying the relative positions of the superior mesen-
teric artery (SMA) and superior mesenteric vein (SMV)
(Fig. 10.26) (6669). The patient is examined in the supine
position with a 5- or 7-MHz transducer. The SMA is iden-
tified at its origin from the abdominal aorta and the SMV
is traced from the portal vein confluence.
Normally, the SMV is anterior and to the right of the
artery (Fig. 10.27). Reversal of this relationship, with the
SMV positioned to the left of the SMA, suggests midgut
malrotation (Fig. 10.28). However, some patients with
malrotation have a normal position of the artery and vein,
and some patients with an abnormal relationship of these
vessels do not have malrotation (6769). Moreover, the
vessel pattern can be indeterminate, with the SMV lying
anterior to the SMA, a pattern that can be seen in patients
with normal as well as abnormal rotation (Fig. 10.29).
Approximately 15% to 20% of patients with midgut mal-
rotation will have a ventral position of the SMV relative
to the SMA. The sensitivity of vascular inversion for the
diagnosis of midgut malrotation ranges from 53% to
87% (6669). Because of the pitfalls, barium upper gas-
trointestinal series remains the study of choice to diagnose
or exclude the presence of malrotation.
Sonographic findings of volvulus are a fluid-filled
proximal duodenum, clockwise twisting of the SMV and
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A B

Midgut malrotation. Transverse gray-scale (A) and color

Fig. 10.28
Doppler (B) images through the upper abdomen demon-
strate reversal in the position of the mesenteric vessels. The superior
mesenteric vein (V) is to the left of the superior mesenteric artery (A).
C  inferior vena cava. C: Upper gastrointestinal tract examination
demonstrates the ligament of Treitz (arrow) located to the right of the
C spine, diagnostic of midgut malrotation.

Indeterminate vascular relationship. Transverse view

Fig. 10.29
through the upper abdomen demonstrates superior
mesenteric vein (V) anterior to the superior mesenteric artery (A). The
upper gastrointestinal series was normal in this patient.
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Midgut volvulus. Transverse color Doppler sonogram
Fig. 10.30
shows clockwise twisting of the superior mesenteric
vein (arrows) around the superior mesenteric artery (A), which is in the
center of the volvulus and lacks flow. (Courtesy of Brian Coley, MD.)
mesentery around the SMA (whirlpool sign) (Fig. 10.30),
peritoneal fluid, thickened echogenic bowel wall from
hemorrhage or edema, and a hyperpulsatile SMA (7073).
Malrotation is treated by a Ladd operation. This
procedure involves resection of peritoneal bands and non-
viable bowel, reduction of volvulus, and placement of small
bowel in the right abdomen and colon in the left abdomen.
INTUSSUSCEPTION
Intussusception is an invagination of a proximal segment of
intestine (the intussusceptum) into a more caudal segment
A B
Intussusception. A: Short-axis view through the right midabdomen demonstrates a large complex mass (arrows) with an echogenic
Fig. 10.31
center (C) and multiple surrounding concentric hypoechoic and hyperechoic rings. B: On a long-axis image, the intussusception has
a reniform shape (arrows). The short-axis diameter and length of the intussusception were 5.0 cm and 8 cm, respectively.
Chapter 10 G A S T R O I N T E S T I N A L T R A C T 355
of bowel (the intussuscipiens) (74). It is the most common
acute abdominal disorder of early childhood. Approxi-
mately 90% of intussusceptions are ileocolic; the remaining
cases are ileoileocolic, colocolic, or ileoileal. Over 90% of
intussusceptions have no pathologic lead point and are
thought to be due to enlarged lymphoid follicles in the ter-
minal ileum. Lead points in the remaining patients include
Meckel diverticulum, intestinal polyps, enteric duplica-
tions, intramural hematoma, and lymphoma (74).
Intussusception occurs most commonly in children
between 3 months and 3 years of age. The peak incidence
is between 5 and 9 months of age, and 75% of children are
under the age of 2 years. The classic clinical findings are
paroxysmal abdominal pain, vomiting, red currant jelly
stools (containing blood and mucus), and a palpable
abdominal mass (75).
Ultrasonography for diagnosis of intussusception is
performed using the graded-compression technique. The
colon is followed from right to left. The entire abdomen
and pelvis are scanned in both longitudinal and trans-
verse planes. On transverse sonograms, the intussuscep-
tion appears as a complex mass with alternating concen-
tric hypoechoic and hyperechoic rings (the doughnut
or target sign) (Fig. 10.31) (7678). The mucosa and
submucosa are echogenic, while the muscularis is hypo-
echoic. The diameter of the intussuscepted bowel exceeds
3 cm in maximal diameter. On longitudinal images, the
intussusception has a reniform appearance (termed the
pseudokidney sign), characterized by alternating
hypoechoic and hyperechoic bands (Fig. 10.31B) (79).
Other findings associated with intussusception are dilated
small bowel proximal to the site of obstruction, peri-
toneal fluid, and inversion of the mesenteric vessels
(80,81).
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356 P E D I AT R I C S O N O G R A P H Y

Intussusception, lead mass. Transverse sonogram

Fig. 10.32
shows an ovoid mass with two layers: an echogenic cen-
tral intussusceptum (I) and hypoechoic intussuscipiens (arrows).
Within the echogenic center, there is a small hypoechoic nodule
(arrowhead), shown to be a hamartoma at surgery. At operation, the
bowel was very edematous, but viable. B  dilated fluid-filled bowel
loops proximal to the intussusception.

Occasionally, a lead mass is apparent. A lead point
appears as a mass in the center of the intussusception
(Figs. 10.32 and 10.33) (82,83). A hypoechoic mass sug-
gests a duplication cyst, polyp, Meckel diverticulum, or
hematoma. However, it is important to recognize that fluid
trapped within the intussuscepted mesentery can mimic a
cyst or hypoechoic mass (84) (Fig. 10.34).
The treatment for intussusception is fluoroscopic-guided
air or hydrostatic reduction. The presence of blood flow on
color Doppler imaging suggests a reducible intussusception
and viable bowel, while the absence of flow suggests a
lower likelihood of reduction and higher likelihood of
ischemia (Figs. 10.35 and 10.36). Wall thickness greater
than 1 cm, large amounts of trapped peritoneal fluid within

A B
Intussusception, lead points. A: Meckel diverticulum. Transverse sonogram shows an echogenic Meckel diverticulum (M) protruding
Fig. 10.33
into the intussusceptum (I). Arrows indicate intussuscipiens. B: Cecal duplication. Transverse sonogram shows a complex mass (the
duplication) (arrowhead) within the intussusceptum (I). Arrows indicate intussuscipiens.
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Chapter 10 G A S T R O I N T E S T I N A L T R A C T 357

Intussusception with trapped peritoneal fluid. Trans-

Fig. 10.34
verse view demonstrates a spherical mass (arrows) rep-
resenting an intussusception. Note fluid (F) trapped in the mesenteric
layer. Differentiation of trapped fluid and a cystic mass can be difficult
by sonography.

Intussusception. Color Doppler sonogram shows flow in

Fig. 10.35
the intussuscepted loop of bowel. This intussusception
was reduced by air-contrast enema.

Intussusception, color Doppler imaging. Long-axis sono-

Fig. 10.36
gram shows no flow within the intussuscepted loop of
bowel (arrows). The intussusception was not reducible by air-contrast
enema. Surgical exploration showed necrotic bowel and a polyp act-
ing as a lead point.
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358 P E D I AT R I C S O N O G R A P H Y
Intussusception, false-positive diagnosis. Transverse
Fig. 10.37
sonogram of the right lower quadrant shows an ovoid
mass (arrows), considered to be an intussusception. Air enema
showed only thickened bowel wall without an intussusception. Cul-
tures grew Escherichia coli.
the intussusception, and lymph nodes greater than 1 cm in
diameter are also associated with a lower reduction rate
(8589).
Sonography has been used to guide reduction with
good results (9092). A liquid or air enema is administered
while the patient is monitored by sonography. The instilled
material is followed as it courses through the large bowel
until the intussusception is no longer visualized and the
A B
Transient intussusception. A, B: Axial and longitudinal sonograms through the left upper quadrant show the typical bulls-eye and
Fig. 10.38
pseudokidney signs, respectively, of intussusception (arrows). The short-axis diameter is 1.5 cm and the length is 2.5 cm, typical of
transient intussusception.
terminal ileum and distal small bowel are filled with fluid
or air. Color Doppler sonography can also confirm a
successful reduction by showing aliasing, related to flow of
fluid through the ileocecal valve (93).
The sensitivity of sonography for the diagnosis of intus-
susception ranges between 95% and 100%, and the speci-
ficity ranges between 88% and 100% (7478,94). False-pos-
itive diagnoses are caused by fecal contents, inflammatory
bowel disease (Fig. 10.37), and intramural hematoma.
Transient Small Bowel Intussusception
Transient small bowel intussusception is a common occur-
rence, particularly in children with hyperperistaltic bowel. It
tends to occur in young children (mean age 4 years) and
most commonly involves proximal small bowel loops (95).
Clinical findings are similar to those of ileocolic intussuscep-
tions and include abdominal pain, vomiting, and diarrhea. A
palpable mass and currant jelly stools are absent.
The transient intussusception is commonly in the
paraumbilical region or left upper quadrant (96),
whereas ileocolic intussusceptions are usually located in
the right upper or lower quadrant of the abdomen. Tran-
sient intussusceptions tend to be shorter than ileocolic
intussusceptions. Mean lengths of transient and ileocolic
intussusceptions are 2.5 cm (range 1.5 to 6.0 cm) and 8.4
cm (range 5.0 to 12.5 cm), respectively (96). The mean
short-axis diameter of transient intussusceptions is 1.5
cm versus 2 to 3.8 cm for ileocolic intussusceptions (Fig.
10.38). Spontaneous resolution of transient intussuscep-
tion usually can be observed with continuous scanning.
OTHER BOWEL OBSTRUCTION
The sonographic features of acquired small bowel obstruc-
tion are hyperperistaltic, dilated, fluid-filled loops proxi-
mal to the site of luminal occlusion (Fig. 10.39). However,
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Small bowel obstruction. Transverse sonogram of the
Fig. 10.39
right lower quadrant shows multiple dilated bowel loops
(B) in a patient with small bowel obstruction secondary to adhesions.
Internal echoes represent gas bubbles and intestinal contents. A
closed loop obstruction was found at operation.
these findings are nonspecific and they may also be
observed in patients with gastroenteritis or ileus. Thick-
ened bowel wall and ascites within the leaves of the small
bowel mesentery are findings suggestive of associated
infarction (62).
A B
Crohn disease. Longitudinal (A) and transverse (B) sonograms of the right lower quadrant show thick-walled terminal ileum (arrows)
Fig. 10.40
(wall thickness 8 mm measured from the mucosal surface to the outer wall). The bowel lumen is narrowed by the apposed thick bowel
walls. Open arrow indicates intraluminal air.
Chapter 10 G A S T R O I N T E S T I N A L T R A C T 359
Small Bowel Wall Thickening
Small bowel wall thickening is defined as wall thickness of
3 mm or greater. It may be caused by inflammatory, infec-
tious, ischemic, or neoplastic conditions. Sonography is
useful for localizing the site of abnormality and for identi-
fying associated complications. However, it rarely allows
for a specific diagnosis to be made without correlation
with clinical history or tissue sampling.
CROHN DISEASE
Crohn disease or regional enteritis is the most common
inflammatory disease of the small bowel. Most children
with Crohn disease are over 10 years of age at the time of
presentation. The systemic symptoms are weight loss,
growth failure (short stature; delayed bone age), anorexia,
malaise and fever of unknown etiology. Common gastroin-
testinal symptoms are abdominal pain (acute and/or
chronic), diarrhea (with or without blood and mucus), and
nausea/vomiting. Other clinical findings include delayed
sexual maturation and osteopenia/osteoporosis. Pathologi-
cally, the acute phase is characterized by enlarged lymphoid
follicles, edema and aphthoid ulceration; the chronic phase
is associated with transmural fibrosis and strictures.
Although contrast examinations and endoscopy remain
the primary diagnostic tools for characterization of mucosal
and luminal changes, sonography plays a role in the evalu-
ation of suspected extraluminal complications, including
biliary and urinary tract disease, peritoneal abscess, and
phlegmon formation.
Sonographic Findings
Crohn disease is characteristically segmental, with spared
areas throughout the bowel. The terminal ileum and prox-
imal colon are the most affected sites, although any part of
the gastrointestinal tract can be affected. The classic find-
ing is concentrically thickened bowel wall, measuring
more than 5-mm in diameter (97101) (Fig. 10.40). Bowel
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360 P E D I AT R I C S O N O G R A P H Y

Crohn disease, creeping fat. Transverse sonogram

Fig. 10.42
shows thickened ileum (I), increased echogenicity of the
Crohn disease. Power Doppler image showing thick- adjacent mesenteric fat (arrows), and an enlarged lymph node (N).
Fig. 10.41
ened, hypervascular terminal ileum (arrows). (Case
courtesy of Kassa Darge, MD.)

stratification (presence of discrete bowel layers) is pre- Complications

served in early disease, but it is lost as the disease pro- Complications of Crohn disease include phlegmon, abscess
gresses and fibrosis develops. The abnormal segment of formation, fistulas and stricture (97,100). Phlegmon
bowel may be partially or noncompressible. Peristalsis is appears as a poorly defined, echogenic mass with irregular
usually present, but it is often diminished. borders adjacent to an area of inflamed bowel. An abscess
Color Doppler imaging shows increased flow in the appears as a well-defined, thick-walled, fluid-filled mass
mucosa and submucosa of affected bowel segments (Fig. (Fig. 10.44). Highly reflective internal echoes, representing
10.41) (102105). Transmural hyperemia can be seen in gas bubbles, may be noted within the abscess.
severe or chronic disease. The presence of hypervascular Fistula formation, the hallmark of Crohn disease, is
bowel wall (3 vessels per square centimeter) usually indi- most common beteween the terminal ileum and cecum,
cates active disease. Another parameter to evaluate inflam- although it can extend from abnormal bowel segments to
matory activity is measurement of superior mesenteric other loops of bowel, bladder or skin. Fistulas appear as
artery (SMA) flow volume with pulsed Doppler sonogra-
phy. Increased SMA flow volume has been noted in patients
with active disease compared with patients with inactive
disease and healthy volunteers: 1,588 mL/min / 576
versus 288 mL/min / 113 and 417 mL/min / 147,
respectively (106,107).
Other sonographic findings of Crohn disease include
increased echogenicity and hyperemia of the mesentery
adjacent to an abnormal segment of bowel, representing
fibrofatty proliferation or creeping fat, and an
increased number of mesenteric lymph nodes (Fig.
10.42) (97,100). Involved mesenteric lymph nodes are
usually 1 cm or less in diameter. Based on meta-analysis
data, the sonographic sensitivity and specificity for the
diagnosis of Crohn disease is 75% to 94% and 67% to
100%, respectively (108).
Appendiceal involvement has been described in approx-
imately 20% of patients with Crohn disease (Fig. 10.43)
(109,110). The sonographic findings include thickened and
hyperemic appendiceal walls. The findings are indistin-
guishable from those of acute appendicitis. Concomitant
thickening and hyperemia of the terminal ileum support Crohn disease with appendiceal involvement. Long-axis
the diagnosis of Crohn disease rather than acute appen- Fig. 10.43
sonogram shows appendiceal wall thickening (9 mm
dicitis (100). diameter) (arrows). (Case courtesy of Brian Coley, MD.)
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Chapter 10 G A S T R O I N T E S T I N A L T R A C T 361

A B
Crohn disease with abscess formation. A, B: Longitudinal sonograms through the right lower quadrant of two different patients demon-
Fig. 10.44
strate a fluid-filled mass (arrows) adjacent to thickened terminal ileum (TI). The surrounding mesentery is echogenic. (Cases courtesy
of Kassa Darge, MD.)

hypoechoic (fluid-filled) or echogenic (gas-filled) linear
bands or tracts adjacent to an actively inflamed segment of
bowel (Fig. 10.45) (97100). Air also may be noted in the
bladder, vagina, retroperitoneum or soft tissues. Strictures
appear as areas of fixed luminal narrowing (97,100). Lumi-
nal dilatation and increased peristalsis may be observed
proximal to the stenotic segment.
Post-treatment Assessment
New or progressive bowel wall thickening or recurrent
hyperemia and high flow velocities in the superior mesenteric
artery are findings of recurrent disease. The sensitivity and
specificity of sonography in demonstrating post-surgical
recurrence is approximately 80% and 100%, respectively
(98,111). During clinical remission, residual hyperemia on
color Doppler sonography appears to correlate with increased
risk of relapse (104).
INFECTIOUS ENTERITISACUTE TERMINAL ILEITIS
Acute bacterial bowel infections that affect the ileocecal
region include Yersinia enterocolitica, Campylobacter
jejuni, Salmonella typhosa and Yersinia pseudotuberculosis.

A B
Enteroenteric fistula. A: Sagittal sonogram shows thickened terminal ileum (TI) with a hypoechoic fistulous tract (arrow) connecting
Fig. 10.45
the diseased bowel to an adjacent small bowel loop (*). The mesentery (M) surrounding the abscess is thick and echogenic (creep-
ing fat). B: Longitudinal sonogram in another patient shows thickened terminal ileum (arrowheads) and a fistula (arrow) extending posteriorly. (Panel
A courtesy of Kassa Darge, MD. Panel B courtesy of Brian Coley, MD.)
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362 P E D I AT R I C S O N O G R A P H Y

Yersinia enterocolitis. Longitudinal sonogram of the right Henoch-Schnlein purpura. Transverse sonogram show-
Fig. 10.46 Fig. 10.47
lower quadrant demonstrates thick-walled loops of dis- ing circumferential thickening of the terminal ileum
tal ileum (arrows). (arrows) (thickness  1 cm).

These conditions usually affect adolescents and young adults.
Patients usually present with mild gastroenteritis, although
in some instances, the pain may mimic acute appendicitis
(112114).
The sonographic findings of terminal ileitis are similar
to those of of Crohn disease, including partially compress-
ible thickened bowel wall, diminished peristalsis and mul-
tiple mesenteric lymph nodes (Fig. 10.46) (112114). The
nodes usually range between 7 and 21 mm in diameter and
are hypoechoic with an echogenic center (112). Color
Doppler imaging shows increased flow within the bowel
mucosa (102,103).
raphy shows hypervascular mucosa and bowel wall
(Fig. 10.48) (102,103,118).
TRAUMATIC INTRAMURAL HEMORRHAGE
Traumatic hematomas result from a direct blow or from
shearing of the bowel against the spine. The common sites
for hematomas are the fixed retroperitoneal portion of the
duodenum directly anterior to the spine and the proximal
jejunum where it is fixed by the ligament of Treitz.
Hematomas can narrow or completely obstruct the bowel

HENOCH-SCHNLEIN PURPURA AND SMALL BOWEL HEMORRHAGE

Intramural hemorrhage in children usually is a result of
accidental or non-accidental trauma or Henoch-Schnlein
purpura. Bleeding diathesis and endoscopic procedures are
less common causes of hemorrhage. Henoch-Schnlein
purpura is a systemic vasculitis characterized by deposition
of immune complexes containing the antibody IgA in the
skin and kidney. It mainly affects young children. The clas-
sic clinical findings are non-thrombocytopenic purpura,
arthritis, abdominal pain, and nephritis (115117).
Abdominal pain is due to bowel wall hemorrhage or intus-
susception, with the hematoma acting as a lead point. The
bowel is affected in approximately one-half of cases. The
stomach and small and large bowel may be affected.
Abdominal pain may precede the onset of skin lesions and
mimic acute appendicitis.
Sonography can demonstrate circumferential bowel
wall thickening (3 mm) in the duodenum, jejunum or
ileum and/or focal intramural hematomas (115118) Henoch-Schnlein purpura. Transverse color Doppler
(Fig. 10.47). Hematomas can be multifocal and they can Fig. 10.48
sonography shows thick-walled, hypervascular loops of
be complicated by intussusception. Color Doppler sonog- jejunum (arrows).
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Chapter 10 G A S T R O I N T E S T I N A L T R A C T 363

A B

Duodenal hematoma. A: Acute hematoma. Transverse

Fig. 10.49
sonogram shows an echogenic mass (arrows), repre-
senting an acute hematoma, medial to the proximal duodenum (D) and
anterior to the spine (SP). The duodenum (D) is dilated. B: Color
Doppler image. The hematoma (arrows) is avascular. C: Chronic
hematoma. Transverse sonogram shows an anechoic mass (arrows)
C compressing and displacing the wall of the transverse duodenum (D).

lumen. Patients typically present with abdominal pain
and vomiting, which may be bilious or nonbilious
depending on the location of the hematoma relative to
the ampulla of Vater.
The sonographic finding of traumatic hematoma is
focal bowel wall thickening (Fig. 10.49) (119121). The
echogenicity of the hemorrhage is dependent on its age.
Acute hemorrhage is hyperechoic. Subacute hematomas
are complex, with hypoechoic and echogenic areas, and
chronic hematomas are anechoic (see Fig. 10.49C). Con-
tiguous proximal bowel is often fluid-filled and dilated.
Hematomas are avascular on color Doppler imaging (see
Fig. 10.49B).
MISCELLANEOUS DISORDERS
Lymphangiectasia, cystic fibrosis, Kawasaki disease, and
graft-versus-host disease are other causes of small bowel
wall thickening in childhood. Primary intestinal lym-
phangiectasia is a congenital protein-losing enteropathy
characterized by dilated lymphatics within the intestinal
villi. Secondary lymphangiectasia results from mesenteric
tumor obstructing segmental lymphatic channels. Sono-
graphic findings include bowel wall thickening, ascites,
and mesenteric edema (Fig. 10.50). Occasionally, dilated
mesenteric lymphatics can be recognized (122). These can
be separated from mesenteric blood vessels by color
Doppler imaging.
In cystic fibrosis, the sonogram can show bowel
wall thickening and highly echogenic bowel contents
(Fig. 10.51). Kawasaki disease is an acute, systemic vas-
culitis affecting medium size arteries. Segmental, non-
stratified bowel wall thickening may be seen on sonog-
raphy (123).
Graft-versus-host disease (GVHD) is a complication of
heterotopic bone marrow transplantation, affecting 50% to
70% of allogeneic transplants. Donor T lymphocytes cause
selected damage to the cellular lining of recipient target
organs, usually the skin, liver, and gastrointestinal tract
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364 P E D I AT R I C S O N O G R A P H Y
Intestinal lymphangiectasia. Longitudinal sonogram of
Fig. 10.50
the right lower quadrant shows thick-walled loops of
ileum projecting into chylous ascites (As).
(124,125). GVDH can affect the entire bowel from the
duodenum to rectum, but more commonly it involves the
small bowel. Sonographic findings are dilated fluid-filled
loops of bowel and bowel wall thickening, usually ranging
between 3 and 5 mm. The increased wall thickness is a
result of an expanded submucosal layer. Bowel wall strati-
Cystic fibrosis. Transverse image of the right lower quad-
Fig. 10.51
rant shows thick-walled distal ileum (arrows).
fication is often preserved. In addition, an additional
echogenic layer may be detected between the mucosal layer
and the bowel lumen, possibly related to severe mucosal
ulceration with coating of the mucosal surface by sloughed
membranes (125).
Benign Small Bowel Masses
ENTERIC DUPLICATION CYSTS
Enteric duplication cysts are congenital anomalies charac-
terized by duplication of the enteric wall (41). The cyst
wall contains all normal bowel layersmucosa, submu-
cosa, and muscularis. The muscularis is typically shared
with the adjacent bowel wall, but the mucosal lining is sep-
arate. They also may contain ectopic gastric mucosa, lym-
phoid aggregates, ganglion cells, and lymphatic tissue.
Duplication cysts of small bowel are most common in the
ileum (41). Most duplications do not communicate with
the lumen of the gastrointestinal tract.
Clinical signs and symptoms include abdominal disten-
sion, pain, or palpable mass; vomiting; and gastrointestinal
bleeding. The latter finding results from ulceration of gas-
tric mucosa within the cyst. Enteric duplication cysts may
be a lead point for intussusception. They can be a cause of
pancreatitis if they are located close to the ampulla of Vater
and obstruct drainage of the pancreatic duct (126).
The sonographic findings are a well-defined, spherical or
tubular hypoechoic mass with an echogenic inner mucosal
lining and an outer hypoechoic muscular wall (Fig. 10.52)
(41,42,127,128). Occasionally, the cyst appears complex as
a result of hemorrhage or inspissated debris. The shape of
the duplication may change with peristalsis (129).
Duodenal duplication cyst. Transverse sonogram
Fig. 10.52
through the upper abdomen just to the right of midline
shows an anechoic mass with an inner layer of echogenic mucosa
(white arrows) and an outer wall of hypoechoic muscle (black arrows).
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Small bowel polyp. Six-year-old boy with Peutz-Jeghers
Fig. 10.53
syndrome, abdominal pain, and clinical suspicion of intus-
susception. Transverse sonogram of the left upper quadrant demon-
strates an intussusception containing an echogenic polyp (arrows).
The combination of a cystic mass with echogenic inner
lining and a hypoechoic rim is specific for duplication. The
presence of these two layers is useful to exclude other cys-
tic masses such as mesenteric or omental cyst, choledochal
cyst, ovarian cyst, and pancreatic pseudocyst, which lack a
mucosal lining. However, the mucosal layer can be
destroyed secondary to ulceration by gastric enzymes. As a
result, the echogenic layer will be absent and the appear-
ance of the cyst will overlap with that of other cystic
lesions.
POLYPS
Polyps are the most common primary tumor of the small
bowel in children. They can be isolated or they can occur
in the multiple polyposis syndromes, such as Peutz-
Jeghers, Cronkhite-Canada, and Gardner syndromes. On
sonography, polyps appear as intraluminal nodules (Fig.
10.53). They may serve as a lead point for intussusception.
Sonography is not meant to replace endoscopy in the
workup of polyps, but these may be first detected by
sonography performed in children with nonspecific symp-
toms or in those who are asymptomatic (130).
Malignant Masses
LYMPHOMA
Lymphoma, usually non-Hodgkin lymphoma, is the most
common small bowel malignancy in childhood. Affected
children present with a palpable abdominal mass or with
abdominal pain and vomiting as the result of intestinal
obstruction. In children, the small bowel is the most fre-
quent site of intestinal involvement by lymphoma, and the
ileum is the most common site of small bowel involvement.
Chapter 10 G A S T R O I N T E S T I N A L T R A C T 365
Non-Hodgkin lymphoma. Longitudinal scan of the lower
Fig. 10.54
abdomen shows hypoechoic circumferential wall thick-
ening of a loop of distal ileum. Arrows indicate compressed mucosa.
The duodenum is the least common site. Multifocal involve-
ment is not uncommon.
At sonography, lymphomatous involvement of bowel
produces hypoechoic circumferential wall thickening or a
focal hypoechoic or complex mass with anechoic areas
related to necrosis (Fig. 10.54) (52). The wall thickness
usually exceeds 1 cm. The lumen may be narrowed due to
extrinsic compression or there may be aneurysmal dilata-
tion, secondary to mucosal invasion and excavation. Intus-
susception is an occasional complication of lymphoma.
Other intra-abdominal findings include splenomegaly and
mesenteric and retroperitoneal adenopathy. The enlarged
nodes are usually hypoechoic and may lack the normal
echogenic hilum.
MISCELLANEOUS
Leiomyosarcoma and adenocarcinoma have been reported
in childhood, but they are extremely rare. On sonography,
these tumors appear as large solid masses with necrotic foci.
MESENTERIC ADENITIS
Mesenteric lymphadenitis is a clinical entity characterized
by benign inflammation of lymph nodes secondary to an
infectious process, and the right lower quadrant is the
most commonly affected site (131134). Lymphadenitis
is commonly viral in origin, but Y. enterocolitica has been
implicated in some cases. Affected patients can present
with acute abdominal pain, mimicking an acute abdomen.
The condition is usually self-limited and treated sympto-
matically.
Sonography shows lymph nodes greater than three in
number and 5 mm in maximum anteroposterior diameter,
with or without bowel wall thickening (133). Enlarged
mesenteric lymph nodes maintain their oval shape. They
are isoechoic or hypoechoic to surrounding tissues and
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366 P E D I AT R I C S O N O G R A P H Y
A B
Mesenteric lymphadenopathy. A: Transverse view through the right lower quadrant shows several enlarged, hypoechoic mesenteric
Fig. 10.55
lymph nodes (arrows). The nodes maintain their normal oval shape. B: Color Doppler imaging shows flow (arrows) within the hilum of
an enlarged lymph node. The nodes maintain their normal oval shape.
demonstrate echogenic central hila (Fig. 10.55), which
may be vascular on color Doppler sonography.
Mesenteric lymph node enlargement is a nonspecific
finding. It can be associated with a variety of infectious,
inflammatory, and neoplastic conditions including acute
appendicitis, inflammatory bowel disease, and lymphoma.
APPENDIX
Appendicitis
Acute appendicitis is the most common indication for emer-
gency surgery in older children and adolescents (135138).
It results from appendiceal luminal obstruction by fecal
impaction or appendiceal calculi, followed by luminal dis-
tension, ischemia, and secondary bacterial infection. Unless
the condition is treated, appendiceal necrosis ultimately
develops, resulting in perforation, abscess formation, and
peritonitis.
The typical clinical findings are abdominal pain that
originates in the periumbilical region and migrates to the
right lower quadrant, abdominal tenderness, fever, and
leukocytosis. However, in about one third of children clin-
ical findings are atypical (135138). This is particularly the
case in adolescent girls, where gynecologic disorders can
produce acute lower abdominal pain that mimics appen-
dicitis.
Sonography has become a principal imaging study for
the diagnosis of appendicitis in children, both to establish
the diagnosis of appendicitis and to aid in the diagnosis of
other abdominal or pelvic conditions that may mimic the
disorder (135141).
The graded-compression method described by Puylaert
is used to evaluate patients with suspected appendicitis. A
linear array transducer (5 or 7.5 MHz) is used to gradually
compress the right lower quadrant (142,143). The use of
graded compression eliminates overlying bowel gas and
reduces the distance from the transducer to the appendix.
Normal air-filled bowel loops are easily compressed and
displaced from the right lower quadrant, whereas the
inflamed, obstructed appendix is not compressible. At the
start of the examination, the patient is asked to point to
the site of maximal tenderness and pain. This self-localiza-
tion expedites the search for an inflamed appendix, espe-
cially an aberrantly located one, and reduces the time of
the examination (144,145). Adequate compression has
been achieved if the iliac vessels and psoas muscle are visu-
alized, as the appendix usually will lie anterior to these
structures (Fig. 10.56). Technically adequate examinations
are achieved in about 95% of patients. Technical failures
are caused by the presence of severe pain, marked ascites,
or obesity, which precludes satisfactory compression. Har-
monic imaging may facilitate demonstration of the appen-
dix and abnormalities in surrounding tissues (146).
NORMAL APPENDIX
The normal appendix is identified in 5% to 10% of
healthy children (147). It is compressible, is blind-ending,
and measures 6 mm or less in maximum diameter. It has a
tubular appearance on long-axis scans and a target appear-
ance in the axial plane. The thin echogenic central layer of
submucosa and the hypoechoic outer zone representing
muscularis propria are usually identifiable (Fig. 10.57).
Occasionally, a small amount of fluid or gas may be noted
within the lumen (148). There usually is no flow or mini-
mal scattered color signal on color Doppler imaging
(149152).
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Chapter 10 G A S T R O I N T E S T I N A L T R A C T 367

A B

Normal right lower quadrant. A: Diagram of right lower quad-

Fig. 10.56
rant showing anatomic landmarks on graded-compression
sonography. A  iliac artery; P  psoas muscle; V  iliac vein. Gray-scale
(B) and color Doppler (C) sonograms show the psoas muscle (P) and iliac
artery (A) anterior to the vein (V). Notice the absence of flow in normal soft
C tissues.

A B
Normal appendix. A: Long-axis scan of the right lower quadrant demonstrates a normal-sized appendix (calipers), measuring 5.4 mm in
Fig. 10.57
diameter. The thin echogenic central mucosa/submucosa (*) and the hypoechoic outer muscularis propria (m) are identifiable. Open
arrow indicates the appendiceal tip. B: Color flow sonogram in another patient shows absence of flow in both the appendix (arrows) (diameter  4 mm)
and adjacent soft tissues. A  iliac artery; P  psoas muscle.
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368 P E D I AT R I C S O N O G R A P H Y
B ence of intact echogenic mucosa usually correlates with
Acute appendicitis. A: Long axis sonogram of the right
Fig. 10.58
lower quadrant shows a tubular fluid-filled appendix (A)
with echogenic submucosal lining (arrowheads). B: On a transverse
scan the appendix (arrows) has a target appearance.
Acute appendicitis, appendicolith. Long-axis scan shows
Fig. 10.59
a fluid-filled appendix (A) containing an echogenic focus
(arrowhead) with well-defined acoustic shadowing (S).
ACUTE APPENDICITIS
In the longitudinal plane, the inflamed appendix is a
fluid-filled, noncompressible, blind-ending tubular struc-
ture with a diameter of 6 mm or more (Fig. 10.58)
(135138,153). In the axial plane, it has a target appear-
ance, reflecting a fluid-filled center, surrounding echogenic
mucosa, and outer hypoechoic muscular wall. The pres-
nonperforated appendicitis. Other findings of appendicitis
include an appendicolith, which appears as a highly
echogenic focus with distal acoustic shadowing (Fig. 10.59);
pericecal or periappendiceal fluid; enlarged mesenteric
Acute appendicitis, phlegmon. Longitudinal scan shows
Fig. 10.60
a dilated appendix (A) and increased periappendiceal
echogenicity representing edema and cellular infiltration (phlegmon)
(arrows).
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A B
Fig. 10.61 Acute appendicitis. Long (A) and short (B) axis color Doppler sonograms show a dilated appendix (arrows) with peripheral hyperemia.
lymph nodes; increased periappendiceal echogenicity rep-
resenting inflamed fat (termed phlegmon) (Fig. 10.60),
abscess and peritonitis. The latter three findings are often
complications of perforation. The inflamed appendix is
hyperemic on color Doppler sonography (Fig. 10.61)
(150152).
Perforation occurs in 20% to 30% of children with
appendicitis. The diagnosis of perforated appendicitis
can be difficult, because the appendix may disintegrate
and hence not be identifiable on sonography. In general,
the appendix is visible in 40% to 60% of children with
perforation (154,155). When the appendix is visualized,
the sonographic features of perforation are loss of
the echogenic submucosa, increased periappendiceal
Periappendiceal abscess. Longitudinal scan shows a
Fig. 10.62
hypoechoic mass (arrows) with low-level echoes in the
right lower quadrant. A separate appendix could not be identified.
Chapter 10 G A S T R O I N T E S T I N A L T R A C T 369
echogenicity (Fig. 10.60), and periappendiceal abscess
(155). No statistically significant association is found
between the presence or absence of perforation and free
pelvic fluid, an appendicolith, or retrocecal location of
the appendix.
Abscess can be limited to the right lower quadrant or
it can extend inferiorly into the pelvis or superiorly into
the peritoneal spaces of the upper abdomen. Appen-
diceal abscess appears as a hypoechoic or complex
mass with internal echoes or septations (Fig 10.62).
Occasionally, the appendiceal stump is displayed as
an echogenic tubular structure projecting into the
hypoechoic fluid-filled abscess. Color flow Doppler
sonography demonstrates flow in the wall of the abscess
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370 P E D I AT R I C S O N O G R A P H Y

A B
Appendiceal abscess. A: Longitudinal sonogram shows a complex fluid collection (arrows) posterior to the bladder (BL). B: Power
Fig. 10.63
Doppler image shows flow in the wall of the abscess (A) and in surrounding soft tissues. BL  bladder.

and surrounding soft tissues (Fig. 10.63) (151,154). PITFALLS IN DIAGNOSIS

Sonography can be used to guide abscess drainage
(156).
Peritonitis is characterized by dilated bowel loops with
thick echogenic walls and ascites (Fig. 10.64). Color
Doppler imaging demonstrates increased blood flow in the
bowel wall and adjacent soft tissues.
Pylephlebitis or suppurative endophlebitis of the portal
vein is a rare complication of appendicitis. Sonographic
findings include thrombus formation within the portal vein
lumen (Fig. 10.65) and dilatation of the intrahepatic portal
vein branches. Pylephlebitis may be complicated by
hepatic abscess formation (157,158).
Causes of a false-negative diagnosis of appendicitis are
focal appendicitis, retrocecal appendicitis, and perforated
appendicitis. In focal appendicitis, inflammation is local-
ized to the distal end (Fig. 10.66) (153,159). Therefore,
it is important to image the entire length of the appendix
to avoid false-negative diagnoses. The appendiceal tip
can be identified on the basis of its blind termination. A
retrocecal appendix may be difficult to visualize, particu-
larly if the ascending colon is air filled. However, graded
compression can usually eliminate the overlying air
(160). If the psoas muscle is visualized, a retrocecal
appendix should be seen (Fig. 10.67). The diagnosis of

A B
Peritonitis. A: Longitudinal view of the right lower quadrant shows thick-walled, fluid-filled small bowel loops (arrows). B: Color
Fig. 10.64
Doppler interrogation in another patient shows increased blood flow within the bowel wall (arrows) and adjacent soft tissues.
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Chapter 10 G A S T R O I N T E S T I N A L T R A C T 371

Pylephlebitis. Transverse view through the porta hepatis

Fig. 10.65
in a patient with perforated appendicitis demonstrates a
thrombus (arrow) in the main portal vein.

A B
Focal appendicitis. A: Long-axis sonogram shows a dilated appendiceal tip (open arrows). A  iliac artery; V  iliac vein. B: Color
Fig. 10.66
Doppler sonogram shows peripheral hyperemia limited to the tip (white arrows).

Retrocecal appendicitis. Transverse scan of the right

Fig. 10.67
lower quadrant shows a dilated appendix (arrow) lateral
to the cecum (C).
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372 P E D I AT R I C S O N O G R A P H Y

A B

D
Meckel diverticulum. A: Long-axis sonogram shows a
Fig. 10.68
blind-ending loop of bowel (arrows) that is adjacent to
the cecum (C) but does not arise from it is. B: Color Doppler image
shows hyperemia of the wall of the Meckel diverticulum (M). C 
cecum. C: Longitudinal sonogram in a 7-year-old girl shows a blind-
ending, tubular, cyst-like structure with internal echoes from debris.
D: Contrast-enhanced computed tomography shows a cystic mass
(arrowheads) connecting to a segment of thickened, distal small
bowel (arrow). (Panels C and D reprinted from Levy AD, Hobbs CM.
Meckel diverticulum: radiologic features with pathologic correla-
C tion. Radiographics 2004;24:565587, with permission.)

appendicitis can be difficult if the appendix perforates
and decompresses. As noted earlier, identification of sec-
ondary signs should help establish the correct diagnosis
(154,155,161).
Causes of a false-positive diagnosis are mistaking a
normal appendix for an abnormal one and appendiceal
inflammation secondary to other inflammatory diseases,
such as Crohn disease, pelvic inflammatory disease, or an
inflamed Meckel diverticulum.
DIAGNOSTIC EFFICACY
The sensitivity of sonography for diagnosing appendicitis
ranges between 80% and 95%; the specificity is 90%
to 100% (135138,141,162166). The sensitivity and
specificity of color Doppler are approximately 90% and
95%, respectively (152). While color Doppler sonography
does not significantly increase the sensitivity of the exami-
nation, it makes interpretation of the gray-scale findings
easier and can increase observer confidence in the diagno-
sis of appendicitis.
Between one fourth and one third of children referred
for sonographic evaluation of suspected appendicitis will
have that condition, and another one fourth to one third
will have other diagnoses, such as gynecologic diseases, gas-
trointestinal tract abnormalities, and renal diseases. The
remaining children will have resolution of abdominal pain
LWBK505-C10_p339-383.qxd 7/7/10 1:32 PM Page 373 Aptara Inc
without a specific diagnosis being established (135138,
167). When sonography fails to identify findings of
appendicitis, it is important to image the pelvis, particu-
larly in female adolescents as gynecologic conditions are
a frequent mimic of appendicitis and also the upper
abdomen.
MECKEL DIVERTICULUM
The omphalomesenteric duct is an in utero tubular struc-
ture that connects the midgut at the level of the ileum to
the yolk sac (168). The duct normally involutes in the
first trimester. Meckel diverticulum develops when the
ileal end of the duct remains open. Patients may present
with abdominal pain due to intussusception with the
diverticulum as the lead point or with bleeding due to the
presence of ulcerated ectopic gastric mucosa in the diver-
ticulum. Uncomplicated Meckel diverticula can be diffi-
cult to diagnose on imaging studies. Sonography of an
inflamed Meckel diverticulum shows a hypoechoic tubu-
lar or cyst-like structure on the antimesenteric border of
the ileum, usually within 60 cm of the ileocecal valve
(Fig. 10.68) (168170). Doppler sonography reveals
hyperemia of the diverticular wall (171). This appearance
can mimic that of appendicitis, but an origin from small
bowel rather than cecum should suggest the diagnosis of
Meckel diverticulum.
COLON
Technique
The graded compression technique is again used to dis-
place adjacent bowel loops and to identify abnormal
bowel loops. A linear or curvilinear 5.0 to 7.0 MHz trans-
ducer is used initially. If wall thickening is detected, a
detailed evaluation with both gray-scale and color Doppler
imaging is performed with a linear or curved high-fre-
quency (7.5 to 12 MHz) transducer.
Normal Anatomy
The colon has a lateral position, contains gas and has
absent or minimal peristalsis. The ileocecal valve is a
hyperechoic fold on the medial side of the cecum. The
appendix is identified as a blind-ending structure at the
lower end of the cecum.
With the exception of the right colon and rectum, most
of the large bowel is not amenable to ultrasound scanning
because the fecal contents and gas produce intense reflec-
tion, with acoustic shadowing (see Fig. 10.20). When the
lumen is fluid-filled, discrete bowel layers with alternating
hypoechoic and hyperechoic bands can be seen. The latter
comprise the moderately echogenic superficial mucosa,
hyperechoic deep mucosa, echogenic submucosa, hypoe-
choic muscularis layer, and outer hyperechoic serosa. The
haustra have a pyramidal shape and homogenous echogenic-
ity, and are spaced at regular intervals. Colonic wall thick-
ness is less than 4 mm.
Chapter 10 G A S T R O I N T E S T I N A L T R A C T 373
Anorectal Malformations
Anorectal malformation, also referred to as imperforate
anus, is the result of abnormal separation of the hindgut
from the genitourinary system, which leads to an abnor-
mal termination of the hindgut. Anorectal malformations
are classified as high or low, depending on whether the rec-
tum terminates above or below the levator ani. In boys
with high lesions, the rectum usually ends with a fistula to
the posterior urethra or, rarely, to the bladder. In girls with
high lesions, the fistula is to the vagina or vestibule. In low
lesions, the rectum has no communication with the geni-
tourinary tract. Patients with low lesions may have a tiny
perineal orifice that is anteriorly positioned relative to the
expected normal position or the rectum may be completely
covered.
Surgical management for a high-type imperforate
anus is an initial diverting colostomy followed by
delayed anorectoplasty. Surgery for a low-type imperfo-
rate anus is often a one-step transperineal anoplasty soon
after birth.
Transperineal sonography is used to identify the
obstructed distal rectal pouch, whether it is high or low,
and any associated neural or spinal anomalies and fistulas
(172174). Longitudinal images are obtained in the mid-
sagittal plane through the perineum with the infant in a
lithotomy position. The distal pouch is identified as a
meconium or gas-filled blind-ending structure (Fig. 10.69).
To determine whether the malformation is high or low, the
examiner places a finger on the perineum at the site of the
anal dimple, and the distance from the distal rectal pouch
to the perineum is measured. A pouch perineum distance
of 10  4 mm (standard deviation [SD]) is consistent with
a low lesion and a distance of 24  6 mm implies a high
High imperforate anus. Longitudinal sonogram demon-
Fig. 10.69
strates a dilated meconium-filled rectum (R), which
abruptly terminates posterior to the bladder (B). Arrow indicates the
end of the pouch.
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374 P E D I AT R I C S O N O G R A P H Y
lesion (172174). Other signs of high lesions are echogenic
foci within the bladder, representing gas or calcifications;
enterolithiasis; and fistulas (175,176).
In normal infants, the rectum courses posteriorly
toward the anus and is separated from the urethra in boys
and the vagina in girls by echogenic fat. Fistulas usually
appear as hypoechoic linear tracts crossing the echogenic
fat plane and extending from the rectum to the bladder,
vagina, or vestibule.
The puborectalis muscle may be identified in low lesions.
It appears as a hypoechoic U-shaped band. The distal rectal
pouch may be seen passing through the muscle. The pub-
orectalis muscle is usually not identified in high lesions
(172,173). The sensitivity of transperineal sonography is
100% with a specificity of 86% and accuracy of 95% (177).
Necrotizing Enterocolitis
Necrotizing enterocolitis (NEC) is an ischemic disease of
bowel, believed to be the result of hypoxia and superim-
posed infection (178). It is primarily seen in premature
infants. When it occurs in term infants, there are usually
associated conditions such as heart disease, sepsis, or
bowel obstruction that predispose to bowel ischemia
(178). NEC begins in the mucosa and submucosa and may
extend through all layers of the bowel wall. The distal
ileum and right colon are involved most often, although
the disease may occur anywhere throughout the colon.
Patients present with abdominal distention, vomiting,
blood in the stool, and irritability.
Plain abdominal radiography remains the traditional
method to establish the diagnosis of necrotizing enterocol-
itis, but sonography can be useful to confirm the diagnosis
when plain radiographs are equivocal (178180). Sono-
graphic findings of necrotizing enterocolitis include thick-
walled fluid-filled loops of bowel; pneumatosis; and portal
Necrotizing enterocolitis. Longitudinal sonogram of the right
Fig. 10.70
colon shows multiple highly echogenic areas with acoustic
shadowing, representing gas (arrows), in the nondependent bowel wall.
Necrotizing enterocolitis. Transverse sonogram through
Fig. 10.71
the liver shows multiple, punctate echogenic foci repre-
senting portal venous air.
vein gas. Pneumatosis intestinalis appears as highly
echogenic intramural echoes with acoustic shadowing (Fig.
10.70) (178182). Portal venous gas appears as mobile
echogenic foci within the portal vein (Fig. 10.71).
Initial color Doppler finding include bowel wall hyper-
emia and increased peak systolic and time average flow
velocity in the celiac and superior mesenteric arteries (183,
184). Absent flow is suggestive of transmural necrosis and
nonviable bowel. Doppler interrogation of portal venous air
shows sharp bidirectional Doppler shifts superimposed on
the portal venous waveforms.
Other findings associated with necrotizing colitis include
ascites, bowel obstruction, pneumoperitoneum and peri-
toneal abscess secondary to perforation (185). Sonographic
findings of pneumoperitoneum are hyperechoic foci with
dirty shadowing between the anterior surface of the liver and
the abdominal wall and ascites with fluid-debris levels (186).
Colonic Wall Diseases
Colonic wall thickening may be caused by inflammatory,
infectious or ischemic, or neoplastic diseases. The role of
sonography is to confirm the presence of colonic disease
and to identify extraluminal abnormalities, such as fistu-
las, sinus tracts, and abscesses (97101,187), rather than
to establish a specific diagnosis.
GRANULOMATOUS COLITIS
Granulomatous colitis or Crohn disease is an inflammatory
condition that characteristically involves the right colon,
terminal ileum, and rectum with areas of normal bowel
(i.e., skip areas) in between. The discontinuous distribution
of disease is characteristic. Diarrhea, abdominal pain,
weight loss and failure to thrive are presenting features.
Sonographic findings include thickened hypoechoic
bowel wall, echogenic pericolonic fat, abscess, and fistulae
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Chapter 10 G A S T R O I N T E S T I N A L T R A C T 375

A B
Granulomatous colitis. A: Transverse sonogram shows thickened right colon (arrows). The wall is hypoechoic relative to surrounding
Fig. 10.72
muscle. M  mucosa. B: Power Doppler image shows increased flow in the bowel wall and surrounding mesentery.

(Fig. 10.72) (97101,187). Colonic wall thickness ranges
between 5 and 15 mm. In acute disease, wall stratification
is usually, but not invariably, maintained. Hyperemia of
mucosal and muscular layers may be noted on color
Doppler sonography.
ULCERATIVE COLITIS
Ulcerative colitis is an idiopathic inflammatory condition
that characteristically begins in the rectum and extends
proximally in a contiguous pattern to involve part of or the
entire colon. Bloody diarrhea and abdominal pain are fre-
quent presenting features. Other findings include arthritis,
spondylitis, and sclerosing cholangitis.
Sonography demonstrates thickened bowel wall, usu-
ally ranging between 6 and 10 mm in diameter (97101,
187). The bowel wall thickening in ulcerative colitis is less
pronounced than that in Crohn disease. Abscess formation
and fistulae are unusual. Color Doppler sonography can
show increased flow in mucosal and muscular layers of the
bowel wall.
involvement. Sonographic findings are moderate to marked
colonic wall thickening with exaggerated haustral markings,
luminal effacement and free peritoneal fluid (Fig. 10.73). All
colonic segments may be involved. Color Doppler sonogra-
phy can show hyperemia in the mucosa and muscularis pro-
pria. Cytomegalovirus colitis can produce findings similar to
those of C. difficile infection.
NEUTROPENIC COLITIS
Neutropenic typhlitis is a necrotizing enteropathy. It
occurs most commonly in severely neutropenic children
who are receiving chemotherapy, immunosuppressed
patients, and patients with acquired immunodeficiency
syndrome (AIDS). The disease is usually limited to the
cecum, ascending colon, appendix, and terminal ileum.

PSEUDOMEMBRANOUS COLITIS
Pseudomembranous colitis is an infectious disease caused by
toxin-producing Clostridium difficile bacteria (188,189).
The toxins attack the membranes and mucosal cells, result-
ing in hemorrhage, inflammation, cellular necrosis, and pro-
tein loss. It occurs almost exclusively in patients who have
been on antibiotic therapy, which alters the microflora of
the colon facilitating colonization by Clostridium difficile.
Symptoms are fever, nausea, vomiting, and ileus; and
colonic perforation in severe cases. The diagnosis is estab-
lished either by endoscopic demonstration of characteristic
yellow plaques or pseudomembranes on the colonic mucosa
or by laboratory documentation of Clostridium difficile in
the feces. Pseudomembranous colitis. Longitudinal sonogram shows
Because these patients are often acutely ill, sonography or Fig. 10.73
thickened right colon (arrows) with exaggerated haustral
CT is often used to assess the presence and extent of colonic markings. The lumen is effaced.
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376 P E D I AT R I C S O N O G R A P H Y

Neutropenic colitis (typhlitis). Longitudinal sonogram

Fig. 10.74
shows thickened right colon (arrows). Although sono-
graphic findings are nonspecific, this patient had a history of immuno-
suppression supporting a diagnosis of typhlitis.

The cecum and ascending colon are at greatest risk for PARASITIC INFECTION AMEBICCOLITIS
involvement because these are the areas of relatively Amebiasis refers to infection caused by the ameba Enta-
greater stasis and distensibility. Involvement of the left moeba histolytica. It is transmitted through contaminated
colon or small bowel is unusual. Affected children pres- food and water. Symptoms range from mild diarrhea to
ent with bloody diarrhea and abdominal pain. severe dysentery with blood and mucus in the stool. The
Sonographic findings include right colonic, distal amebae can enter the bloodstream and may affect other
ileal, and appendiceal wall thickening (Fig. 10.74) and organs, particularly the liver. Sonographic findings include
increased pericecal echogenicity, representing edema and bowel wall thickening and hypervascularity of the submu-
inflammation of the pericecal fat. Color Doppler imaging cosal and muscle layers. All the colonic segments may be
shows hypervascularity of the mucosal and muscular affected or the infection may be limited to the right-sided
layers. colon. Bowel wall thickening is similar to that seen in
HEMOLYTIC UREMIC SYNDROME
Hemolytic uremic syndrome is a disorder characterized
by a prodrome of bloody diarrhea followed by acute
renal failure, hemolytic anemia, and thrombocytopenia
(190). The cause is thought to be an antigen-antibody
reaction to bacterial toxins, E. coli serotype O 157:H7
being one of the most frequent pathogens. This serotype
produces a verotoxin, which attaches to endothelium
causing damage to blood vessels, which in turn causes
deposition of fibrin thrombi in the microvasculature in
multiple organs.
Sonographic findings are a markedly thickened colonic
wall, usually affecting the entire colon from the cecum to
the anus (Fig. 10.75). In the prodromal stage, the colon is
avascular. The bowel can appear hypervascular during the
recovery stage.

INFECTIOUS COLITIS
A variety of organisms, including Yersinia enterocolitica,
Salmonella species, Shigella, and Escherichia coli, may
result in colitis. Sonographic findings in these conditions
include bowel wall thickening (Fig. 10.76), a fluid-filled
lumen, mesenteric lymphadenopathy, and free peritoneal Hemolytic uremic syndrome, prodromal phase. Longitu-
fluid. The mucosa and occasionally the muscular layers are Fig. 10.75
dinal view of the right flank shows a thickened, hypo-
hypervascular on color Doppler imaging. echoic right colonic wall (arrows). Wall thickness (calipers)  2.2 cm.
LWBK505-C10_p339-383.qxd 7/7/10 1:32 PM Page 377 Aptara Inc
Infectious colitis. Transverse sonogram shows concen-
Fig. 10.76
tric thickening of the sigmoid colon (arrows). Cultures
grew Shigella.
Crohn disease and ulcerative colitis, but clinical history of
travel or residence in an endemic should raise suspision of
amebic colitis (191).
Cystic Fibrosis
Cystic fibrosis is an inherited disease characterized by a
generalized dysfunction of the exocrine glands. The result
is inspissation of thick fecal contents with secondary
inflammatory changes in the bowel wall. Clinical findings
include abdominal pain, constipation, and a palpable right
lower quadrant mass.
A B
Rectal duplication cyst. A: Longitudinal sonogram of the pelvis shows a tubular structure (arrows), with echogenic mucosa and hypo-
Fig. 10.77
echoic wall characteristic of gut, posterior to the uterus (Ut) and anterior to the rectum (R). BL  bladder. B: Contrast enema shows
retrograde flow of contrast from the rectum (R) into the tubular duplication (arrows).
Chapter 10 G A S T R O I N T E S T I N A L T R A C T 377
Sonographic findings include thickened ascending
colon, cecum, and distal small bowel; increased echogenic-
ity of the pericolonic and mesenteric fat; and mesenteric
lymphadenopathy (192194). The appendix may be
enlarged, measuring greater than 6 mm in diameter, with
the lumen containing echogenic mucoid contents (195,196).
Sinus tracts, fistulas, abscesses, and extensive small bowel
involvement are not typical of cystic fibrosis and help to
differentiate it from Crohn disease.
Benign Masses
JUVENILE POLYPS
Juvenile polyps are the most frequent benign colonic tumor
in childhood. They are inflammatory lesions and are
thought to represent mucus retention cysts that result when
the orifices of the mucous glands are blocked. Juvenile
polyps typically occur in the rectosigmoid area and are usu-
ally large (1 to 5 cm) and pedunculated, although they may
be small or sessile. Affected children are usually between 2
and 10 years of age and present with painless bright red rec-
tal bleeding or with rectal prolapse of the polyp.
Sonographic findings are a hyperechoic mass projecting
into the anechoic fluid-filled bowel lumen (197). Polyps
need to be differentiated from fecal material, which also
appears highly echogenic. Fecal material is mobile and will
change position in the colon.
ENTERIC DUPLICATION CYSTS
Duplication cysts can occur in the colon, although they are
more common in the small intestine. Colonic duplication
has an appearance similar to that of other gastrointestinal
duplications. Sonographic findings include a hypoechoic
tubular mass with gut signature (i.e., an inner echogenic
lining and an outer hypoechoic rim) (Fig. 10.77).
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378 P E D I AT R I C S O N O G R A P H Y

A B
Adenocarcinoma. A: Longitudinal sonogram shows a thickened right colonic wall (arrows). B: Contrast-enhanced computed
Fig. 10.78
tomography scan confirms marked circumferential thickening of the ascending colon (arrows). The tumor protrudes into the
colonic lumen (*).

Malignant Masses occurrence. It is usually detected on barium enema studies

LYMPHOMA
Colonic involvement by lymphoma is rare, but when it
occurs the cecum is the most common site of tumor. As
noted previously, most bowel lymphoma in children is
the non-Hodgkin subtype. On sonography, the appear-
ance is that of hypoechoic bowel wall thickening (52).
The wall thickening may be eccentric or circumferential.
Enlarged mesenteric nodes may be noted adjacent to the
bowel. Complications of colonic lymphoma include
intussusception, mucosal ulcerations, and perforation.
CARCINOMA
Adenocarcinoma is a rare tumor in childhood, although it
can be seen in polyposis syndromes or it can be an isolated
or colonoscopy. In some cases, the tumor may be an
unsuspected finding in children referred for evaluation of
a palpable mass. Sonographic findings of adenocarcinoma
include eccentric or circumferential colonic wall thicken-
ing (Fig. 10.78), an exophytic wall mass, luminal narrow-
ing, increased echogenicity of adjacent mesenteric fat indi-
cating tumor infiltration, and mesenteric adenopathy.
FOREIGN BODY LOCALIZATION
Although conventional radiography is sensitive in detect-
ing radio-opaque ingested foreign bodies, it may not be
as reliable for determining the precise location of the for-
eign body, particularly whether it is in bowel lumen or in
the peritoneal cavity. With its high-resolution capability,

A B
Ingested foreign body. A: Longitudinal view of the appendix demonstrates the intraluminal position of a straight pin with its head
Fig. 10.79
(arrow) against the tip of the appendix. B: Transverse view of the appendix (calipers) demonstrates the intraluminal position of the pin.
(Reprinted from Piotto L, Gent R, Kirby CP, et al. Preoperative use of ultrasonography to localize an ingested foreign body. Pediatr Radiol
2009;39:299301, with permission.)
LWBK505-C10_p339-383.qxd 7/7/10 1:32 PM Page 379 Aptara Inc
sonography has the potential to define the precise loca-
tion of an ingested foreign body, thus facilitating surgical
removal (Fig. 10.79) (198). It appears to be particularly
valuable in cases where there is no progressive movement
of the foreign body through the alimentary tract or if the
foreign body is radiolucent or sharp.
REFERENCES
1. Siegel MJ. Pediatric general abdomen. In: Meire HB, Cosgrove
D, Dewbury K, eds. Clinical ultrasound. London: Churchill
Livingstone, In press.
2. Gomes H, Menanteau B. Gastro-esophageal reflux: compara-
tive study between sonography and pH monitoring. Pediatr
Radiol 1991;21:168174.
3. Gomes H, Lallenmand A, Lallenmand P. Ultrasound of the gas-
troesophageal junction. Pediatr Radiol 1993;23:9499.
4. Westra SJ, Wolf BHM, Staalman CR. Ultrasound diagnosis of
gastroesophageal reflux and hiatal hernia in infants and young
children. J Clin Ultrasound 1990;18:477485.
5. Wright LL, Baker KR, Meny RG. Ultrasound demonstration of
gastroesophageal reflux. J Ultrasound Med 1988;7:471475.
6. Koumanidou C, Vakaki M, Pitsoulakis G, et al. Sonographic
measurements of the abdominal esophagus length in infancy: a
diagnostic tool for gastroesophageal reflux. AJR Am J
Roentgenol 2004;183:801807.
7. Hirsch W, Kedar R, Preiss U. Color Doppler in the diagnosis of
the gastroesophageal reflux in children: comparison with pH
measurements and B-mode ultrasound. Pediatr Radiol 1996;
26:232235.
8. Jang HS, Lee JS, Lim GY, et al. Correlation of color Doppler
sonographic findings with pH measurements in gastroesophageal
reflux in children. J Clin Ultrasound 2001;29:212217.
9. Swischuk LE, Hayden CK Jr, Stansberry SD. Sonographic pit-
falls in imaging of the antropyloric region in infants. Radi-
ographics 1989;9:437447.
10. Argyropoulou MI, Hadjigeorgi CG, Kiortsis DN. Antro-pyloric
canal values from early prematurity to full-term gestational age:
an ultrasound study. Pediatr Radiol 1998;28:933936.
11. OKeeffe FN, Stansberry SD, Swischuk LE, et al. Antropyloric
muscle thickness at US in infants: what is normal? Radiology
1991;178:827830.
12. Aintablian NH, Slim MS, Antoun BW. Congenital microgastria.
Case report and review of the literature. Pediatr Surg Int 1987;
2:307310.
13. Hernanz-Schulman M. Infantile hypertrophic pyloric stenosis.
Radiology 2003;227:319331.
14. Hernanz-Schulman M. Vomiting in the infant. In: Bluth EI, Ben-
son CB, Ralls PW, et al., eds. Ultrasound: a practical approach
to clinical problems. 2nd ed. New York: Thieme, 2007:
489400.
15. Hernanz-Schulman M, Sells LL, Ambrosino MM, et al. Hyper-
trophic pyloric stenosis in the infant without a palpable olive: accu-
racy of sonographic diagnosis. Radiology 1994;193:771776.
16. Rohrschneider WK, Mittnacht H, Darge K, et al. Pyloric mus-
cle in asymptomatic infants: sonographic evaluation and dis-
crimination from idiopathic hypertrophic pyloric stenosis. Pedi-
atr Radiol 1998;28:429434.
17. Cohen HL, Blumer SL, Zucconi WB. The sonographic double
track sign. Not pathognomonic for hypertrophic pyloric steno-
sis; can be seen in pylorospasm. J Ultrasound Med 2004;23:
641646.
18. Hernanz-Schulman M, Dinauer P, Ambrosino MM, et al. The
antral nipple sign of pyloric mucosal prolapse: endoscopic cor-
relation of a new sonographic observation in patients with
pyloric stenosis. J Ultrasound Med 1995;14:283287.
Chapter 10 G A S T R O I N T E S T I N A L T R A C T 379
19. Hernanz-Schulman M, Zhu Y, Stein SM, et al. Hypertrophic
pyloric stenosis in infants: US evaluation of vascularity of the
pyloric canal. Radiology 2003;229:389393.
20. Bisset RAL, Gupta SC. Hypertrophic pyloric stenosis, ultra-
sonic appearances in a small baby. Pediatr Radiol 1988;18:
405.
21. Haider N, Spicer R, Grier D. Ultrasound diagnosis of infantile
hypertrophic pyloric stenosis: determinants of pyloric length
and the effect of prematurity. Clin Radiol 2002;57:136139.
22. Lowe LH, Banks W, Shyr Y. Efficacy in the diagnosis of hyper-
trophic pyloric stenosis. J Ultrasound Med 1999;18:773777.
23. Westra SJ, deGroot CJ, Smits NJ, et al. Hypertrophic pyloric
stenosis: use of the pyloric volume measurement in early US
diagnosis. Radiology 1989;172:615619.
24. Finkelstein MS, Mandell GA, Tarbell KV. Hypertrophic pyloric
stenosis: volumetric measurement of nasogastric aspirate to
determine the imaging modality. Radiology 1990;177:759761.
25. Mandell GA, Wolfson PJ, Adkins ES, et al. Cost-effective imag-
ing approach to the nonbilious vomiting infant. Pediatrics
1999;103:11981202.
26. Kaminsky CK, Cleveland RH. Midgut malrotation. In: Siegel BA,
Proto AV, eds. Pediatric disease (fourth series) test and syllabus.
Reston, VA: American College of Radiology, 1993:376404.
27. Calahan MJ, Mccauley RG, Patel H, et al. The development of
hypertrophic pyloric stenosis in patients with prostaglandin-
induced foveolar hyperplasia. Pediatr Radiol 1999;29:748751.
28. Bhargava P, Parisi M. Gastric pneumatosis and portal venous
gas: benign findings in hypertrophic pyloric stenosis. Pediatr
Radiol 2009;39:413.
29. Muramori K, Nagasaki A, Kawanami T. Ultrasonographic serial
measurements of the morphologic resolution of the pylorus after
Ramstedt pyloromyotomy for infantile hypertrophic pyloric
stenosis. J Ultrasound Med 2007;26:16811687.
30. Yoshizawa J, Eto T, Higashimoto Y, et al. Ultrasonographic fea-
tures of normalization of the pylorus after pyloromyotomy for
hypertrophic pyloric stenosis. J Pediatr Surg 2001;36:582586.
31. Cohen HL, Zinn HL, Haller JO, et al. Ultrasonography of
pylorospasm: findings may simulate hypertrophic pyloric steno-
sis. J Ultrasound Med 1998;17:705711.
32. Gilet AG, Dunkin J, Cohen HL. Pylorospasm (simulating
hypertrophic pyloric stenosis) with secondary gastroesophageal
reflux. Ultrasound Q 2008;24:9396.
33. Chew AL, Friedwald JP, Donovan C. Diagnosis of congenital
antral web by ultrasound. Pediatr Radiol 1992;22:342343.
34. Mostbeck G, Mallek R, Gebauer A, et al. Hepatic penetration
by duodenal ulcer: sonographic diagnosis. J Clin Ultrasound
1990;18:726729.
35. Lee DH, Lim JH, Ko YT, et al. Sonographic detection of pneu-
moperitoneum in patients with acute abdomen. AJR Am J
Roentgenol 1990;154:107109.
36. Chang-Chien CS, Lin HH, Yen CL, et al. Sonographic demonstra-
tion of free air in perforated peptic ulcers: comparison of sonogra-
phy with radiography. J Clin Ultrasound 1989;17:95100.
37. Gassner I, Strasser K, Bart G, et al. Sonographic appearance of
Mntriers disease in a child. J Ultrasound Med 1990;9:
537539.
38. Goldwag SS, Bellah RD, Ward KJ, et al. Sonographic detection
of Mntriers disease in children. J Clin Ultrasound 1994;22:
55675570.
39. Blankenberg FG, Parker BR, Sibley E, et al. Evolving asymmet-
ric hypertrophic pyloric stenosis associated with histologic evi-
dence of eosinophilic gastroenteritis. Pediatr Radiol 1995;25:
310311.
40. Snyder JD, Rosenblum N, Wershil B, et al. Pyloric stenosis and
eosinophilic gastroenteritis in infants. J Pediatr Gastroenterol
Nutr 1987;6:543547.
41. Macpherson RI. Gastrointestinal tract duplications: clinical,
pathologic, etiologic, and radiologic considerations. Radi-
ographics 1993;13:10631080.
LWBK505-C10_p339-383.qxd 7/7/10 1:32 PM Page 380 Aptara Inc
380 P E D I AT R I C S O N O G R A P H Y
42. Hur J, Yoon C-S, Kim M-J, et al. Imaging features of gastroin-
testinal tract duplications in infants and children: from oesoph-
agus to rectum. Pediatr Radiol 2007;37:691699.
43. Segal SR, Sherman NH, Rosenberg HK, et al. Ultrasonographic
features of gastrointestinal duplications. J Ultrasound Med
1994;13:863870.
44. Dunlap JP, James CA, Maxson RT, et al. Gastric teratoma with
intramural extension. Pediatr Radiol 1995;25:383384.
45. Herman TE, Siegel MJ. Congenital gastric teratoma. J Perina-
tol 2008;28:786787.
46. Bowen B, Ros PR, McCarthy MJ, et al. Gastrointestinal ter-
atomas: CT and US appearance with pathologic correlation.
Radiology 1987;162:431433.
47. Maves CK, Johnson JF, Bove K, et al. Gastric inflammatory
pseudotumor in children. Radiology 1989;173:381383.
48. Hanquinet S, Damry N, Dassonville M, et al. Gastric outlet
obstruction: unusual ultrasonographic findings in the pyloric
and antral regions. Pediatr Radiol 1995;25:S163S166.
49. Nakazawa S, Yoshino J, Nakamura T, et al. Endoscopic ultra-
sonography of gastric myogenic tumor. A comparative study
between histology an ultrasonography. J Ultrasound Med 1989;
8:353359.
50. Rohrer K, Murphy R, Thresher C, et al. Infantile myofibro-
matosis: a most unusual cause of gastric outlet obstruction.
Pediatr Radiol 3005;35:808811.
51. Schroeder BA, Wells RG, Sty JR. Inflammatory fibroid polyp of
the stomach in a child. Pediatr Radiol 1987;17:7172.
52. Georg C, Schwerk WB, Goerg K. Gastrointestinal lymphoma:
sonographic findings in 54 patients. AJR Am J Roentgenol
1990;155:795798.
53. Miettinen M, Lasota J, Sobin LH. Gastrointestinal stromal
tumors of the stomach in children and young adults: a clinico-
pathologic, immunohistochemical, and molecular genetic study
of 44 cases with long-term follow-up and review of the litera-
ture. Am J Surg Pathol 2005;29:13731381.
54. Levy AD, Remotti HE, Thompson WM, et al. Gastrointestinal
stromal tumors: radiologic features with pathologic correlation.
Radiographics 2003;23:283304.
55. Egloff A, Lee EY, Dillon JE. Gastrointestinal stromal tumor
(GIST) of stomach in a pediatric patient. Pediatr Radiol 2005;
35:728729.
56. Hughes JA, Cook JV, Said A, et al. Gastrointestinal stromal
tumour of the duodenum in a 7-year-old boy. Pediatr Radiol
2004;34:10241027.
57. Park J, Rubinas TC, Fordahn LA, et al. Multifocal gastroin-
testinal tumor (GIST) of the stomach in an 11-year-old girl.
Pediatr Radiol 2006;36:12121214.
58. Ripolles T, Garcia-Aguayo J, Martinez M-J, Gil P. Gastroin-
testinal bezoars: sonographic and CT characteristics. AJR
2001;177:6569.
59. Naik DR, Bolia A, Boon AW. Demonstration of a lactobezoar
by ultrasound. Br J Radiol 1987;60:506508.
60. Epifanio M, Baldisserotto M, Spolidoro, et al. Gray-scale and
color Doppler sonography in the evaluation of children with
suspected bowel inflammation: correlation with colonoscopic
and histologic findings. Clin Radiology 2008;63:968978.
61. Splainger J, Patriquin H, Miron MC, et al. Doppler US in
patients with Crohn disease: vessel density in the diseased
bowel reflects disease activity. Radiology 2000;217:787791.
62. Ko YT, Lim JH, Lee DH, Lee HW, Lim JW. Small bowel obstruc-
tion: sonographic evaluation. Radiology 1993;188:649653.
63. Neal MR, Seibert JJ, Vanderzalm MD, et al. Neonatal ultra-
sonography to distinguish between meconium ileus and ileal
atresia. J Ultrasound Med 1997;16:263266.
64. Lawrence PW, Chrispin A. Sonographic appearances in two
neonates with generalized meconium peritonitis: the snowstorm
sign. Br J Radiol 1984;57:340342.
65. Wu CC. Sonographic findings of generalized meconium peritonitis
presenting as neonatal ascites. J Clin Ultrasound 1988;16:4851.
66. Strouse PJ. Disorders of intestinal rotation and fixation (mal-
rotation). Pediatr Radiol 2004;34:837851.
67. Dufour D, Delaet MH, Dassonville M, et al. Midgut malrota-
tion, the reliability of sonographic diagnosis. Pediatr Radiol
1992;22:2123.
68. Weinberger E, Winters WD, Liddell RM, et al. Sonographic
diagnosis of intestinal malrotation in infants: importance of the
relative positions of the superior mesenteric artery and vein.
AJR Am J Roentgenol 1992;159:825828.
69. Epelman M. The whirlpool sign. Radiology 2006;240:910911.
70. Patino MO, Munden MM. Utility of the sonographic whirlpool
sign in diagnosing midgut volvulus in patients with atypical
clinical presentations. J Ultrasound Med 2004;23:397401.
71. Pracros JP, Sann L, Genin G, et al. Ultrasound diagnosis of midgut
volvulus: the whirlpool sign. Pediatr Radiol 1992;22:1820.
72. Shimanuki Y, Aihara T, Takano H, et al. Clockwise whirlpool
sign at color Doppler US: an objective and definite sign of
midgut volvulus. Radiology 1996;199:261264.
73. Smet MH, Marchal G, Ceulemans R, et al. The solitary hyper-
dynamic pulsating superior mesenteric artery: an additional
dynamic sonographic feature of midgut volvulus. Pediatr
Radiol 1991;21:156157.
74. Beasley S. Intussusception. Pediatr Radiol 2004;34:302304.
75. Daneman A, Navarro O. Intussusception. Part I: a review of
diagnostic approaches. Pediatr Radiol 2003;33:7985.
76. del-Pozo G, Albillos JC, Tejedor D. Intussusception: US findings
with pathologic correlationthe crescent-in-doughnut sign.
Radiology 1996;199:688692.
77. Verschelden P, Filiatrault D, Garel L, et al. Intussusception in
children: reliability of US in diagnosisa prospective study.
Radiology 1992;184:741744.
78. Weinberger E, Winters WD. Intussusception in children: the
role of sonography. Radiology 1992;184:601602.
79. Anderson DR. The pseudokidney sign. Radiology 1999;211:
395397.
80. Swischuk LE, Stansberry SD. Ultrasonographic detection of free
peritoneal fluid in uncomplicated intussusception. Pediatr
Radiol 1991;21:350351.
81. Papadopoulou F, Efremidis SC, Raptopoulou A, et al. Distal
ileocolic intussusception: another cause of inversion of superior
mesenteric vessels in infants. AJR Am J Roentgenol 1996;
167:12431246.
82. Itagaki A, Uchida M, Ueki K, et al. Double target sign in ultra-
sonic diagnosis of intussuscepted Meckel diverticulum. Pediatr
Radiol 1991;21:148149.
83. Patenaude Y, Jquier S, Russo P. Pediatric case of the day. Dupli-
cation cyst of distal ileum. Radiographics 1993;13:218220.
84. Kenney IJ. Ultrasound in intussusception: a false cystic lead
point. Pediatr Radiol 1990;20:348.
85. del-Pozo G, Gonzlez-Spinola J, Gmez-Ansn B, et al. Intussus-
ception: trapped peritoneal fluid detected with USrelationship
to reducibility and ischemia. Radiology 1996;201:379383.
86. John SD. The value of ultrasound in children with suspected
intussusception. Emerg Radiol 1998;5:297305.
87. Kong MS, Wong HF, Lin SL, et al. Factors related to detection
of blood flow by color Doppler ultrasonography in intussus-
ception. J Ultrasound Med 1997;16:141144.
88. Lim HK, Bae SH, Lee KH, et al. Assessment of reducibility of
ileocolic intussusception in children: usefulness of color
Doppler sonography. Radiology 1994;191:781785.
89. Koumanidou C, Vakaki M, Pitsoulakis G, et al. Sonographic
detection of lymph nodes in the intussusception of infants and
young children. Clinical evaluation and hydrostatic reduction.
AJR Am J Roentgenol 2002;178:445450.
90. Riebel TW, Wasir R, Weber K. US-guided hydrostatic reduction
of intussusception in children. Radiology 1993;188:513516.
91. Woo SK, Kim JS, Suh SJ, et al. Childhood intussusception:
US-guided hydrostatic reduction. Radiology 1992;182:
7780.
LWBK505-C10_p339-383.qxd 7/7/10 1:32 PM Page 381 Aptara Inc
92. Yoon CH, Kim HJ, Goo HW. Intussusception in children: US-
guided pneumatic reduction-initial experience. Radiology
2001;218:8588.
93. Crystal P, Barki Y. Using color Doppler sonography-guided
reduction of intussusception to differentiate edematous ileoce-
cal valve and residual intussusception. AJR Am J Roentgenol
2004;182:1345.
94. Hryhorczuk AL, Strouse PJ, Validation of US as a first-line diag-
nostic test for assessment of pediatric ileocolic intussusception.
Pediatr Radiol 2010;39:10751079.
95. Kim JH. US features of transient small bowel intussusception in
pediatric patients. Korean J Radiol 2004;5:178184.
96. Wiersma F, Allema JH, Holscher HC. Ileoilial intussusception
in children: ultrasonographic differentiation from ileocolic
intussusception. Pediatr Radiol 2006;36:11771181.
97. Alison M, Kheniche A, Azoulay R, et al. Ultrasonography of
Crohn disease in children. Pediatr Radiol 2007;37:10711082.
98. Faure C, Belarbi N, Mougenot JF, et al. Ultrasonographic
assessment of inflammatory bowel disease in children: compar-
ison with ileocolonoscopy. J Pediatr 1997;130:147151.
99. Lim JH, Ko YT, Lee DH. Sonography of inflammatory bowel
disease: findings and value in differential diagnosis. AJR Am J
Roentgenol 1994;163:343347.
100. Sarrazin J, Wilson SR. Manifestations of Crohns disease at US.
Radiographics 1996;16:499520.
101. Siegel MJ, Friedland JA, Hildebolt CF. Bowel wall thickening in
children: differentiation with US. Radiology 1997;203:
631635.
102. Quillin SP, Siegel MJ. Color Doppler US of children with acute
lower abdominal pain. Radiographics 1993;13:12811293.
103. Quillin SP, Siegel MJ. Gastrointestinal inflammation in chil-
dren: color Doppler ultrasonography. J Ultrasound Med
1994;13:751756.
104. Ripolles T, Martinez MJ, Barrachina MM. Crohns disease and
color Doppler sonography: response to treatment and its rela-
tionship with long-term prognosis. J Clin Ultrasound 2008;36:
267272.
105. Sholbach T, Herrero I, Scholbach J. Dynamic color Doppler
sonography of intestinal wall in patients with Crohn disease
compared with healthy subjects. Pediatr Gastoenterol Nutr
2004;39:524528.
106. Van Oostayen JA, Wasser MN, van Hogezand RA, et al. Activity
of Crohn disease assessed by measurement of superior mesenteric
artery flow with Doppler US. Radiology 1994;193:551554.
107. Yekler E, Danalioglu A, Movasseghi B, et al. Crohn disease
activity evaluated by Doppler ultrasonography of the superior
mesenteric artery and affected small-bowel segments. J Ultra-
sound Med 2005;24:5965.
108. Fraquilli M, Colli A, Casazza G, et al. Role of US in detection
of Crohn disease: meta-analysis. Radiology 2005;236:95101.
109. Agha FP, Ghahremani GG, Panella JA, et al. Appendicitis as the
initial manifestation of Crohns disease: radiologic features and
prognosis. AJR Am J Roentgenol 1987;149:515158.
110. Ripolles T, Martinez MJ, Morote V, et al. Appendiceal involve-
ment in Crohns disease: gray-scale sonography and color Doppler
flow features. AJR Am J Roentgenol 2006;186:10711078.
111. Ruess L, Blask ARN, Bulas DI, et al. Inflammatory bowel disease
in children and young adults: correlation of sonographic and
clinical parameters during treatment. AJR Am J Roentgenol
2000;175:7984.
112. Matsumoto T, Iida M, Sakai T, et al. Yersinia terminal ileitis:
sonographic findings in eight patients. AJR Am J Roentgenol
1991;156:965967.
113. Puylaert JCBM. Mesenteric adenitis and acute terminal ileitis:
US evaluation using graded compression. Radiology 1986;161:
691695.
114. Tuohy AMM, OGorman M, Byington C, et al. Yersinia ente-
rocolitis mimicking Crohns disease in a toddler. Pediatrics
1999;104:e36.
Chapter 10 G A S T R O I N T E S T I N A L T R A C T 381
115. Bmelburg T, Claasen U, vonLengerke H-J. Intestinal ultra-
sonographic findings in Schnlein-Henoch syndrome. Eur J
Pediatr 1991;150:158160.
116. Couture A, Veyrac C, Baud C, et al. Evaluation of abdominal
pain in Henoch-Schonlein syndrome by high frequency ultra-
sound. Pediatr Radiol 1992;22:1217.
117. John SD SL, Hayden DK Jr. Gastrointestinal sonographic find-
ings in Henoch-Schonlein purpura. Emerg Radiol 1996;3:48.
118. Nichimi A, Khamis J, Paquoit I, et al. Significance of bowel wall
abnormalities at ultrasound in Henoch-Schonlein purpura.
Pediatr Gastroenterol Nutr 2008;46:4853.
119. Hayashi K, Futagawa S, Kozaki S, et al. Ultrasound and CT
diagnosis of intramural duodenal hematoma. Pediatr Radiol
1988;18:167168.
120. Hernanz-Schulman M, Genieser NB, Abrosino M. Sonographic
diagnosis of intramural duodenal hematoma. J Ultrasound Med
1989;8:273276.
121. Orel SG, Nussbaum AR, Sheth S, et al. Duodenal hematoma in
child abuse: sonographic detection. AJR Am J Roentgenol
1988;151:147149.
122. Dorne HL, Jequier S. Sonography of intestinal lymphangiecta-
sis. J Ultrasound Med 1986;5:1316.
123. Maurer K, Unsinn KM, Waltner-Romen M, et al. Segmental
bowel-wall thickening on abdominal ultrasonography: an addi-
tional diagnostic sign in Kawasaki disease. Pediatr Radiol
2008;38:10131016.
124. Benya EC, Sivit CJ, Quinones RR. Abdominal complications
after bone marrow transplantation in children: sonographic
and CT findings. AJR Am J Roentgenol 1993;161:10231027.
125. Haber HP, Schlegel PG, Dette S, et al. Intestinal acute graft-
versus-host disease: findings on sonography. AJR Am
J Roentgenol 2000;174:118120.
126. Magnano GM, Occhi M, Mattioli G, et al. Pancreatitis caused
by duodenal duplication. Pediatr Radiol 1998;28:524526.
127. Saxena A, Singla V, Gupta P. Sonographic evaluation of enteric
duplication cysts. Pediatr Radiol 2007;37:691699.
128. Cheng G, Soboleskdi D, Daneman A, et al. Sonographic pitfalls
in the diagnosis of enteric duplication cysts. AJR Am J
Roentgenol 2005;184:521525.
129. Spottswood SE. Peristalsis in duplication cyst: a new sono-
graphic finding. Pediatr Radiol 1994;24:344345.
130. Parra DA, Navarro OM. Sonographic diagnosis of intestinal
polyps in children. Pediatr Radiol 2008;38:680684.
131. Puylaert JB, van der Zant FM. Mesenteric lymphadenitis or
appendicitis? AJR Am J Roentgenol 1995;165:490.
132. Sivit CJ, Newman KD, Chandra RS. Visualization of enlarged
mesenteric lymph nodes at US examination: clinical signifi-
cance. Pediatr Radiol 1993;23:471475.
133. Swischuk LE, John SD. Mesenteric adenitisacute ileitis: a
constellation of findings definable with ultrasound. Emerg
Radiol 1998;5:210218.
134. Vayner N, Coret A, Plliack G, et al. Mesenteric lymphadenopa-
thy in children examined by US for chronic and/or recurrent
abdominal pain. Pediatr Radiol 2003;33:864867.
135. Siegel MJ. Acute appendicitis in childhood: the role of US.
Radiology 1992;185:341342.
136. Siegel MJ, Carel C, Surratt S. Ultrasonography of acute abdom-
inal pain in children. JAMA 1991;266:19871989.
137. Sivit CJ, Siegel MJ, Applegate KE, et al. When appendicitis is
suspected in children. Radiographics 2001;21:247262.
138. Sivit CJ. Imaging the child with right lower quadrant pain and
suspected appendicitis: current concepts. Pediatr Radiol 2004;
34:447453.
139. Axelrod DA, Sonnad SS, Hirschl RB. An economic evaluation
of the sonographic examination of children with suspected
appendicitis. J Pediatr Surg 2000;35:12361241.
140. Kaneko K, Tsudo M. Ultrasound-based decision making in the
treatment of acute appendicitis in children. J Pediatr Surg
2004;39:13161320.
LWBK505-C10_p339-383.qxd 7/7/10 1:32 PM Page 382 Aptara Inc
382 P E D I AT R I C S O N O G R A P H Y
141. Sivit CJ, Applegate KE, Stallion A, et al. Imaging evaluation of sus-
pected appendicitis in a pediatric population: effectiveness of
sonography versus CT. AJR Am J Roentgenol 2000;175:977980.
142. Puylaert JBCM, Rutgers PH, Lalisang RI. A prospective study
of ultrasonography in the diagnosis of appendicitis. N Engl J
Med 1987;317:666669.
143. Puylaert JBCM. Acute appendicitis: US evaluation using graded
compression. Radiology 1986;158:355360.
144. Chesbrough RM, Burkhard TK, Balsara ZN, et al. Self-local-
ization in US of appendicitis: an addition to graded compres-
sion. Radiology 1993;187:349351.
145. Soda K, Nemoto K, Yoshizawa S, et al. Detection of pinpoint
tenderness on the appendix under ultrasonography is useful to
confirm acute appendicitis. Arch Surg 2002;136:11361140.
146. Rompel O, Huelsse B, Bodenschatz K, et al. Harmonic US
imaging of appendicitis in children. Pediatr Radiol 2006;36:
12571264.
147. Wiersma F, Sramek A, Hoscher HC. US features of the normal
appendix and surrounding area in children. Radiology
2005;235:10181022.
148. Rettenbacher T, Hollerweger A, Macheiner P, et al. Presence or
absence of gas in the appendix: additional criteria to rule out or
confirm acute appendicitisevaluation with US. Radiology
2000;214:183187.
149. Baldisserotto M, Peletti AB. Is colour Doppler sonography a
good method to differentiate normal and abnormal appendices
in children? Clin Radiol 2007;62:365369.
150. Lim HK, Lee WJ, Kim TH, et al. Appendicitis: usefulness of
color Doppler US. Radiology 1996;200:221225.
151. Quillin SP, Siegel MJ. Appendicitis in children: color Doppler
sonography. Radiology 1992;184:745747.
152. Quillin SP, Siegel MJ. Appendicitis: efficacy of color Doppler
sonography. Radiology 1994;191:557560.
153. Sivit CJ. Diagnosis of acute appendicitis in children: spectrum of
sonographic findings. AJR Am J Roentgenol 1993;151:147152.
154. Quillin SP, Siegel MJ. Diagnosis of appendiceal abscess in chil-
dren with acute appendicitis: value of color Doppler sonogra-
phy. AJR Am J Roentgenol 1995;164:12511254.
155. Quillin SP, Siegel MJ, Coffin CM. Acute appendicitis in chil-
dren: value of sonography in detecting perforation. AJR Am J
Roentgenol 1992;159:12651268.
156. McCann JW, Maroo S, Wales P, et al. Image-guided drainage of
multiple intraabdominal abscesses in children with perforated
appendicitis: an alternative to laparotomy. Pediatr Radiol
2008;38:661668.
157. Levin C, Koren A, Miron D, et al. Pylephlebitis due to perforated
appendicitis in a teenager. Eur J Pediatr. 2009;168:633635.
158. Slovis TL, Haller JO, Cohen HL, et al. Complicated appen-
diceal inflammatory disease in children: pylephlebitis and liver
abscess. Radiology 1989;171:823825.
159. Lim HK, Lee WJ, Lee SJ, et al. Focal appendicitis confined to
the tip: diagnosis at US. Radiology 1996;200:799801.
160. Ceres L, Alonso I, Lpez P, et al. Ultrasound study of acute
appendicitis in children with emphasis upon diagnosis of retro-
cecal appendicitis. Pediatr Radiol 1990;20:258261.
161. Wiersma F, Toorenvliet BR, Bloem JL, et al. US examination
of the appendix in children with suspected appendicitis: the
additional value of secondary signs. Eur Radiol 2009;
19:455461.
162. Applegate KE, Sivit CJ, Salvator AE, et al. Effect of cross-sec-
tional imaging on negative appendectomy and perforation rates
in children. Radiology 2001;220:103107.
163. Hahn HB, Hoepner FU, Kalle TV, et al. Sonography of acute
appendicitis in children: 7 years experience. Pediatr Radiol
1998;28:147151.
164. Hernandez JA, Swischuk LE, Angel CA, et al. Imaging of acute
appendicitis: US as the primary imaging modality. Pediatr
Radiol 2005;35:392395.
165. Sivit CJ, Applegate KE, Stallion A, et al. Imaging evaluation of
suspected appendicitis in a pediatric population: effectiveness of
sonography. AJR Am J Roentgenol 2000;175:977980.
166. Wong ML, Casey SO, Leonidas JC, et al. Sonographic diagno-
sis of acute appendicitis in children. J Pediatr Surg 1994;29:
13561360.
167. Sung T, Callahan MJ, Taylor GA. Clinical and imaging mim-
ickers of acute appendicitis in the pediatric population. AJR Am
J Roentgenol 2006;186:6774.
168. Levy AD, Hobbs CM. Meckel diverticulum: radiologic features
with pathologic correlation. Radiographics 2004;24:565587.
169. Baldisserotto M, Mffazzoni DR, Dora MD. Sonographic find-
ings of Meckels diverticulitis in children. AJR Am J Roentgenol
2003;180;425428.
170. Daneman A, Lobo A, Alton DJ, et al. The value of sonography,
CT and air enema for detection of complicated Meckel diver-
ticulum in children with nonspecific clinical presentation. Pedi-
atr Radiol 1998;28:928932.
171. Baldisserotto M. Color Doppler sonographic findings of
inflamed and perforated Meckel diverticulum. J Ultrasound
Med 2004;23:843848.
172. Han T, Kim I-O, Kim WS, et al. US identification of the anal
sphincter complex and levator ani muscle in neonates: infra-
coccygeal approach. Radiology 2000;217:392394.
173. Han T, Kim I-O, Kim WS. Imperforate anus: US determination
of the type with infracoccygeal approach. Radiology 2003;228:
226229.
174. Donaldson JS, Black CT, Reynolds M, et al. Ultrasound of the
distal pouch in infants with imperforate anus. J Pediatr Surg
1989;24:465468.
175. Anderson S, Savader B, Barnes J, et al. Enterolithiasis with imper-
forate anus. Report of two cases with sonographic demonstration
and occurrence in a female. Pediatr Radiol 1988;18:130133.
176. Kim I-O, Han TI, Kim WS, et al. Transperineal ultrasonogra-
phy in imperforate anus: identification of the internal fistula. J
Ultrasound Med 2000;19:211216.
177. Haber HP, Seitz G, Warmann SW, et al. Transperineal sonogra-
phy for determination of the type of imperforate anus. AJR Am
J Roentgenol 2007;189:15251529.
178. Epelman M, Daneman A, Navarro OM, et al. Necrotizing ente-
rocolitis: review of state-of-the-art imaging findings with patho-
logic correlation. Radiographics 2007;27:285305.
179. Goske MJ, Goldblum JR, Applegate KE, et al. The circle
sign: a new sonographic sign of pneumatosis intestinalis
clinical, pathologic and experimental findings. Pediatr Radiol
1999;29:530535.
180. Kim WY, Kim WS, Kim IO, et al. Sonographic evaluation of
neonates with early-stage necrotizing enterocolitis. Pediatr
Radiol 2005;35:10561061.
181. Miller SF, Seibert JJ, Kinder DL, et al. Use of ultrasound in the
detection of occult bowel perforation in neonates. J Ultrasound
Med 1993;12:531535.
182. Patel U, Leonidas JC, Furie D. Sonographic detection of necrotiz-
ing enterocolitis in infancy. J Ultrasound Med 1990;9:673675.
183. Faingold R, Daneman A, Tomlilson G, et al. Necrotizing ente-
rocolitis assessment of bowel viability with color Doppler US.
Radiology 2005;235:587594.
184. Deeg KH, Rupprecht T, Schmid E. Doppler sonographic detec-
tion of increased flow velocities in the celiac trunk and superior
mesenteric artery in infants with necrotizing enterocolitis. Pedi-
atr Radiol 1993;23:578582.
185. Silva CT, Daneman A, Navarro OM, et al. Correlation of sono-
graphic findings and outcome in necrotizing enterocolitis. Pedi-
atr Radiol 2007;37:274282.
186. Brill PW, Olson SR, Winchester P. Neonatal necrotizing entero-
colitis: air in Morison pouch. Radiology 1990;174:469471.
187. Baud C, Saguintaah M, Veyrac C, et al. Sonographic diagnosis
of colitis in children. Eur Radiol 2004;14:21052119.
LWBK505-C10_p339-383.qxd 7/7/10 1:32 PM Page 383 Aptara Inc
188. Downey DB, Wilson SR. Pseudomembranous colitis: sono-
graphic features. Radiology 1991;180:6164.
189. Ros PR, Buetow PC, Pantograg-Brown L, et al. Pseudomem-
branous colitis. Radiology 1996;198:19.
190. Friedland JA, Herman TE, Siegel MJ. Escherichia coli 0157:H7-
associated hemolytic-uremic syndrome: value of colonic color
Doppler sonography. Pediatr Radiol 1995;25:865867.
191. Tsujimoto T, Kuriyama S, Yoshiji H, et al. Ultrasonographic
findings of amebic colitis. J Gastroenterol 2003;38:8286.
192. Dialer I, Hundt C, Bertele-Harms RM, et al. Sonographic eval-
uation of bowel wall thickness in patients with cystic fibrosis. J
Clin Gastroenterol 2003;37:5560.
193. Fields TM, Michel SJ, Butler CL, et al. Abdominal manifesta-
tions of cystic fibrosis in older children and adults. AJR Am J
Roentgenol 2006;187:11991203.
Chapter 10 G A S T R O I N T E S T I N A L T R A C T 383
194. Haber HP, Benda N, Fitzke G, et al. Colonic wall thickness
measured by ultrasound. Striking differences in patients with
cystic fibrosis versus healthy controls. Gut 1997;49:406411.
195. Lardenoye SW, Puylaert JB, Smit MJ, et al. Appendix in children
with cystic fibrosis: US features. Radiology 2004;232: 187189.
196. Menten R, Lebecque P, Saint-Martin C, et al. Outer diameter of
the vermiform appendix: not a valid sonographic criterion for
acute appendicitis in patients with cystic fibrosis. AJR Am J
Roentgenol 2005;184:19011903.
197. Walter DF, Govil S, Korula A, et al. Pedunculated colonic polyp
diagnosed by colonic sonography. Pediatr Radiol 1992;22:
148149.
198. Piotto L, Gent R, Kirby CP, et al. Preoperative use of ultra-
sonography to localize an ingested foreign body. Pediatr Radiol
2009;39:299301.
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CHAPTER

11 Urinary Tract
MARILYN J. SIEGEL

Technique Renal Cystic Disease Hemolytic Uremic Disease

Gray Scale Bilateral Cystic Disease Henoch-Schnlein Purpura
Doppler Imaging Unilateral Cystic Disease Acute Tubular Necrosis
Acute Renal Cortical Necrosis
Normal Anatomy Malignant Renal Neoplasms
Acute Interstitial Nephritis
Measurements Wilms Tumor
Neonate Nephroblastomatosis Renal Vascular DIsease
Children and Adolescents Renal Cell Carcinoma Renal Artery Stenosis
Vascular Anatomy Lymphoma Renal Artery Thrombosis and Infarction
Doppler Flow Patterns Leukemia Arteriovenous Fistula
Ureters Malignant Medullary Tumors Pseudoaneurysm
Other Rare Tumors Renal Vein Thrombosis
Anatomic Variants
Secondary Tumor Deposits Urinary Tract Calcifications
Fetal Lobulation
(Metastases) Nephrocalcinosis
Column of Bertin
Cortical Fusion Defects Benign Renal Tumors Urolithiasis
Compound Calyces Mesoblastic Nephroma Sonography
Dromedary Hump Angiomyolipoma Juxtarenal Processes
Rare Benign Renal Tumors Renal Trauma
Congenital Anomalies
Doppler Sonography
Renal Agenesis Renal Transplant
Renal Hypoplasia Acute Urinary Tract Infection Normal Renal Allograft
Renal Ectopia Imaging Guidelines Pathology
Horseshoe Kidney Acute Bacterial Pyelonephritis Parenchymal Complications
Duplication Anomalies Complicated Acute Pyelonephritis Vascular Complications
Renal Vascular Fungal Infection Perinephric Fluid Collections
Variants Acquired Immunodeficiency Syndrome Ureteral Obstruction
Lymphoproliferative Disorder
Congenital Hydronephrosis Chronic Renal Infections
Miscellaneous Complications
General Imaging Approach Chronic Pyelonephritis
Ureteropelvic Junction Xanthogranulomatous Pyelonephritis Bladder and Urethra
Obstruction Scanning Techniques and
Treatment Procedures for Normal Anatomy
Primary Megaureter
Vesicoureteral Reflux Pathology
Vesicoureteral Reflux
Ureteral Reimplantation Congenital Anomalies
Ureteral Duplication
Endoscopic Treatment Neurogenic Bladder
Simple Ureterocele
Posterior Urethral Valves Medical Renal Disease Bladder Calculi
Prune Belly Syndrome Sonographic Findings Neoplasms
Retrocaval Ureter Hypotension (Prerenal Disease) Cystitis
Stasis Nephropathy Postsurgical Findings
Acquired Renal Obstruction Trauma
Glomerulonephritis

onography plays an increasingly important role in the and thin adolescents, a 5.0- to 7.5-MHz transducer usually

S evaluation of urinary tract disease, particularly the eval-

uation of prenatal hydronephrosis, renal masses, and
urinary tract infection. Other indications include renal fail-
ure, renal vascular diseases, stone disease, renal allografts,
and bladder and perivesical abnormalities.
TECHNIQUE
Gray Scale
The highest-possible-frequency, curved or linear array trans-
ducer should be used to maximize resolution. In children
384
suffices. In larger adolescents, a. 3.0- to 3.5-MHz transducer
may be required for adequate penetration. Each kidney
should be examined in transverse and longitudinal planes.
The right kidney is best seen using a ventral scanning
approach with the patient in the supine or left lateral
decubitus position. The left kidney can be imaged with
the patient in the supine or right lateral decubitus posi-
tion, using the spleen as an acoustic window. Scanning
the patient in the prone position with a dorsal approach,
especially with the use of harmonic imaging, may be
advantageous when bowel gas obscures visualization of
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Chapter 11 U R I N A R Y T R A C T 385

the kidneys via an anterior approach (1). In some NORMAL ANATOMY

patients, intercostal and subcostal approaches can
improve visualization of the upper poles of the kidneys,
particularly the upper pole of the left kidney.
Doppler Imaging
Pulsed and color flow Doppler imaging are useful to evalu-
ate the integrity of the renal vessels and the vascular resist-
ance (2). The resistive index (RI) (peak systolic frequency
shift minus the minimum diastolic frequency shift divided
by the peak systolic frequency shift) provides an estimate of
arterial resistance. RI values are usually obtained in the
main renal artery and the intraparenchymal arcuate and
interlobar arteries. At least three different areas in the kid-
ney should be sampled to obtain a mean RI.
Measurements
Sonographic measurements of renal length and volume in
relation to patient age, weight, height, and/or body surface
have been established and have facilitated evaluation of
the abnormal kidney (3,4). Measurements of renal length
obtained with the patient lying supine or in a contralateral
decubitus position appear to be slightly higher than those
obtained with the patient prone (5).
Neonate
The neonatal and infant kidneys have three unique features
that differentiate them from the kidneys of older children and
adults (Fig. 11.1) (6). First, in term infants the echogenicity of

RT. Kidney : Liver RT. Kidney : Spleen

35 35

30 30

25 25
No. Children
No. Children

20 20

15 15

10 10

5 5

Age Newborn 1-6 mo. 7-11 mo. 1-3 yr. 4-9 yr. > 10 yr. Age Newborn 1-6 mo. 7-11 mo. 1-3 yr. 4-9 yr. > 10 yr.
B
Kidney = Liver Kidney = Spleen

Kidney < Liver Kidney < Spleen

A

35

30

25 35
No. Children

30
20
No. Children

25
15
20

10 15

10
5
5

Age Newborn 1-6 mo. 7-11 mo. 1-3 yr. 4-9 yr. > 10 yr. CSE 0+1+2+3 0+1+2+3 0+1+2+3 0+1+2+3 0+1+2+3 0+1+2+3
Age Newborn 1-6 mo. 7-11 mo. 1-3 yr. 4-9 yr. > 10 yr.
+ prominent MP D
- prominent MP
C
Normal anatomy. A: Renal cortical echogenicity relative to the liver. B: Renal cortical echogenicity relative to the spleen. Cortical
Fig. 11.1
echogenicity is increased at birth and usually equal to that of the liver or spleen. The cortex becomes less echogenic with age.
C: Prominence of medullary pyramids (MP). Medullary pyramids are hypoechoic and prominent in neonates and young infants. By 6 months of age,
the pyramids have attained a more adult-like pattern. D: Central sinus echogenicity (CSE). Intensity of CSE is classified into four groups: 0, intensity
equal to cortex; 1, intensity slightly more echogenic than cortex; 2, intensity moderately more echogenic than cortex; 3, highly echogenic. The
echogenicity of the central sinus gradually increases with age. (Adapted from Han BK, Babcock DS. Sonographic measurements and appearance of
normal kidneys in children. AJR Am J Roentgenol 1985;145:611616, with permission.)
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386 P E D I AT R I C S O N O G R A P H Y

A B
Normal renal anatomy. Neonatal kidney, longitudinal scans. A: The echogenicity of the cortex (arrows) is equal to that of the adjacent
Fig. 11.2
liver (L). The pyramids (P) are prominent. There is minimal separation of the central renal sinus (S). B: In the premature infant, the cor-
tical echogenicity can be greater than that of liver (L). Note again the prominent pyramids (arrows).

the renal cortex is increased and usually equal to or slightly echogenic area in the second half of the first decade
greater than that of the liver or spleen (Fig. 11.2), whereas in (Fig. 11.3).
older children and adults the cortex is hypoechoic relative to The renal pelvis may dilate with changes in patient posi-
these structures. In the neonatal kidney, the glomeruli occupy tion. Individuals with a nondilated collecting system in the
about 20% of the cortical volume compared to about 9% of supine position can show a dilated renal pelvis in the prone
the cortical volume in the adult (6). The increased number of position. The dilatation presumably reflects shifting of
glomeruli leads to more acoustic interfaces that are believed urine from normal-sized calyces to the redundant renal
to account for the increased cortical echogenicity. The renal pelvis in the prone position. The renal pelvis should be 10
cortex usually becomes less echogenic than liver or spleen by mm or less in maximum anteroposterior measurement (8).
12 months of age. Of note, in premature infants, the renal
cortex can be moderately hyperechoic to liver. In fact, the Vascular Anatomy
more premature the infant, the higher the likelihood is that The main renal arteries arise from the lateral aspect
the renal cortex will be very echogenic (Fig. 11.2B). of the abdominal aorta immediately distal to the origin of
The second difference between infant and adult kidneys is the superior mesenteric artery and course posterior to the
that in the former the medullary pyramids are moderately or renal veins to reach the renal hilum, where they give rise
markedly hypoechoic and strikingly prominent (Fig. 11.2).
This is believed to reflect the larger medullary and smaller
cortical volume in neonates relative to that seen in older chil-
dren and adults (6). By the time the infant is 12 months of
age, the pyramids are substantially less prominent.
The third unique feature of the kidney in neonates and
young infants is that the renal sinus is not as echogenic as
in older adolescents and adults, because of the paucity of
fat in this area (Fig. 11.2). The echogenicity of the central
sinus increases with age (6).
The renal pelvis usually measures 10 mm or less in
anteroposterior diameter and is not associated with calyceal
dilatation. A diameter greater than 10 mm is more likely to
be associated with obstructive uropathy (7). Prominent hilar
vessels can mimic a dilated renal pelvis, but these can be rec-
ognized with the use of color Doppler imaging.

Children and Adolescents
During the first year of life, the renal cortex becomes
hypoechoic or isoechoic to adjacent liver and spleen. The
medullary pyramids are minimally hypoechoic relative to
the cortex. The renal sinus begins to appear as a central
Normal renal anatomy, older child. Longitudinal sonogram
Fig. 11.3
of the right kidney reveals a more mature pattern. The
renal cortex (arrows) is less echogenic than the liver (L); the renal pyr-
amids are imperceptible; and the central renal sinus (open arrows) is
moderately echogenic.
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Chapter 11 U R I N A R Y T R A C T 387

A B
Color Doppler sonography. A: Color Doppler image demonstrates the segmental artery in the renal hilum (straight arrow), interlobar
Fig. 11.4
arteries along the sides of the pyramids (open arrow), and arcuate arteries around the corticomedullary junction, separating the base
of the pyramids from the cortex (arrowheads). B: Power Doppler enhances visualization of the vascular tree. Compared with color Doppler imaging,
power Doppler imaging has increased sensitivity for flow detection, but it does not provide information about flow direction.

to parenchymal branches that supply the medulla and cor-
tex. These intrarenal branches include the segmental renal
arteries, which lie within the renal hilum; the interlobar
arteries, which course along the sides of the pyramids; the
arcuate arteries, which course around the corticomedullary
junction, separating the base of the pyramids from the cor-
tex; and the interlobular arteries, which radiate into the
cortex toward the renal capsule (Fig. 11.4). Power or
Doppler imaging enhances visualization of the entire vascu-
lar tree from the main renal artery to the cortical branches.
The main renal veins lie anterior to the renal arteries.
They empty into the inferior vena cava. The left renal vein
courses between the superior mesenteric artery and the
aorta to reach the inferior vena cava. The right renal vein
is shorter than the left and courses directly to the inferior
vena cava from the renal hilum. The intrarenal venous cir-
culation parallels that of the arteries.
Doppler Flow Patterns
On pulsed Doppler interrogation, the main renal artery
has a low-impedance waveform and demonstrates a rapid
upstroke in systole, a sharp systolic peak, and gradual
drop-off with continuous forward flow above the baseline
during diastole (Fig. 11.5) (2). Maximum systolic velocity
varies with patient age. Peak systolic velocity in the main
renal artery is approximately 30 to 52 cm/sec in neonates
and as high as 100 to 110 cm/sec in older children, with
flow velocity decreasing as the vessel branches distally
into the renal parenchyma (9,10). Similar waveforms are
seen in the interlobular and arcuate arteries, although the
systolic peak is lower in the intrarenal vessels than in the
main renal arteries. The systolic acceleration time (AT),
measured from the start of the systolic upstroke to the
first or early systolic peak (ESP), is usually equal to or less
than 0.07 seconds (10).

Arterial waveform. Doppler waveform

Fig. 11.5
obtained from a segmental renal artery
shows a low-resistance waveform with sharp systolic
upstroke and gradual descent and continuous dias-
tolic flow. Peak systolic velocity is 62 cm/sec and sys-
tolic acceleration time is 0.07 seconds.
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388 P E D I AT R I C S O N O G R A P H Y
The RI varies during the first year of life. Preterm infants
can have RIs as high as 0.9. In neonates under 4 months of age,
the RI can be as high as 0.85 (range 0.56 to 0.85) (11). The rel-
atively high RI is attributed to the physiologic lower glomeru-
lar filtration rate in infants compared with older children and
adults. During the first year of life, the RI gradually decreases
and by the end of the first year of life it is generally less than
0.70 (range 0.50 to 0.67) (1113). Patent ductus arteriosus,
aortic coarctation, intrinsic renal disease, renovascular disease,
hydronephrosis, and large subcapsular or perinephric fluid col-
lections can elevate intrarenal RIs. In the setting of a patent
ductus arterious, there is a decrease or reversal in diastolic
flow, with diastolic flow reappearing after ductal closure (14).
Doppler interrogation of the main and intrarenal veins
shows continuous flow throughout the cardiac cycle. The
direction and color signal are opposite that of the renal artery.
The venous waveforms can show fluctuations in velocity
related to cardiac and respiratory motions (Fig. 11.6).
A B
Fig. 11.7 Ureteral jets. Color flow Doppler images in two patients show signal from right ureteral jets. The jets course anteriorly and to the left.
Venous waveform. Doppler sonogram shows
Fig. 11.6
continuous venous flow (arrows) with mini-
mal variation in velocity related to respiratory motion.
Ureters
The ureters course anterior to the common or external
iliac artery to enter the bladder, where they have an
oblique course in the bladder wall. The normal distal
ureters are difficult to identify unless a peristaltic wave
passes through them or a ureteric jet is seen. The ureteric
jet appears as an intermittent stream of echoes flowing
anteromedially from the ureteral orifice into the urine-
filled bladder. It is believed that the differences in density
between the bladder and ureteric urine allow the jet to be
seen at sonography. The duration of the jet ranges from
0.4 to 7.5 seconds and varies with fluid intake (15). The
jets should be symmetric bilaterally. They can be seen on
real-time imaging but are better demonstrated on color
flow Doppler sonography (Fig. 11.7). Hydration prior to
the study and a full bladder increase sensitivity of the
examination.
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Fetal lobulations. Longitudinal scan of the right kidney
Fig. 11.8
shows a lobulated renal margin (arrows). Fetal lobulations
lie between the renal pyramids or calyces, unlike cortical scars, which
lie directly over the calyces.
ANATOMIC VARIANTS
Fetal Lobulation
The kidney develops from embryonic parenchymal masses
termed renunculi, which develop during the second trimester
(16). Each renunculus consists of a large central pyramid
that contains renal tubules and that is enveloped by a layer of
cortex containing glomeruli. Fusion of the renunculi produces
a single kidney with lobulated margins, referred to as fetal lob-
ulation. During the third trimester, the renal surface becomes
smoother, although fetal lobulation can persist in postnatal life
(Fig. 11.8). Fetal lobulation should not be mistaken for renal
scarring, which is associated with parenchymal thinning.
Column of Bertin
The adjacent cortices of the contiguous renunculi fuse to
form a thick layer of cortex, termed a column of Bertin.
The fused parenchyma usually resorbs during in utero
development. If resorption is incomplete, the column of
Bertin can hypertrophy and cause splaying of the calyces,
A B
Fusion lines. A: Junctional parenchymal defect. Longitudinal sonogram of the right kidney shows a triangular echogenic focus (arrow)
Fig. 11.10
peripherally in the parenchyma of the upper pole without cortical loss. B: Junctional parenchymal line, appearing as an oblique
echogenic line (arrow) in the upper pole of the kidney.
Chapter 11 U R I N A R Y T R A C T 389
Hypertrophied column of Bertin. Longitudinal sonogram
Fig. 11.9
shows a mass-like structure (M), representing the column of
Bertin extending from the renal cortex to the renal sinus (S). The hypertro-
phied column typically has an echogenicity similar to that of normal cortex.
mimicking a mass. At sonography, the column of Bertin
appears as a round or oval mass with an echogenicity equal
to or slightly greater than that of normal adjacent cortex
(Fig. 11.9). It extends from the renal cortex to the renal
sinus and is located between two medullary pyramids, and
it is frequently bordered by a junctional parenchymal defect
and/or junctional parenchymal line (16,17). The absence of
renal contour abnormality is a useful feature in differenti-
ating a hypertrophied column of Bertin from a true mass.
Cortical Fusion Defects
The junctional parenchymal defect and junctional parenchy-
mal line (also called the interrenuncular septum) represent
the plane of embryologic fusion between the renunculi
(16,18). The junctional parenchymal defect appears as a
triangular echogenic focus, usually near the junction of the
upper and middle thirds of the kidney. The junctional
parenchymal line appears as an echogenic line, running from
the junctional defect to the renal hilum or medulla
(Fig. 11.10) (16). The junctional parenchymal defect and line
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390 P E D I AT R I C S O N O G R A P H Y
Compound calyx. Longitudinal scan of the left kidney
Fig. 11.11
(calipers) shows a hypoechoic area (arrow) in the upper
pole, representing a compound pyramid.
are seen more often on the right than on the left side. The
junctional defect should not be mistaken for a parenchymal
scar. The scar is associated with parenchymal thinning; the
junctional defect is not associated with parenchymal loss, but
occasionally it may indent the cortex (16).
Compound Calyces
Compound calyces are present in the upper and lower poles
of the kidney and are associated with compound pyramids.
At sonography, they appear as prominent anechoic or hypoe-
choic areas in the polar region of the kidney (Fig. 11.11).
They can be distinguished from an obstructed upper pole of
a duplex system, focal caliectasis, simple renal cyst, or hypoe-
choic mass by their characteristic location and the absence of
calyceal distortion, mass effect, and cortical thinning.
Dromedary Hump
A dromedary hump is a bulge in the lateral margin of the
midpole of the left kidney. The calyces subadjacent to the
hump extend further into the cortex than the other calyces
and the echotexture of the hump is similar to that of the
surrounding normal parenchyma.
CONGENITAL ANOMALIES
Congenital anomalies can be classified as abnormalities in
number (renal agenesis), position (ptosis or ectopia), and
fusion (horseshoe kidney, crossed fused ectopia, and renal
duplication).
Renal Agenesis
Renal agenesis is defined as complete absence of renal tissue.
It results when there is absence of the metanephric blastema,
absence of ureteral bud development, or failure of the ureteric
bud to induce metanephric differentiation (19). The corre-
sponding ureter and hemitrigone of the bladder are absent,
although occasionally a short remnant of distal ureter may be
identified. This event usually occurs between the fifth and sev-
enth week of gestation and it may be bilateral or unilateral.
Bilateral renal agenesis is rare (incidence of 0.02% to
0.04%) (19,20). This condition is incompatible with life,
and affected infants are either stillborn or die in the imme-
diate postnatal period of respiratory insufficiency or renal
failure. Almost all patients have pulmonary hypoplasia as
a result of oligohydramnios and uterine compression of the
fetal thorax. At sonography, the kidneys and renal arteries
are absent and the bladder often is small or absent. The
adrenals usually are present but typically elongated.
Unilateral renal agenesis occurs in 0.01% of live births
(20). Affected individuals commonly have associated
anomalies of the cardiovascular, gastrointestinal, or skele-
tal systems. Genital anomalies also are common. These
include absence of the seminal vesicles or vas deferens,
cysts of the epididymis and seminal vesicle, undescended
testes, unicornuate and bicornuate uterus, and imperfo-
rate vagina with secondary hydrometrocolpos (19,20).
Sonographic findings of renal agenesis are an empty
renal fossa, absent renal arteries, a small bladder, an elon-
gated ipsilateral adrenal gland, and adjacent organ dis-
placement (Fig. 11.12). On the right, the proximal small
bowel, hepatic flexure, liver, or pancreatic head may fill the
Renal agenesis. An elongated right adrenal gland (arrows)
Fig. 11.12
is noted on a longitudinal image. The right kidney could not
be identified.
LWBK505-C11_p384-460.qxd 7/7/10 1:35 PM Page 391 Aptara Inc
empty renal fossa. On the left, small bowel loops, the
splenic flexure, or the pancreatic tail fills the corresponding
space. The contralateral kidney is normal in size at birth,
but within 6 to 12 months of life it usually begins to show
compensatory hypertrophy.
Renal Hypoplasia
Renal hypoplasia refers to a normally formed but small
kidney (2 standard deviations [SD] below the expected
mean for age) (20). It is usually unilateral and is char-
acterized by a decreased number of renal lobes, pyra-
mids, calyces, and nephrons. Patients with unilateral
hypoplasia tend to be asymptomatic and the anomaly is
detected as an incidental finding. Patients with bilateral
hypoplasia can have renal insufficiency. At sonography,
the hypoplastic kidney is present in the renal fossa
and is small, but otherwise normal in appearance.
There is compensatory hypertrophy of the contralateral
kidney.
Renal Ectopia
SIMPLE ECTOPIA
In utero, the kidneys arise in the pelvis and then migrate
cranially. By the eighth gestational week, the fetal kidneys
have achieved their expected position in the renal fossa.
Ectopic kidneys occur when there is failure of complete
ascent.
Renal ectopia may be simple or crossed. In simple
ectopia, the kidneys and ureter are on their expected sides
of the spine. The simple ectopic kidney is most commonly
located in the pelvis. It is usually small and malrotated and
frequently has a dysmorphic configuration, such as a pan-
cake, disc, or lump shape (Fig. 11.13). The calyces,
infundibula, and pelvis are positioned near the surface of
A B
Pelvic kidney. A: Transverse sonogram shows an ectopic kidney (calipers) posterior to the bladder (BL). Scans of the upper abdomen
Fig. 11.13
had not shown a left kidney. B: Transverse view in another patient shows a pelvic kidney with dilated calyces (C). SP  spine. A nor-
mally positioned right kidney was not identified.
Chapter 11 U R I N A R Y T R A C T 391
the kidney, not in the deeper parenchyma, as occurs in the
normal kidney. The result is that the normal sinus echo
complex is absent or eccentric (21). The ureters are short.
The blood supply is from regional arteries, usually the com-
mon or internal iliac arteries, and multiple arteries are com-
mon.
Rarely, the ectopic kidney is found in the posterior tho-
rax, with the left hemithorax being affected more often than
the right. The congenital intrathoracic kidney is covered by
a thin membrane, in contradistinction to the thoracic kidney
associated with a Bochdalek hernia or a traumatic rupture
of the diaphragm, which lacks a membranous cover. Sonog-
raphy is useful to determine whether or not the diaphragm
is intact.
CROSSED ECTOPIA
In crossed ectopia, both kidneys are located on the same
side of the spine. The left kidney is more often ectopic than
the right. The crossed ectopic kidney is smaller than the
normal kidney and malrotated, and it usually lies caudal to
the orthotopic kidney. Ninety percent of crossed ectopic
kidneys are fused to the normal ipsilateral kidney. Typi-
cally, the upper pole of the ectopic kidney is fused to the
lower pole of the orthotopic unit. The ureter draining the
ectopic kidney returns across the midline and enters
the bladder at the contralateral trigone, while the ureter of
the orthotopic component enters the ipsilateral trigone.
There is an increased incidence of multicystic dysplasia,
hydronephrosis, infection, and calculus formation in the
crossed unit.
The sonographic findings of crossed fused ectopia
include a sigmoid or S-shaped mass with two renal sinuses
and absence of the kidney in the contralateral renal fossa.
The fused upper pole unit is positioned medially, extending
anteriorly to the spine (Fig. 11.14). Both distal ureters are
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392 P E D I AT R I C S O N O G R A P H Y
Crossed fused ectopia. Oblique scan of the right lower
Fig. 11.14
flank in a neonate demonstrates fusion of the lower pole
of the normal right kidney (RK) to the upper pole of the ectopic left
kidney (LK), which crosses the midline anterior to the spine (S).
P  anteriorly positioned right renal pelvis.
A B
C pole of the normally positioned left kidney (LK).
normally located. In patients with cystic dysplasia, a mul-
ticystic mass is contiguous with the lower pole of the nor-
mally positioned kidney (Fig. 11.15).
Horseshoe Kidney
Horseshoe kidney is the most common renal anomaly,
with an incidence of 0.2% to 0.25% (1 in 400 births) and
a 2:1 male predominance (22). The site of fusion usually is
at the lower poles of the kidneys. The two poles are con-
nected by an isthmus, which may contain functioning
parenchyma or fibrous tissue. The ureters cross in front of
the isthmus, descending from anteriorly positioned renal
pelves. The arterial supply is variable, arising from either
the lower aorta or the common iliac arteries. Associated
anomalies of the genitourinary, cardiovascular, and skele-
tal systems as well as the gastrointestinal tract occur in
about one third of patients. The genitourinary anomalies
include ureteropelvic junction obstruction, vesicoureteral
reflux, duplicated collecting system, and renal dysplasia.
There also is a slightly increased incidence of Wilms tumor
and renal cell carcinoma.
Crossed fused ectopia with dysplastic kidney. A: Longi-
Fig. 11.15
tudinal sonogram shows bowel gas (arrows) filling the
empty right renal fossa. B: Transverse sonogram through the midab-
domen shows a cystic mass (arrows) anterior to the spine (SP).
C: Longitudinal sonogram further to the left shows the cystic mass
(arrows), representing a dysplastic right kidney, fused to the lower
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Horseshoe kidney. Transverse scan shows an isthmus of
Fig. 11.16
tissue (ISTH) anterior to the spine (S) connecting the
lower poles of the kidneys. RK  right kidney; LK  left kidney.
Sonographic findings include an abnormal axis of each
kidney with medial orientation of the lower poles of the
kidneys, anteriorly located renal pelves, and an isthmus of
tissue crossing the midline anterior to the spine and great
vessels (Fig. 11.16). Pelvocaliectasis and stone formation
are other occasional findings.
Duplication Anomalies
Duplication of the renal collecting system is the most com-
mon congenital anomaly of the urinary tract, with an inci-
dence of 0.8% to 5% in autopsy series (19,22). It can be
partial or complete. The former is more common and
accounts for over 95% of the duplication anomalies (19).
The spectrum of partial duplication ranges from a bifid
renal pelvis to Y-shaped ureters with the two ureters fusing
somewhere along their course, producing a single common
ureter distally. In complete duplication, the kidney has two
pelvicaliceal systems and two ureters that enter the bladder
through separate orifices. The ureter from the lower pole
collecting system is normally located in the trigone. The
ureter from the upper pole moiety usually inserts ectopi-
cally and often is obstructed. Complete duplications are
discussed in more detail later in the chapter.
Partial or incomplete duplication anomalies are gener-
ally not clinically significant, and the incidence of infection
in these patients is not significantly different from that of
the general population. At sonography, the partially dupli-
cated kidney is larger than the normal single-system kid-
ney, and it has two separate echogenic renal sinuses with
intervening renal parenchyma and a single distal ureter
(Fig. 11.17).
Renal Vascular Variants
In approximately 30% of individuals, one or both kidneys
are supplied by more than one renal artery. Accessory
arteries usually arise from the abdominal aorta near the
main renal artery, but they can arise lower on the aorta
and from the common iliac arteries. They are usually infe-
Chapter 11 U R I N A R Y T R A C T 393
Partial ureteral duplication. Longitudinal sonogram
Fig. 11.17
shows an enlarged kidney with two echodense renal
sinuses (S). Asterisk indicates intervening normal parenchyma.
rior to the main renal artery. Accessory right renal arteries
are more likely to be detected by sonography than acces-
sory left renal arteries. On longitudinal views, they appear
as two round structures posterior to the inferior vena cava
and in front of the right diaphragmatic crus.
A retroaortic left renal vein, passing posterior to the
aorta instead of between the aorta and superior mesenteric
vein, is another common vascular variant. On longitudinal
views, it appears as an anechoic ovoid structure posterior
to the aorta. The renal vein may be circumaortic, dividing
before reaching the aorta, with one branch coursing ante-
riorly and another posteriorly around the aorta.
CONGENITAL HYDRONEPHROSIS
Congenital hydronephrosis may be secondary to mechani-
cal or functional causes. Mechanical causes of obstruction
include ureteropelvic junction obstruction, primary megau-
reter, duplex collecting system anomalies, and posterior
urethral valves. Functional causes include prune belly syn-
drome and vesicoureteral reflux. Congenital hydronephro-
sis is nearly always diagnosed on prenatal sonography.
Occasionally, patients present with a palpable abdominal
mass or with complications of obstruction, including flank
pain, hematuria, and urinary tract infection.
General Imaging Approach
When intrauterine hydronephrosis is diagnosed, a postpar-
tum sonogram is indicated to confirm the diagnosis. It is
recommended that sonography not be performed until 4 to
5 days after delivery (23,24). A sonogram performed earlier
may be falsely negative or may underestimate the severity of
hydronephrosis, due to a relative state of dehydration and
decreased glomerular filtration rate immediately after deliv-
ery. After patient rehydration in the first few days of life, the
glomerular filtration rate increases, thereby increasing urine
flow. Pelvicaliceal dilatation secondary to an obstructing
lesion then becomes more apparent (Fig. 11.18).
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394 P E D I AT R I C S O N O G R A P H Y
A B
Hydronephrosis. A: Longitudinal sonogram of the left kidney obtained on the first day of life shows mild dilatation of the renal pelvis
Fig. 11.18
(RP) and upper pole calyx (C). B: A scan on the fourth day of life reveals marked dilatation of the renal pelvis (RP) and calyces (C).
If the postnatal sonogram shows moderate or severe
hydronephrosis, further evaluation is usually undertaken
and a voiding cystourethrogram (VCUG) and diuretic
scintigraphy are performed. Voiding cystography
assesses the presence of reflux and diuretic scintigraphy
assesses differential renal function. When the initial
postnatal sonogram is normal or shows mild dilatation,
it is generally repeated at 6 weeks of age. If follow-up
sonography shows mild hydronephrosis, a VCUG is per-
formed.
The diagnosis of hydronephrosis is usually based on
classic gray-scale findings of separation and dilatation of
the central echo complex and caliectasis. The degree of
dilatation is dependent on the duration of obstruction, the
amount of urine production, and the presence or absence
of spontaneous decompression of the collecting system. It
needs to be recognized that dilatation of the collecting
system does not necessarily indicate obstruction. Vesi-
coureteral reflux, infection, postobstructive pelvocaliecta-
sis, and diabetes insipidus may result in nonobstructed
dilatation of the collecting system. In addition, prominent
vessels in the region of the renal hilum can mimic
hydronephrosis.
Pulsed Doppler examination of the intrarenal vessels
has been used to differentiate between obstructed and
nonobstructed (reflux) pyelocaliectasis. In the setting of
renal obstruction, renin and angiotensin as well as other
hormones cause diffuse arteriolar vasoconstriction, thus
decreasing diastolic arterial flow velocities and elevating
the RI (25). Several authors have reported that an RI
greater than 0.85 in neonates and greater than 0.70 in chil-
dren and adolescents is suggestive of renal obstruction,
while an RI less than 0.70 supports a diagnosis of nonob-
structed dilatation (2527). However, elevated RIs are not
specific for obstruction. Medical renal disease is another
cause of an abnormally high RI. In addition, the RI can be
normal in partial obstruction and in severe chronic
obstruction (25,28).
Initial experience with three-dimensional (3D) sonog-
raphy suggests that it may be useful for assessment of renal
parenchymal volume and relative renal size in patients
with hydronephrosis, provided that there is no acute renal
disease (29).
Ureteropelvic Junction Obstruction
Ureteropelvic junction obstruction is the most common
cause of congenital urinary tract obstruction. It is
believed to be due to abnormal development of a short
segment of the ureteral smooth muscle at the uretero-
pelvic junction. Extrinsic factors, such as bands, adhe-
sions, or aberrant vessels crossing the upper ureter or
renal pelvis, have also been implicated as causes of
obstruction (20,30). Ureteropelvic junction obstruction
may coexist with other urinary tract abnormalities,
including vesicoureteral reflux, ureterovesical junction
obstruction, horseshoe kidney, and duplex kidney. In duplex
kidney, the obstruction usually occurs in the upper pole
moiety.
Ureteropelvic junction obstruction, like other congeni-
tal causes of hydronephrosis, is commonly diagnosed on
prenatal sonograms, although it can present at any age.
Clinical findings in the neonate include a palpable mass
and abdominal distention. Clinical findings in the older
child include abdominal pain, hematuria or urinary tract
infection, and recurrent flank pain, associated with
increased fluid intake.
The characteristic sonographic findings include multi-
ple dilated calyces of uniform size that communicate with
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A B
C scan through the bony pelvis. BL  bladder.
a moderate or large renal pelvis; visible renal parenchyma
of varying thickness; lack of visualization of a distal ureter;
and a normal bladder (Fig. 11.19). The renal pelvis dilates
more than the calyces. Rarely, ipsilateral ureteral dilatation
is present owing to associated vesicoureteral reflux or dis-
tal ureteral obstruction. Severe in utero obstruction has
been associated with rupture of the renal collecting system
and renal dysplasia. Sonographic findings of renal dyspla-
sia are increased cortical echogenicity and cortical cysts.
The sonographic findings of urine leakage are subcapsular
urinomas and urine ascites (Fig. 11.20).
A large extrarenal pelvis should not be mistaken for
ureteropelvic junction obstruction. The former is associated
with a normal parenchymal thickness and nondilated
calyces (Fig. 11.21). The latter is associated with both
pelvic and calyceal dilatation, and on occasion parenchy-
mal loss. False-negative diagnoses are unusual, but as noted
previously, the diagnosis can be difficult in the immediate
postnatal period when the infant is relatively dehydrated.
The treatment of ureteropelvic junction obstruction in
infants and young children is a dismembered pyeloplasty,
where the redundant renal pelvis is trimmed and reinserted
into the ureter. In some adolescent patients, endopyelo-
tomy has replaced the pyeloplasty. Endourologic repair is
Chapter 11 U R I N A R Y T R A C T 395
Ureteropelvic junction (UPJ) obstruction. Longitudinal
Fig. 11.19
(A) and transverse (B) sonograms of the left kidney
demonstrate moderately dilated calyces (C) communicating with a
markedly dilated renal pelvis (RP). A thin rim of normal parenchyma
surrounds the dilated collecting system. C: No ureter is identified on a
associated with an increased risk of vascular complications
because of the blind incision into the periureteral tissues.
Color Doppler imaging can depict crossing vessels at the
ureteropelvic junction and hence can aid in planning sur-
gical management (31).
Primary Megaureter
The term megaureter refers to a dilated ureter. The con-
dition can be secondary to a congenital or primary
obstruction of the ureter or to reflux. In the obstructed
megaureter, the most distal 0.5 to 4 cm of ureter is nar-
rowed and unable to conduct a peristaltic wave, produc-
ing a functional obstruction (32,33). Histologic studies
have shown absence of ganglion cells and in some cases
muscle hypoplasia and atrophy, mural fibrosis, and
increased collagen deposition in the adynamic segment
(32,33).
A refluxing megaureter results when the intramural
portion of the ureter is short and has an oblique course.
These structural abnormalities lead to incompetence of
the ureterovesical junction and consequent reflux (see later
discussion).
The sonographic findings of primary megaureter are
ureterectasis and variable degrees of pelviectasis and
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396 P E D I AT R I C S O N O G R A P H Y

Ureteropelvic junction obstruction with forniceal rup-

Fig. 11.20
ture. Longitudinal sonogram demonstrates a dilated
renal pelvis (RP) surrounded by echogenic dysplastic parenchyma (P).
The adjacent hypoechoic fluid collection represents urinoma (U).

caliectasis. Fusiform dilatation of the distal third of the
affected ureter prior to its insertion into the bladder is typ-
ical of primary megaureter (Fig. 11.22). The narrowed dis-
tal segment is adynamic on real-time examination. The
proximal ureter may show normal or increased peristalsis
with a to-and-fro motion at real-time imaging. The ipsilat-
eral ureteral jet is absent or shows diminished velocity on
Doppler examination (15).
Patients with moderate and severe primary megaureter
are usually treated with ureteral tapering and reimplanta-
tion. Patients with mild megaureter are often followed
clinically and may not undergo reimplantation.
Other causes of a dilated ureter are the refluxing megau-
reter, ureteral obstruction due to neurogenic bladder, poste-
rior ureteral valves, ureterocele or calculi, and high urine flow
and volume, such as that occurring in diabetes insipidus.

A B
Extrarenal pelvis. A: Longitudinal and B: transverse sonograms of the left kidney show a prominent renal pelvis (RP). The absence of
Fig. 11.21
calyceal dilatation and preserved cortical thickness excludes obstructive uropathy. Arrows indicate renal margins.
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Chapter 11 U R I N A R Y T R A C T 397

A B

Megaureter. A: Longitudinal scan of the right flank reveals

Fig. 11.22
dilated calyces (C) communicating with a dilated renal
pelvis (RP). B: Longitudinal image through the lower pelvis shows fusiform
dilatation of the distal right ureter (U), which tapers posterior to the blad-
der (BL). C: Color Doppler image shows a normal left ureteral jet (arrow).
C The right ureteral jet is absent.

estimates of sensitivity and specificity for diagnosis of

Vesicoureteral Reflux
Vesicoureteral reflux is the retrograde flow of urine from
the urinary bladder into the ureter or renal collecting sys-
tem. The normal ureter enters the bladder at an oblique
angle and courses submucosally to the ureteral orifice.
Most reflux is primary and is due to an abnormal angle of
insertion of the distal ureter into the bladder and a short-
ened submucosal course, leading to an incompetent antire-
flux flap-valve mechanism. Secondary causes of reflux
include bladder outlet obstruction, voiding dysfunction,
neurogenic disease, and prune belly syndrome. The sono-
graphic features of reflux are described in this section. The
complications of reflux related to urinary tract infection
are discussed later in this chapter. The significance of vesi-
coureteral reflux is that in the setting of infection, it pre-
disposes to pyelonephritis and scarring.
Various sonographic techniques are available for diag-
nosing vesicoureteral reflux, including non-contrast and
contrast-enhanced techniques. The most reliable non-
contrast, gray-scale findings of reflux are ureteral, pelvic
and/or urinary tract dilatation (i.e., combined ureteral and
pelvic dilatation), which may increase or decrease follow-
ing micturition or catheterization (Fig. 11.23) (34). The
reflux have varied greatly, from 11% to 91% and 15% to
94%, respectively (34,35). It is important to recognize that
a normal sonogram of the urinary tract does not exclude
reflux.
Color Doppler findings of reflux include retrograde
flow of urine from the bladder to distal ureter, seen as a
change in color signal, and lateral positioning of the
ureteral orifice (36). In patients with reflux, the mean dis-
tance of the ureteral orifice from the midline is 10.25 mm
 2.40 mm (SD) versus 7.98 mm  2.40 mm (SD) in a
nonrefluxing population.
Sonographically guided cystography with microbub-
bles is a more recent technique for diagnosing reflux. This
technique involves bladder catheterization and intravesical
instillation of saline or a contrast agent. The diagnosis of
reflux is based on detection of retrograde passage of
microbubbles from bladder to ureter and/or renal pelvis
during bladder filling or voiding (Fig. 11.24) (3739). The
addition of harmonic imaging to contrast enhanced sonog-
raphy appears to improve detection of reflux (40,41). In
general, regardless of the technique ultrasound results are
not considered dependable enough for routine clinical
investigation of reflux.
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398 P E D I AT R I C S O N O G R A P H Y

A B

C D
Refluxing megaureter. A: Longitudinal sonogram of the left kidney shows a dilated renal pelvis (RP). B: Longitudinal image through the
Fig. 11.23
pelvis demonstrates a dilated distal ureter (arrows) posterior to the bladder (BL). C: Longitudinal sonogram of the left kidney in another
patient with known grade V reflux shows marked dilatation of the renal calyces, pelvis (RP), and proximal ureter (U). D: Longitudinal sonogram of
the left kidney (arrows) in the same patient following bladder catheterization shows minimal fluid in the renal pelvis (arrowhead) and resolution of
the collecting system dilatation.

A B
Refluxing ureter, contrast enhanced. A: Precontrast sonogram shows a dilated distal left ureter (U). BL  bladder. B: Sonogram after
Fig. 11.24
instillation of contrast agent into the bladder shows echoes in the dilated ureter (U) and bladder (BL), indicating reflux. (Case courtesy
of Kassa Darge, MD.)
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Chapter 11 U R I N A R Y T R A C T 399

Ureteral Duplication
Complete ureteropelvic duplications have two separate
pelvicaliceal systems and two ureters, each with its own
ureteral orifice and site of insertion. The upper pole ureter
often has an ectopic insertion and is prone to obstruction.
It typically inserts medial and inferior to the trigone and to
the ureter draining the lower pole moiety (Weigert-Meyer
rule). The ureter from the lower pole moiety is orthotopic
and inserts into the trigone. It lies lateral and superior to
the ureter draining the upper pole moiety and often has a
perpendicular course (rather than the normal oblique
course), predisposing it to reflux.
Complete duplication anomalies are more common in
girls than in boys. If the diagnosis is not made in utero,
patients often present later in life with signs of urinary
tract infection. Girls also present with incontinence if the
ureter inserts below the external sphincter, and boys can
present with prostatitis or epididymitis.
The termination of the ureter from the upper pole can
end as an ectopic ureter or ectopic ureterocele. The ectopic
ureter either inserts extravesically or intravesically below
the trigone. In girls, ectopic ureters insert into the
vestibule, vagina, or urethra, and, less commonly, into the
uterus, cervix, or rectum. In boys, the ectopic ureteral
opening may enter the bladder neck, the trigone inferome-
dial to the normal location, the posterior urethra, the gen-
ital structures (i.e., ejaculatory ducts, seminal vesicles, vas
deferens), or the rectum. The ureterocele terminates intra-
vesically.
The sonographic features of an obstructed duplicated
system include a variable degree of dilatation of the upper
pole collecting system, cortical thinning, and a dilated
ureter that is continuous with the upper pole renal pelvis
(Figs. 11.25 and 11.26). Occasionally, the upper pole moi-
ety will appear highly echogenic with small cysts due to
dysplasia or it may be hypoplastic, rather than dilated, and

A B

C D
Ureteral duplication with ureterocele. A: Longitudinal sonogram of the left kidney demonstrates dilated upper pole (UP) and lower pole
Fig. 11.25
(LP) moieties. B: Longitudinal sonogram through the lower abdomen shows a dilated distal left ureter (U) from the upper pole moiety.
C: Longitudinal sonogram through the pelvis shows a cyst with an echogenic wall, representing the ureterocele (Uret) entering the base of the blad-
der (BL). D: Voiding cystourethrogram demonstrates the ureterocele (arrowheads) at the bladder base.
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400 P E D I AT R I C S O N O G R A P H Y

A B

Ureteral duplication with an ectopic ureter. A: Longitudi-

Fig. 11.26
nal view of the right kidney shows dilatation of the upper
pole (UP) collecting systems. B: Longitudinal sonogram through the
pelvis shows the dilated distal right ureter (U) from the upper pole moi-
ety extending below the bladder (BL) base. The dilated refluxing ureter
(arrow) from the lower renal pole inserts into the trigone. C: Voiding
cystourethrogram demonstrates ectopic insertion of the right ureter
C (U) into the prostatic urethra (arrow).

have a diminutive ureter (42). The lower pole moiety may
be normal or dilated secondary to reflux. Ureteropelvic
junction obstruction has been described in the lower pole
of a duplicated collecting system (43).
The ectopic ureter appears as a dilated ureter that
ends intravesically below the trigone or extravesically
(Fig. 11.26). The ectopic ureterocele appears as a round,
thin-walled, anechoic mass in the bladder (Fig. 11.25C).
Occasionally, the ureterocele will evert or intussuscept
into or adjacent to its own ureter, mimicking a bladder
diverticulum. Most ureteroceles are located at the blad-
der base, but large ureteroceles can fill the bladder,
obstructing the ureter on the contralateral side or the
bladder neck.
Ectopic ureteroceles are treated by endoscopic incision
and unroofing. Heminephrectomy may be performed in
patients with severe upper pole hydronephrosis and poor
renal function. In patients with mild hydronephrosis, the
ureter from the upper pole moiety is reimplanted into the
ureter from the lower pole moiety. Following unroofing,
the ureterocele collapses and can appear as an echogenic
mass at the bladder base (Fig. 11.27).
Simple Ureterocele
The simple ureterocele is the result of obstruction of a nor-
mally positioned ureteral orifice. This leads to ballooning of
the segment of ureter immediately proximal to the obstruc-
tion. The cause of the ureteral narrowing can be a congen-
ital stenosis or an inflammatory stricture. Simple or ortho-
topic ureteroceles are associated with single collecting
systems. In adults, simple ureteroceles are usually asympto-
matic and found incidentally on examinations performed
for other clinical indications. In children, they are more
often associated with obstruction and occasionally with
renal dysplasia (44). Symptoms are those of urinary
infection.
Sonography shows a round, cyst-like structure within
the trigone (Fig. 11.28). The ureterocele may partially col-
lapse during peristalsis. Associated findings include
hydronephrosis and hydroureter.
Posterior Urethral Valves
Posterior urethral valves are the most common cause of ure-
thral obstruction in boys, occurring in 1 in 8000 to 25,000
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Chapter 11 U R I N A R Y T R A C T 401

A B
Postoperative ureterocele. A: Preoperative transverse sonogram shows a large ureterocele (Uret) at the bladder (BL) base. B: Sono-
Fig. 11.27
gram following unroofing of the ureterocele shows an echogenic mass (arrows), representing the collapsed ureter. BL  bladder.

live male births (45). Three types of valves have been
described, although the existence of type 2 and type 3 valves
is controversial. The type 1 valves, the most common, are
folds that attach below the verumontanum, usually at
the level of the membranous urethra. The type 2 valves
are mucosal folds that arise above the verumontanum. The
type 3 valve is a diaphragm with a central aperture that
arises distal to the verumontanum. Posterior urethral valves
increase resistance to urine outflow, leading to proximal ure-
thral dilatation and hypertrophy of the muscles in the blad-
der wall and neck. The prostatic utricle, prostatic ducts, and
ejaculatory ducts dilate when there is severe obstruction.
Clinical findings in neonates include large palpable kid-
neys and pulmonary hypoplasia secondary to maternal
oligohydramnios. Clinical findings in infants and children
include growth retardation, failure to thrive, urinary tract
infection, and voiding abnormalities, such as urinary fre-
quency, a poor stream, and incontinence.
Characteristic sonographic findings include bilateral
hydronephrosis and hydroureter; parenchymal thinning; a
dilated, thick-walled urinary bladder; and a dilated prosta-
tic urethra (Fig. 11.29) (46). The dilated posterior urethra
and occasionally the valve itself can be demonstrated with
transabdominal scanning, using the distended urinary blad-
der as an acoustic window, or with transperineal imaging
(4649). Even with the perineal approach, the urethra may
be difficult to visualize if it is not distended with urine. The
valve appears as an area of linear echogenicity within the
dilated posterior urethra.
Other findings include renal dysplasia, urinary ascites,
and subcapsular or perirenal urinomas. Renal dysplasia is
the result of high-pressure in utero reflux. The sonographic

A B
Simple ureterocele. A: Longitudinal sonogram of the right kidney demonstrates mild dilatation of the calyces and renal pelvis (RP) in a
Fig. 11.28
nonduplicated collecting system. B: Longitudinal scan of the bladder (BL) shows the echogenic wall of the ureterocele (open arrows)
at the level of the trigone.
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402 P E D I AT R I C S O N O G R A P H Y
A B
C D
E
features of renal dysplasia are increased cortical echogenic-
ity and cortical cysts (Fig. 11.30). The presence of dyspla-
sia implies an unfavorable prognosis.
Urinary ascites and urinoma formation result when
there is calyceal rupture (Fig. 11.31). The distal obstruc-
Posterior urethral valves in a neonate. A, B: Longitudi-
Fig. 11.29
nal views of the right and left kidneys, respectively,
show bilaterally dilated calyces and renal pelves (RP). C: Longitudi-
nal sonogram through the lower pelvis demonstrates a thickened
bladder wall (arrows). Thickness  8 mm (normal thickness  3 mm).
D: Longitudinal sonogram below the bladder shows the narrowed
bladder neck (arrow) and dilated prostatic urethra (PU). E: Voiding
cystourethrogram shows a narrow bladder neck and dilated prosta-
tic urethra (PU). Arrow indicates the site of valves.
tion of the urinary tract causes the fornix of a calyx to rup-
ture, which allows urine to enter the subcapsular or perire-
nal space. The urine may remain in these spaces, produc-
ing a urinoma, or it may escape into the retroperitoneum
and peritoneal cavity, due either to a tear in the renal
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Chapter 11 U R I N A R Y T R A C T 403

A B
Posterior urethral valves, associated dysplasia. A: Longitudinal scan of the right kidney shows pelvicaliceal dilatation and diffusely
Fig. 11.30
echogenic parenchyma (arrows) secondary to dysplasia. B: Longitudinal sonogram in another patient shows dilated renal pelvis and
upper pole calyces (C) and diffusely echogenic cortex with small cysts (arrows).

capsule or to transudation. The perforation serves as a
method to decompress the collecting system; thus,
hydronephrosis may be minimal or barely apparent sono-
graphically. Treatment of posterior valves is early cysto-
tomy followed by later valve resection.
Prune Belly Syndrome
The prune belly or Eagle-Barrett syndrome is characterized
by the triad of hypoplastic or absent abdominal wall muscu-
lature, urinary tract anomalies, and cryptorchidism. It is usu-
ally diagnosed in the neonatal period and occurs almost
exclusively in male infants. Pathologic findings include a
decreased number of functioning nephrons, parenchymal
dysplasia, and absence of smooth muscle in the ureters and
bladder. The cause is unknown, but a number of theories
have been suggested, including high-grade urethral obstruc-
tion, a primary defect in the mesoblast, and a complex chro-
mosomal mutation.
Patients with the prune belly syndrome have been arbi-
trarily divided into three groups. Group 1 is the most
severe. Affected patients have urethral valves or atresia,
marked hydroureteronephrosis, and bilateral cystic renal
dysplasia, which results in death shortly after birth. Group
2 and 3 patients have less severe urinary tract involvement
and no obstructing urethral lesions. In group 2 patients, the
ureters and renal pelvis are moderately to markedly dilated;
the calyces are dysmorphic and often minimally dilated.
Group 3 patients have mild involvement with features
ranging between those of group 2 and those of a normal
urinary tract. Infants in groups 2 and 3 survive the neona-
tal period, but they have recurrent urinary tract infections
or failure to thrive. Other anomalies associated with the
prune belly syndrome include intestinal malrotation or
atresia, imperforate anus, Hirschsprung disease, congenital
heart disease, clubfeet, and congenital hip dislocation.
Sonographic findings include varying degrees of
hydronephrosis, dilated tortuous ureters, a large urinary
bladder, a urachal diverticulum, a dilated posterior and/or
anterior urethra (megalourethra), and a dilated prostatic
utricle (Fig. 11.32). The renal parenchyma may be echogenic

A B
Posterior urethral valves with ascites and subcapsular urinoma. A: Longitudinal image of the right kidney (arrows) shows mild dilata-
Fig. 11.31
tion of the renal pelvis (P), subcapsular fluid collection (F), and ascites (open arrows). B: Longitudinal sonogram of the left kidney in a
second patient shows dilatation of the calyces (C), renal pelvis (RP), and proximal ureter (U) with a subcapsular urinoma (arrow) and echogenic
parenchyma indicating dysplasia.
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404 P E D I AT R I C S O N O G R A P H Y

A B

C D

Prune belly syndrome. A, B: Longitudinal sonograms of

Fig. 11.32
the right kidney and left kidney, respectively, reveal
dilated renal pelves (RP) and calyces (C). C: Longitudinal sonogram of
the pelvis shows a dilated distal ureter (U) posterior to the bladder
(BL). D: A dilated urethra (arrows) can be noted on a more caudad
scan. Note that the bladder (BL) is thin walled, in contrast to the thick-
walled bladder seen with posterior urethral valves. E: Voiding cys-
tourethrogram shows a smooth-walled dilated bladder (BL), dilated
E ureters (arrows), and dilated left renal pelvis (RP).
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A B
Ureteral calculus. A: Longitudinal view of the right kidney shows mild dilatation of the renal collecting system and an echogenic cal-
Fig. 11.33
culus (arrow) with acoustic shadowing (open arrows). B: Longitudinal view through the distal right ureter shows a ureteral calculus
(straight arrow) with distal acoustic shadowing (open arrow). The ureter (U) proximal to the stone is dilated.
and contain small cysts due to associated dysplasia. Of note,
the bladder wall is thin (3 mm) in contrast to the thick-
walled bladder in patients with posterior valves.
Retrocaval Ureter
Retrocaval ureter is a rare congenital anomaly. Normally,
the infrarenal vena cava arises from the supracardinal vein.
If the infrarenal segment of the cava arises from either the
postcardinal or right subcardinal vein, the ureter will cross
posterior to the inferior vena cava and then re-emerge lat-
erally before entering the bladder in a normal location.
This abnormality may be clinically silent or produce symp-
toms related to obstruction caused by constriction of the
retrocaval segment of the ureter by the inferior vena cava.
Sonography shows pelvocaliectasis and a dilated proximal
right ureter to the level where the ureter turns medially to
pass behind the inferior vena cava.
ACQUIRED RENAL OBSTRUCTION
Acquired obstruction can be intraluminal or extraluminal.
The causes of intrinsic obstruction include stones, blood
clot, and benign polyps. Gray-scale images show a dilated
ureter and an echogenic intraluminal mass with varying
amounts of distal acoustic shadowing (Fig. 11.33). Color
Doppler imaging in high-grade obstruction shows either
absence of a ureteral jet or diminished flow velocity on the
abnormal side. The ureteral jets disappear immediately in
the setting of acute obstruction and reappear immediately
when the obstruction is relieved. In low-grade obstruction,
ureteral flow may be normal or diminished (50).
The causes of extrinsic ureteral obstruction include
inflammatory lesions, such as abscess or phlegmon most
commonly secondary to appendicitis or Crohn disease;
retroperitoneal tumors; and neurogenic bladder.
Chapter 11 U R I N A R Y T R A C T 405
RENAL CYSTIC DISEASE
Cystic diseases of the kidney can be inherited or sporadic,
unilateral or bilateral, and symptomatic at birth or
detected later in life (51). This section will approach the
differential diagnosis from the standpoint of unilateral and
bilateral disease.
Bilateral Cystic Disease
AUTOSOMAL RECESSIVE POLYCYSTIC DISEASE
Autosomal recessive polycystic disease, previously known
as infantile polycystic kidney disease, as the name implies,
is inherited as a recessive characteristic. Pathologically,
numerous small cysts, 1 to 2 mm in diameter, are seen in
the medulla. Microdissection studies have shown that
these cysts are predominantly dilated collecting tubules,
which are radially arranged, extending from the medulla
to the subcapsular cortex. The nephrons are normal or
minimally altered (20). Virtually all patients with autoso-
mal recessive cystic disease have hepatic abnormalities,
characterized by ductal plate lesions, especially biliary duc-
tal ectasia and periportal fibrosis.
Autosomal recessive polycystic disease is a spectrum of
abnormality, with the renal disease and hepatic fibrosis
varying inversely (52). Neonates tend to have more severe
renal disease and milder hepatic disease. Patients who sur-
vive the neonatal period and come to clinical attention
later in life have milder renal disease and more severe
hepatic disease (usually cirrhosis and portal hypertension).
The sonographic findings of autosomal recessive poly-
cystic disease in the neonate are bilateral renal enlargement,
diffusely increased parenchymal echogenicity, poor corti-
comedullary differentiation, and dilated bile ducts (Figs.
11.34 to 11.36) (53,54). Occasionally, there is a thin rim of
hypoechoic parenchyma at the periphery of the kidney. The
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A B
Neonatal autosomal recessive polycystic disease. Longitudinal (A) and transverse (B) sonograms of the right kidney (RK) show renal
Fig. 11.34
enlargement, diffusely increased parenchymal echogenicity and loss of corticomedullary differentiation.

A B
Neonatal autosomal recessive polycystic disease. A, B: Longitudinal sonograms through both flanks show enlarged echogenic kid-
Fig. 11.35
neys with absent corticomedullary differentiation, dilated tubules extending from the medulla to the cortex, and a small medullary cyst
(C). RP  dilated renal pelvis.

Neonatal autosomal recessive polycystic disease and

Fig. 11.36
hepatic fibrosis. Transverse sonogram shows dilated
intrahepatic ducts and echogenic hepatic parenchyma.
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A B
C small medullary cysts (C).
increased parenchymal echogenicity is produced by the
innumerable fluidtubular wall interfaces, while the hypoe-
choic rim has been attributed to a remnant of compressed
normal renal cortex. Discrete macrocysts representing
markedly dilated tubules are occasionally seen in the
medullary region (Fig. 11.35). Rarely, unilateral renal
enlargement is noted (55).
In older children, the sonographic findings include nor-
mal-size or mildly enlarged kidneys, hyperechoic pyra-
mids, small medullary cysts, and loss of corticomedullary
differentiation (Fig. 11.37) (5658). Findings in the liver
include dilated bile ducts and increased hepatic parenchy-
mal echogenicity, nodular hepatic margins, splenomegaly,
and esophageal varices, consistent with cirrhosis and por-
tal hypertension (Fig. 11.38).
AUTOSOMAL DOMINANT POLYCYSTIC DISEASE
Autosomal dominant polycystic disease, previously
known as adult polycystic renal disease, is a hereditary
disorder resulting from an abnormality on the short arm
Chapter 11 U R I N A R Y T R A C T 407
Autosomal recessive polycystic disease. A: Longitudi-
Fig. 11.37
nal sonogram in a 7-year-old girl shows a normal-size
right kidney (arrows) with loss of corticomedullary differentiation. B:
Longitudinal sonogram of the right kidney in another young child
demonstrates hyperechoic medullary pyramids (arrows). C: Sono-
gram of the right kidney (arrows) in a third patient shows multiple
of chromosome 16 or on the long arm of chromosome 4
(52,59). Patients with an abnormality on chromosome 16
account for approximately 90% of cases. Autosomal
dominant disease has 100% penetrance but variable
expression. Up to 50% of cases are due to spontaneous
mutations.
Pathologically, cysts of varying size are present in the
cortex and medulla, with islands of normal tissue inter-
spersed between the cystic areas. Microdissection studies
show that the cysts communicate with the nephrons as
well as with the collecting tubules (20). Cysts can also
develop in the liver, pancreas, lungs, spleen, ovaries,
testes, and seminal vesicles (52). Clinical findings include
palpable abdominal masses in neonates, and hyperten-
sion, flank pain, and hematuria in children and adoles-
cents.
In the neonate, sonography demonstrates enlarged,
diffusely echogenic kidneys with multiple small cysts
(Fig. 11.39) (60). The sonographic findings are similar to
those of autosomal recessive polycystic disease, and the
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408 P E D I AT R I C S O N O G R A P H Y

Autosomal recessive polycystic disease with liver dis-

Fig. 11.38
ease. Transverse sonogram in an adolescent shows
dilated intrahepatic ducts (D) and nodular liver margins (arrows) con-
sistent with cirrhosis.

diagnosis needs to be based on family history or renal GLOMERULOCYSTIC DISEASE

biopsy.
In older children and adolescents, the more classic
changes develop. The kidneys may be normal size or
enlarged and contain multiple bilateral cortical cysts,
causing calyceal distortion (Fig. 11.40) (60). Hemorrhage
into the renal cysts can result in low-level internal echoes,
fluid-blood levels, septations, and thick walls. Calcifica-
tion of the cyst walls may be seen later in life. Cysts can
also be seen in other organs, particularly the liver.
Sonography is used to screen children in affected
families to determine whether they have the disease. Cri-
teria for diagnosing the disease include the presence of at
least two cysts in one kidney or one cyst in each kidney
(61).
Glomerulocystic disease is a rare cystic renal disorder. It
usually occurs as an isolated renal disease (52), but it also
may occur in association with other malformations, such
as Zellweger syndrome, trisomy 13, oral-facial-digital syn-
drome, and renal-retinal dysplasia. Histologic examination
shows cystic dilatation of Bowman spaces with a variable
degree of dilatation of the proximal collecting tubules (60).
The medulla is normal. Periportal hepatic fibrosis, bile
duct hyperplasia and dilatation, and hepatic cysts are seen
in a minority of patients. Affected patients typically pres-
ent in the neonatal period with large palpable kidneys and
renal failure.
Sonographic findings are similar to those of autosomal
recessive and dominant polycystic disease in the neonate

A B
Autosomal dominant cystic disease in a newborn. Longitudinal (A) and transverse (B) scans of the right flank show an enlarged,
Fig. 11.39
echogenic kidney with multiple small cysts. The left kidney had a similar appearance.
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Chapter 11 U R I N A R Y T R A C T 409

A B
Autosomal dominant polycystic disease, older child. A: Longitudinal sonogram of the right kidney shows multiple cortical cysts of vary-
Fig. 11.40
ing size. B: Sonogram in another child shows multiple cysts. One cyst (C) contains internal echoes due to hemorrhage.

and include enlarged hyperechoic kidneys, poor corti-
comedullary differentiation, and small cortical cysts, usually
1 cm or less in diameter (51,62). The cysts are predomi-
nantly subcapsular or in the peripheral cortex, although the
entire cortex may be involved (Fig. 11.41). Other abnor-
malities include hepatic adenomas and cysts (62).
CYSTIC DISEASE OF THE RENAL MEDULLA
Medullary cystic diseases include medullary sponge kidney,
juvenile nephronophthisis, and uremic medullary cystic dis-
ease. Medullary sponge kidney, also known as medullary
tubular ectasia, is a sporadic rather than an inherited disor-
der. Pathologically, there is cystic dilatation of the collecting
tubules in the area of the renal pyramids. The condition is
asymptomatic, unless complications, such as infection or
urolithiasis, occur. Symptomatic patients present with renal
colic, flank pain, or hematuria. Uncomplicated tubular ecta-
sia is difficult to recognize sonographically. When nephro-
calcinosis occurs, sonography shows hyperechoic pyramids;
acoustic shadowing may or may not be seen (Fig. 11.42).
Juvenile nephronophthisis and uremic medullary cystic
disease are hereditary diseases characterized by polyuria,
polydipsia, salt wasting, severe anemia, and ultimately
renal failure (51). Pathologically, the kidneys are small or
normal sized and a variable number of small cysts are pres-
ent in the medulla and at the corticomedullary junction.
Juvenile nephronophthisis is inherited as an autosomal
recessive trait and becomes symptomatic in childhood or
adolescence. Medullary cystic disease is inherited as an
autosomal dominant trait and usually becomes sympto-
matic after the second decade. Sonography shows small
kidneys, loss of corticomedullary differentiation, increased
cortical and/or medullary echogenicity, and medullary or
corticomedullary cysts (Fig. 11.43).

A B
Glomerulocystic disease. A, B: Sagittal sonograms of the right and left kidneys, respectively, in a neonate show enlarged, echogenic
Fig. 11.41
kidneys containing multiple cysts.
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410 P E D I AT R I C S O N O G R A P H Y
Medullary sponge kidney. Longitudinal sonogram of the
Fig. 11.42
right kidney shows hyperechoic renal pyramids (arrow-
heads), due to multiple small calculi.
RENAL CYSTS ASSOCIATED WITH MULTISYSTEM DISORDERS
Tuberous sclerosis is an inherited autosomal dominant
condition resulting from a defect on chromosome 9. Clas-
sic clinical features are seizures, mental retardation, and
adenoma sebaceum (63). Other abnormalities include
cardiac lesions (rhabdomyomas), pulmonary lesions
(lymphangiomyomatosis and parenchymal cysts), central
nervous system lesions (periventricular subependymal
glial nodules, giant cell astrocytomas, and retinal and
cortical hamartomas), and renal lesions. Renal cysts are
common in infants and young children, while angiomy-
olipomas are a more frequent manifestation in adoles-
cents and adults. In the pediatric population, both types
of lesions are usually small, multiple, and bilateral (Fig.
11.44). Renal cysts are hypoechoic or anechoic and
angiomyolipomas are hyperechoic to surrounding
parenchyma.
Medullary cystic disease. Longitudinal sonogram in a
Fig. 11.43
child shows a small right kidney (cursors) with thinned
cortex and increased corticomedullary echodensities (arrowheads)
arising from numerous tiny cysts.
Tuberous sclerosis. Longitudinal sonogram of the right
Fig. 11.44
kidney shows multiple cortical cysts (arrows).
Von Hippel-Lindau disease is an inherited autosomal
dominant trait due to an error on the short arm of chro-
mosome 3. Clinically, it is associated with retinal and cen-
tral nervous system hemangioblastomas, pancreatic cysts
and islet cell tumors, and pheochromocytoma. There is an
increased incidence of renal cell carcinomas. The renal cysts
range in size from 0.5 to 3.0 cm and occur in approxi-
mately 60% of patients with von Hippel-Lindau disease.
Renal cysts are also associated with a variety of
other syndromes, including Turner syndrome (Fig. 11.45),
Meckel syndrome (microcephaly, polydactyly, posterior
encephalocele), Jeune asphyxiating thoracic dystrophy
(small chest, respiratory failure, renal dysplasia),
oral-facial-digital syndrome, and Zellweger syndrome
(cerebrohepatorenal syndrome). Their sonographic charac-
teristics are identical to those of simple cysts. Correlation
with clinical findings usually permits the correct diagnosis.
Turner syndrome. Longitudinal sonogram of the right kid-
Fig. 11.45
ney shows an anechoic cyst (arrow) in the lower pole of
the right kidney.
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Acquired renal cystic disease. Longitudinal sonogram in
Fig. 11.46
an adolescent patient on chronic dialysis demonstrates
a small kidney (cursors) with multiple parenchymal cysts.
ACQUIRED RENAL CYSTIC DISEASE
Acquired cystic disease of the kidney is usually seen in
patients with chronic renal failure who are on hemodialy-
sis. The incidence increases with the years on dialysis, and
is approximately 10% to 20% after 3 years of dialysis,
increasing to 90% after 5 to 10 years. The cause is believed
to be hyperplasia of the tubular epithelium with resulting
nephron dilatation. Pathologic examination shows multi-
ple small cysts in both the cortex and medulla.
Sonography shows small echogenic kidneys containing
multiple cortical-based cysts (Fig. 11.46). Complications
include hemorrhage into the cysts, the subcapsular space,
or the perinephric space and the development of renal cell
carcinoma. Hemorrhagic cysts and renal cell cancer appear
as solid echogenic masses. Color Doppler can be helpful in
separating these two lesions. The presence of internal vas-
cularity suggests neoplasm, while absence of color flow is
more consistent with a hemorrhagic cyst. Calcifications
also can occur in the cyst walls or in the renal interstitium.
The cysts in acquired cystic disease are isolated to the kid-
neys. Other organs are not involved by this condition.
Unilateral Cystic Disease
SIMPLE RENAL CYSTS
Simple cysts are rare in children, with an incidence of less
than 1% (64). Pathologically, they are unilocular, lined by
a single layer of flattened epithelium, and contain clear
serous fluid. Simple cysts arise in the renal cortex, do not
communicate with the collecting system, and are more
often solitary than multiple. They are usually asympto-
matic and detected during imaging examinations per-
formed for other indications. However, very large cysts can
present as palpable abdominal masses. Simple renal cysts
have also been reported as a manifestation of acquired
immunodeficiency syndrome (65).
The classic sonographic findings of a simple cyst
include a round or oval shape, thin or imperceptible walls,
Chapter 11 U R I N A R Y T R A C T 411
Simple renal cyst. Longitudinal sonogram shows an an-
Fig. 11.47
echoic cyst (C) arising from the upper pole of the right
kidney (RK).
smooth margins, anechoic contents, and posterior acoustic
enhancement (Fig. 11.47) (64). If these sonographic find-
ings are present, no additional evaluation is required.
Occasionally, simple cysts are complicated by hemor-
rhage, infection, or calcification. In these instances, sonog-
raphy shows a complex mass with thick walls, internal
echoes or septations, and distal acoustic shadowing. In this
scenario, cyst puncture and percutaneous aspiration under
ultrasound guidance may be both diagnostic and thera-
peutic.
Lesions that can mimic a simple cyst on gray-scale
imaging include aneurysm, pseudoaneurysm, lymphoma,
and upper pole duplication. Color Doppler imaging can
confirm the vascular nature of the first two lesions. Lym-
phoma can appear anechoic but it usually lacks posterior
acoustic enhancement. The upper pole duplication can be
recognized by the associated findings of a dilated ureter
and distal ureteral ectopia or ureterocele.
MULTICYSTIC DYSPLASTIC KIDNEY
Multicystic dysplastic kidney is a nonhereditary develop-
mental anomaly that is believed to be the consequence of
early in utero urinary tract obstruction (66). When this
occurs in the first 10 weeks of gestation, atresia of the
renal pelvis and the proximal ureter occurs, producing the
classic multicystic dysplastic kidney. The more unusual
hydronephrotic form of multicystic dysplastic kidney
results if the obstruction occurs after the 10th week of ges-
tation. Ureteral atresia occurs, but the renal pelvis and
calyces are not atretic. Histologic examination of both
forms shows noncommunicating cysts of various sizes,
separated by fibrous tissue containing primitive dysplastic
elements. The cysts are believed to represent greatly dilated
collecting ducts. Contralateral renal abnormalities are
common and include vesicoureteral reflux, ureteropelvic
junction obstruction, primary megaureter, and obstructed
duplex systems (67,68). Most cases are diagnosed on pre-
natal sonography.
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412 P E D I AT R I C S O N O G R A P H Y

A B
Multicystic dysplastic kidney. Longitudinal (A) and transverse (B) sonograms in a neonate reveal multiple oval and round cysts of vary-
Fig. 11.48
ing size with a random distribution in the right renal fossa. There is no central renal pelvis or normal renal parenchyma noted.

The sonographic features of the classic multicystic dys-
plastic kidney are multiple cysts of varying size with a ran-
dom distribution, absence of communication between the
cysts, no discernible renal pelvis or sinus, and absent or
dysplastic renal parenchyma (Figs. 11.48 and 11.49).
Occasionally, multicystic dysplastic kidney may appear as
a solitary cystic mass in the renal fossa. Calcifications may
be noted in the cyst walls or in the septations between
cysts. The contralateral kidney usually shows compensa-
tory hypertrophy. Doppler waveforms are either absent or
show low-velocity systolic peaks with absent diastolic flow
(69). The hydronephrotic form of multicystic dysplastic
kidney appears as a mass with multiple small peripheral
cysts and a larger central cyst (70).
Multicystic dysplasia usually involves the entire kid-
ney. In rare cases, it may be confined to one segment of
the kidney. Most cases of segmental dysplasia occur in
crossed fused ectopic kidneys (see Fig. 11.15) or in the
upper pole moiety of a duplicated collecting system (71).
The sonographic appearance is that of a multiloculated
cystic mass.
Multicystic dysplastic kidney is treated nonoperatively,
because the natural history is spontaneous decrease in size
during the first year of life, presumably related to the grad-
ual resorption of the residual urine in the cysts (72).
Surgery is performed if there is respiratory distress because
of thoracic compression by the large cystic kidney or if
complications of infection, hypertension, or pain related to
compression of adjacent organs develop.
MULTILOCULAR CYSTIC RENAL TUMOR
Multilocular cystic renal tumor, previously called multiloc-
ular cystic nephroma, benign cystic nephroma, cystic
hamartoma, cystic Wilms tumor, cystic lymphangioma,

A B
Multicystic dysplastic kidney. Longitudinal sonogram through the right renal fossa shows a large cyst and multiple smaller cysts,
Fig. 11.49
which do not communicate with each other. B: Follow-up sonogram 3 months later shows bowel loops (arrows) filling the empty
renal fossa.
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A B
Multilocular cystic renal tumor. A: Transverse sonogram of the left kidney shows a complex mass (arrows) containing anechoic locules
Fig. 11.50
separated by echogenic septae. B: Computed tomography confirms a water attenuation mass with thin septations and a small amount
of enhancing parenchyma posteriorly.
and partially polycystic kidney, is a nonhereditary cystic
mass. The lesion has a biphasic age and sex distribution,
affecting boys under 4 years of age and women over 40
years of age. Presenting signs are a nonpainful abdominal
mass or hematuria, which results from herniation of a por-
tion of the tumor into the renal pelvis. On pathologic
examination, the tumor is an encapsulated mass contain-
ing multiple noncommunicating epithelial-lined cysts sepa-
rated by fibrous septa. The cysts contain clear fluid. Hem-
orrhage and necrosis are uncommon. Histologically, there
are two distinct types: (a) cystic nephroma, characterized
by mature septal elements, and (b) cystic partially differ-
entiated nephroblastoma, which contains immature septal
elements (i.e., blastemal cells) or, rarely, foci of Wilms
tumor (7376).
The sonographic findings of multilocular cystic
nephroma are a well-circumscribed mass with multiple,
fluid-filled cysts separated by echogenic septations (Fig.
11.50) (73,74,76,77). The echogenicity of the locules may
increase if the contents are hemorrhagic or mucoid. When
the cysts are small or contain mucoid material, the multi-
locular nature may not be apparent and the tumor can
appear echogenic, mimicking other solid renal tumors.
Curvilinear calcifications may be seen within the wall or
the septa. Multilocular cystic nephromas are treated by
nephrectomy or heminephrectomy.
MALIGNANT RENAL NEOPLASMS
Because of its high sensitivity and ease of performance,
ultrasonography remains the imaging study of choice for
initial evaluation of suspected or known renal masses. If
the sonogram shows a benign condition such as a
hydronephrotic kidney or renal cystic disease, serial sonog-
raphy can be performed to assess stability of the lesion or
Chapter 11 U R I N A R Y T R A C T 413
renal scintigraphy can be performed to evaluate function.
If the mass is solid and a malignant neoplasm is suspected,
computed tomography (CT) or magnetic resonance imag-
ing (MRI) should be performed to better delineate the
extent of the disease.
Wilms Tumor
Wilms tumor (nephroblastoma) is the most common renal
malignancy in children, accounting for approximately
90% of all pediatric renal malignancies. Affected children
usually present before 5 years of age (mean age, 3 years)
(76,7880). Rarely, Wilms tumor is encountered prenatally
or in the neonatal period (81). The common clinical find-
ing is a palpable abdominal mass. Other findings include
abdominal pain, fever, microscopic or gross hematuria,
and hypertension. Hypertension has been attributed either
to production of renin by the tumor or to renal ischemia
due to compression of hilar vessels. Occasionally, patients
present with the Budd-Chiari syndrome secondary to
hepatic vein invasion by tumor, pulmonary emboli (82), or
varicocele, which occurs when the tumor obstructs the
gonadal vein (83).
Syndromes with increased incidence of Wilms tumor
include Beckwith-Wiedemann syndrome, congenital hemihy-
pertrophy, WAGR syndrome (Wilms tumor, sporadic
aniridia, genital malformations, and retardation), Drash syn-
drome (male pseudohermaphroditism and nephritis), and
Perlman syndrome (fetal overgrowth, neonatal macrosomia,
macrocephaly, dysmorphic facial features, visceromegaly,
nephroblastomatosis) (80,8486). Most Wilms tumors arise
in otherwise normal kidneys. However, this malignancy can
arise in an abnormal kidney, such as a horseshoe kidney or
multicystic kidney (87,88), and in extrarenal sites, such as
the inguinal canal, sacrococcygeal region, genital structures,
retroperitoneum, and chest wall (83,89).
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414 P E D I AT R I C S O N O G R A P H Y
Table 11.1 National Wilms Tumor Study Group Staging System
I. Tumor limited to kidney and completely excised
II. Tumor extends beyond the kidney but is completely removed
III. Residual nonhematogenous tumor confined to abdomen, including:
A. Lymph nodes in the hilus, the periaortic chains, or beyond
B. Implants on the peritoneal surfaces
C. Tumor beyond the surgical margins either microscopically or
grossly
IV. Hematogenous metastases to lung, liver, bone, and brain
V. Bilateral renal involvement at diagnosis
PATHOLOGY
On gross examination, Wilms tumor is a large mass (aver-
age 12 cm) that is sharply delineated by a pseudocapsule
composed of compressed renal tissue. It arises within the
cortex and grows in an exophytic fashion, with the bulk of
the tumor protruding from the kidney. It often contains
areas of hemorrhage or necrosis and, rarely, fat or calcifi-
cation (91).
Histologically, approximately 85% of Wilms tumors
have a favorable triphasic histology, containing primitive
blastemal, stromal, and epithelial elements (80,92). The
remaining 15% of tumors have unfavorable histology,
with anaplastic or sarcomatous elements. Patients with
unfavorable histology tumors have a much poorer progno-
sis than those with favorable histology and higher resis-
tance to chemotherapy.
Knowledge of the system for staging Wilms tumor is
important for understanding the many appearances of
this tumor and for patient planning treatment. Staging of
Wilms tumor is determined by surgical findings. The
anatomic staging of Wilms tumor is stage I, tumor limited
to the kidney and completely resected; stage II, tumor
extending beyond the kidney but completely resected;
stage III, residual tumor confined to the abdomen with-
out hematogenous spread; stage IV, hematogenous metas-
tases to lung, liver, bone, or brain; and stage V, bilateral
renal involvement at the time of diagnosis (Table 11.1)
(80).
SONOGRAPHIC FEATURES
Imaging Features of the Primary Tumor
The characteristic sonographic findings of Wilms tumor
are (a) a large echogenic mass with a homogeneous or a
heterogeneous echotexture related to areas of hemorrhage,
necrosis, fat, or calcification (Fig. 11.51); (b) a sharp
parenchymal interface; (c) a hypoechoic or hyperechoic
rim (pseudocapsule) representing compressed renal
parenchyma at the tumor interface; and (d) secondary
characteristics, such as renal vein or inferior vena caval
enlargement or invasion, enlarged lymph nodes, and
metastases (76,9396). In some instances, the bulk of the
tumor occupies the renal pelvis instead of the parenchyma
(9799). On rare occasions, Wilms tumor will extend
down the ureter and protrude into the bladder as a botry-
oid mass (100). The extrarenal Wilms tumors appears
as a solid echogenic mass. Color Doppler sonography
usually demonstrates increased flow in the compressed
parenchyma (pseudocapsule) and varying amounts of neo-
vascularity or arteriovenous shunting in the tumor itself
(Fig. 11.51C).
Local Tumor Spread
Wilms tumor may extend directly through the renal cap-
sule into perinephric tissues, adjacent organs, or lymph
nodes; invade the renal vein and inferior vena cava; or
metastasize to the lungs, liver, or distant lymph nodes.
Perinephric extension appears as a thickened renal cap-
sule or as nodular or streaky echogenicity in the per-
inephric space. Tumor extension into the perinephric
space can be difficult to visualize by sonography because
of the minute size of the perirenal infiltration. Since radi-
cal nephrectomy with en bloc resection of the kidney,
perirenal fat, and Gerota fascia is the surgical treatment
of choice, failure to visualize this extension does not
affect treatment.
Spread to regional lymph nodes occurs in about 20%
of cases. Detection of lymphadenopathy is important
because it can direct the surgeon to the area of abnormal
lymph nodes for surgical sampling. Lymph nodes are not
usually seen in the retroperitoneum of young children.
The demonstration of hilar, periaortic, paracaval, or other
retroperitoneal nodes, regardless of size, should be con-
sidered abnormal and suspicious for tumor metastases.
Occasionally, enlarged lymph nodes are due to reactive
hyperplasia and are a cause of false-positive interpreta-
tions.
Intrarenal venous invasion by tumor is difficult to
demonstrate by sonography, but main renal vein and infe-
rior vena caval involvement can be detected. Invasion of
the renal vein occurs in 5% to 10% of children with Wilms
tumor. Tumor thrombus also can extend from the inferior
vena cava into the right atrium. Vascular invasion does not
adversely affect prognosis if the thrombus can be resected,
but it can alter the surgical approach. Preoperative knowl-
edge of tumor extension above the hepatic veins is impor-
tant because removal may require cardiopulmonary bypass
to prevent tumor embolization to the lungs. Tumors that
are below the hepatic veins can be resected by an abdomi-
nal approach alone. The gray-scale diagnosis of venous
thrombosis is based on the demonstration of a focally
enlarged renal vein or inferior vena cava with an
echogenic, intraluminal mass (Fig. 11.52). Complete caval
occlusion may be accompanied by the development of
perivertebral collaterals. Color Doppler imaging shows
absence of flow in the occluded vessel. In some instances,
color Doppler scans may show internal vascularity within
the thrombus, confirming that the mass represents tumor
thrombus rather than bland thrombus.
Bilateral synchronous tumors occur in 5% to 10% of
patients, making evaluation of both kidneys mandatory.
Sonography can show a dominant mass in one kidney with
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A B

C D
Wilms tumor. Transverse (A) and longitudinal (B) sonograms of the right kidney show a large, homogeneous echogenic mass (M) aris-
Fig. 11.51
ing from the midpole and distorting dilated calyces (C). C: Color Doppler image shows flow in the rim of compressed normal
parenchyma (i.e., the pseudocapsule) with no flow in the tumor itself. D: Computed tomography reveals a soft tissue mass (M) in the upper pole of
the right kidney and dilated calyces (C).

A B
Wilms tumor with invasion of the inferior vena cava. A: Longitudinal sonogram of the inferior vena cava shows intraluminal tumor
Fig. 11.52
thrombus (arrows). RA  right atrium. B: Contrast-enhanced computed tomography scan shows a right Wilms tumor and thrombus
(arrow) in the inferior vena cava.
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416 P E D I AT R I C S O N O G R A P H Y
A B
C shows large bilateral Wilms tumors.
a smaller contralateral tumor or a large, dominant mass in
each kidney (Fig. 11.53).
Metastatic Disease
Metastases are to lungs, liver, or distant lymph nodes. The
liver is the most common intra-abdominal site of
hematogenous spread of Wilms tumor. Hepatic metastases
occur in up to 10% of patients at time of diagnosis. They
usually appear as hypoechoic masses. CT is the method of
choice to detect pulmonary metastases.
TREATMENT
Treatment of Wilms tumor is radical nephrectomy and
chemotherapy. Treatment of stage V (bilateral) disease is
usually preoperative chemotherapy with delayed resec-
tion after tumor shrinkage. Partial nephrectomy or
nephron-sparing surgery may be performed for small
lesions (101).
Bilateral Wilms tumors. Gray-scale sonogram of the
Fig. 11.53
right kidney (A) and color Doppler image of the left
kidney (B) shows large echogenic masses (arrows) replacing most
of the parenchyma. C: Contrast-enhanced computed tomography
FOLLOW-UP IMAGING
After therapy, sonography can be used to detect local recur-
rence and hepatic metastases. Patients with incomplete resec-
tion of tumor, lymph node involvement, and vascular inva-
sion have the highest risk for recurrence. The features that
suggest localized recurrence are a soft tissue mass in the
empty renal fossa, enlarged lymph nodes, and ipsilateral
psoas muscle enlargement. A peritoneal or pelvic mass can be
seen if tumor spillage occurred at surgery. Recurrence within
the kidneys can be associated with partial nephrectomy.
Imaging Surveillance of High-risk Patients
Screening for Wilms tumor in patients with associated syn-
dromes (Beckwith-Wiedemann syndrome, nonfamilial
aniridia, congenital hemihypertrophy, and Drash syn-
drome) should begin at 6 months of age with sonography
and followed by serial sonography every 3 to 4 months
until the patient is 8 years of age (85,86). Nephromegaly is
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Chapter 11 U R I N A R Y T R A C T 417

a strong risk factor for the development of Wilms tumor in
patients with Beckwith-Wiedemann syndrome (85). Chil-
dren who are screened for tumor nearly always have stage
I or II disease, while almost 50% of unscreened children
have stage III or IV disease (85).
Nephroblastomatosis
Nephroblastomatosis is an abnormality of nephrogenesis
characterized by persistence of fetal renal blastema or
nephrogenic rests beyond 36 weeks of gestation
(102104). Nephroblastomatosis is not a malignant tumor
per se, but it is a precursor to Wilms tumor. Foci of
nephroblastomatosis have been found in nearly all kidneys
with bilateral Wilms tumors and in approximately 25% of
children with unilateral Wilms tumor (76,78). Nephro-
blastomatosis has been found in Beckwith-Wiedemann
syndrome, hemihypertrophy, Perlman syndrome, chromo-
somal abnormalities in the 11p15 and 11p13 loci, sporadic
aniridia, and Drash syndrome.
Nephrogenic rests may be classified as intralobar, perilo-
bar, or mixed (20). Intralobar rests occur within a renal lob-
ule. They may be found in the superficial cortex, the pelvi-
caliceal wall, or the renal sinus. Perilobar rests occur at the
periphery of the renal lobule. They may be found in a sub-
capsular location, within the columns of Bertin, or along the
cortical surface lining the renal sinus (20). Perilobar rests are
more common than intralobar rests, but intralobar rests
have a higher association with Wilms tumor development.
Both forms of nephrogenic rests may be focal, multifocal,
or diffuse. Infants with diffuse nephroblastomatosis are usu-
ally under 2 years of age and commonly present with bilateral
nephromegaly or flank masses. Occasionally, tumor infiltra-
tion is unilateral. Focal and multifocal nephroblastomatosis
is generally asymptomatic and found during imaging evalua-
tion of Wilms tumor, at operation for Wilms tumor, or dur-
ing a screening examination in high-risk patients. It does not
necessarily produce significant nephromegaly.
The sonographic appearance is variable (103,105,106).
Diffuse disease typically presents as a peripheral rind of
hypoechoic tissue or multiple masses. The kidneys main-
tain their reniform shape, but they are enlarged. Corti-
comedullary differentiation is absent (Fig. 11.54). Focal

A B

Diffuse nephroblastomatosis. Transverse (A) and longitudinal

Fig. 11.54
(B) sonograms of the right kidney show nephromegaly
(arrows), hypoechoic subcapsular tumor compressing the medulla (arrow-
head), and loss of corticomedullary differentiation. C: Contrast-enhanced
computed tomography demonstrates renal enlargement with a large con-
fluent mass replacing the cortex and compressing the enhancing renal
C medulla (arrowhead).
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418 P E D I AT R I C S O N O G R A P H Y
C (arrow).
disease typically presents as hypoechoic masses (Fig.
11.55). Occasionally, the nephrogenic rests are isoechoic
or hyperechoic compared to normal renal parenchyma
(103,105107). Isoechoic lesions will be detected only if
they alter the renal contour or displace the collecting sys-
tem. A subcapsular location of the tumor is highly sugges-
tive of nephroblastomatosis.
Patients with nephroblastomatosis are usually treated
with chemotherapy (identical to that used to treat stage I
Wilms tumor). However, the management of nephrogenic
rests is controversial and arguments exist for and against
the use of chemotherapy.
Renal Cell Carcinoma
Renal cell carcinoma is rare in the first two decades of life,
accounting for 2% to 6% of all malignant renal tumors in
children (76,108). Mean patient age at presentation is
approximately 10 years. There is a 2:1 male predominance.
Clinical findings are nonspecific and include abdominal or
flank pain (50% to 60%), a palpable abdominal mass
(50% to 60%), and hematuria (30% to 60%). Hyperten-
sion, polycythemia, dysuria, and fever may also be present.
Focal nephroblastomatosis. Longitudinal (A) and trans-
Fig. 11.55
verse (B) sonograms in a 3-year-old girl with a right
Wilms tumor show an echogenic, contour-deforming, subcapsular
mass (arrows) in the upper pole of the left kidney. C: Contrast enhanced
computed tomography shows a low-attenuation soft tissue mass
Renal cell carcinoma is associated with von Hippel-Lindau
syndrome, tuberous sclerosis, urogenital malformations,
Beckwith-Wiedemann syndrome (109), and treated neu-
roblastoma. The mean time interval after treatment of neu-
roblastoma and development of renal cell carcinoma is
approximately 11 years (110,111).
Renal cell carcinoma arises from epithelial cells of the
renal tubule, with the clear cell subtype being most com-
mon. Pathologically, the tumor can be well circumscribed
by a pseudocapsule or unencapsulated and infiltrating.
Renal vein invasion is common. Metastases are to lung,
liver, and bone.
Sonography can show a hypoechoic, isoechoic, or
hyperechoic intrarenal mass (Fig. 11.56) (112,113). The
average diameter of the tumor at the time of diagnosis is
4 cm. The tumors may be homogeneous or heterogeneous
because of areas of necrosis, hemorrhage, and calcifica-
tion. Renal cell carcinoma can invade locally into the
retroperitoneum, invade the renal vein and inferior vena
cava, and metastasize to local or distant lymph nodes,
liver, or lung. Differentiation between renal cell carcinoma
and Wilms tumor is not possible on the basis of the
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Chapter 11 U R I N A R Y T R A C T 419

A B
Renal cell carcinoma. A: Longitudinal sonogram in a 9-year-old boy demonstrates an echogenic mass (cursors) in the left kidney.
Fig. 11.56
B: Computed tomography scan shows an enhancing soft tissue mass (M) causing hydronephrosis. C  dilated calyces.

sonographic findings, but the age of the patient is usually
helpful in suggesting the correct diagnosis. Treatment is
radical nephrectomy. Nephron-sparing partial nephrec-
tomy may be performed for small tumors.
Lymphoma
Renal involvement is a late manifestation of lymphoma
and is more common in non-Hodgkin lymphoma than
Hodgkin lymphoma (114,115). Affected patients are usu-
ally over 5 years of age. Since the kidneys do not contain
lymphatic tissue, renal involvement by lymphoma occurs
either as a result of hematogenous spread or direct exten-
sion of retroperitoneal tumor. Symptoms are rare and the
diagnosis is often made only at imaging or autopsy.
Four patterns of renal involvement by lymphoma can
be observed on imaging studies: multiple cortical masses
(60% to 70%) (Fig. 11.57), direct invasion from contigu-
ous lymph nodes (10% to 20%), solitary renal masses (5%
to 10%), and diffuse infiltration (5% to 10% of cases)
(Fig. 11.58) (116120). Additionally, perinephric involve-
ment (Fig. 11.57) with fascial thickening or compression
of the renal cortex can be noted. Hydronephrosis and
ureteral dilatation may be observed if the retroperitoneal
nodes compress the ureter.
Typically, lymphomatous masses are homogeneous and
hypoechoic or anechoic, but they can be isoechoic or
hyperechoic to normal parenchyma. Anechoic lesions can
simulate renal cysts, but in most instances, the absence of
distal acoustic enhancement should suggest that the mass
is solid rather than cystic. In rare cases, acoustic enhance-
ment can be seen despite the solid nature of the tumor. The
sonographic appearance of solitary renal lymphoma is

A B
Lymphoma. A: Longitudinal sonogram in a patient with non-Hodgkin lymphoma shows two anechoic mass (cursors) within the left kid-
Fig. 11.57
ney and a hypoechoic perinephric mass (arrows). Biopsy of both lesions confirmed lymphoma. B: Longitudinal sonogram in a
9-year-old boy shows a bilobed hypoechoic mass (M) within the right kidney. L  liver.
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420 P E D I AT R I C S O N O G R A P H Y

A B
Lymphoma. A: Longitudinal sonogram in a child with non-Hodgkin lymphoma shows an enlarged, echogenic right kidney (arrows).
Fig. 11.58
B: Contrast-enhanced computed tomography scan shows bilateral renal enlargement.

indistinguishable from that of other solid intrarenal
masses, but the diagnosis is possible when there is coexist-
ing splenomegaly or widespread lymph node enlargement.
Leukemia
Acute lymphoblastic leukemia is the most common malig-
nancy of childhood, usually occurring in children between
3 and 5 years of age. The kidneys can be involved by
leukemia during the active stages of disease or they may
serve as a sanctuary for disease during bone marrow remis-
sion. Renal infiltration by leukemia usually is clinically
occult, although it can result in abdominal pain, hema-
turia, hypertension, or renal failure.
Renal involvement can be diffuse or focal; the former
pattern is more common. The sonographic findings of dif-
fuse leukemic involvement include nephromegaly with
smooth renal contours; normal to decreased parenchymal
echogenicity; and loss of corticomedullary differentiation
(Fig. 11.59A). The kidneys maintain their reniform shape
(121). Focal involvement presents as solitary or multiple
masses (Fig. 11.59B) (122). Hydronephrosis can be present
due to ureteral obstruction by enlarged retroperitoneal
lymph nodes.
Malignant Medullary Tumors
RHABDOID TUMOR
Rhabdoid tumor is an uncommon, highly aggressive malig-
nancy arising in the renal medulla and accounting for about
2% of renal malignancies in children (76,78,123). It occurs
most often in young infants, with mean age at diagnosis
of 18 months (124). Clinical signs include an abdominal
mass, hematuria, fever, hypertension, and hypercalcemia

A B
Leukemia. A: Longitudinal sonogram in a 1-year-old boy demonstrates an enlarged right kidney. The parenchymal echogenicity is nor-
Fig. 11.59
mal, but there is loss of corticomedullary differentiation. The left kidney had a similar appearance. B: Longitudinal sonogram of the
right kidney in another patient shows echogenic masses (arrows) representing leukemic infiltration.
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C sular fluid (F).
(123126). Rhabdoid tumor is associated with synchro-
nous or metachronous primary intracranial tumors, most
commonly primitive neuroectodermal tumor, and brain
metastases.
The sonographic features of malignant rhabdoid tumor
are those of a large, heterogeneous intrarenal mass with
indistinct margins and infiltration of the renal hilum (Fig.
11.60). Additional findings include renal capsular thicken-
ing and subcapsular or perinephric fluid collection with
tumor implants (123,125127) (Fig. 11.60). The tumor
may contain calcification and it may extend into the renal
vein or inferior vena cava. Uncommonly, there is bilateral
renal involvement (123,127). Metastatic spread is to lungs,
liver, brain, and lymph nodes. Rhabdoid tumor has a
highly aggressive behavior and a poor prognosis.
CLEAR CELL SARCOMA
Clear cell sarcoma is another aggressive tumor that arises
in the renal medulla, accounting for about 4% to 5% or
primary renal tumors in childhood (76,128). The peak age
incidence is 1 to 4 years of age, but the tumor can present
in the fetus and in neonates (124).
Chapter 11 U R I N A R Y T R A C T 421
Rhabdoid tumor. A: Longitudinal sonogram of the right
Fig. 11.60
kidney demonstrates an ill-defined heterogeneous mass
(M) replacing the renal parenchyma and infiltrating the renal hilum. A
subcapsular fluid collection with tumor nodules (arrows) surrounds the
mass. B: Transverse sonogram in another 2-year-old boy shows a
poorly defined, irregular heterogeneous mass (arrows) in the left kid-
ney and subcapsular fluid (F). C: Contrast-enhanced computed tomog-
raphy scan shows a lobulated, infiltrating mass (arrows) with subcap-
The sonographic features of clear cell sarcoma are a
poorly circumscribed, heterogeneous intrarenal mass with
cystic changes (Fig. 11.61). Infiltration of the renal medulla
and pelvis is another common finding (128). Metastatic
spread is to bone, lymph nodes, brain, liver, and lungs
(125). Medullary infiltration and bone metastases are clues
to the diagnosis.
RENAL MEDULLARY CARCINOMA
Renal medullary carcinoma is a highly aggressive malig-
nant tumor of epithelial origin that originates in the
medulla and almost always occurs in patients with sickle
cell trait or hemoglobin SC disease, but not with homozy-
gous hemoglobin sickle cell disease (129,130). Patients are
usually in the second or third decade of life and present
with flank or abdominal pain or gross hematuria and occa-
sionally with a palpable mass, weight loss, or fever. The
tumor appears to affect the right kidney more than the left
kidney.
At sonography, renal medullary carcinoma is a heteroge-
neous, hypovascular mass containing hemorrhage and exten-
sive necrosis. It is located deep in the parenchyma, invading
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422 P E D I AT R I C S O N O G R A P H Y
A B
Clear cell sarcoma. A: Transverse sonogram in a 2-year-old boy reveals a large, heterogeneous mass with cystic components replac-
Fig. 11.61
ing most of the left kidney. A rim of renal tissue (arrows) extends around the tumor. B: Computed tomography image also shows the
large heterogeneous mass with a rim of enhancing renal tissue (arrow).
and encasing the renal pelvis and causing caliectasis
(76,130). It can invade the perinephric fat, regional lymph
nodes, retroperitoneal soft tissues, and renal vein with prop-
agation into the inferior vena cava. Distant metastases are to
lung and liver. The prognosis is extremely poor, and most
patients have advanced disease at time of diagnosis.
Other Rare Tumors
PRIMITIVE NEUROECTODERMAL TUMOR
Primitive neuroectodermal tumor (PNET) is a rare malig-
nant renal tumor that has been associated with transloca-
tion of tissue from chromosome 11 to 22 (131). On histo-
logic examination, the tumor contains round blue cells with
large areas of necrosis. Imaging findings are nonspecific.
Sonography shows a poorly circumscribed, solid, infiltrative
mass with hyperechoic foci owing to calcifications and
hypoechoic areas representing necrosis or hemorrhage. This
tumor can extend into the renal vein and inferior vena cava.
PRIMARY SARCOMA
Primary renal sarcomas are rare malignant renal tumors.
Subtypes include leiomyosarcoma, angiosarcoma, heman-
giopericytoma, rhabdomyosarcoma, fibrosarcoma, and
osteosarcoma. At imaging, renal sarcomas are indistin-
guishable from other renal tumors (125). They may appear
as well-circumscribed, expansile masses or as diffusely
infiltrative neoplasms with widespread nodal and systemic
metastases at presentation.
Secondary Tumor Deposits (Metastases)
Renal metastases are uncommon, although occasionally,
they have been reported in children with primary tumors
who have widespread metastases elsewhere (132,133).
Spread to the kidneys can be from a hematogenous route
or from invasion by adjacent retroperitoneal tumors (132).
Direct invasion usually occurs in association with neuro-
blastoma or lymphoma. Hematogenous metastases are
commonly from the undifferentiated sarcomas. Renal
metastases are usually small and noncontour deforming,
appearing as hypoechoic or hyperechoic masses.
BENIGN RENAL TUMORS
Mesoblastic Nephroma
Mesoblastic nephroma, also termed fetal renal hamartoma,
leiomyomatous hamartoma, and mesenchymal hamartoma
of infancy, is the most common renal tumor of infancy, usu-
ally presenting during the first 6 months of life (76). It has
been associated with cytogenetic abnormalities on chromo-
some 11 and translocations (t14;15), (t12;15), and
(p13;q25) (90). On cut-section, the tumor is a solid unen-
capsulated mass, measuring 5 to 8 cm in diameter. Micro-
scopically, mesoblastic nephroma contains intersecting bun-
dles of spindle cells, which infiltrate between and entrap
glomeruli, and renal tubules (20). Hemorrhage, necrosis,
and calcifications are relatively uncommon. Most tumors
are histologically benign. However, a cellular variant with
an increased incidence of local recurrence and metastases to
lung, liver, and brain has been reported. (134,135). The
common presentation is an abdominal mass. Hypertension
is an occasional presenting feature (136).
The sonographic features are usually those of a large,
echogenic mass with a homogeneous echopattern or het-
erogeneous echotexture related to areas of necrosis or
hemorrhage (Fig. 11.62) (137). Occasional findings
include concentric hypoechoic and hyperechoic rings
surrounding the tumor and central highly reflective areas
related to the presence of fat (136,138). Mesoblastic
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Chapter 11 U R I N A R Y T R A C T 423

A B

C D
Mesoblastic nephroma. A: Longitudinal sonogram shows a heterogeneous mass (arrowheads) in the right kidney. B: Transverse sono-
Fig. 11.62
gram in another patient shows a relatively homogeneous mass (arrows) arising from the upper pole of the right kidney. C: Color Doppler
imaging in the patient in panel B shows minimal neovascularity in the tumor and flow in compressed renal parenchyma. D: Contrast-enhanced com-
puted tomography scan shows a mass (M) in the upper pole of the right kidney.

nephroma can invade the perinephric connective tissue,
but it typically does not infiltrate the vascular pedicle or
extend into the renal pelvis. Color Doppler sonography
demonstrates flow in the compressed parenchyma and
varying amounts of neovascularity in the tumor itself.
Treatment is nephrectomy or heminephrectomy.
Chemotherapy is reserved for those patients with locally
recurrent tumors or metastatic disease.
Angiomyolipoma
Angiomyolipoma, also called renal hamartoma, is a benign
renal neoplasm that contains varying amounts of mature adi-
pose tissue, smooth muscle, and blood vessels. It is rare as an
isolated lesion in the general pediatric population, but it is
present in as many as 80% of children with tuberous sclero-
sis (mental retardation, epilepsy, sebaceous adenomas). The
lesions usually are small, bilateral, and asymptomatic and
are detected as incidental findings. Large tumors can cause
clinical findings, including hematuria, abdominal pain, and
anemia secondary to intratumoral or retroperitoneal hem-
orrhage. There appears to be a relationship between the
size of the angiomyolipoma and the risk of bleeding.
Angiomyolipomas larger than 3.5 cm in diameter have a
higher risk of hemorrhage (139). Renal failure is unusual
but can occur if the tumors replace most of the renal
parenchyma.
Renal angiomyolipomas typically appear as multiple,
small hyperechoic foci in the renal cortex (Fig. 11.63). The
increased echogenicity is related to fat within the tumor as
well as the complex interfaces created by the angiomatous
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424 P E D I AT R I C S O N O G R A P H Y

A B
Angiomyolipomas. A: Longitudinal sonogram in a patient with tuberous sclerosis shows multiple echogenic masses in the right kidney.
Fig. 11.63
B: Longitudinal image in another patient shows a solitary echogenic angiomyolipoma (arrows) in the upper pole of the right kidney.

and myomatous tissues. Less commonly, they appear as soli-
tary intrarenal masses (Fig. 11.63B). The tumor may extend
to regional lymph nodes or into the inferior vena cava (140).
Fatty tissue is not specific for the diagnosis of angiomy-
olipoma and it also can be present in other renal tumors,
including Wilms tumor, lipoma, and teratoma. The clinical
history and presence of concomitant cysts should suggest
the diagnosis of angiomyolipoma with tuberous sclerosis.
Rare Benign Renal Tumors
METANEPHRIC ADENOMA
Metanephric adenoma, also called embryonal adenoma,
metanephric adenofibroma, and nephrogenic adenofi-
broma, is part of a spectrum of benign renal neoplasms
with varying proportions of epithelial and stromal compo-
nents (141,142). Clinical features include flank mass, pain,
hematuria, hypertension, hypercalcemia, and polycythemia
resulting from increased secretion of erythropoietin (143).
Metanephric adenomas are usually small, sharply
defined, round, solid masses that are isoechoic, hypo-
echoic, or hyperechoic to normal parenchyma. They may
contain highly echogenic areas related to psammomatous
calcifications or hypoechoic foci related to necrosis or
myxoid contents (76,143,144). The tumors are hypovas-
cular on color imaging (144).
OSSIFYING RENAL TUMOR OF INFANCY
Ossifying renal tumor of infancy is a rare benign neoplasm
of early infancy, usually occurring in the first year of age
(145,146). Most patients are under 14 months of age at
the time of diagnosis and present with a palpable abdomi-
nal mass or gross hematuria. The tumor is usually less than
2 to 3 cm in diameter (76,145). Histologically, it contains
osteoid, osteoblasts, and spindle cells. Involvement of the
collecting system is common.
Sonography shows a solid hypoechoic mass containing
more intensely reflective foci with acoustic shadowing (i.e.,
calcifications) (Fig. 11.64). Extension into the collecting
system leads to varying degrees of hydronephrosis. Treat-
ment is nephrectomy or heminephrectomy.

A B
Ossifying renal tumor of infancy. Longitudinal (A) and transverse (B) sonograms in a 5-month-old girl with hematuria show a hypo-
Fig. 11.64
echoic mass (calipers) with highly reflective areas (arrows) representing calcifications in the upper pole of the right kidney.
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INFLAMMATORY PSEUDOTUMOR
Inflammatory pseudotumor, also known as inflammatory
myoblastic tumor, plasma cell granuloma, and pseudosar-
comatous fibromyxoid tumor, is a benign tumor-like con-
dition of unknown cause (147,148). It is characterized by
an admixture of spindle-shaped cells and inflammatory
cells, including plasma cells, lymphocytes, and histiocytes.
Clinical features include hematuria and abdominal pain.
Sonographic findings are nonspecific with the tumor
appearing as a homogeneous or heterogeneous mass in the
parenchyma or in the renal pelvis (148).
Doppler Sonography
Malignant lesions often demonstrate Doppler frequency
shifts exceeding 2.5 kHz. Benign renal masses show a
smaller Doppler shift (0.57  0.65) or no Doppler signal
(149,150). An elevated systolic frequency shift, however, is
not specific for malignant neoplasm, and it also can be seen
with inflammatory masses (150).
ACUTE URINARY TRACT INFECTION
Infection is the most common disorder of the urinary tract in
children. Urinary tract infection in children can involve the
upper urinary tract (kidney), lower urinary tract (bladder), or
both areas. In most cases, clinical signs and laboratory eval-
uation provide the diagnosis of acute urinary tract infection.
The role of imaging is not to diagnose acute pyelonephritis
but to identify underlying anatomic factors that predispose
to infection, such as hydronephrosis and vesicoureteral reflux
(see earlier discussion), to demonstrate resultant damage to
the urinary tract, or to diagnose a complication of the infec-
tion such as a renal abscess or pyonephrosis.
Imaging Guidelines
Current practice is to evaluate all infants and children
younger than 5 years of age with first-time febrile urinary
tract infection (151155). The most commonly used imaging
Acute pyelonephritis. Longitudinal sonogram shows an
Fig. 11.65
enlarged right kidney in a 3-year-old girl. The echogenicity
is increased and greater than that of the liver (L).
Chapter 11 U R I N A R Y T R A C T 425
examinations are sonography and a voiding cystourethro-
gram. In most cases, no further imaging is required if the cys-
togram and sonogram are normal. When hydronephrosis is
demonstrated in the absence of reflux, further evaluation
with diuretic renography may be useful to quantify renal
function. A renal cortical scan with 99mdimercaptosuccinic
acid (DSMA) may be helpful in children who are suspected
of having acute pyelonephritis but in whom laboratory tests
are equivocal (156).
Because the likelihood of reflux is low, older children
and adolescents with infection are usually evaluated by
a sonogram alone. If sonography is normal, further imag-
ing is unnecessary. If, however, sonography shows either
hydronephrosis or parenchymal scarring, voiding cys-
tourethrography may be indicated.
Acute Bacterial Pyelonephritis
Acute bacterial pyelonephritis is an infection of the uroep-
ithelium of the collecting system and renal interstitium
(152155). It usually is a result of an ascending infection
and is associated with vesicoureteral reflux. The common
inciting microorganism is Escherichia coli, which elabo-
rates a protein termed P fimbriae that facilitates bacter-
ial adhesion to the cells of the uroepithelium. Less com-
monly, infection is due to Proteus species, Staphylococcus
saprophyticus, or Pseudomonas aeruginosa.
Symptoms and signs of acute pyelonephritis vary with
patient age. Neonates and infants under 2 years of age usu-
ally present with nonspecific systemic manifestations, such
as temperature instability or fever, irritability, vomiting,
jaundice, poor feeding, and failure to gain weight. Older
children and adolescents usually present with flank pain,
fever, and costovertebral tenderness.
SONOGRAPHIC FINDINGS
Ultrasonography is normal in most children with uncom-
plicated acute pyelonephritis. Severe infection can alter the
appearance of the kidney, producing global or focal
enlargement (Figs. 11.65 and 11.66), areas of increased or
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426 P E D I AT R I C S O N O G R A P H Y
decreased echogenicity, loss of corticomedullary differenti-
ation, and thickening of the walls of the renal pelvis or
ureter (Fig. 11.67) (157160). Color or power Doppler
sonography shows decreased blood flow in the involved
areas, secondary to vascular compression by inflammatory
cells (Fig. 11.68).
The sensitivity of gray-scale sonography for the diag-
nosis of renal inflammation is only 25% to 40%
(161163). With the addition of color Doppler tech-
niques, the sensitivity increases to 65% to 75%, and with
the addition of power Doppler imaging, the sensitivity
and specificity increase to 75% and 86% to 100%,
respectively (161164). Newer applications such as tissue
harmonic imaging have been reported to have sensitivities
and specificities as high as 97% and 80%, respectively
(165).
Acute pyelonephritis. Longitudinal sonogram demon-
Fig. 11.67
strates an enlarged kidney with thickened, echogenic
epithelial lining (arrowheads) in the renal pelvis.
Acute pyelonephritis, focal involvement. Longitudinal sono-
Fig. 11.66
gram demonstrates a focal area of increased echogenicity
(arrows) without evidence of liquefaction in the upper pole of the right
kidney.
Complicated Acute Pyelonephritis
ABSCESS
A renal abscess is a necrotic cavity filled with purulent
material. Most renal abscesses are the result of inade-
quately treated interstitial infection that ultimately lique-
fies. Less often they are the result of contiguous spread
from other organs or a complication of trauma or sur-
gery. Clinical findings include fever, abdominal or flank
pain, and pyuria. Abscesses may be intraparenchymal
and/or extraparenchymal (i.e., in the perinephric space).
Sonography shows a hypoechoic mass with thick, irreg-
ular walls and distal acoustic enhancement (Fig. 11.69).
The abscess fluid often contains septations and mobile
debris, and it may contain highly echogenic foci with
dirty shadowing if the infection is due to a gas-forming
Acute pyelonephritis. Power Doppler image shows
Fig. 11.68
diminished flow in the right lower pole (arrowheads).
Normal flow is noted in the remaining parenchyma.
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Chapter 11 U R I N A R Y T R A C T 427

A B

Renal abscess. A: Longitudinal sonogram in a 5-year-old

Fig. 11.69
girl shows a hypoechoic mass (M) with internal echoes in
the left kidney. B: Power Doppler image shows absence of internal flow
and normal flow in the surrounding parenchyma. C: Contrast-enhanced
computed tomography shows a low-attenuation mass (M) with sur-
C rounding edema posteriorly.

organism. The perinephric fat can appear hypoechoic
owing to edema.
Perinephric abscess results when renal parenchymal
infection extends through the renal capsule. It also can be
secondary to direct extension from an infection in the
retroperitoneum or an adjacent organ. The imaging fea-
tures are similar to those of intrarenal abscesses.
Small abscesses are treated conservatively with antibi-
otic therapy. Large abscesses are treated with percutaneous
or surgical drainage. In such cases, sonography can be use-
ful to guide percutaneous drainage and monitor resolution
of the abscess.
PYONEPHROSIS
Pyonephrosis is the accumulation of purulent exudate
within a hydronephrotic kidney. In children, the common
cause is an obstructive uropathy, and less often distal
ureteral calculi or stricture. The most common causative
organism is E. coli. Pyonephrosis is a urologic emergency
and requires urgent percutaneous or surgical drainage. If
left untreated, it can lead to gram-negative bacteremia,
septic shock, and progressive parenchymal destruction
with loss of renal function.
The sonographic findings of pyonephrosis are a dilated
collecting system containing mobile echoes in the urine, a
fluid-debris level, or bright echoes with dirty shadowing
(i.e., gas) (Fig. 11.70). Echogenic debris is the most reliable
sign of pyonephrosis with a sensitivity of 90% and speci-
ficity of 97% (157). False-negative diagnoses occur when
the pyogenic material is predominantly anechoic rather than
echogenic, while false-positive diagnoses occur when the
collecting system is filled with noninflammatory protein or
debris, mimicking pus. Ultrasonography can be used to
guide aspiration for diagnosis and drainage.
Fungal Infection
Infants and children who have indwelling catheters for
hyperalimentation, or who are on prolonged antibiotics or
immunosuppression or who are immunocompromised (i.e.,
transplant recipients, patients with acquired immunodefi-
ciency syndrome [AIDS], patients with malignancies) are at
increased risk for fungal infections of the urinary tract.
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428 P E D I AT R I C S O N O G R A P H Y
A B
Pyonephrosis. A: Longitudinal sonogram shows a dilated renal pelvis (RP) containing debris. LK  left kidney. B: On a posterior oblique
Fig. 11.70
sonogram, the dependent debris (arrows) shifts in position. LK  left kidney. The patient had an underlying ureteropelvic junction
obstruction.
Most fungal infection is the result of hematogenous seed-
ing, with the most common organism being Candida albi-
cans. Early pathologic findings are microabscesses and
inflammatory infiltrates in the renal cortex, interstitium,
and tubules. Later findings include necrotizing papillitis
and fungal ball formation (owing to mycelial clumping).
Sonographic findings can mimic acute bacterial
pyelonephritis and include enlarged kidneys, increased
parenchymal echogenicity, parenchymal abscess, and
pyonephrosis. Fungal balls are highly suggestive of fungal
infection. Fungal balls appear as nonshadowing echogenic
masses within the renal pelvis, calyces, or urinary bladder
(Fig. 11.71). They may shift position with changes in
patient position and they may obstruct the collecting
Renal candidiasis. Longitudinal sonogram in an infant
Fig. 11.71
with Candida urinary tract infection shows an echogenic
left kidney. The collecting system is mildly dilated and contains several
nonshadowing echogenic masses (arrows) representing fungal balls.
The masses shifted position with changes in patient position.
system. Other findings are thickening of the perinephric
soft tissues, urinary ascites, and microabscesses in the
spleen or liver (166).
Acquired Immunodeficiency Syndrome
Patients with AIDS are susceptible to a number of
opportunistic infections, including Pneumocystis carinii,
Mycobacterium avium-intracellulare, and cytomegalovirus.
The sonographic findings are nonspecific and include
nephromegaly, increased parenchymal echogenicity, small
highly reflective foci representing parenchymal calcifica-
tions, and fungal balls (167). Multiple calcifications also
occur in lymph nodes and other abdominal viscera
(167,168).
CHRONIC RENAL INFECTIONS
Chronic Pyelonephritis
Chronic pyelonephritis is the term used to describe the
parenchymal scarring that is the result of a single or mul-
tiple episodes of acute pyelonephritis. The parenchymal
abnormalities can be unilateral or bilateral, but they typi-
cally are found in the polar regions of the kidneys. The
sonographic findings include a small kidney, focal or dif-
fuse cortical atrophy overlying a dilated blunted calyx, and
loss of corticomedullary differentiation (Fig. 11.72). Com-
pensatory hypertrophy of normal parenchyma occurs
between areas of renal scarring. Large areas of hypertro-
phied tissue can simulate a tumor.
The major differential diagnostic consideration for an
irregular renal contour is fetal lobulation. The cortical
indentations in fetal lobulation are interpolar in distribu-
tion; there is no parenchymal loss and the underlying calyces
are normal (see Fig. 11.8). Cortical scarring in chronic
pyelonephritis has a polar distribution and it overlies a
blunted calyx. Other diagnostic considerations for small
kidneys include primary renal hypoplasia and atrophy
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Chapter 11 U R I N A R Y T R A C T 429

TREATMENT PROCEDURES FOR

VESICOURETERAL REFLUX
Patients with reflux are usually treated with prophylactic
antibiotic therapy. Most low-grade vesicoureteral reflux
will resolve spontaneously, unless there is an anatomic
abnormality. Surgical reimplantation of the ureter or an
endoscopic injection of a bulking agent is performed in
children who fail to maintain a sterile urine while on pro-
phylactic antibiotics or whose reflux has not resolved over
a reasonable time period.

Ureteral Reimplantation
Sonographic findings after reimplantation include focal
bladder wall thickening or a hyperechoic nodule along the
expected course of the reimplanted ureter, bladder saccula-
tions, and transient hydroureteronephrosis (172). Early
surgical complications include urinoma and hematoma at
Chronic pyelonephritis. Longitudinal sonogram of a 10-
the surgical site, ureteral obstruction, and injury to adja-
Fig. 11.72
year-old boy shows a small echogenic left kidney with a cent organs. Bladder lithiasis is a late complication (172).
dilated calyx (C) and overlying parenchymal atrophy (arrows).
Endoscopic Treatment
In this procedure, a bulking agent is injected submucosally
underneath the intravesical portion of the ureter using cysto-
secondary to renal vein thrombosis, ischemia, obstruction,
scopic guidance. The bulking agent elevates the ureteral ori-
or irradiation. In these conditions the kidney is small, but
fice and distal ureter, narrowing the ureteral orifice and pre-
the contours are smooth and there is uniform parenchymal
venting reflux of urine but still allowing antegrade urine
loss. Calyceal morphology is normal.
flow. Bulking agents include polytetrafluoroethylene (PTFE
Xanthogranulomatous Pyelonephritis or Teflon), collagen, autologous fat, silicone, and, more
Xanthogranulomatous pyelonephritis is a chronic granulo- recently, a solution of dextranomer/hyaluronic acid (Deflux).
matous process induced by recurrent infection in the Sonographically, bulking agents appear as round, hyper-
presence of urinary tract obstruction (157,169171). echoic areas with variable acoustic shadowing (Fig. 11.73)
Pathologically, there is destruction of renal parenchyma (172,173). Complications are rare and include transient
and replacement by necrotic debris with numerous inflam- ureteral obstruction, infection, and particle migration
matory cells and lipid-laden macrophages (xanthoma through the ureteral wall and into the ureter. Refluxed mate-
cells) (157). The inflammatory zone is bordered by a rial appears as echogenic material within the collecting sys-
band of fibrous tissue. In children, the disease is usually tem with posterior shadowing (172,174).
focal, involving the upper or lower poles. This form is
sometimes referred to as tumefactive xanthogranuloma-
tous pyelonephritis, since it can mimic a mass. Occasion-
ally, the process involves the entire kidney (157,169171).
Symptoms are nonspecific and include fever, flank pain,
and hematuria. The most common organisms are Proteus
species and E. coli.
In focal xanthogranulomatous pyelonephritis, sonogra-
phy shows a hypoechoic cortical mass, which may be asso-
ciated with a shadowing stone in the adjacent calyx and
parenchymal calcifications. The remainder of the kidney is
normal.
The classic sonographic findings of diffuse infiltration
are nephromegaly; multiple hypoechoic masses represent-
ing either dilated calyces, areas of parenchymal destruc-
tion, or xanthoma collections; stones in the renal sinus and
parenchyma; and perinephric fluid collections. An amor-
phous central echogenic focus representing a staghorn cal-
culus is also common (157). Treatment is usually nephrec- Endoscopic injection of bulking agent. Transverse sono-
tomy for diffuse disease and partial nephrectomy for focal Fig. 11.73
gram shows round echogenic foci (arrows) protruding
disease. into the bladder lumen.
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430 P E D I AT R I C S O N O G R A P H Y
MEDICAL RENAL DISEASE
Medical renal disease is a cause of acute or chronic renal
failure (175). Renal parenchymal disease can be classified
as prerenal, renal (intrinsic), or postrenal. In the neonatal
period, it is most often prerenal, resulting from hypoper-
fusion due to severe dehydration, shock, respiratory dis-
tress syndrome, or heart failure. Less commonly, it is due
to renal abnormalities, including renal cystic disease, uri-
nary tract obstruction, renal artery or vein thrombosis,
and congenital nephrotic syndrome, or to postrenal abnor-
malities, such as posterior urethral valves. A transient
cause of renal parenchymal disease and oliguria is stasis
nephropathy (see below).
In older children, renal parenchymal disease is com-
monly due to prerenal causes and also intrinsic causes
such as acute glomerulonephritis, nephrotic syndrome,
hemolytic uremic syndrome, Henoch-Schnlein purpura,
and acute tubular or cortical necrosis (175,176). Other
causes include hypersensitivity reaction to administered
medications, sickle cell disease, glycogen storage disease,
tyrosinemia, polycystic disease, lymphoma, leukemia,
amyloidosis, and nephrosclerosis. Patients present with
decreased or absent urine output, hematuria, protein-
uria, or hypertension.
Sonographic Findings
The sonographic hallmark of acute medical renal disease is
increased parenchymal echogenicity (Fig. 11.74) (176).
Cortical echogenicity is considered increased when the kid-
neys are more echogenic than the liver or the spleen. The
degree of echogenicity correlates loosely with the severity
of the disease, but not with a specific histopathologic diag-
nosis. Other findings include loss of corticomedullary dif-
ferentiation and a perinephric hypoechoic rim, thought to
represent edema (177). Increased renal echogenicity is a
nonspecific finding and can be seen in children with acute
abdominal illnesses or pneumonia but no history of renal
abnormalities, possibly related to dehydration (178).
Medical renal disease, acute glomerulonephritis. Longi-
Fig. 11.74
tudinal sonogram shows an enlarged echogenic kidney
(calipers). The cortical echogenicity is greater than that of the liver (L).
Doppler flow may be normal in mild disease and dimin-
ished, reversed, or absent in severe disease. The RI is usu-
ally normal in diseases limited to the glomeruli, regardless
of severity (mean RI 0.58 to 0.67). It can be elevated in dis-
eases involving the tubulointerstitial compartment (acute
tubular necrosis, interstitial nephritis) (mean RI 0.75)
(179,180).
The primary role of sonography is to exclude anatomic
abnormalities as the cause of renal failure and to determine
renal size, which is helpful information for limiting the dif-
ferential diagnosis. Some of the more common renal
parenchymal diseases are discussed next.
Hypotension (Prerenal Disease)
Prerenal disease secondary to hypoperfusion accounts for
most cases of acute renal failure in the pediatric age group.
The sonographic appearance of the hypoperfused kidney is
normal unless cortical necrosis occurs. The RI is also nor-
mal in most cases (180).
Stasis Nephropathy
Stasis nephropathy is found in neonates. It is the result of
glycoprotein deposition (e.g., the Tamm-Horsfall protein)
within the tubules, leading to transient tubular obstruc-
tion. Characteristically, patients present with oliguria. The
precipitated proteins cause increased echogenicity of the
medullary pyramids (Fig. 11.75) (18). The kidneys are of
normal size. Stasis nephropathy generally resolves sponta-
neously within the first week of postnatal life.
Glomerulonephritis
Acute glomerulonephritis is an immune complexmediated
condition. Pathologic examination shows cellular infiltrate
in the glomerular tufts and interstitial edema. Patients
present with hematuria and hypertension. Mean patient
age is 6 to 7 years. Sonography demonstrates normal or
bilaterally enlarged kidneys with increased cortical
echogenicity (see Fig. 11.74). The medullary area may be
spared. Following successful medical treatment, renal size
and echogenicity return to normal. Chronic glomeru-
lonephritis occurs when there is progression of acute dis-
ease. In chronic disease, the kidneys are small, are diffusely
echogenic, and have poor or absent corticomedullary dif-
ferentiation.
Hemolytic Uremic Disease
Hemolytic uremic syndrome is a vasculitis that is believed
to be caused by an antigen-antibody reaction to bacterial
toxins, most commonly the E. coli 0157:H7 strain (181).
Histologically, there is narrowing and obstruction of small
arteries and capillaries by thrombi, swollen endothelial
cells, and intimal inflammation. Most children are under
5 years of age and present with a prodromal phase of diar-
rhea, which is frequently bloody in nature, followed by the
onset of renal failure. Patients have a triad of microangio-
pathic hemolytic anemia, thrombocytopenia, and renal fail-
ure. Spontaneous recovery generally occurs within 3 weeks,
although during that time the patient may need dialysis.
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Chapter 11 U R I N A R Y T R A C T 431

A B
Stasis nephropathy secondary to precipitation of Tamm-Horsfall proteins. A, B: Longitudinal sonograms of the right and left kidneys,
Fig. 11.75
respectively, show hyperechoic renal pyramids (arrows). The parenchymal echogenicity is normal for a neonate.

During the phase of oliguria or anuria, sonography
shows normal or slightly enlarged kidneys. The renal cor-
tex is hyperechoic to liver and the pyramids are hypo-
echoic and prominent. Diastolic flow is absent, reversed,
or diminished, reflecting the reduced size of the arteriolar
lumen (Fig. 11.76). During the recovery phase, character-
ized clinically by diuresis, intrarenal resistance decreases
and diastolic flow returns to normal (182).
Henoch-Schnlein Purpura
Henoch-Schnlein purpura is a vasculitis with IgA deposits
in the walls of small vessels in the skin, gastrointestinal
tract, and kidney, associated with arthralgias and arthritis.
It is generally a self-limited disorder that follows an inter-
current illness, usually an upper respiratory infection.
Most affected children are under 10 years of age. Clinical
findings include rash, abdominal pain, renal involvement
ranging from hematuria to acute renal failure, and arthral-
gia or arthritis. Sonography shows increased parenchymal
echogenicity and high RIs, similar to other medical renal
diseases.
Acute Tubular Necrosis
Acute tubular necrosis refers to a nephrotoxic or ischemic
injury to the renal tubules accompanied by clinical mani-
festations of acute renal failure. Nephrotoxic injury can
follow the administration of antibiotics, nonsteroidal anti-
inflammatory drugs, or chemotherapeutic agents. Acute
tubular necrosis due to ischemic injury usually produces
no change in renal size or cortical or medullary echogenic-
ity. Nephrotoxic injury can result in renal enlargement,
hyperechoic cortex, and enlarged and hypoechoic renal
pyramids. Doppler evaluation may show reduced diastolic
flow and an elevated RI (180).

A B
Hemolytic uremic syndrome. A: Longitudinal sonogram of the right kidney (RK) shows increased renal cortical echogenicity relative to
Fig. 11.76
the liver (L). B: Pulsed Doppler waveform from a segmental artery shows diminished systolic and reversed diastolic arterial flow, indi-
cating high resistance.
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432 P E D I AT R I C S O N O G R A P H Y

Acute Renal Cortical Necrosis
Acute cortical necrosis results from an ischemic injury to the
renal cortex; the medullary pyramids are usually spared.
The causes of renal cortical necrosis include severe dehydra-
tion, sepsis, blood loss, glomerulonephritis, hemolytic ure-
mic syndrome, and sickle cell disease. Sonographic findings
include normal-size kidneys, increased cortical echogenicity,
and prominent hypoechoic pyramids. Cortical calcifications
can be noted in chronic disease.
Acute Interstitial Nephritis
Acute interstitial nephritis is a rare cause of reversible renal
failure. Most interstitial nephritis is secondary to an acute
hypersensitivity reaction to drugs. Renal failure resolves
with termination of drug therapy. The kidneys are enlarged
and echogenic.
RENAL VASCULAR DISEASE
Renal Artery Stenosis
Renal artery stenosis is a cause, albeit rare, of hypertension
in children. Fibromuscular dysplasia is the most common
cause of renal artery stenosis in children, accounting for
50% to 70% of cases (183,184). Other causes of arterial
stenosis include Takayasu arteritis, moyamoya, neurofi-
bromatosis, midaortic syndrome (coarctation of the aorta),
tuberous sclerosis, and Williams syndrome (idiopathic
infantile hypercalcemia) (183186).
Fibromuscular dysplasia is a noninflammatory vascular
disease that most commonly affects the renal and internal
carotid arteries (187). Medial fibroplasia is the most com-
mon histologic subtype of this lesion. Renal disease is
bilateral in about 65% of cases. The stenosis commonly
involves the mid- to distal part of the main renal artery
with occasional extension into segmental branches. Steno-
sis also can be seen in the mesenteric, splenic, and hepatic
vessels
The gray-scale findings of renal artery stenosis are a
size discrepancy in the two kidneys due to ischemia,
increased cortical echogenicity of the normal contralat-
eral kidney, and a small renal artery (Fig. 11.77) (188).
A length differential of greater than 1 cm between the
two kidneys in a hypertensive child is considered abnor-
mal.

A B

Renal artery stenosis. A: Longitudinal sonogram shows a

Fig. 11.77
small right kidney (arrows) measuring 8 cm. B: Normal
left kidney (arrows) for comparison measures 13 cm. C: Transverse
color Doppler sonogram shows segmental narrowing of the right renal
C artery (arrow). A  aorta. Peak systolic flow was 220 cm/sec.
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Chapter 11 U R I N A R Y T R A C T 433

A B
Renal artery stenosis. A: Pulsed Doppler waveform in an adolescent girl with hypertension and fibromuscular dysplasia shows increased
Fig. 11.78
peak systolic velocity (223 cm/sec) and bidirectional flow at the site of stenosis in the main right renal artery. B: Pulsed Doppler waveform
of an intrarenal artery shows delayed upstroke with decreased amplitude and flattening of the systolic peak (tardus parvus effect).

Pulsed Doppler findings of significant stenosis of the Occlusion of the main renal artery causes global infarc-
main renal artery (60% vessel diameter narrowing) include tion of the kidney. In the acute phase, the kidney is normal
(a) an increased peak systolic velocity (150 cm/sec) at in size, but it is echogenic secondary to hemorrhage and
the site of stenosis (Fig. 11.78A), (b) poststenotic turbulence edema (Fig. 11.80). An echogenic filling defect, represent-
causing spectral broadening and bidirectional flow (above ing thrombus, may be seen in the lumen of the affected ves-
and below the baseline), and (c) renal arterytoaorta peak sel. Absent, diminished, or reversed flow in the main or
systolic velocity ratio greater than 3.5 (189191). segmental renal arteries on pulsed or color Doppler sonog-
Doppler findings in the intrarenal arteries (i.e., the down- raphy supports the diagnosis of occlusion (Fig. 11.80B).
hill circulation) include the tardus-parvus waveform (Fig. The end result of arterial thrombosis depends on the extent
11.78B) and systolic acceleration time greater than 0.07 sec- of the insult and the presence or absence of recanalization
onds (189,192). The tardus-parvus waveform shows a and collateral channels. The chronically ischemic kidney is
slowed systolic upstroke (300 cm/sec) and rounding or flat- small with a smooth outline and increased or normal
tening of the systolic peak. This pattern is not specific for echogenicity. An end-stage small kidney caused by arterial
renal artery stenosis. Other causes include proximal abdom- thrombosis is indistinguishable from that caused by renal
inal aortic stenosis from Takayasu disease and thoracoab- vein thrombosis.
dominal aortic coarctation (193).
Color Doppler findings of renal artery stenosis include
(a) a narrowed vascular lumen (Fig. 11.77C) and (b)
perivascular flow artifacts caused by soft tissue vibrations,
appearing as random color assignment in the parenchyma
adjacent to the stenosis (Fig. 11.79) (10).
Multiple renal arteries and segmental lesions account
for almost all false-negative Doppler results. Neither
pulsed nor color Doppler examinations are sensitive for
detecting stenoses in accessory renal arteries or in small
branch vessels.

Renal Artery Thrombosis and Infarction

Renal artery thrombosis is found in infants of diabetic
mothers and in infants with sepsis, dehydration, hemocon-
centration, and indwelling umbilical artery catheters. In
older children, thrombosis is most often a complication of
traumatic dissection, vasculitis, or embolus from an
indwelling arterial line or cardiac valvular vegetation (194). Renal artery stenosis. Color Doppler image shows soft
Fig. 11.79
The clinical features are acute flank pain and hematuria. tissue vibrations around the left renal artery. A  aorta.
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434 P E D I AT R I C S O N O G R A P H Y

LK

A B
Renal artery thrombosis. A: Longitudinal sonogram in a neonate with hematuria and an umbilical artery catheter shows an echogenic
Fig. 11.80
left kidney (LK). Renal size is normal. S  spleen. B: Transverse pulsed Doppler image of the main renal artery shows high arterial
impedance with narrowed systolic peaks and reversed diastolic flow.

Segmental occlusion causes a hypoechoic, wedge-
shaped, cortical defect with the apex of the infarct at the
renal hilum and the base at the renal capsule. Pulsed and
color Doppler interrogation show absent or diminished
flow in the hypoechoic area. Following the administration
of contrast agents, color signal intensity in the normally
perfused areas increases, whereas the signal intensity in the
ischemic areas remains unchanged (195). Late sequelae are
an echogenic cortical mass and cortical scaring.
Arteriovenous Fistula
An arteriovenous fistula is a direct connection between an
artery and vein without an intervening capillary network.
It can be congenital or acquired due to a biopsy or pene-
trating injury (196,197). Small fistulas are often asympto-
matic and resolve spontaneously. Large fistulas can be a
cause of hypertension, hematuria, or high-output cardiac
failure and may need surgical ligation or interventional
radiologic embolization.
The gray-scale sonogram is usually normal. Doppler
imaging confirms the diagnosis by showing the character-
istic waveform related to loss of the intervening capillary
bed and the absence of impedance to arterial flow. Pulsed
Doppler abnormalities include (a) high-velocity systolic
flow and elevated diastolic flow in the feeding artery (Fig.
11.81), (b) turbulent flow at the shunt site, and (c) arteri-
alization of the draining vein (196). Color Doppler abnor-
malities include a dilated feeding artery and draining vein,

A B
Arteriovenous fistula. A: Pulsed Doppler sonogram in a young adult with hematuria following renal biopsy shows high-velocity systolic
Fig. 11.81
flow (peak velocity, 400 cm/sec) and elevated diastolic flow in a lower pole artery. B: Doppler sonogram from a normal intrarenal artery
for comparison shows a normal waveform.
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A B
Pseudoaneurysm. A: Transverse image shows a hypoechoic mass (arrow) in the lower pole of the right kidney. B: Color and Doppler
Fig. 11.82
image shows a swirling pattern of internal blood flow with high systolic and diastolic flow (above baseline) and pulsatile venous wave-
forms (below baseline).
an intervening tangle of vessels, and perivascular soft tis-
sue vibrations adjacent to the fistula.
Pseudoaneurysm
Pseudoaneurysms occur as a result of laceration of an
artery, usually related to percutaneous needle biopsy. Most
are clinically occult, although they can produce bleeding if
they rupture into the perinephric space or into the collect-
ing system.
The gray-scale finding of a pseudoaneurysm is a hypo-
echoic mass (198). Color and spectral Doppler imaging
show a swirling, disorganized pattern of internal blood
flow with high-velocity arterial flow and pulsatile venous
waveforms (Fig. 11.82). A to-and-fro pattern of flow may
be seen in the neck of the pseudoaneurysm.
Renal Vein Thrombosis
Renal vein thrombosis is predominantly a disease of the
newborn, although it can occur in any age group, includ-
ing the fetus (199,200). Heterozygosity for factor V Leiden
is a risk factor for in utero renal vein thrombosis. In
neonates, renal vein thrombosis is usually a complication
of severe dehydration and associated hemoconcentration,
secondary to blood loss, diarrhea, or sepsis. Because they
are relatively water depleted, infants of diabetic mothers
are also prone to thrombosis. In neonates, the venous
thrombosis usually begins in small intrarenal veins and
extends proximally into larger veins or into the inferior
vena cava. In older children, thrombosis of the renal vein
may occur as a result of trauma, neoplastic invasion of the
renal vein, or dehydration, and it is common in nephrotic
syndrome. In this group of patients, the thrombus usually
begins in the inferior vena cava and propagates into the
renal vein.
The classic clinical findings are flank pain, a palpable
flank mass, hematuria, and proteinuria. Most renal vein
thrombosis is unilateral, but bilateral involvement does
occur. Pathologic findings include edema and hemorrhage
Chapter 11 U R I N A R Y T R A C T 435
in the acute phase, followed by cellular infiltration and
fibrosis. Adrenal hemorrhage may coexist, particularly if
the left renal vein is involved.
Immediately after obstruction of the renal vein, the kid-
ney becomes enlarged with increased parenchymal
echogenicity and absent corticomedullary differentiation
(Fig. 11.83). Echogenic streaks thought to be thrombosed
vessels may be seen in the intrarenal vessels and echogenic
thrombus may be identified in the renal vein or inferior
vena cava (Figs. 11.83B and 11.83C) (201). Additional
findings include thickening of Gerota fascia and perirenal
venous collateral vessels.
Doppler imaging shows either the absence of venous
signal or partial flow around the thrombus in the main
renal vein and/or inferior vena cava. When present, flow in
the renal vein is steady, without any pulsations reflected
from the right atrium. The venous outflow obstruction
also increases interstitial pressure and diminishes arterial
flow, which leads to a narrow systolic arterial peak and
absent, reduced, or reversed diastolic flow in the segmen-
tal renal arteries (Fig. 11.84) (202).
Over the next 1 to 2 weeks the echogenicity of the kid-
ney decreases; the corticomedullary junction remains indis-
tinct. The parenchyma may appear heterogeneous with
hypoechoic and hyperechoic areas. As cellular infiltration
and fibrosis develop, the kidney again becomes echogenic
and of variable size. The ultimate fate of the kidney
depends on the extent of venous occlusion and the forma-
tion of venous collateral channels. If there is early forma-
tion of collateral channels, allowing continued arterial per-
fusion, the outcome is more favorable. If the kidney lacks
collateral veins, there is a higher incidence of hemorrhagic
infarction. The end-stage kidney is small, smoothly mar-
ginated, and hyperechoic (Fig. 11.85). At this stage, it may
contain calcifications, which typically are linear and pres-
ent throughout the parenchyma. Calcified thrombus may
also be seen in the renal vein and inferior vena cava
(203206).
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436 P E D I AT R I C S O N O G R A P H Y

Acute renal vein thrombosis. A: Longitudinal sonogram

Fig. 11.83
in an infant with severe dehydration shows an enlarged
echogenic left kidney (arrows) and loss of corticomedullary differenti-
ation. SPL  spleen. B: Longitudinal sonogram in another infant with
acute onset of hematuria shows a large left kidney and branching lin-
ear echodensities related to thrombosed vessels. A similar appear-
ance can be seen in chronic renal vein thrombosis when the vessels
calcify. The diagnosis depends on clinical correlation with the age of
the insult. C: Longitudinal sonogram shows echogenic thrombus in the
C inferior vena cava (arrows). GB  gallbladder.

A B
Acute renal vein thrombosis. A: Longitudinal sonogram of a 2-month-old boy who presented with acute severe dehydration shows an
Fig. 11.84
enlarged, echogenic right kidney (cursors) with absent corticomedullary differentiation. B: Pulsed Doppler imaging of an intrarenal
artery demonstrates narrowed systolic peaks and reversal of diastolic flow, reflecting increased intrarenal impedance.
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Chronic renal vein thrombosis. Longitudinal sonogram in
Fig. 11.85
a neonate 1 month after acute renal vein occlusion
shows a small kidney (cursors) with increased renal sinus echoes.
URINARY TRACT CALCIFICATIONS
Nephrocalcinosis
Nephrocalcinosis refers to a pathologic deposition of cal-
cium in the renal parenchyma. Calcification is more com-
mon in the medulla than in the cortex. The common causes
of medullary nephrocalcinosis in neonates and infants are
chronic diuretic therapy for bronchopulmonary dysplasia,
corticosteroid administration, and metabolic disturbances
such as hypercalciuria and hypercalcemia (207209).
Other causes include renal tubular acidosis (RTA), Bartter
syndrome, and Williams syndrome (idiopathic infantile
hypercalcemia). In older children and adolescents, causes
of medullary calcification include (a) metabolic disorders
such as hyperoxaluria, hypercalcemic states (hyper-
parathyroidism, hypervitaminosis D, Williams syndrome),
A B
Medullary nephrocalcinosis. A: Longitudinal views of the right kidney in a 16-year-old boy with renal tubular acidosis show an
Fig. 11.86
echogenic focus (arrowhead) with acoustic shadowing (arrows) in a lower pole renal pyramid. B: Longitudinal sonogram in a patient
with Williams syndrome shows echogenic renal pyramids (arrows) without acoustic shadowing.
Chapter 11 U R I N A R Y T R A C T 437
cystinuria, and renal tubular acidosis; (b) structural abnor-
malities causing stasis/obstruction, such as congenital
hydronephrosis, autosomal recessive and dominant renal
diseases, medullary sponge kidney, and tyrosinemia; and
(c) infection (210214). No cause (idiopathic) is found in
approximately 25% of patients (207).
Cortical calcifications occur in hypercalcemic states,
chronic glomerulonephritis, acute cortical or tubular necro-
sis, renal vein thrombosis, and infection with P. carinii,
M. avium-intracellulare, and cytomegalovirus.
Urolithiasis
Urolithiasis refers to the presence of stones in the collect-
ing system of the kidney or in the ureter. It often is idio-
pathic, but it also may be a complication of underlying uri-
nary tract obstruction and associated infection, prolonged
immobilization, renal tubular syndromes (renal tubular
acidosis, cystinuria, glycinuria), enzyme disorders (hyper-
oxaluria, xanthinuria), uric acid lithiasis due to hereditary
hyperuricosuria (Lesch-Nyhan syndrome), myeloprolifera-
tive states, hypercalcemic states, and enteric abnormalities.
The most common type of stone is calcium oxalate, fol-
lowed by calcium phosphate, struvite, and cystine stones.
Sonography
Nephrocalcinosis and urolithiasis appear as areas of
increased echogenicity with or without acoustic shadowing
(Figs. 11.86 and 11.87). Acoustic shadowing can usually
be seen if the stone is 5 mm or greater in size (215). Small
stones (5 mm) may not shadow, especially if they are not
located in the focal zone of the transducer. The sensitivity
and specificity of sonography for detecting renal calculi
is approximately 95% and 85%, respectively (216,217).
Differentiation of the various types of renal calculi is not
possible on the basis of their sonographic appearance.
Nonopaque stones, such as uric acid calculi, can produce
as much acoustical shadowing as opaque or calcium-
containing renal calculi.
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438 P E D I AT R I C S O N O G R A P H Y
Urolithiasis. Longitudinal sonogram shows a well-
Fig. 11.87
defined echogenic focus (arrow) with distal acoustic
shadowing, representing a distal ureteral calculus.
Although stones can be identified in the proximal or
middle thirds of the ureter, they are easier to identify in the
distal ureter, especially near the ureterovesical junction.
Color Doppler evaluation of the ureteric jet may be of
value in diagnosing the degree of obstruction. In high-
grade obstruction, the jet is absent or has diminished
velocity. In partial or low-grade obstruction, the jet may be
normal or show low-level flow (50).
PITFALLS
It is important to recognize that not all hyperechoic pyra-
mids are the result of crystalloid deposition, although
this probably causes the brightest medullary pyramids.
Increased echogenicity in the renal medulla can also be seen
in dehydration states, Tamm-Horsfall proteinuria, sickle cell
anemia, papillary necrosis, autosomal recessive polycystic
disease, and C. albicans pyelonephritis.
A pitfall in the diagnosis of urolithiasis is air in the col-
lecting system following urinary diversion. Air produces
increased echogenicity with dirty or poorly defined
acoustic shadowing, whereas urolithiasis produces clean
or sharply marginated shadowing (Fig. 11.88).
JUXTARENAL PROCESSES
Disease processes that affect the juxtarenal spaces include
infection and inflamation, hemorrhage, and urine leakage.
Pararenal infection is usually an extension of underlying
parenchymal disease, but it can be a complication of an
extrinsic inflammatory process, such as pancreatitis. The
sonographic finding of an inflammatory mass is a hypoe-
choic or echogenic pararenal fluid collection with irregular
or smooth walls.
Hemorrhage into the pararenal spaces usually follows
blunt trauma or a penetrating injury, such as renal biopsy
Intrarenal collecting system air. Transverse image of the
Fig. 11.88
left kidney shows an echogenic focus (arrow) with
poorly defined posterior shadowing (arrowheads), reflecting air in the
renal pelvis.
or percutaneous nephrolithotomy. Less frequently it is
associated with a bleeding diathesis. Acute hematomas
appear hyperechoic. Subacute hematomas are heteroge-
neous masses containing an admixture of serous fluid, fi-
brin, and clot. Chronic hematomas are hypoechoic.
Urine leakage into the perirenal space may be a com-
plication of urinary tract obstruction or renal trauma. Uri-
nomas usually appear as anechoic or hypoechoic fluid col-
lections and they often contain septations or debris (see
Figs. 11.20 and 11.31).
RENAL TRAUMA
The kidney is the third most frequently injured organ in
blunt abdominal trauma, after the liver and spleen (218).
Children with marked hematuria (50 red blood cells per
high-power field) are more likely to have renal injuries than
those with minimal hematuria (50 red blood cells per
high-power field). CT is the study of choice in patients who
are clinically stable and suspected of having serious renal
injuries. Although sonography is capable of identifying
renal and perirenal hematomas as well as the integrity of
the main renal vessels, it is inferior to CT in revealing the
extent of injury. Technical problems, such as bandages,
ileus, and broken ribs, also make it difficult to obtain high-
quality sonograms. Sonography, however, may be of value
in following the course of renal injury.
Renal injuries are classified into four major categories:
(a) minor lesions, consisting of hematomas or contusions
and small corticomedullary lacerations that do not extend
to the collecting system; (b) major injuries, including lacer-
ations that extend into the collecting system and fractures
that separate the kidney into two parts; (c) catastrophic
injuries, consisting of shattered kidneys and injuries to the
renal vascular pedicle, such as arterial occlusion and
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Chapter 11 U R I N A R Y T R A C T 439

A B

Renal fracture. Sonography was performed to follow a

Fig. 11.89
fracture seen on computed tomography. A: Longitudinal
sonogram shows increased echogenicity (arrows) in the lower pole of
the kidney and the perinephric area (curved arrow). B: Color Doppler
sonogram shows absent flow in the lower pole parenchyma (arrows).
C: Contrast-enhanced CT scan shows a fracture line separating the
C kidney into two parts (arrow).

avulsion; and (d) avulsion or laceration of the ureteropelvic
junction or renal pelvis (219,220). Perirenal hematomas
frequently accompany major and catastrophic injuries.
At sonography, hematomas are round or ovoid
parenchymal lesions. Lacerations and fractures appear as
linear or branching defects in the renal parenchyma (Fig.
11.89). Perirenal hematomas are recognizable as crescent-
shaped fluid collections (Fig. 11.90). Absent flow signal in
the renal vessels or in part or all of the parenchyma suggests
vascular injury.

A B
Acute perirenal hematoma. A: Longitudinal sonogram of the right kidney shows an echogenic extrarenal fluid collection (arrows).
Fig. 11.90
RP  renal pelvis. B: Contrast-enhanced computed tomography scan confirms a perirenal hematoma (arrows).
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440 P E D I AT R I C S O N O G R A P H Y

A B
Diagram showing surgical anastomoses for renal transplantation. A: In small children, an anastomosis is created between the distal
Fig. 11.91
aorta and donor renal artery and between the inferior vena cava and the donor renal vein. B: In older children, an anastomosis is cre-
ated between the internal iliac artery (IA) and donor renal artery (RA) and between the external iliac vein (EV) and donor renal vein (RV).

Hematomas vary in echogenicity, depending on age.
Freshly extravasated blood may be isoechoic or hyper-
echoic relative to adjacent parenchyma (see Fig. 11.89).
Within hours of the acute injury, clot formation begins,
and within several days of the hemorrhage, clot lysis
begins and the echogenicity of the blood starts to decrease.
The subacute hematoma is heterogeneous with anechoic
and echogenic areas. After 2 to 3 weeks, the lysed
blood appears anechoic or hypoechoic relative to normal
parenchyma.
RENAL TRANSPLANT
Renal transplant is performed for patients with chronic
renal failure who are maintained on peritoneal dialysis or
hemodialysis. Three types of allografts are possible: cadav-
eric, living-related donor, and living-unrelated donor.
differentiation, echogenic central sinus, and minimally
hypoechoic medullary pyramids (Fig. 11.92).
VASCULAR IMAGING
The normal renal allograft has a low-impedance capillary
bed and continuous antegrade flow throughout the car-
diac cycle (Fig. 11.93) (221). Pulsed Doppler evaluation of
the anastomosed main renal artery shows a rapid rise in
systole followed by a gradual decline in diastole.
Intrarenal arterial signals (in the renal sinus, arcuate ves-
sels, and interlobar vessels) are similar to those of the
main renal artery, although they are dampened in ampli-
tude. The resistive index varies from 0.4 to 0.8, with a
mean of 0.6. Doppler signals from the main renal vein are
in a direction opposite to that of arterial flow. Flow in the

Normal Renal Allograft

MORPHOLOGIC CHARACTERISTICS
In small children, the transplanted kidney is placed intra-
abdominally (i.e., intraperitoneally) with anastomosis of
the donor renal artery and vein to the recipient distal aorta
and inferior vena cava, respectively (Fig. 11.91A). In older
children, the allograft is placed in the iliac fossa in a
retroperitoneal position. The donor renal artery is anasto-
mosed either to the recipient external or internal iliac
artery and the donor vein is anastomosed to the recipient
external iliac vein (Fig. 11.91B). The donor ureter is anas-
tomosed to the recipient urinary bladder (ureteroneocys-
tostomy).
The sonographic appearance of the normal allograft is
similar to that of a normal native kidney, although the Normal renal allograft. Longitudinal sonogram through
morphology is more clearly identified because of the close Fig. 11.92
the right iliac fossa shows an extraperitoneal renal allo-
proximity of the allograft to the body surface. The normal graft (calipers) with smooth margins, distinct corticomedullary differ-
allograft has a smooth contour, distinct corticomedullary entiation, and echogenic renal sinus fat.
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Renal allograft, normal Doppler waveforms. Pulsed
Fig. 11.93
Doppler display of the waveform from the main renal
artery shows a sharp upstroke in systole followed by a gradual decrease
in diastole. The main renal vein (below the baseline) shows continuous
blood flow with minimal respiratory variation.
main renal vein is continuous: minimal variation can be
noted with respiratory and cardiac motion. More marked
venous pulsations can occur with right heart failure or
fluid overload.
Color flow and power (energy) Doppler imaging tech-
niques are useful to localize the vascular anatomy for
pulsed interrogation. Power Doppler has the added advan-
tage of enabling visualization of the interlobular vessels as
they course from their arcuate origin to the proximity of
the renal capsule (222224). These vessels are not as easily
seen on conventional color flow Doppler.
Pathology
Complications of allograft failure can be divided into
parenchymal complications (acute and chronic rejection,
acute tubular necrosis, drug toxicity), renal vascular
lesions, peritransplant fluid collections, ureuteral obstruc-
tion, and lymphoproliferative disorder.
The role of sonography in patients with renal trans-
plants and deteriorating renal function is to identify
hydronephrosis, peritransplant fluid collections, and vas-
cular complications. Ultrasonography cannot accurately
indicate parenchymal dysfunction. Biopsy remains the
gold standard for establishing the diagnosis of rejection
and other parenchymal complications.
Parenchymal Complications
REJECTION
Rejection is the most common cause of allograft failure.
Histologically, there are two types of rejection: (a) inter-
stitial or cellular, mediated by T cells, and (b) vascular or
humoral, mediated by B cells. Interstitial rejection is
Chapter 11 U R I N A R Y T R A C T 441
characterized by cellular infiltration of the cortex, inter-
stitial edema, and tubular necrosis. Inflammatory cells
are found within capillaries, venules, and lymphatics, but
the arterioles and glomeruli are spared so that vascular
impedance and diastolic flow are not altered. The vascu-
lar form of rejection is characterized by an endovasculi-
tis, which results in swelling and inflammation of the
endothelium, with resultant vessel wall damage, throm-
bus formation, and luminal obliteration. Vascular imped-
ance is increased, leading to decreased or absent diastolic
flow.
Based on temporal patterns, graft rejection can be
classified as hyperacute, accelerated, acute, or chronic.
Hyperacute rejection occurs immediately at the time of
transplantation, is mediated by humoral antibodies, and
occurs in recipients who have been sensitized by previ-
ous blood transfusions or a prior graft. The recipients
circulating antibodies bind to antigens on the graft vas-
cular endothelium, leading to vessel thrombosis. Hyper-
acute rejection is usually not imaged because the diag-
nosis is evident during surgery. Accelerated rejection
occurs between 1 and 7 days after transplantation and is
similar in pathogenesis to hyperacute rejection, but less
severe.
Acute rejection generally occurs within the first
3 months of transplantation. It can be cellular or humoral
mediated, but the cellular form is more common. Clinical
findings include oliguria, fever, graft enlargement and ten-
derness, and elevated serum creatinine levels. These find-
ings are nonspecific and mimic those of the other causes of
allograft failure.
Chronic rejection begins 3 months to years after
transplantation and is the sequela of previous episodes
of untreated or unsuccessfully treated acute rejection.
Histologically, it is characterized by interstitial fibrosis
and sclerosing arteritis with narrowing or occlusion of
small arteries. Clinical signs include azotemia, protein-
uria, and hypertension. In general, the changes are irre-
versible.
Sonographic Findings
Gray-scale imaging of accelerated and acute rejection, both
vascular and interstitial types, is usually normal. Findings
when present include increased renal volume, enlarged
hypoechoic medullary pyramids, loss of corticomedullary
differentiation, increased parenchymal echogenicity, thick-
ening of the uroepithelium lining of the renal pelvis (Fig.
11.94), and mild dilatation of the intrarenal collecting
system.
Acute vascular rejection affects the vascular impedance
to a greater degree than other forms of rejection and most
other parenchymal processes. This is reflected by a high-
resistance waveform, seen as elevated peak _systolic flow,
decreased or reversed diastolic flow, and elevated RIs
(range 0.7 to 1.0, mean 0.83) (Fig. 11.95) (225,226). The
RIs in acute interstitial rejection are usually normal (range
0.4 to 0.85, mean 0.6), because there is no increased vas-
cular impedance (221).
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442 P E D I AT R I C S O N O G R A P H Y
Acute rejection. The extraperitoneal allograft (calipers)
Fig. 11.94
is enlarged with thickened uroepithelium in the renal
pelvis (arrows). Parenchymal echogenicity is normal.
With a resistive index of 0.7 or greater, the sensitivity
for diagnosing acute rejection in children is about 90%
and the specificity is approximately 70%. At a resistive
index of 0.80 or greater, the specificity for rejection
increases to 90%, but the sensitivity decreases to 65%
(221). In general, elevated resistive indices are nonspecific
and can be caused by rejection, pyelonephritis, acute tubu-
lar necrosis, drug toxicity, renal vein thrombosis, and
parenchymal compression by a perirenal fluid collection
(227). Because of this overlap, the role of the RI in diag-
nosing parenchymal disease remains controversial. Renal
biopsy is required to definitively determine the specific
cause of graft dysfunction.
Acute vascular rejection. Pulsed Doppler waveform from
Fig. 11.95
the main renal artery shows decreased diastolic flow
due to high impedance. The resistive index is elevated, measuring 0.88.
Chronic allograft rejection. Longitudinal sonogram shows
Fig. 11.96
an irregular cortical margin with focal parenchymal loss
(arrow) consistent with an old infarct. Resistive indices were normal.
The gray-scale findings of chronic rejection are a
small allograft, decreased cortical thickness, increased
cortical echogenicity, loss of corticomedullary differenti-
ation, and cortical scarring related to focal infarctions
(Fig. 11.96). The RIs are usually normal (range 0.4 to
0.85, mean 0.59) (221).
TUBULAR NECROSIS AND DRUG TOXICITY
Acute tubular necrosis generally occurs in the first
24 hours after transplantation and is the result of pro-
longed ischemia of the transplanted kidney (228). Histo-
logically, there is swelling and disruption of tubular cells.
The process usually is self-limited, with renal function
eventually returning to normal. Clinical findings include
oliguria, increasing creatinine levels, and enlargement and
tenderness of the graft.
The sonographic findings of acute tubular necrosis are
similar to those of acute rejection and include allograft
enlargement, increased cortical echogenicity, loss of corti-
comedullary differentiation, and enlarged hypoechoic pyr-
amids. Reversed diastolic flow and high RIs can be seen in
patients with severe tubular necrosis.
Drug nephrotoxicity is another cause of graft failure
and diminished renal function. Cyclosporine-induced
nephropathy produces tubular damage as well as interstitial
nephritis, glomerular thrombi, and endothelial swelling,
usually within 1 to 4 months after transplantation. Gray-
scale and Doppler findings are usually normal (221,227).
Because the arterioles are spared, diastolic flow is main-
tained and RIs are generally normal, ranging from 0.4 to
0.8.
Vascular Complications
Vascular complications include renal artery thrombosis
and stenosis, arteriovenous fistula, pseudoaneurysm, and
renal vein thrombosis (229231).
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Chapter 11 U R I N A R Y T R A C T 443

A B
Transplant, renal artery thrombosis. A: Longitudinal sonogram from the upper pole of the allograft shows normal Doppler waveforms.
Fig. 11.97
B: A waveform could not be obtained from the lower pole of the renal allograft. This patient had two renal arteries. At re-exploration,
the lower pole renal artery was occluded by thrombus.

ARTERIAL THROMBOSIS AND INFARCTION
Main renal artery thrombosis occurs in up to 1% of allo-
grafts. It usually occurs in the immediate postoperative
period (within the first week) and causes either global or
segmental infarction of the transplant with resultant loss
of the graft (232). Causative factors are twisting or kink-
ing of the renal artery, intraoperative intimal damage,
hyperacute or acute rejection, and hypercoagulable states.
Gray-scale sonography shows global or focal cortical
hyperechogenicity and loss of corticomedullary differenti-
ation. Pulsed and color Doppler imaging demonstrate
absent flow in the involved renal artery and within the
graft parenchyma (Fig. 11.97).
producing spectral broadening and reversed diastolic flow,
and (d) dampened intrarenal arterial waveforms distal to
the site of stenosis (tardus-parvus waveform) (229233).
Color Doppler findings include (a) a narrowed vascular
lumen; (b) perivascular soft tissue vibrations, appearing as
an admixture of arterial and venous flow, around the
stenotic segment; and (c) spectral broadening.
Although sonography is a sensitive technique for the eval-
uation of stenosis, it cannot differentiate between arterial
kinking and main renal artery stenosis. MRI or arteriography
is required for differentiation.

RENAL ARTERY STENOSIS

Renal artery stenosis occurs in up to 10% of allografts in
children. The stenosis usually is at the anastomotic site,
but it can occur in the distal donor or recipient artery.
Anastomotic stenoses occur more often in allografts with
end-to-end anastomoses; distal donor stenosis occurs fre-
quently in those grafts with end-to-side anastomoses; and
stenosis of the recipient artery occurs with either end-to-
end or end-to-side anastomoses. The diagnosis is suspected
clinically when there is recent onset of severe hypertension
in association with graft dysfunction or a bruit over the
iliac artery. Since stenoses can occur anywhere along the
course of the artery, the entire length of the renal artery
from the renal hilum to the iliac arteries must be evaluated
sonographically.
Gray-scale findings are usually normal. Pulsed Doppler
findings are similar to those previously described for native Transplant, main renal artery stenosis. Doppler waveform
arterial stenosis and include (a) rapid systolic acceleration Fig. 11.98
shows high systolic flow (388 cm/sec) and decreased
with a high peak frequency systolic shift at the stenotic diastolic flow at the stenotic site. Flow turbulence causes perivascular
site, greater than 180 cm/sec (Fig. 11.98); (b) diastolic soft tissue vibrations, which are seen as low-frequency reflections
damping at the stenotic site; (c) poststenotic turbulence (arrows) on each side of the baseline.
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444 P E D I AT R I C S O N O G R A P H Y

ARTERIOVENOUS FISTULA
Arteriovenous fistula usually follows percutaneous renal
biopsy. Small fistulas are commonly asymptomatic. Large
fistulas can be a cause of hypertension, hematuria, or high-
output cardiac failure. Small asymptomatic fistulas usually
resolve spontaneously; large symptomatic fistulas may
require surgical ligation or embolization.
In most cases, the gray-scale sonogram is normal.
Pulsed Doppler abnormalities include (a) increased systolic
and end-diastolic velocities in the supplying artery; (b) tur-
bulent flow at the site of the fistula, resulting from the
large pressure drop from the supplying artery to the drain-
ing vein; and (c) increased flow velocities and arterializa-
tion in the efferent vein (see Fig. 11.81). Color Doppler
abnormalities include an enlarged supplying artery and
draining vein with turbulence in the affected vessels and
perivascular soft tissue vibrations resulting in random
color assignment in the parenchyma adjacent to the fistula.

PSEUDOANEURYSM
A pseudoaneurysm is a localized rupture of an artery con-
tained by surrounding soft tissues. It is usually a late compli-
cation and can occur at the anastomotic site or in the allo-
graft. Anastomotic pseudoaneurysms are the result of suture
rupture, leakage, or vessel wall ischemia. Intrarenal pseudoa-
neurysms are caused by percutaneous needle biopsy and usu-
ally involve the arcuate arteries. Most pseudoaneurysms are
clinically occult, although they can produce hematuria if they
rupture into the collecting system. Pseudoaneurysms usually
involute spontaneously.
Sonographically, a pseudoaneurysm appears as a
hypoechoic mass at the anastomotic site or within the allo-
graft. Pulsed and color Doppler imaging at the neck of the
pseudoaneurysm shows high-velocity, to-and-fro flow with
blood entering the pseudoaneurysm during systole (flow
above baseline) and leaving during diastole (flow below
baseline). Doppler imaging of the pseudoaneurysm itself
shows a disorganized, swirling pattern of mixed arterial
and venous blood flow (Fig. 11.99), which may contain
areas of signal void due to clot formation (221).
RENAL VEIN THROMBOSIS
Renal vein thrombosis is a rare complication of renal
transplantation and is usually the result of ischemic
changes in the vein wall at the anastomotic site. Other pre-
disposing factors are diminished intrarenal flow due to
acute vascular rejection, shock or dehydration, and
cyclosporine therapy, which enhances platelet aggregation.
Clinical findings of renal vein thrombosis include hema-
turia, hypertension, renal failure, and graft tenderness.
Prompt diagnosis of renal vein thrombosis is important
because immediate thrombectomy may save the graft.
Gray-scale sonography shows allograft enlargement;
increased cortical echogenicity reflecting edema secondary
to obstructed venous outflow; and cortical heterogeneity,
usually indicating hemorrhagic infarction. The demonstra-
tion of echogenic material within a renal vein is diagnostic
of thrombosis.
Pseudoaneurysm. Color Doppler waveform shows a
Fig. 11.99
swirling pattern of internal color flow in the pseudo-
aneurysm (arrows). Pulsed Doppler waveform shows to-and-fro flow.
Flow above the baseline indicates blood entering the pseudoaneurysm
during systole and flow below the baseline indicates blood exiting dur-
ing diastole.
Pulsed Doppler interrogation of the main and segmental
veins shows absent Doppler signals or decreased flow if
there is nonocclusive thrombus. Doppler sonography of the
main and intrarenal arteries shows (a) sharply peaked,
spike-like, systolic arterial frequency shifts and (b) absent or
reversed diastolic arterial flow. The RI exceeds 1.0 because
of the reversed diastolic flow (see Fig. 11.84) (221,224,228).
Perinephric Fluid Collections
Peritransplant fluid collections include lymphoceles, uri-
nomas, hematomas, and abscesses. The sonographic
appearances of these fluid collections are largely indistin-
guishable, and final diagnosis often requires clinical cor-
relation or needle aspiration of the fluid (221,228). Most
peritransplant fluid collections are small and clinically
insignificant.
LYMPHOCELE
Lymphoceles are the most common perinephric fluid col-
lections, occurring in approximately 20% of transplants
(221). They are the result of seepage of lymph from sev-
ered lymphatic vessels in the transplant bed and usually
develop within 2 to 8 weeks of surgery (221,228). Large
lymphoceles may cause local findings, such as a palpable
pelvic or inguinal mass, ipsilateral lower extremity edema,
or decreased renal function secondary to ureteral com-
pression.
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Chapter 11 U R I N A R Y T R A C T 445

A B
Lymphocele. A: Longitudinal sonogram shows a septated fluid collection (calipers) beneath the transplanted kidney (TX). B: Trans-
Fig. 11.100
verse sonogram in another patient shows a unilocular fluid collection (FL) inferior to the allograft. TX  transplanted kidney.

At sonography, lymphoceles typically appear as well- ones are hypoechoic. The RI can be elevated if diastolic
defined complex hypoechoic masses with internal septations flow decreases secondary to the compressive effect of the
(Fig. 11.100). Occasionally, they are unilocular (Fig. fluid collection.
11.100B). Most lymphoceles are located inferomedial to the
allograft between the kidney and the bladder. Hydronephro- ABSCESS
sis can be observed if the lymphocele compresses the ureter. Abscesses usually result from superimposed infection of a
lymphocele, hematoma, or urinoma. Less commonly they
URINOMA are a complication of graft pyelonephritis. Most occur
Urinomas occur in about 3% of transplants. The most within 2 months of surgery. Patients present with fever,
common cause of urine leakage is a defect at the uretero- leukocytosis, and pain over the allograft.
neocystostomy. Other causes are renal biopsy or ureteral
necrosis from vascular compromise. Urinomas almost
always form within the first 2 weeks of transplantation
and produce clinical findings of oliguria, pain, and
swelling over the allograft (221,228).
Sonography shows an anechoic fluid collection inter-
posed between the allograft and bladder. Unlike lympho-
celes, they rarely contain septations (Fig. 11.101). Since
most urinomas are located near the lower margin of the
allograft, they can compress the ureter, leading to
hydronephrosis. Renal scintigraphy or percutaneous nee-
dle aspiration and biochemical analysis of the lesion can
help to establish the diagnosis.

HEMATOMA
Hematomas can occur in the immediate postoperative
period as a normal sequela of surgery or they can develop
later as a complication of percutaneous biopsy. They can
be perirenal, subcapsular, or intrarenal in location. Small
hematomas are usually clinically insignificant. Large
hematomas may result in a decreased hematocrit, dimin-
ished urine output secondary to ureteral compression, and
graft and back pain. Urinoma. Longitudinal sonogram shows the urinoma as
The sonographic appearance varies with the age of Fig. 11.101
a unilocular fluid collection (FL). In the absence of sep-
the hemorrhage. Acute hematomas are hyperechoic tations, differentiation from lymphocele requires needle aspiration or
(Fig. 11.102), subacute ones are complex, and chronic scintigraphy.
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446 P E D I AT R I C S O N O G R A P H Y
Acute subcapsular hematoma. Longitudinal sonogram
Fig. 11.102
following a biopsy shows an echogenic fluid collection
(calipers) compressing the renal parenchyma. Percutaneous aspira-
tion of the fluid collection revealed blood.
The sonographic appearance is nonspecific and
includes a hypoechoic fluid collection (Fig. 11.103), com-
plex mass containing debris and/or septations, and hyper-
echoic fluid collection containing highly reflective echoes
with acoustic shadowing secondary to a gas-producing
organism. Specific diagnosis requires aspiration.
Ureteral Obstruction
Ureteral obstruction occurs in 1% to 10% of transplants
and can be caused by intrinsic lesions, such as ureteral stric-
ture, clot or calculi, or extrinsic compression by a lympho-
cele, urinoma, or hematoma. Ureteral stricture is a late
complication of transplantation and can be the result of
ischemia, rejection, or infection. Most strictures (80% to
85%) are located in the distal ureter near the ureterovesical
junction. Patients present with deteriorating renal function.
A B
Ureteral stricture. A: Sonogram of the allograft shows a dilated renal pelvis and calyces. B: Longitudinal sonogram below the allo-
Fig. 11.104
graft shows a dilated distal ureter (calipers).
Abscess. Longitudinal sonogram shows a hypoechoic
Fig. 11.103
fluid (FL) collection anterior to the allograft. Aspiration
yielded purulent fluid.
The dilated intra- and extrarenal collecting system is easily
recognized by sonography (Figs. 11.104 and 11.105).
It is important to recognize that mild degrees of dilata-
tion may not represent obstruction (228). Immediately
posttransplant, mild dilatation is a normal occurrence and
can be due to transient edema at the ureteroneocystostomy
site or reduced peristalsis related to denervation of the col-
lecting system during allograft harvest. A distended blad-
der, which increases resistance to ureteral emptying, can
result in dilatation of the collecting system. The dilatation
in this instance usually resolves after the patient empties
the bladder. Mild dilatation of the collecting system in the
absence of anatomic obstruction also has been described in
allograft rejection. The ureteral musculature is infiltrated
by edema and mononuclear cells during acute rejection,
leading to decreased peristalsis and eventual dilatation.
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Hydroureter. Longitudinal sonogram shows a dilated
Fig. 11.105
distal left ureter (calipers) extending from the renal
transplant (TX) to a fluid collection, proven to be a lymphocele (L).
Lymphoproliferative Disorder
Posttransplant lymphoproliferative disorder (PTLD) repre-
sents a spectrum of abnormal lymphocytic proliferation that
ranges from polymorphic hyperplasia to monomorphic
lesions and lymphoma (234). Immunosuppression, particu-
larly with antilymphocyte antibodies, and infection with
Epstein-Barr virus are well-recognized factors that predispose
patients to lymphoproliferative disorder. This disorder can
involve the native kidney or renal allograft. Treatment is reduc-
tion in immunosuppression. Allograft involvement by PTLD
or lymphoma causes either an isoechoic or hypoechoic mass or
diffuse cortical thickening (Fig. 11.106) (234).
Miscellaneous Complications
Calculi and urinary tract infections are unusual complica-
tions of transplantation. Calcifications usually are late
complications (6 months after transplantation) and
Allograft posttransplant lymphoproliferative disease.
Fig. 11.106
Longitudinal view of a transplanted right kidney shows
a focal hypoechoic mass (calipers) measuring 2.6  2.0 cm. Biopsy
proved lymphoproliferative disease.
Chapter 11 U R I N A R Y T R A C T 447
Allograft calcification. An echogenic focus (arrow),
Fig. 11.107
measuring 2.5 mm, represents a calculus, possibly
related to prior biopsy.
occur in less than 1% of allografts. Risk factors include
biopsy, recurrent urinary tract infections, ureteral stricture,
and altered calcium metabolism (renal tubular acidosis,
hypercalcemia, hypophosphatemia). Stones also may be
present in the donor kidney. Sonography shows echogenic
foci with acoustic shadowing, either in the renal
parenchyma or the collecting system (Fig. 11.107).
Infection can be an early or late complication. The
common causative organisms are cytomegalovirus, herpes
simplex virus, C. albicans, and E. coli. Sonography usually
is normal, although occasionally increased parenchymal
echogenicity (Fig. 11.108), hydronephrosis, or a fungal
ball can be observed in the allograft. The RI can be ele-
vated in severe infection, reflecting intrarenal edema.
Allograft infection. Transverse sonogram of a right lower
Fig. 11.108
quadrant allograft shows areas of patchy increased
echogenicity (arrows). Cultures grew Candida albicans.
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448 P E D I AT R I C S O N O G R A P H Y

A B
Normal urinary bladder. A: Transverse sonogram demonstrates a fluid-filled bladder (BL). The wall is imperceptible. B: With the blad-
Fig. 11.109
der incompletely filled, the walls (arrows) appear falsely thickened. The thickness measures 5 mm.

BLADDER AND URETHRA
Scanning Techniques and Normal Anatomy
The bladder is best evaluated when it is moderately filled,
which is achieved either by having the patient not void for
several hours prior to the examination or by instilling ster-
ile water into the bladder via catheterization. Overdisten-
tion of the bladder should be avoided since it increases
patient discomfort. High-frequency linear array or curved
array transducers are used to obtain transverse and sagit-
tal views of the bladder.
The bladder is an ovoid structure in the bony pelvis,
inferior and anterior to the peritoneal cavity and partially
posterior to the pubic bones. The innermost layer of the
bladder is lined by mucosa. Adjacent to the mucosa are the
muscular layers of the bladder, including an inner longitu-
dinal muscle layer, a middle circular muscle layer, and an
outer longitudinal muscle layer. A subserosal layer com-
posed of loose connective tissue covers the muscular lay-
ers. The normal bladder wall is smooth and of uniform
thickness. The wall thickness depends on the degree of
bladder distention; the upper limits are 3 and 5 mm for a
full or empty bladder, respectively (Fig. 11.109) (235).
Bladder volume can be estimated by the following for-
mula: depth  height  width  a correction factor (236).
Sonographic evaluation of bladder volume is a noninvasive
method to evaluate bladder capacity and estimate the
amount of residual urine volume, which can be abnormal
in bladder dysfunction disorders such as meningomyelo-
cele, sacral agenesis, and myelitis (237).
The male and female urethra as well as the seminal
vesicles and prostate gland in the male patient can be
scanned with a transabdominal approach acquired with
the transducer angled caudally or with transperineal or
translabial approaches (Fig. 11.110) (46,48,49). A trans-
vaginal approach may be useful in pubertal girls.

A B
Normal seminal vesicles and prostate gland. A: Transverse caudally angled view shows oval seminal vesicles (arrowheads). B: More
Fig. 11.110
caudally angled view demonstrates the echogenic prostate gland (arrows). The cystic area represents a prostatic utricle (arrowhead).
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Congenital bladder diverticulum. Longitudinal sonogram
Fig. 11.111
demonstrates a thin-walled, fluid-filled diverticulum
(calipers) arising from the superior aspect of the bladder (B). Note the
smooth bladder wall.
Pathology
Abnormalities of the bladder may be of congenital, inflamma-
tory, neoplastic, postsurgical, or posttraumatic origin (238).
Congenital Anomalies
BLADDER DUPLICATION
Bladder duplication is a rare anomaly that consists of two
distinct bladder chambers, each drained by a separate ure-
thra. The septa may divide the bladder in the sagittal or
transverse planes (239).
BLADDER DIVERTICULA
Bladder diverticula are herniations of bladder mucosa
through fibers of the detrusor muscle. They are usually asso-
ciated with reflux, neurogenic bladders, or obstructed ure-
A B
Bladder augmentation. A: Transverse sonogram shows a normal-size bladder with irregular walls. B: Longitudinal image shows an
Fig. 11.112
echogenic inner lining representing mucosa (arrowheads) and a hypoechoic outer wall (arrows). Internal echoes (*) represent
mucus produced by the intestinal lining.
Chapter 11 U R I N A R Y T R A C T 449
thras, but they can be congenital. Diverticula secondary to
obstruction tend to be multiple and associated with bladder
cellules and trabeculation. Congenital diverticula are solitary,
and are often larger than those caused by obstruction or neu-
rogenic bladder. Congenital diverticula are associated with
Menkes syndrome (an abnormality of copper metabolism),
cutis laxa, Williams syndrome, and Ehlers-Danlos syndrome
(239). Patients with bladder diverticula present with urinary
tract infection, incontinence, or urinary retention.
At sonography, diverticula appear as round or oval an-
echoic fluid collections arising from the bladder base or
around the ureteric orifice. A dilated distal ureter secondary
to ureterovesical obstruction or reflux can be an associated
finding. Congenital diverticula usually occur with smooth-
walled bladders, while acquired ones are found with trabec-
ulated bladders (Fig. 11.111). Complications include infec-
tion, stone formation, and ureteral obstruction. Purulent
material and stones may increase the echogenicity of the
diverticular lumen.
BLADDER EXSTROPHY
Exstrophy of the bladder is the result of failure of midline clo-
sure of the infraumbilical abdominal wall, thus exposing the
anterior wall of the bladder. The bladder neck and urethra
also may be exposed. The bladder is small, but otherwise
normal at birth. Bladder exstrophy is obvious on physical
examination and sonography is not required for diagnosis,
although it is used to detect associated hydronephrosis due to
poor bladder emptying.
The surgery for exstrophy is a primary closure of the
abdominal wall and bladder with bladder augmentation.
In the augmentation procedure, a segment of bowel is
attached to the native bladder, which acts as the bladder
base or neck. The bladder is then more normal in size, but
it can still have irregular walls and it may contain echogenic
debris due to mucus production by the intestinal lining. The
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450 P E D I AT R I C S O N O G R A P H Y
walls may show the signature of bowel: a hypoechoic outer
wall and echogenic inner mucosa (Fig. 11.112).
URACHAL ANOMALIES
During fetal development, the anterior bladder wall and
umbilicus communicate with each other via a tubular
channel, known as the urachus. The urachus normally
closes during the fourth or fifth month of gestation
(238240). Incomplete obliteration of the urachal lumen
results in four major types of abnormalities: patent ura-
chus, urachal sinus, urachal diverticulum, and urachal
cyst. A patent urachus develops when there is failed oblit-
eration of the urachal lumen, resulting in a persistent chan-
nel between the bladder and umbilicus. The urachal sinus
is a persistence of the urachus only at its umbilical end.
The bladder end of the urachus is obliterated. Patients with
patent urachal channels or urachal sinuses present with
umbilical drainage or periumbilical infections.
The urachal diverticulum develops when there is failed
obliteration of the urachus at its bladder end, while the
Patent urachus. Longitudinal sonogram shows a par-
Fig. 11.113
tially fluid-filled fistulous tract (arrows) extending from
the bladder (BL) to the area of the umbilicus (U).
urachal cyst develops when both the cranial and caudal
urachal ends close and fluid accumulates in the central por-
tion, which remains open. Urachal diverticula and cysts
are usually clinically asymptomatic, although they may
present as palpable masses (239).
At sonography, the persistent urachus and the urachal
sinus are small-caliber tubular structures that are contigu-
ous with the umbilicus. The patent urachus also commu-
nicates with the bladder (Fig. 11.113). The urachal diver-
ticulum has a communication with the bladder dome,
does not communicate with the umbilicus, and empties
when the bladder is emptied (Fig. 11.114). The urachal
cyst appears as a midline, thin-walled, fluid-filled mass
located between the umbilicus and dome of the bladder
(Fig. 11.115). Internal echoes or debris may be seen in
both the diverticulum and cyst if they are infected or if
they contain calculi.
Complications associated with urachal remnants
include infection (termed pyourachus) and, rarely, ade-
nocarcinoma (241). Findings of pyourachus include an
Urachal diverticulum. Longitudinal sonogram shows a
Fig. 11.114
tubular fluid collection (arrows) arising from the dome
of the bladder (BL). The cyst did not communicate with the abdominal
wall. Asterisk indicates the rectus abdominis muscle.
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Urachal cyst. Longitudinal sonogram shows a round
Fig. 11.115
fluid collection (C) in the midline of the pelvis just
cephalad to the bladder (BL) and beneath the rectus abdominis mus-
cles (*). The cyst did not communicate with the bladder or the abdom-
inal wall.
echogenic mass contiguous with the bladder dome, rectus
muscle thickening, intraperitoneal abscess, ascites, and
bladder wall thickening (Fig. 11.116).
PROSTATIC UTRICLE
Prostatic utricles are remnants of the mllerian duct sys-
tem that persist in the midline between the bladder and
rectum (239). They are derived from mllerian ducts. The
normal prostatic utricle is 8 to 10 mm in length; it has a
tiny orifice (2 mm) at the verumontanum and a blind end-
ing. Small utricles are usually asymptomatic and detected
incidentally during imaging studies (see Fig. 11.110B).
Enlarged prostatic utricles can be seen with severe
Pyourachus. Longitudinal sonogram shows an echogenic
Fig. 11.116
mass (M) containing internal debris just superior to dome
of the bladder (BL), causing thickening of the bladder wall (arrowheads).
Chapter 11 U R I N A R Y T R A C T 451
Utricle in an infant with perineal hypospadias. Longitu-
Fig. 11.117
dinal sonogram shows a midline fluid-filled utricle (U)
posterior to the bladder (B) base.
hypospadias, undescended testis, and renal agenesis (239).
Large utricles can present with signs of bladder outlet
obstruction. Sonography shows a midline cyst with or
without internal echoes, posterior and caudal to the blad-
der base (Fig. 11.117).
CONGENITAL MEGACYSTIS
Congenital megacystis, megacystis-megaureter syndrome,
and megacystis-microcolon-hyperperistalsis syndrome
are functional disorders of the bladder. Congenital
megacystis is characterized by a large bladder in the
absence of obstruction, reflux, or other pathology.
Megacystis-megaureter syndrome refers to a large
bladder, dilated ureteral orifices, and dilated refluxing
ureters. During micturition, large volumes of urine flow
back up into the ureters from the bladder. Between mic-
turition cycles, the urine flows back into the bladder,
eventually producing an atonic, thin-walled and dilated
bladder (239).
Megacystis-microcolon-hyperperistalsis syndrome
is an uncommon functional obstruction of the
bladder and intestine, which occurs almost exclusively in
girls. This syndrome is characterized by a dilated blad-
der, hydroureters, hydronephrosis, a small colon, and
dilated small bowel. The entire gastrointestinal tract is
hypoperistaltic. The condition is invariably fatal unless
the patient can be maintained on total parenteral hyper-
alimentation.
Neurogenic Bladder
Normally, all parts of the lower urinary tract (i.e., the
detrusor, internal, and external sphincter mechanism)
function together to allow storage and evacuation of urine.
A neurogenic bladder results when these components fail
to act as a coordinated unit. The neurogenic bladder in
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452 P E D I AT R I C S O N O G R A P H Y
Neurogenic bladder. Longitudinal sonogram shows
Fig. 11.118
residual urine and an irregular, thick bladder wall
(arrows). Wall thickness measures 8 mm.
childhood is most often congenital due to a meningocele or
a myelomeningocele or to sacral agenesis. Acquired causes
are rarer and include traumatic paraplegia, encephalitis, or
meningitis. The lower motor neuron lesions result in
smooth, large-capacity, thin-walled bladders. Lesions
above the sacral reflux produce a trabeculated, small,
thick-walled bladder (Fig. 11.118). Complications, such as
bladder calculi, can be identified by sonography. Postvoid
images of the bladder are useful in evaluating bladder
function and usually demonstrate varying amounts of
residual urine due to inability of patients to empty the
bladder completely.
Bladder augmentation is an operation designed to
increase the volume of the small or high-pressure neuro-
A B
Bladder calculi. A: Sonogram in the left decubitus position shows multiple shadowing stones (arrows) within the bladder (BL). B: On
Fig. 11.119
a transverse sonogram, the stones layer on top of one another, producing a larger echogenic focus (arrows) with acoustic shadow-
ing. BL  bladder.
genic bladder. The technique uses a loop of bowel as a con-
duit attached to the bladder. Sonography shows an irregu-
larly shaped bladder and echogenic bowel mucosa (see
Fig. 11.112), which may exhibit peristalsis at real-time
imaging. Mucus produced by the bowel lining causes intra-
luminal echoes.
Bladder Calculi
The factors associated with formation of bladder calculi
include an intravesical foreign body, infection with urea-
splitting organisms (usually Proteus), exstrophy of the
bladder, bladder augmentation, stasis of urine, and hyper-
calciuria. Affected patients can present with symptoms and
signs of infection or bladder neck obstruction. Bladder cal-
culi are echogenic, producing sharp acoustic shadowing
(Fig. 11.119). They shift to the dependent portion of the
bladder with changes in patient position. The endoscopic,
submucosal injection of bulking agents for treatment of
reflux can cause a hyperechoic focus with distal shadowing
that mimics bladder calculi, but bulking agents do not shift
position (See Fig. 11.73).
Neoplasms
MALIGNANT TUMORS
Bladder tumors in children are rare and more often malig-
nant than benign, with rhabdomyosarcoma being the most
common. Bladder rhabdomyosarcoma typically involves
the submucosal region of the trigone; less often, it origi-
nates in the dome of the bladder. There are two peak age
incidences: the first between 2 and 6 years and the second
between 14 and 18 years (242,243). Affected children usu-
ally present with urinary retention or painless gross hema-
turia. Transitional cell carcinoma and leiomyosarcomas
are rare bladder tumors in children (244,245).
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Chapter 11 U R I N A R Y T R A C T 453

A B
Rhabdomyosarcoma of the bladder wall. A: Longitudinal sonogram shows an echogenic, polypoid intravesicular mass (arrows) aris-
Fig. 11.120
ing from the bladder base. The cystic changes are secondary to necrosis. B: Longitudinal color Doppler sonogram in another patient
shows an echogenic mass (arrows) with increased vascularity at the bladder base.

Sonographically, rhabdomyosarcoma appears either
as an echogenic pedunculated soft tissue mass projecting
into the bladder lumen, referred to as a botryoid or
bunch of grapes appearance, or as focal wall thicken-
ing. Polypoid lesions often are complex with cystic areas
representing areas of hemorrhage or necrosis (see Fig.
11.120A). Infiltrating tumors produce irregular wall
thickening with an echogenicity equal to or less than that
of the bladder wall. With deep invasion, the bladder wall
is markedly deformed and rigid, and bladder capacity is
diminished. Hydronephrosis and invasion of perivesical
structures also can be noted. Metastases to pelvic lymph
nodes can be diagnosed when the involved nodes are
enlarged. Transitional cell cancer and other sarcomas
also can manifest as intraluminal polypoid masses or wall
thickening.
Diffuse bladder wall thickening by rhabdomyosarcoma
can be confused with cystitis, although the thickening usu-
ally is uniform in cystitis, whereas it is irregular in tumor
infiltration.
of tumor along the neurovascular bundles is a clue to the
diagnosis of neurofibromatosis. In most cases, tissue
sampling is needed for diagnosis. Bladder wall thicken-
ing due to ureteral reimplantation, submucosal injection
of bulking agents, or infection can be mistaken for blad-
der neoplasm, but the clinical history should allow dif-
ferentiation.
URETHRAL POLYPS
Congenital urethral polyp is the most common urethral
tumor (46,48,49). Histologically, it is composed of fibrous
tissue covered by epithelium. It arises near the verumon-
tanum and is attached to it by a stalk. Pedunculated polyps

BENIGN LESIONS
Benign bladder lesions include hemangioma, neurofi-
broma, paraganglioma (pheochromocytoma), papilloma,
nephrogenic adenoma, and leiomyoma. On sonography,
these tumors appear as well-circumscribed, sessile or poly-
poid masses arising within the bladder wall and projecting
into the bladder lumen (Fig. 11.121) (246248). They
may be homogeneous or complex, containing cystic areas
corresponding to old hemorrhage and necrosis or hypere-
choic areas related to acute hemorrhage. The diagnosis of Benign bladder tumor. Transverse sonogram of the
hemangioma or paraganglioma should be suspected when Fig. 11.121
bladder in a 10-year-old boy with hematuria shows a
Doppler shows hypervascularity. A history of micturition polypoid mass (arrow) near the right ureteral orifice. Cystoscopic
syncope should suggest pheochromocytoma. Distribution resection revealed a benign papilloma.
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454 P E D I AT R I C S O N O G R A P H Y

Trauma
Injury to the bladder and urethra in childhood most often
occurs with blunt trauma, but it can also be a complication
of surgery or penetration by a foreign body. CT is the
study of choice in evaluating suspected bladder trauma,
but sonography may be of value in follow-up evaluation.
Sonographic findings of bladder trauma include focal or
diffuse wall thickening, intraluminal clot, and free pelvic
and/or abdominal fluid.

Cystitis. Transverse sonogram shows diffuse bladder
Fig. 11.122
wall thickening (arrows). The greatest thickness mea-
sured from the inner to outer wall was 8 mm.
can prolapse into the bladder, obstructing the bladder neck
or urethra. Symptoms are nonspecific and include hema-
turia, urinary retention, infection, and enuresis. Urethral
polyps appear as echogenic masses in the bladder or pro-
static or bulbous urethra.
Cystitis
Inflammation of the urinary bladder or cystitis is usually
bacterial or viral in origin, but other causes include fungal
infection; drug therapy, particularly cyclophosphamide
(249); and indwelling catheters. Patients present with
dysuria and hematuria. The common sonographic findings
are diffuse bladder wall thickening (i.e., 3 mm) and
echogenic debris or a fluid-fluid level in the bladder lumen
(Fig. 11.122). Occasionally, cystitis produces focal wall
thickening or a polypoid mass (inflammatory pseudotu-
mor) that is difficult to differentiate from tumor based on
imaging findings alone, and biopsy may be needed for
diagnosis.
Cystitis cystica is an inflammatory process of the
mucosa that is usually localized to the trigone and ureteral
orifices. Sonography shows a broad-based irregular, isoe-
choic or hyperechoic soft tissue mass. Large inflammatory
lesions can protrude into the bladder lumen, mimicking
rhabdomyosarcoma.
Postsurgical Findings
The changes of ureteral reimplantation and injection of
bulking agents are focal bladder wall irregularity and an
echogenic mound of tissue (i.e., mucosal pseudomass) (see
Fig. 11.73). The changes of surgical or endoscopic unroof-
ing of ectopic ureterocele are a pseudomass, focal mucosal
thickening, and a residual ureterocele (see Fig. 11.27)
(250).
REFERENCES
1. Bartram U, Darge K. Harmonic versus conventional ultrasound
imaging of the urinary tract in children. Pediatr Radiol
2005;35:655660.
2. Govind B, Chavhan GB, Parra DA, et al. Normal Doppler spec-
tral waveforms of major pediatric vessels: specific patterns.
Radiographics 2008;28:691706.
3. Kadioglu A. Renal measurements including length, parenchy-
mal thickness and medullary pyramid thickness in healthy chil-
dren: what are the normative ultrasound values? AJR 2010;
194:509514.
4. Leung VY-F, Chu WC-W, Yeung C-K, et al. Nomograms of
total renal volume, urinary bladder volume and bladder wall
thickness index in 3,376 children with a normal urinary tract.
Pediatr Radiol 2007;37:181188.
5. Carrico CWT, Zerin JM. Sonographic measurement of renal
length in children: does the position of the patient matter?
Pediatr Radiol 1996;26:553555.
6. Han BK, Babcock DS. Sonographic measurements and appear-
ance of normal kidneys in children. AJR Am J Roentgenol 1985;
145:611616.
7. Bouzada MCF, Oliveira EA, Pereira AK, et al. Diagnostic
accuracy of postnatal renal pelvic diameter as a predictor of
uropathy: a prospective study. Pediatr Radiol 2004;34:
798804.
8. Tsai TC, Lee HC, Huang FY. The size of the renal pelvis on
ultrasonography in children. J Clin Ultrasound 1989;17:
647651.
9. Stavel M, Zibolen M, Kolarovzka H, et al. Comparison of
Doppler parameters of central versus intraparenchymal renal
arteries in physiologically normal newborns. Pediatr Radiol
2004;34:552555.
10. Helenon O, Rody FE, Correas J-M, et al. Color Doppler US of
renovascular disease in native kidneys. Radiographics 1995;15:
833854.
11. Bude RO, DiPietro MA, Platt JF, et al. Age dependence of the
renal resistive index in healthy children. Radiology 1992;184:
469473.
12. Andriani G, Persico A, Tursini S, et al. The renal-resistive index
from the last 3 months of pregnancy to 6 months old. BJU Int
2001;87:562564.
13. Kuzmic A, Brkljacic B, Ivankovic D, et al. Doppler sonographic
renal resistance index in healthy children. Eur Radiol 2000;10:
16441648.
14. Armstrong D, Teele R, Kuschel C, et al. The use of renal
Doppler ultrasonography to diagnose patent ductus arteriosus
in preterm infants. J Ultrasound Med 2001;20:10051010.
15. Leung VY-F, Chu WC-W, Yeung C-K, et al. Doppler waveforms
of the ureteric jet: and overview and implications for the pres-
ence of a functional sphincter at the vesico-ureteric junction.
Pediatr Radiol 2007;37:417425.
16. Patriquin H, Lefaivre J-F, Lafortune M, et al. Fetal lobation. An
anatomo-ultrasonographic correlation. J Ultrasound Med
1990;9:191197.
LWBK505-C11_p384-460.qxd 7/7/10 1:36 PM Page 455 Aptara Inc
17. Yeh HC, Halton KP, Shapiro RS, et al. Junctional parenchyma:
revised definition of hypertrophic column of Bertin. Radiology
1992;185:725732.
18. Patriquin H. Stasis nephropathy. In: Siegel BA, Proto AV, eds.
Pediatric disease (fourth series) test and syllabus. Reston, VA:
American College of Radiology, 1993:556583.
19. Bernstein J, Risdon RA, Gilbert-Barness E. Renal. In:
Gilbert-Barness E, ed. Potters pathology of the fetus and
infant. St. Louis, MO: Mosby-Year Book, Inc., 1997:
863935.
20. Husain AN, Pysher TJ, Dehner LP. The kidney and lower uri-
nary tract. In: Stocker JT, Dehner LP, eds. Pediatric pathology.
2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins,
2001:835903.
21. Barnewolt CE, Lebowitz RL. Absence of a renal sinus echo
complex in the ectopic kidney of a child: a normal finding. Pedi-
atr Radiol 1996;26:318323.
22. Decter RM. Renal duplication and fusion anomalies. Pediatr
Clin North Am 1997;44:13231341.
23. Clautice-Engle T, Anderson NG, Allan RB, et al. Diagnosis of
obstructive hydronephrosis in infants: comparison of sono-
grams performed 6 days and 6 weeks after birth. AJR Am J
Roentgenol 1995;164:963967.
24. Elder JS. Antenatal hydronephrosis. Pediatr Clin North Am
1997;44:12991321.
25. Platt JF. Duplex Doppler evaluation of native kidney dysfunc-
tion: obstructive and nonobstructive disease. AJR Am J
Roentgenol 1992;158:10351042.
26. Kessler RM, Quevedo H, Lankau CA, et al. Obstructive vs.
nonobstructive dilatation of the renal collecting system in chil-
dren: distinction with duplex sonography. AJR Am J Roentgenol
1993;160:353357.
27. Platt JF, Rubin JM, Ellis JH. Acute renal obstruction: evaluation
with intrarenal duplex Doppler and conventional US. Radiol-
ogy 1993;186:685688.
28. Coley BD, Arellano RS, Talner LB, et al. Renal resistive index
in experimental partial and complete ureteral obstruction. Acad
Radiol 1995;2:373378.
29. Riccabona M, Fritz GA, Schollnast H, et al. Hydronephrotic
kidney: pediatric three-dimensional US for relative renal size
assessment-initial experience. Radiology 2005;236:276283.
30. Rooks V, Lebowitz R. Extrinsic ureteropelvic junction obstruc-
tion from a crossing renal vessel: demography and imaging.
Pediatr Radiol 2001;31:120124.
31. Veyrac C, Baud C, Lopez C, et al. The value of color Doppler
ultrasonography for identification of crossing vessels in children
with pelvi-ureteric junction obstruction. Pediatr Radiol 2003;
33:745751.
32. Massad C, Smith E. Megaureter. In: Gonzales ET, Bauer SB,
eds. Pediatric urology practice. Philadelphia, PA: Lippincott
Williams & Wilkins, 1999:205221.
33. Meyer JS, Lebowitz RL. Primary megaureter in infants and chil-
dren: a review. Urol Radiol 1992;14:296305.
34. Leroy S, Vantalon S, Larakeb A, et al. Vesicoureteral reflux in
children with urinary tract infection: comparison of diagnostic
accuracy of renal US criteria. Radiology 2010;255:890898.
35. Tiballs JM, DeBruyn R. Primary vesicoureteral reflux-how
useful is postnatal ultrasound. Arch Dis Child 1996;75:
444447.
36. Marshall JL, Johnson ND, De Campo MP. Vesicoureteric reflux
in children: prediction with color Doppler imaging. Radiology
1990;175:355358.
37. Berrocal T, Gava F, Arjonilla A, et al. Vesicoureteral reflux:
diagnosis and grading with echo-enhanced cystosonography
versus voiding cystourethrography. Radiology 2001;221:
359365.
38. Darge K. Voiding urosonography with ultrasound contrast
agents for the diagnosis of vesico-ureteric reflux in children. I.
Procedure. Pediatr Radiol 2008;38:4053.
Chapter 11 U R I N A R Y T R A C T 455
39. Darge K. Voiding urosonography with ultrasound contrast
agents for the diagnosis of vesico-ureteric reflux in children. I.
Comparison with radiological examinations. Pediatr Radiol
2008;38:5463.
40. Papadopoulou F. Harmonic voiding urosongraphy with a second-
generation contrast agent for the diagnosis of vesicoureteral
reflux. Pediatr Radiol 2009;39:239244.
41. Darge K, Moeller RT, Trusen A, et al. Diagnosis of vesi-
coureteric reflux with low-dose contrast-enhanced harmonic
ultrasound imaging. Pediatr Radiol 2005;35:7378.
42. Share JC, Lebowitz RL. Ectopic ureterocele without ureteral
and calyceal dilatation (ureterocele disproportion): findings on
urography and sonography. AJR Am J Roentgenol 1989;152:
567571.
43. Fernbach SK, Zarwin JK, Lebowitz RL. Complete duplication of
the ureter with ureteropelvic junction obstruction of the lower
pole of the kidney: imaging findings. AJR Am J Roentgenol
1995;164:701704.
44. Zerin JM, Baker DR, Casale JA. Single-system ureteroceles in
infants and children: imaging features. Pediatr Radiol 2000;30:
139146.
45. Casale AJ. Posterior urethral valves and other obstructions of
the urethra. In: Gonzales ET, Bauer SB, eds. Pediatric urology
practice. Philadelphia, PA: Lippincott Williams & Wilkins,
1999:223244.
46. Levin TL, Han B, Little BP. Congenital anomalies of the male
urethra. Pediatr Radiol 2007;37:851862.
47. Cohen HL, Susman M, Halloer JO, et al. Posterior urethral
valve: transperineal US for imaging and diagnosis in male
infants. Radiology 1994;192:261264.
48. Berrocal T, Gaya F, Arjonilla A. Vesicoureteral reflux: can
the urethra by adequately assessed by using contrast-
enhanced voiding US of the bladder. Radiology 2005;234:
235241.
49. Duran C, Valera A, Alguersuari A, et al. Voiding urosonogra-
phy: the study of the urethra is no longer a limitation of the
technique. Pediatr Radiol 2009;39:124131.
50. Burge HJ, Middleton WD, McClennan BL, et al. Ureteral jets
in healthy subjects and in patients with unilateral ureteral cal-
culi: comparison with color Doppler US. Radiology 1991;180:
437442.
51. Wood BP. Renal cystic disease in infants and children. Urol
Radiol 1992;14:284295.
52. Dell KM. Polycystic disease. In: Kaplan BS, Meyers KEC, eds.
Pediatric nephrology and urology: the requisites in pediatrics.
Elsevier Mosby, 2004:214222.
53. Lonergan GJ, Rice RR, Suarez ES. Autosomal recessive poly-
cystic kidney disease: radiologic-pathologic correlation. Radi-
ographics 2000;20:837855.
54. Turkbey B, Ocak I, Daryanani K, et al. Autosomal recessive
polycystic kidney disease and congenital hepatic fibrosis
(ARPKD/CHF). Pediatr Radiol 2009;39:100111.
55. Kogutt MS, Robichaux WH, Boineau FG, et al. Asymmetric
renal size in autosomal recessive polycystic kidney disease: a
unique presentation. AJR Am J Roentgenol 1993;160:835836.
56. Blickman JG, Bramson RT, Herrin JT. Autosomal recessive
polycystic kidney disease: long-term sonographic findings in
patients surviving the neonatal period. AJR Am J Roentgenol
1995;164:12471250.
57. Herman TE, Siegel MJ. Pyramidal hyperechogenicity in autoso-
mal recessive polycystic kidney disease resembling medullary
nephrocalcinosis. Pediatr Radiol 1991;21:270271.
58. Traubici J, Daneman A. High-resolution renal sonography in
children with autosomal recessive polycystic kidney disease.
AJR Am J Roentgenol 2005;184:16301633.
59. Longa L, Scolari F, Brusco A, et al. A large TSC2 and PKD1
gene deletion is associated with renal and extrarenal signs of
autosomal dominant polycystic kidney disease. Nephrol Dial
Transplant 1997;12:19001907.
LWBK505-C11_p384-460.qxd 7/7/10 1:36 PM Page 456 Aptara Inc
456 P E D I AT R I C S O N O G R A P H Y
60. Jain M, LeQuesne GW, Bourne AJ, et al. High-resolution ultra-
sonography in the differential diagnosis of cystic diseases of the
kidney in infancy and childhood: preliminary experience.
J Ultrasound Med 1997;16:235240.
61. Ravine D, Gibson RN, Walker RG, et al. Evaluation of ultra-
sonographic criteria for autosomal dominant polycystic kidney
disease. Lancet 1994;343:824.
62. Fredericks BJ, de Campo M, Chow CW, et al. Glomerulocystic
renal disease: ultrasound appearances. Pediatr Radiol 1989;19:
184186.
63. Cook JA, Oliver K, Sampson MJ. A cross sectional study of
renal involvement in tuberous sclerosis. J Med Genet 1996;33:
480484.
64. McHugh K, Stringer DA, Hebert D, et al. Simple renal cysts in
children: diagnosis and follow-up with US. Radiology 1991;178:
383385.
65. Zinn HL, Rosberger ST, Haller JO, et al. Simple renal
cysts in children with AIDS. Pediatr Radiol 1997;27:
827828.
66. Beck AD. The effect of intra-uterine urinary obstruction upon
the development of the fetal kidney. J Urol 1971;105:
784789.
67. Atiyeh B, Husmann D, Baum M. Contralateral renal abnor-
malities in multicystic-dysplastic kidney disease. J Pediatr
1992;121:6567.
68. Karmazyn B, Zerin JM. Lower urinary tract abnormalities in
children with multicystic dysplastic kidney. Radiology 1997;203:
223226.
69. Hendry PL, Hendry GMA. Observations on the use of Doppler
ultrasound in multicystic dysplastic kidney. Pediatr Radiol
1991;21:203204.
70. Kountz PD, Siegel MJ, Shapiro E. Flank mass in a newborn.
Urol Radiol 1989;11:6164.
71. Jeon A, Cramer BC, Walsh E, et al. A spectrum of segmental
multicystic renal dysplasia. Pediatr Radiol 1999;29:
309315.
72. Strife JL, Souza AS, Kirks DR, et al. Multicystic dysplastic
kidney in children: US follow-up. Radiology 1993;186:
785788.
73. Agrons GA, Wagner BJ, Davidson AJ, et al. Multilocular cystic
renal tumor in children: radiologic-pathologic correlation.
Radiographics 1995;15:653669.
74. Hopkins JK, Giles HW, Wyatt-Ashmead J, et al. Best cases
from the AFIP: cystic nephroma. Radiographics 2004;24:
589593.
75. Joshi VV, Beckwith JB. Multilocular cyst of the kidney (cystic
nephroma) and cystic, partially differentiated nephroblastoma.
Terminology and criteria for diagnosis. Cancer 1989;64:
466479.
76. Lowe LH, Isuani BH, Heller RM, et al. Pediatric renal
masses: Wilms tumor and beyond. Radiographics 2000;20:
15851603.
77. Gervais DA, Whitman GJ, Chew FS. Multilocular cyst of the
kidney. AJR Am J Roentgenol 1993;161:600.
78. Shamberger RC. Pediatric renal tumors. Semin Surg Oncol
1999;16:105120.
79. Geller E, Smergel EM, Lowry PA. Renal neoplasms of child-
hood. Radiol Clin North Am 1997;35:13911413.
80. Dome JS, Perlman EJ, Richey ML, et al. Renal tumors. In: Pizzo
PA, Poplack DG, eds. Principles and practice of pediatric oncol-
ogy. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins,
2006:905932.
81. Richey ML, Azizkhan J, Beckwith B, et al. Neonatal Wilms
tumor. J Pediatr Surg 1995;30:856859.
82. Bulas DI, Thompson R. Pulmonary emboli as a primary mani-
festation of Wilms tumor. AJR Am J Roentgenol 1991;156:
155156.
83. Navoy JE, Royal SA, Vaid YN, et al. Wilms tumor: unusual
manifestations. Pediatr Radiol 1995;25:S76S86.
84. DeBaun MR, Siegel MJ, Choyke PL. Nephromegaly in
infancy and early childhood: a risk factor for Wilms tumor
in Beckwith-Wiedemann syndrome. J Pediatr 1998;132:
401404.
85. Choyke PL, Siegel MJ, Craft AW, et al. Screening for Wilms
tumor in children with Beckwith-Wiedemann syndrome or
idiopathic hemihypertrophy. Med Ped Oncol 1999;32:
196200.
86. Green D, Breslow N, Beckwith J, et al. Screening of children
with hemihypertrophy, aniridia, and Beckwith-Wiedemann
syndrome in patients with Wilms tumor: a report from the
National Wilms Tumor Study. Med Pediatr Oncol 1993;21:
188192.
87. Neville H, Ritchey ML, Shamberger RC, et al. The occurrence
of Wilms tumor in horseshoe kidneys: a report from the
National Wilms Tumor Study Group (NWTSG). J Pediatr Surg
2002;37:11341137.
88. Oddone M, Marino C, Sergi C, et al. Wilms tumor arising in a
multicystic kidney. Pediatr Radiol 1994;24:236238.
89. Song JH, Hansen K, Wallach MT. Extrarenal Wilms tumor.
J Ultrasound Med 1997;16:149151.
90. Charles AK, Vujanic GM, Berry BJ. Renal tumours of child-
hood. Histopathology 1998;32:293309.
91. Williams MA, Schropp KP, Noe HN. Fat containing renal mass
in childhood: a case report of teratoid Wilms tumor. J Urol
1994;151:16621663.
92. Aquisto TM, Yost R, Marshall KW. Best cases from the AFIP:
anaplastic wilms tumor: radiologic and pathologic findings.
Radiographics 2004;24:17091713.
93. Reiman TA, Siegel MJ, Shackelford GD. Wilms tumor in chil-
dren: abdominal CT and US evaluation. Radiology 1986;160:
501505.
94. White KS, Grossman H. Wilms and associated renal tumors of
childhood. Pediatr Radiol 1991;21:8188.
95. Brise HJ, Smets AM, Kaste C, Owens CM. Imaging in unilat-
eral Wilms tumour. Pediatr Radiol 2008;38:1829.
96. Park CM, Kim WS, Cheon JE, et al. Teratoid Wilms tumor in
childhood: CT and ultrasonographic appearances. Abdom
Imaging 2003;28:440443.
97. Johnson KM, Horvath LJ, Gaisie G, et al. Wilms tumor occur-
ring as a botryoid renal pelvicalyceal mass. Radiology 1987;163:
385386.
98. Nagahara A, Kawagoe M, Matsumoto F, et al. Botryoid Wilms
tumor of the renal pelvis extending into the bladder. Urology
2006;67:845.e15e17.
99. Yanai T, Okazaki T, Yamataka A, et al. Botryoid Wilms tumor:
a report of two cases. Pediatr Surg Int 2005;21:4346.
100. Mitchell CS, Yeo TA. Noninvasive botryoid extension of
Wilms tumor into the bladder. Pediatr Radiol. 1997;27:
818820.
101. Brown SD, Vansonnenberg E, Morrison PR, et al. CT-guided
radiofrequency ablation of pediatric Wilms tumor in a solitary
kidney. Pediatr Radiol 2005;35:923928.
102. Fernbach SK, Feinstein KA, Donaldson JS, et al. Nephroblas-
tomatosis: comparison of CT with US and urography. Radiol-
ogy 1988;166:153156.
103. Lonergan GJ, Martinez-Leon MI, Agrons GA, et al. Nephro-
genic rests, nephroblastomatosis, and associated lesions of the
kidney. Radiographics 1998;18:947968.
104. Machin GA, McCaughey WT. A new precursor lesion of Wilms
tumour (nephroblastoma): intralobar multifocal nephroblas-
tomatosis. Histopathology 1984;8:3553.
105. Rohrschneider WK, Weirich A, Rieden K, et al. US, CT and MR
imaging characteristics of nephroblastomatosis. Pediatr Radiol
1998;28:435443.
106. White KS, Kirks DR, Bove KE. Imaging of nephroblastomato-
sis: an overview. Radiology 1992;182:15.
107. Gallant JM, Barnewolt CE, Taylor GA, et al. Radiologic-
pathologic conference of Childrens Hospital Boston: bilateral
LWBK505-C11_p384-460.qxd 7/7/10 1:36 PM Page 457 Aptara Inc
asymptomatic renal enlargement. Pediatr Radiol 1997;27:
614617.
108. Selle B, Furtwangler R, Graf N, et al. Population-based study
of renal cell carcinoma in children in Germany, 19802005:
more frequently localized tumors and underlying disorders
compared with adult counterparts. Cancer 2006;107:
29062914.
109. Kraushaar G, Wiebe S. Renal cell carcinoma as a second malig-
nant neoplasm in a patient with non-syndromic hemihypertro-
phy and previous Wilms tumor. Pediatr Radiol 2005;35:
12081211.
110. Donnelly LF, Rencken IO, Shardell K, et al. Renal cell carcinoma
after therapy for neuroblastoma. AJR Am J Roentgenol 1996;
167:915917.
111. Fleitz JM, Wootton-Gorges SL, Wyatt-Ashmead J, et al. Renal
cell carcinoma in long-term survivors of advanced stage
neuroblastoma in early childhood. Pediatr Radiol 2003;33:
54545.
112. Sostre G, Johnson JF III, Cho M. Ossifying renal cell carci-
noma. Pediatr Radiol 1998;28:458460.
113. Kabala JE, Shield J, Duncan A. Renal cell carcinoma in child-
hood. Pediatr Radiol 1992;22:203205.
114. Hudson MM, Onciu M, Donaldson SS. Hodgkin lymphoma.
In: Pizzo PA, Poplack DG, eds. Principles and practice of pedi-
atric oncology. 5th ed. Philadelphia, PA: Lippincott Williams &
Wilkins, 2006:695721.
115. Link MP, Weinstein HJ. Malignant non-Hodgkin lymphoma in
children. In: Pizzo PA, Poplack DG, eds. Principles and practice
of pediatric oncology. 5th ed. Philadelphia, PA: Lippincott
Williams & Wilkins, 2006:722747.
116. Hugosson C, Mahr MA, Sabbah R. Primary unilateral renal
lymphoblastic lymphoma. Pediatr Radiol 1997;27:2325.
117. McGuire PM, Merritt CRB, Ducos RS. Ultrasonography of pri-
mary renal lymphoma in a child. J Ultrasound Med 1996;15:
479481.
118. Ng YY, Healy JC, Vincent JM, et al. The radiology of non-
Hodgkins lymphoma in childhood: a review of 80 cases. Clin
Radiol 1994;49:594600.
119. Sheth S, Ali S, Fishman E. Imaging of renal lymphoma: patterns
of disease with pathologic correlation. Radiographics 2006;26:
11511168.
120. Weinberger E, Rosenbaum DM, Pendergrass TW. Renal
involvement in children with lymphoma: comparison of
CT with sonography. AJR Am J Roentgenol 1990;155:
347349.
121. Hemmaway C, Walker MM, Deal J, et al. Teaching cases from
the Royal Marsden and St Marys Hospitals case 25. A young
boy with massive bilateral renal enlargement. Leuk Lymphoma
2004;45:13011303.
122. Jayagopal S, Cohen HL, Bhagat J, et al. Hyperechoic renal cor-
tical masses: an unusual sonographic presentation of acute lym-
phoblastic leukemia in a child. J Clin Ultrasound 1991;19:
425429.
123. Agrons GA, Kingsman KD, Wagner BJ, et al. Rhabdoid tumor
of the kidney in children: a comparative study of 21 cases. AJR
Am J Roentgenol 1997;168:447451.
124. Issacs H. Fetal and neonatal renal tumors. J Pediatr Surg 2008;
43:15871595.
125. Prasad SR, Humphrey PA, Menias CO, et al. Neoplasms of the
renal medulla: radiologic-pathologic correlation. Radiographics
2005;25:369380.
126. Winger DI, Buyuk A, Bohrer S, et al. Radiology-Pathology Con-
ference: rhabdoid tumor of the kidney. Clin Imaging 2006;30:
132136.
127. Sisler CL, Siegel MJ. Malignant rhabdoid tumor of the kidney:
radiologic features. Radiology 1989;172:211212.
128. Glass RB, Davidson AJ, Fernbach SK. Clear cell sarcoma of the
kidney: CT, sonographic, and pathologic correlation. Radiol-
ogy 1991;180:715717.
Chapter 11 U R I N A R Y T R A C T 457
129. Wesche WA, Wilmas J, Khare V, et al. Renal medullary carci-
noma: a potential sickle cell nephropathy of children and ado-
lescents. Pediatr Pathol Lab Med 1998;18:97113.
130. Blitman NM, Berkenblit RG, Rozenblit AM, et al. Renal
medullary carcinoma: CT and MRI features. AJR Am J
Roentgenol 2005;185:268272.
131. Ng AW, Lee PS, Howard RG. Primitive neuroectodermal kidney
tumour. Australas Radiol 2004;48:211213.
132. Filiatrault D, Hoyoux C, Benoit P, et al. Renal metastases from
neuroblastoma. Report of two cases. Pediatr Radiol 1987;17:
137138.
133. Ayres R, Curry NS, Gordon L, et al. Renal metastases from
osteogenic sarcoma. Urol Radiol 1985;7:3941.
134. Schlesinger AE, Rosendfield NS, Castle VP, et al. Congenital
mesoblastic nephroma metastatic to the brain: a report of two
cases. Pediatr Radiol 1995;25S:7375.
135. Vujani GM, Delemarre JFM, Moeslichan S, et al. Mesoblastic
nephroma metastatic to the lungs and heart another face of
this peculiar lesion: case report and review of the literature.
Pediatr Pathol 1993;13:143153.
136. Khashu M, Osiovich H, Sargent MA. Congenital mesoblastic
nephroma presenting with neonatal hypertension. J Perinatol
2005;25:433435.
137. Chaudry G, Perez-Atayde AR, Ngan BY, et al. Imaging of con-
genital mesoblastic nephroma with pathological correlation.
Pediatr Radiol 2009;39:10801086.
138. Riebel T, Kebelmann-Betzing C, Sarioglu N, et al. Unusual
mesoblastic nephroma in a young child. Pediatr Radiol 2003;
33(1):6265.
139. Kennelly MJ, Grossman HB, Cho KJ. Outcome analysis
of 42 cases of renal angiomyolipoma. J Urol 1994;152:
19881991.
140. Arenson AM, Graham RT, Shaw P, et al. Angiomyolipoma of
the kidney extending into the inferior vena cava: sonographic
and CT findings. AJR Am J Roentgenol 1988;151:11591161.
141. Amodio JB, Shapiro E, Pinkney L, et al. Metanephric adenoma
in an 8-year-old child: case report and review of the literature.
J Pediatr Surg 2005;40:e25e28.
142. Davis CJ Jr, Barton JH, Sesterhenn IA, et al. Metanephric ade-
noma: clinicopathological study of fifty patients. Am J Surg
Pathol 1995;19:11011114.
143. Comerci SC, Levin TL, Ruzal-Shapiro C, et al. Benign adeno-
matous kidney neoplasms in children with polycythemia: imag-
ing findings. Radiology 1996;198:265268.
144. Navarro O, Conolly B, Taylor G, et al. Metanephric adenoma
of the kidney: a case report. Pediatr Radiol 1999;29:
100103.
145. Sotelo-Avila C, Beckwith JB, Johnson JE. Ossifying renal tumor
of infancy: a clinicopathologic study of nine cases. Pediatr
Pathol Lab Med 1995;15:745762.
146. Vazquez JL, Barnewolt CE, Shamberger RC, et al. Ossifying
renal tumor of infancy presenting as a palpable abdominal
mass. Pediatr Radiol 1998;28:454457.
147. Tarhan F, Gul AE. Inflammatory pseudotumor of the kidney: a
case report. Int Urol Nephrol 2004;36:137140.
148. Ho PH, Chen SY, Hsueh C, et al. Inflammatory myofibroblas-
tic tumor of renal pelvis presenting with prolonged fever and
abdominal pain in children: report of 1 case and review of lit-
erature. J Pediatr Surg 2005;40:e35e37.
149. Kier R, Taylor KJW, Feyock AL, et al. Renal masses: character-
ization with Doppler US. Radiology 1990;176:703707.
150. Van Campenhout I, Patriquin H. Malignant microvasculature
in abdominal tumors in children: detection with Doppler US.
Radiology 1992;183:445448.
151. AAP Committee on Quality Improvement, Subcommittee on
Urinary Infection. Practice parameter: the diagnosis, treat-
ment and evaluation of the initial urinary tract infection in
febrile infants and young children. Pediatrics 1999;103:
843852.
LWBK505-C11_p384-460.qxd 7/7/10 1:36 PM Page 458 Aptara Inc
458 P E D I AT R I C S O N O G R A P H Y
152. Christensen AM, Shaw K. Urinary tract infection. In: Kaplan
BS, Meyers KEC, eds. Pediatric nephrology and urology: the
requisites in pediatrics. Elsevier Mosby, 2004:317325.
153. Hoberman A, Charron M, Hickey RW, et al. Imaging studies
after the first febrile urinary tract infection in young children.
N Engl J Med 2003;348:195202.
154. Rosenberg HK, Hakan I, Finkelstein M. Work-up of urinary
tract infection in infants and children. Ultrasound Q 2001;17:
87102.
155. Siegel MJ. Pediatric urinary tract infection. In: Pollack HM,
McClennan BL, eds. Clinical urography. Philadelphia, PA: WB
Saunders, 2000:11031121.
156. Majd M, Blask ARN, Markle BM, et al. Acute pyelonephritis:
comparison of diagnosis with 99mT c-DMSA, SPECT, spiral
CT, MR imaging and power Doppler US in an experimental pig
model. Radiology 2001;218:101108.
157. Craig WD, Wagner BJ, Travis MD. Pyelonephritis: radiologic-
pathologic review. Radiographics 2008;28:255276.
158. Dacher J-N, Avni F, Francois A, et al. Renal sinus hypere-
chogenicity in acute pyelonephritis: description and pathologi-
cal correlation. Pediatr Radiol 1999;29:179182.
159. Vourganti S, Agarwal PK, Bodner DR, et al. Ultrasonographic
evaluation of renal infections. Radiol Clin North Am.
2006;44:763775.
160. Sorantin E, Fotter R, Aigner R, et al. The sonographically thick-
ened wall of the upper urinary tract system: correlation with
other imaging methods. Pediatr Radiol 1997;27:667671.
161. Dacher J-N, Pfister C, Monroe M, et al. Power Doppler sono-
graphic pattern of acute pyelonephritis in children: comparison
with CT. AJR Am J Roentgenol 1996;166:14511455.
162. Lavocat MP, Granjon D, Allard D, et al. Imaging of
pyelonephritis. Pediatr Radiol 1997;27:159165.
163. Stogianni A, Nikolopoulos P, Oikonomou I, et al. Childhood
acute pyelonephritis: comparison of power Doppler sonogra-
phy and T c-DMSA scintigraphy. Pediatr Radiol 2007;37:
685690.
164. Winters WD. Power Doppler sonographic evaluation of
acute pyelonephritis in children. J Ultrasound Med 1996;15:
9196.
165. Kim B, Lim HK, Choi MH, et al. Detection of parenchymal
abnormalities in acute pyelonephritis by pulse inversion harmonic
imaging with or without microbubble ultrasonographic contrast
agent: correlation with computed tomography. J Ultrasound Med
2001;20:514.
166. Sie AH, Patel N, Spenceley N. Neonatal urinary ascites in
renal candidal infection. J Paediatr Child Health 2006;42:
387388.
167. Miller FH, Parikh S, Gore RM, et al. Renal manifestations of
AIDS. Radiographics 1993;13:587596.
168. Feuerstein IM, Francis P, Raffeld M, et al. Widespread calcifi-
cation in disseminated Pneumocystis carinii infection: CT char-
acteristics. J Comput Assist Tomogr 1990;14:149151.
169. Cousins C, Somers J, Broderick N, et al. Xanthogranulomatous
pyelonephritis in childhood: ultrasound and CT diagnosis.
Pediatr Radiol 1994;24:210212.
170. Hayes WS, Hartman DS, Sesterbenn IA. From the archives of
the AFIP. Xanthogranulomatous pyelonephritis. Radiographics
1991;11:485498.
171. Kim JC. US and CT findings of xanthogranulomatous
pyelonephritis. Clin Imaging 2001;25:118121.
172. Rypens F, Avni EF, Bank WO, et al. The ureterovesical junction
in children: sonographic findings after surgical or endoscopic
treatment. AJR Am J Roentgenol 1992;158:837842.
173. Gore MD, Fernbach SK, Donaldson JS, et al. Radiographic
evaluation of subureteric injection of Teflon to correct vesi-
coureteral reflux. AJR Am J Roentgenol 1989;152:115119.
174. Giuliano CT, Cohen HL, Haller JO, et al. The sting procedure
and its complications: sonographic evaluation. J Clin Ultra-
sound 1990;18:415420.
175. Flynn JT. Acute renal failure. In: Kaplan BS, Meyers KEC, eds.
Pediatric nephrology and urology: the requisites in pediatrics.
Elsevier Mosby, 2004:241249.
176. Kraus RA, Gaisie G, Young LW. Increased renal parenchymal
echogenicity causes in pediatric patients. Radiographics 1990;10:
10091018.
177. Yassa NA, Peng M, Ralls PW. Perirenal lucency (kidney sweat):
a new sign of renal failure. AJR Am J Roentgenol 1999;173:
10751077.
178. Wiersma F, Toorenvliet BR, Ruige M, et al. Increased echogenic-
ity of renal cortex: a transient feature in acutely ill children. AJR
Am J Roentgenol 2008;190:240243.
179. Platt JF, Ellis JH, Rubin JM, et al. Intrarenal arterial Doppler
sonography in patients with nonobstructive renal disease: cor-
relation of resistive index with biopsy findings. AJR Am J
Roentgenol 1990;154:12231227.
180. Platt JF, Rubin JM, Ellis JH. Acute renal failure: possible role
of duplex Doppler US in distinction between acute prerenal
failure and acute tubular necrosis. Radiology 1991;179:
419423.
181. Andreoli SP, Trachtman H, Acheson DWK, et al. Hemolytic
uremic syndrome: epidemiology, pathophysiology, and therapy.
Pediatr Nephrol 2002;17:293298.
182. Patriquin HB, ORegan S, Robitaille P, et al. Hemolytic-uremic
syndrome: intrarenal arterial Doppler patterns as a useful guide
to therapy. Radiology 1989;172:625628.
183. Sorof JM. Hypertension: principles for the practitioner. In:
Kaplan BS, Meyers KEC, eds. Pediatric nephrology and urol-
ogy: the requisites in pediatrics. Elsevier Mosby, 2004:
110121.
184. Roth C, Spottswood S, Chan J, et al. Evaluation of the hyper-
tensive infant: a rational approach to diagnosis. Radiol Clin
North Am 2003;41:931944.
185. Ingelfinger JR, Dillon MJ. Evaluation of secondary hyperten-
sion. In: Holliday-Barratt A, eds. Pediatric nephrology. 3rd ed.
Baltimore, MD: Williams & Wilkins, 1994:11461150.
186. Vo NJ, Hammelman BD, Racadio JM, et al. Anatomic distri-
bution of renal artery stenosis in children: implications for
imaging. Pediatr Radiol 2006;36:10321036.
187. Slovut DP, Olin JW. Fibromuscular dysplasia. N Engl J Med
2004;350:18621871.
188. Enriquez G, Castello F, Sousa P, et al. Increased cortical
echogenicity of the normal kidney in infants with unilateral
renal artery stenosis: report of two cases. J Ultrasound Med
1997;16:5963.
189. Lee H, Grant EG. Sonography in renovascular hypertension.
J Ultrasound Med 2002;21:431441.
190. Williams GJ, Macaskill P, Chan SF, et al. Comparative accuracy
of renal duplex sonographic parameters in the diagnosis of
renal artery stenosis: paired and unpaired analysis. AJR Am
J Roentgenol 2007;188:798811.
191. Stein M, Koenigsberg M, Grigoropoulos J, et al. Aortic coarc-
tation diagnosed in a hypertensive child undergoing Doppler
sonography for suspected renal artery stenosis. Pediatr Radiol
2002;32:384386.
192. Patriquin H, Lafortune M, Jquier JC, et al. Stenosis of the
renal artery: assessment of slowed systole in the downstream
circulation with Doppler sonography. Radiology 1992;184:
479485.
193. McLeary MS, Rouse GA. Tardus-parvus Doppler signals
in the renal arteries: a sign of pediatric thoracoabdominal
aortic coarctations. AJR Am J Roentgenol 1996;167:
521523.
194. Kuzmanovska DB, Sahpazova EM, Grujovska SJ, et al. Renal
infarction in a child with systemic lupus erythematosus. Pediatr
Nephrol 2004;19:685687.
195. Taylor GA. Potential pediatric applications for US contrast
agents: lessons from the laboratory. Pediatr Radiol 2000;30:
101109.
LWBK505-C11_p384-460.qxd 7/7/10 1:36 PM Page 459 Aptara Inc
196. Donmez FY, Coskun M, Uyusur A, et al. Noninvasive imaging
findings of idiopathic renal arteriovenous fistula. Diagn Interv
Radiol 2008;14:103105.
197. Riccabona M, Schwinger W, Ring E. Arteriovenous fistula after
renal biopsy in children. J Ultrasound Med 1998;17:505508.
198. More B, Chandran H, Pimpalwar A, et al. A traumatic intra-
renal pseudo-aneurysm in a child. Pediatr Surg Int 2004;20:
729730.
199. Lau KK, Garcia EF, Kwan WY, et al. Bilateral renal venous
thrombosis and adrenal hemorrhage: sequential prenatal US
with postnatal recovery. Pediatr Radiol 2007;37:912915.
200. Zigman A, Yazbeck S, Emil S, et al. Renal vein thrombosis: a 1-
year review. J Pediatr Surg 2000;35:15401542.
201. Wright NB, Blanch G, Walkinshaw S, et al. Antenatal and
neonatal renal vein thrombosis: new ultrasonic features with
high frequency transducers. Pediatr Radiol 1996;26:686689.
202. Laplante S, Patriquin HB, Robitaille P, et al. Renal vein throm-
bosis in children: evidence of early flow recovery with Doppler
US. Radiology 1993;189:3742.
203. Toma P, Rossi U, Mengozzi E. Bilateral calcified renal vein
thromboses in a newborn: a case associated with dual outcome.
Pediatr Radiol 2002;32:212213.
204. Wilkinson A, Murphy A, Stewart G. Renal venous thrombosis
with calcification and preservation of renal function. Pediatr
Radiol 2001;31:140143.
205. Jayogapal S, Cohen HL, Brill PW, et al. Calcified neonatal renal
vein thrombosis demonstration by CT and US. Pediatr Radiol
1990;20:160162.
206. Sodhi KS, Khandelwal S, Ray M, et al. Calcified neonatal renal
vein and vena caval thrombosis. Pediatr Radiol 2006;36:
437439.
207. Milliner DS. Calculi. In: Kaplan BS, Meyers KEC, eds. Pediatric
nephrology and urology: the requisites in pediatrics. Elsevier
Mosby, 2004:361374.
208. Milliner DS, Murphy ME. Urolithiasis in pediatric patients.
Mayo Clin Proc 1993;68:241248.
209. Hernanz-Schulman M. Hyperechoic renal medullary pyramids
in infants and children. Radiology 1991;181:911.
210. Dialoo O, Janssens F, Hall M, et al. Type 1 primary hyperox-
aluria in pediatric patients. Renal sonographic patterns. AJR
Am J Roentgenol 2004;183:17671770.
211. Cote G, Jequier S, Kaplan P. Increased renal medullary
echogenicity in patients with Williams syndrome. Pediatr Radiol
1989;19:481483.
212. Burton EM, Hanna JD, Mercado-Deane MG. Nephrocalcinosis
in a child with autosomal dominant polycystic kidney disease
and a prolapsing ectopic ureterocele. Pediatr Radiol 1995;25:
462465.
213. Lucaya J, Enriquez G, Nieto J, et al. Renal calcifications in
patients with autosomal recessive polycystic kidney disease:
prevalence and cause. AJR Am J Roentgenol 1993;160:359362.
214. Forget S, Patriquin HB, Dubois J, et al. The kidney in children
with tyrosinemia: sonographic, CT and biochemical findings.
Pediatr Radiol 1999;29:104108.
215. Kraus SJ, Lebowitz RL, Royal SA. Renal calculi in children:
imaging features that lead to diagnoses: a pictorial essay. Pedi-
atr Radiol 1999;29:624630.
216. Cramer B, Husa L, Pushpanathan C. Nephrocalcinosis in
rabbits correlation of ultrasound, computed tomography,
pathology and renal function. Pediatr Radiol 1998;28:913.
217. Middleton WD, Dodds WJ, Lawson TL, et al. Renal calculi:
sensitivity for detection with US. Radiology 1988;167:
239244.
218. Siegel MJ. Thoracoabdominal trauma. In: Siegel MJ, ed. Pedi-
atric body CT. 2nd ed. Philadelphia, PA: Lippincott Williams &
Wilkins, 2008:429457.
219. Kawashima A, Sandler CM, Corl FM, et al. Imaging of renal
trauma: a comprehensive review. Radiographics 2001;21:
557574.
Chapter 11 U R I N A R Y T R A C T 459
220. Pollack HM, Wein AJ. Imaging of renal trauma. Radiology
1989;172:297308.
221. Surratt JT, Siegel MJ, Middleton WD. Sonography of compli-
cations in pediatric renal allografts. Radiographics 1990;10:
687699.
222. Martinoli C, Crespi G, Bertolotto M, et al. Interlobular vascu-
lature in renal transplants: a power Doppler US study with MR
correlation. Radiology 1996;200:111117.
223. Turetschek K, Nasel C, Wunderbaldinger P, et al. Power
Doppler versus color Doppler imaging in renal allograft evalu-
ation. J Ultrasound Med 1996;15:517522.
224. Claudon M, Lefevre F, Hestin D, et al. Power Doppler imaging:
evaluation of vascular complications after renal transplanta-
tion. AJR Am J Roentgenol 1999;173:4146.
225. Baxter GM. Imaging and renal transplantation. Br Int Radiol
2002;14:285298.
226. Kaveggia LP, Perrella RR, Grant EG, et al. Duplex Doppler
sonography in renal allografts: the significance of reversed flow
in diastole. AJR Am J Roentgenol 1990;155:295298.
227. Drake DG, Day DL, Letourneau JG, et al. Doppler evaluation
of renal transplants in children: a prospective analysis with
histopathologic correlation. AJR Am J Roentgenol 1990;154:
785787.
228. Brown ED, Chen MY, Wolfman NT, et al. Complications of
renal transplant: evaluation with US and radionuclide imaging.
Radiographics 2000;20:607622.
229. Taylor KJ, Marks WH. Use of Doppler imaging for evaluation
of dysfunction in renal allografts. AJR Am J Roentgenol
1990;155:536537.
230. Dodd GD III, Tublin ME, Shah A, et al. Imaging of vascular
complications associated with renal transplants. AJR Am J
Roentgenol 1991;157:449459.
231. Snider JF, Hunter DW, Moradian GP, et al. Transplant renal
artery stenosis: evaluation with duplex sonography. Radiology
1989;172:10271030.
232. Herz D, McLorie G, Hafez A, et al. High resolution ultra-
sound characterization of early allograft hemodynamics in
pediatric living related renal transplantation. J Urol 2001;166:
18531858.
233. Mutze S, Trk I, Schnberger B, et al. Colour-coded duplex
sonography in the diagnostic assessment of vascular complica-
tions after kidney transplantation in children. Pediatr Radiol
1997;27:898902.
234. Pickhardt PJ, Siegel MJ. Abdominal manifestations of posttrans-
plantation lymphoproliferative disorder. AJR Am J Roentgenol
1998;171:10071013.
235. Jequier S, Rousseau O. Sonographic measurements of the nor-
mal bladder wall in children. AJR Am J Roentgenol 1987;149:
563566.
236. Bis KG, Slovis TL. Accuracy of ultrasonic bladder volume
measurement in children. Pediatr Radiol 1990;20:457460.
237. Tereza MF, Lima EM, Sanchez TM, et al. Bladder dysfunction:
diagnosis with dynamic US. Radiology 2003;227:33403344.
238. Fernbach SK, Feinstein KA. Abnormalities of the bladder in
children: imaging findings. AJR Am J Roentgenol 1994;162:
11431150.
239. Nasrallah PF, McMahon DR. Anatomic abnormalities of the
bladder. In: Gonzales ET, Bauer SB, eds. Pediatric urology prac-
tice. Philadelphia, PA: Lippincott Williams & Wilkins, 1999:
13321.
240. Cacciarelli AA, Kass EJ, Yang SS. Urachal remnants: sonographic
demonstration in children. Radiology 1990;174:473475.
241. Herman TE, Shackelford GD. Pyourachus: CT manifestations.
J Comput Assist Tomogr 1995;19:440443.
242. Argons GA, Wagner BJ, Lonergan GJ, et al. Genitourinary
rhabdomyosarcoma in children: radiologic-pathologic correla-
tion. Radiographics 1997;17:919937.
243. Wexler LH, Meyer WH, Helman LJ. Rhabdomyosarcoma and
the undifferentiated sarcomas. In: Pizzo PA, Poplack DG, eds.
LWBK505-C11_p384-460.qxd 7/7/10 1:36 PM Page 460 Aptara Inc
460 P E D I AT R I C S O N O G R A P H Y
Principles and practice of pediatric oncology. Philadelphia, PA:
Lippincott Williams & Wilkins, 2006:9711001.
244. Lalmand B, Avni EF, Simon J, et al. Transitional cell papillary
carcinoma of the bladder in a child. Pediatr Radiol 1987;17:
7779.
245. Quillin SP, McAlister WH. Transitional cell of the bladder in
children: radiologic appearance and differential diagnosis. Urol
Radiol 1991;13:107109.
246. Crecelius SA, Bellah R. Pheochromocytoma of the bladder in an
adolescent: sonographic and MR imaging findings. AJR Am J
Roentgenol 1995;165:101103.
247. Jquier S, Bugmann P, Brndler M-A. Nephrogenic adenoma of
the bladder: ultrasound demonstration. A case report. Pediatr
Radiol 1999;29:185187.
248. Shapeero LG, Vordermark JS. Bladder neurofibromatosis in child-
hood: noninvasive imaging. J Ultrasound Med 1990;9:177180.
249. McCarville MB, Hoffer FA, Gingrich JR, et al. Imaging findings
of hemorrhagic cystitis in pediatric oncology patients. Pediatr
Radiol 2000;30:131138.
250. Keesling CA, OHara SM, Chavez DR, et al. Sonographic
appearance of the bladder after endoscopic incision of uretero-
celes. AJR Am J Roentgenol 1998;170:759763.
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CHAPTER

Adrenal Glands, Pancreas, and

Other Retroperitoneal Structures
12
MARILYN J. SIEGEL AND ELLEN M. CHUNG

Adrenal Glands Adrenal Hyperplasia Retroperitoneal Great Vessels

Scanning Techniques Wolman Disease Scanning Techniques
Embryology Aorta
Pancreas
Normal Anatomy Inferior Vena Cava
Scanning Technique
Congenital Anomalies
Normal Anatomy Crura and Psoas Muscles
Adrenal Masses
Embryology Normal Anatomy
Adrenal Medullary Neoplasms
Congenital Anomalies Pathology
Metastases
Congenital Systemic Diseases
Adrenocortical Tumors Retroperitoneal Lymph Nodes
Congenital Hyperinsulinism
Myelolipoma Normal Anatomy
Tumors
Adrenal Hemangioendothelioma Pathology
Acute Pancreatitis
Adrenal Hemorrhage Primary Retroperitoneal Tumors
Chronic Pancreatitis
Adrenal Cysts
Trauma Retroperitoneal Hemorrhage
Infection
Retroperitoneal Fibrosis

he retroperitoneum is bordered superiorly by the

T
diaphragm, inferiorly by the pelvic brim, anteriorly by
the parietal peritoneum, and posteriorly by the trans-
versalis fascia. Within the retroperitoneum are larger struc-
tures, such as the adrenal glands, pancreas, kidneys,
ureters, duodenal loop, ascending and descending colon,
and great vessels and their branches, as well as smaller
structures, such as the lymph nodes, lymphatic channels,
and nerves. This chapter reviews the normal anatomy and
common pathologic disorders of the adrenal glands, pan-
creas, lymph nodes, major vascular structures, and other
soft tissue structures. The psoas muscles and adjacent sym-
pathetic trunks, which lie posterior to the retroperitoneum
within the retrofascial space, are included in the discussion
because conditions affecting these structures can involve
the retroperitoneal compartment. Diseases of the kidney
and duodenum and colon have been covered elsewhere in
this book.
ADRENAL GLANDS
Scanning Techniques
In neonates and young infants, the right adrenal gland can
be visualized by an anterolateral or right flank approach,
using the right hepatic lobe as an acoustic window. The left
adrenal gland is usually best seen from a left flank
approach. In older children and adolescents, the right adre-
nal gland is best evaluated with an intercostal approach in
the anterior axillary or midaxillary line, using the liver as
an acoustic window. The left adrenal gland is best evalu-
ated with an intercostal approach in the posterior axillary
or midaxillary line, using the spleen or left kidney as an
acoustic window. Ideally, patients should have nothing by
mouth for several hours before the study to minimize the
amount of intervening bowel gas.
The normal right adrenal gland can be visualized in
97% to 100% of neonates and young infants and the left
adrenal gland in 83% to 98% (1). The corresponding
numbers for adults and presumably older children are
92% and 71%, respectively (2).
Embryology
The adrenal gland has a dual origin. The fetal adrenal
medulla develops from neuroectodermal tissue and the
cortex arises from peritoneal mesoderm. During fetal and
early postnatal development, the adrenal cortex is com-
posed of two layers: a thick inner fetal cortex, comprising
approximately 80% of the adrenal cortex, and a thin outer
zone, which becomes the adult cortex (3). The large bulk
of the fetal cortex is responsible for the relatively large size
of the adrenal gland at birth (up to one-third the size of the
kidney). The fetal cortex begins to atrophy almost imme-
diately after birth by a process of hemorrhagic necrosis
and is completely resorbed by the end of the first year of

461
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462 P E D I AT R I C S O N O G R A P H Y

life (1,3). The adrenal glands do not reach their birth weight
again until the third year of life.
Simultaneously with the involution of the fetal cortex,
the outer cortex destined to become the permanent cortex
differentiates into three zones: glomerulosa, fasciculata, and
reticularis (3). The glomerulosa (outermost zone) secretes
aldosterone. The zona fasciculata (middle zone) and zona
reticularis (innermost zone) synthesize glucocorticoids
(principally cortisol) and androgens. The adrenal medulla
produces catecholamines. Adrenal cortical steroid hormone
synthesis requires an intact hypothalamic-pituitary-adrenal
axis. The hypothalamus secretes corticotrophin-releasing
hormone, which stimulates the pituitary to secrete adreno-
corticotropic hormone (ACTH). ACTH stimulates the adre-
nal cortex to produce the three major types of hormones.
Normal Anatomy
The adrenal glands lie within the confines of the perirenal
fascia, anteromedial to the upper pole of each kidney. The
right adrenal gland is located lateral to the diaphragmatic
crus, medial to the right lobe of the liver, posterior to the
inferior vena cava, and anterosuperior to the upper pole of
the right kidney. The left adrenal gland is located lateral to
the aorta and left diaphragmatic crus, medial to the spleen,
posterior to the splenic vessels and pancreatic tail, and
anteromedial to the upper pole of the left kidney. Changes
in the normal anatomic relationship may occur as a result
of nephrectomy or displacement by adjacent organs, such
as liver or pancreas.
Each gland is composed of medial and lateral limbs and
an anteromedial apex, where they fuse. The glands are sur-
rounded by varying amounts of fatty tissue.
SHAPE
In neonates, the adrenal glands have a V or Y shape
in coronal and longitudinal planes. In the transverse plane,
the glands assume a linear, V, Y, or L configuration
(Fig. 12.1) (4).
ECHO TEXTURE
The sonographic appearance of the normal adrenal gland
varies with age. In newborns, the adrenal medulla is rela-
tively thin and hyperechoic and is surrounded by a thicker
hypoechoic cortex (Fig. 12.1) (5,6). Soon after birth, the

A B

Neonatal adrenal glands, variants in shape. A: Transverse

Fig. 12.1
sonogram of the right adrenal gland shows a linear shape.
D  duodenum. B: Transverse sonogram of the left adrenal gland shows
an inverted V configuration. C: Transverse sonogram in another patient
shows the inverted Y configuration. C  inferior vena cava. In the
neonate, the medulla is echogenic and is surrounded by hypoechoic cor-
C tex. Arrowheads indicate the adrenal glands.
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Chapter 12 A D R E N A L G L A N D S , PA N C R E A S , A N D O T H E R R E T R O P E R I T O N E A L S T R U C T U R E S 463

A B
Normal adrenal gland, 13-year old boy. A: Transverse sonogram. The right adrenal gland is a thin, linear structure (arrows) that is isoe-
Fig. 12.2
choic to liver (L). Note absent corticomedullary differentiation. The gland lies posterior to the inferior vena cava (C). PV  portal vein;
SP  spine. B: Corresponding computed tomography scan shows similar anatomy. Arrow indicates the right adrenal gland. PV  portal vein; C 
inferior vena cava.

fetal cortex starts to atrophy and by 5 or 6 months of age,
the gland is hyperechoic and smaller, with poor or absent
differentiation between the cortex and medulla. The adult
appearance is reached by 1 to 3 years of age. At this time,
the adrenal gland appears as a very thin linear structure
that is isoechoic to liver and lacks corticomedullary differ-
entiation (Fig. 12.2).
SIZE
The method used to measure the glands is illustrated in Fig-
ure 12.3. In neonates, the length of each adrenal gland is
between 0.9 and 3.6 cm (mean 1.5 to 1.7 cm), and the thick-
ness ranges between 0.2 and 0.5 cm (mean 0.3 cm) (Fig. 12.3)
(1). There is no statistically significant difference in the size of
the two glands. Postnatally, the glands involute, and by 6
weeks of postnatal life, there is a 40% to 50% decrease in size
(1). In older children and adults, the adrenal glands are 4 to
6 cm in length, 0.2 to 0.6 cm in thickness, and 2 to 3 cm in
width (4). The limbs have a uniform thickness except at the
apex of the gland, where they unite and may appear larger.
In general, the presence or absence of adrenal disease
can be established by subjective assessment of shape,
margins, and relative size of the gland. Given the consid-
erable variability in the lengths of the adrenal glands in
normal individuals, focal or diffuse enlargement is a more
important finding than any measurement. The surface of
the glands should be smooth, without nodular protuber-
ances, and the thickness of the limbs should be uniform.
In adolescents and young adults, an area of the adrenal
gland with a thickness greater than 10 mm is probably
abnormal.
Congenital Anomalies
AGENESIS/HYPOPLASIA
Unilateral adrenal agenesis is rare and usually occurs in
association with ipsilateral renal agenesis. The incidence of
ipsilateral adrenal gland absence in patients with renal age-
nesis is about 6% to 9% (7).
Congenital adrenal hypoplasia has been described in
anencephalic infants and in infants with prenatal pituitary
and central nervous system degenerative disorders, pre-
sumably secondary to inadequate production of ACTH,
leading to failure of normal development of the fetal adre-
nal cortex (8).

Method used to measure the

Fig. 12.3
normal neonatal adrenal glands.
L  length; W  width. (Adapted from W W
Oppenheimer EH, Carroll BA, Yousem S.
Sonography of the normal neonatal adrenal
L L
gland. Radiology 1983;146:157160.)
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464 P E D I AT R I C S O N O G R A P H Y

A B
Fusion anomalies. A: Circumrenal adrenal gland. Transverse sonogram of the right adrenal gland demonstrates fusion of the two limbs
Fig. 12.4
of the gland (arrowheads) around the upper pole of the right kidney (K). B: Horseshoe adrenal gland. Transverse scan shows fusion of
the right and left adrenal glands (arrows) across the midline (arrowheads). A  aorta; SP  spine.

ACCESSORY GLANDS (ADRENAL RESTS)
Accessory adrenal glands, also known as adrenal rests,
arise when fragments of tissue separate from the adrenal
gland during the time of neural crest cell migration in utero
(9,10). They may contain both cortical and medullary tis-
sue or only cortical tissue (3,9). Adrenal rests are com-
monly found near the celiac plexus, but they can occur
along the course of the spermatic and ovarian veins and in
the testes, ovary, broad ligament, tail of the epididymis,
and inguinal canals (9,10). These cells can form tumor-like
masses in response to increased levels of adrenocortical
hormones, usually associated with congenital adrenal
hyperplasia and cushing syndrome.
Testicular adrenal rests are usually bilateral, multifocal,
and less than 5 mm in size. At sonography, they appear as
round, hypoechoic, nodular masses, most commonly
located near the mediastinum testis (10) (See Fig. 14.25,
Chapter 14, Male Pelvis). At color Doppler sonography,
they may be hypervascular to normal parenchyma (10).
shape, and assuming a flattened or discoid configuration
(Fig. 12.5) (5,7,9,12). The mean length of the elongated
right and left adrenal glands in neonates is 3.4 and 2.9 cm,
respectively (normal, 1.5 cm); mean thickness of each gland
is 0.5 cm (normal, 0.3 cm) (13). The elongated gland
retains its characteristic corticomedullary differentiation.
The adrenal gland retains its normal shape in patients
who have had a nephrectomy. Other organs, such as bowel,
tail of the pancreas, and spleen, may move into the empty
renal fossa.
Adrenal Masses
Adrenal masses may be caused by neoplasms, hemorrhage,
abscesses, and cysts. Adrenal neoplasms can arise from the

FUSION ANOMALIES
Two anomalies of adrenal fusion have been described at
sonography: fusion of the two wings of one gland, produc-
ing a circumrenal adrenal gland, and fusion of the two
adrenal glands across the midline, resulting in a horse-
shoe adrenal gland. In the circumrenal gland, the fused
limbs encircle the upper pole of the ipsilateral kidney. In the
horseshoe adrenal gland, the limbs are connected by an
isthmus of tissue (Fig. 12.4) (11). The latter anomaly has
been associated with horseshoe kidney, renal agenesis, neu-
ral tube defects, and asplenia syndrome (5).

ADRENAL HYPERTROPHY WITH RENAL AGENESIS

In patients with renal agenesis, the ipsilateral adrenal gland Renal agenesis. Longitudinal sonogram shows an elon-
is nearly always present in its expected location, but it elon- Fig. 12.5
gated and discoid right adrenal gland (arrowheads). Cor-
gates and increases in thickness, losing its Y or V ticomedullary differentiation is preserved.
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adrenal medulla or the cortex, with the former being more
common. Neoplasms of the adrenal medulla include neu-
roblastoma, ganglioneuroblastoma, ganglioneuroma, and
pheochromocytoma. Adrenal cortical neoplasms include
carcinoma, adenoma, and myelolipoma.
Adrenal Medullary Neoplasms
NEUROBLASTOMA
Neuroblastoma is the most common solid, extracranial
malignant tumor in children, accounting for 8% to 10% of
all childhood cancers (14,15). Most children with neuro-
blastoma are between 1 and 5 years of age, with a median
age at diagnosis of 22 months. Neuroblastomas may arise
in the adrenal medulla or anywhere along the sympathetic
ganglion chain (14,16). Up to 75% of neuroblastomas
arise in the abdomen, and two thirds of these lesions arise
in the adrenal medulla. The remaining abdominal and
pelvic tumors usually originate in the paravertebral sym-
pathetic ganglia, presacral area, or organ of Zuckerkandl.
On cut section, neuroblastoma is usually well demar-
cated, although it lacks a capsule. It commonly contains
areas of necrosis, hemorrhage, cystic degeneration, and
calcification. Microscopically, the tumor is composed of
small, darkly staining, round cells that are characteristi-
cally arranged in rosettes. Average size is approximately
8 cm at the time of presentation.
In rare cases, neuroblastoma is familial, exhibiting an
autosomal dominant inheritance pattern, possibly related to
an abnormality in the short arm of chromosome 16 (16p12-
13) (17). In this subset, median patient age at diagnosis is 9
months. Neuroblastoma has been associated with neurofi-
bromatosis type I and with aganglionosis of the colon.
Children with abdominal neuroblastomas present with
an abdominal mass or findings of metastases. Between 60%
and 70% of children have evidence of metastatic disease
when initially diagnosed (1416). Common sites of metas-
tases are lymph nodes, liver, skeleton, bone marrow, and
skin. The pattern of metastases varies with age. Cutaneous
lesions are more common in infants than in older children.
Conversely, skeletal metastases are common in older infants
and children but rare in neonates. Hepatic metastases can
occur at any age, but extensive hepatic involvement tends to
occur in young infants. Extra-adrenal abdominal tumors
arising from the paravertebral sympathetic chain have a par-
ticular predilection for direct intraspinal extension.
Rarely, presenting manifestations are those of a para-
neoplastic syndrome. Two paraneoplastic syndromes have
been described in association with neuroblastoma (18,19).
One is myoclonic encephalopathy of infancy, which
includes the triad of cerebellar ataxia, myoclonus, and
opsomyoclonus. The precise cause of this syndrome is
unknown, but it has been postulated that an immune
response to the primary tumor leads to production of anti-
neural antibodies that cross-react with cerebellar tissue.
The second syndrome consists of intractable watery diar-
rhea and hypokalemia caused by excess production of
vasoactive intestinal peptides (VIPs) and catecholamines.
465
Table 12.1 International Neuroblastoma Staging System
Stage Definition
I Localized tumor with complete resection, with or without
microscopic residual disease; representative ipsilateral
lymph nodes negative for tumor microscopically
II-A Localized tumor with incomplete gross excision;
representative ipsilateral nonadherent lymph nodes
negative for tumor microscopically
II-B Localized tumor with or without complete gross excision,
with representative ipsilateral nonadherent lymph
nodes positive for tumor. Enlarged contralateral lymph
nodes must be negative microscopically.
III Unresectable unilateral tumor infiltrating across the midline,
with or without regional lymph node involvement; or
localized unilateral tumor with contralateral regional
lymph node involvement; or midline tumor with bilateral
extension by infiltration (unresectable) or by lymph node
involvement
IV Any primary tumor with dissemination to distant lymph
nodes, bone, bone marrow, liver, skin, and/or other
organs (except as defined for stage IV-S)
IV-S Localized primary tumor (as defined for stage I, II-A, or
II-B), with dissemination limited to skin, liver, and/or
bone marrow. Bone marrow involvement should be
minimal (10% of total nucleated cells identified as
malignant on bone marrow biopsy or on marrow
aspirate). Limited to infants younger than 1 year of age
Serum or urinary levels of catecholamines or their metabo-
lites, particularly vanillylmandelic acid (VMA) and
homovanillic acid (HVA), are increased in approximately
90% of patients with neuroblastoma.
The International Neuroblastoma Staging System
(INSS), based on a combination of clinical, radiographic,
and surgical findings, is the most widely used staging system
for neuroblastoma (Table 12.1) (20,21). Distribution of
stages based on the INSS is approximately as follows: I,
20%; II, 10%; III, 15%; IV, 50%; and IV-S, 4% (21,22).
The treatment of neuroblastoma varies with the stage
of the tumor (16,21,22). Patients with tumors that are
localized to one side of the midline or cross the midline
without encasement of major vessels undergo primary sur-
gical resection. Chemotherapy is the treatment of choice in
patients with initially unresectable disease followed by
delayed surgical resection. The use of radiation therapy is
limited to patients with localized disease that cannot be
resected and does not regress completely with chemother-
apy. Once unresectable tumors decrease sufficiently in vol-
ume, delayed surgical resection is performed. Infants with
IV-S disease may not be treated since spontaneous regres-
sion sometimes occurs in these patients.
Prognosis is dependent on clinical and biologic markers.
Important clinical factors are stage, site of the primary
tumor, patient age, and histology. Children aged younger
than 1 year with localized tumors and stroma-rich histol-
ogy have 2-year survival rates of up to 90%. Children aged
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466 P E D I AT R I C S O N O G R A P H Y
older than 1 year with skeletal metastases and undifferenti-
ated histology can have survival rates less than 25%
(21,22). Several biologic markers of tumor tissue also influ-
ence survival rate. Favorable factors include triploid kary-
otypes, well-differentiated stroma, an unamplified N-myc
oncogene, and absence of abnormalities of chromosome 1.
Unfavorable prognostic signs are a diploid (decreased
DNA) karyotype, N-myc amplification (more than 10 copy
numbers), and allelic loss of chromosome 1p (23,24).
Sonographic Evaluation of the Primary Tumor
The evaluation of patients with palpable abdominal
masses, including neuroblastoma, usually begins with
A B
C a left suprarenal mass (M), displacing the kidney inferiorly.
sonography. Sonography is performed to confirm the pres-
ence of a mass and its site of origin. Depending on the site
of origin, neuroblastoma appears either as a suprarenal
(Fig. 12.6) or paraspinal mass (Fig. 12.7) (20,25). The
retroperitoneal location of the mass can be confirmed by
demonstration of anterior displacement of the inferior
vena cava and aorta or displacement of other retroperi-
toneal organs. Neuroblastomas in infants and children are
echogenic and isoechoic or hyperechoic to surrounding
tissues. They can be homogeneous (Figs. 12.6 and 12.7) or
heterogeneous and contain highly reflective areas second-
ary to calcification (Fig. 12.8) and very hypoechoic areas
secondary to hemorrhage, necrosis, cystic change, or some
Suprarenal neuroblastoma. A: Transverse sonogram in a
Fig. 12.6
2-year-old boy shows a suprarenal mass (M) inferior to
the pancreas (PANC) and superior to the left kidney (LK). The tumor is
isoechoic to surrounding structures and homogeneous. A  aorta;
C  inferior vena cava. B: Color Doppler image shows an avascular
mass (M). C: Contrast-enhanced computed tomography scan confirms
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A B

Extra-adrenal neuroblastoma. A: Longitudinal sonogram

Fig. 12.7
in an 8-week-old girl shows a homogeneous echogenic
mass (*) compressing and displacing the right kidney (calipers) supe-
riorly. L  liver. B: Transverse sonogram shows the tumor (calipers)
displacing the right kidney (K) anteriorly. L  liver. On both images, the
tumor is isoechoic to surrounding viscera. C: Fat-saturated, T2-
weighted magnetic resonance image shows a low-signal-intensity
right paraspinal mass (M). The tumor arose in the sympathetic gan-
C glia. A second tumor is noted in the left adrenal gland (arrow).

Suprarenal neuroblastoma with calcifications. Longitudi-

Fig. 12.8
nal sonogram shows a heterogeneous mass (arrowheads)
superior to the left kidney (LK) and just below the stomach (ST). The
bright hyperechoic areas represent calcifications.
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468 P E D I AT R I C S O N O G R A P H Y

A B

C D
Cystic neuroblastoma. A: Longitudinal sonogram in a neonate shows an anechoic mass (M) superior to the right kidney (RK). B: Com-
Fig. 12.9
puted tomography scan shows a cystic mass (M), which has displaced the right kidney inferiorly. C: Transverse sonogram in a 3-month-
old girl shows a small, nearly anechoic right paraspinal mass (arrowhead). SP  spine. D: Axial T2-weighted magnetic resonance image shows a
well-circumscribed hyperintense mass (arrowhead). Both tumors were highly necrotic.

combination thereof (15,20,25,26). Tumor margins

may be smooth or irregular. Absent, peripheral, or cen-
tral vascularity may be observed on color Doppler
sonography.
In neonates, neuroblastomas can be markedly hypo-
echoic and may even appear cystic (Fig. 12.9). On patho-
logic sections, this appearance reflects either degenerative
change in the tumor or clusters of microcysts in the tumor
cells. Calcification is relatively uncommon in cystic tumors
(2729).
Imaging Intra-abdominal Tumor Spread
Patterns of intra-abdominal extension of tumors include
midline extension (Fig. 12.10), vessel encasement, spread
to regional lymph nodes, intraspinal extension, and
hepatic metastases (Fig. 12.11). Inferior vena caval and
aortic displacement are common (30). Color Doppler
sonography is useful in displaying vessel encasement and
displacement. Rarer patterns of spread include peritoneal
seeding with ascites (31), intravascular invasion (32), and
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Adrenal neuroblastoma, midline extension. Transverse

Fig. 12.10
view shows a large left suprarenal mass extending
across the midline anterior to the aorta (AO) and left renal vein (RV).
Within the mass are two hyperechoic foci, one of which demonstrates
posterior acoustic shadowing, corresponding to areas of calcification
(arrowheads). LK  left kidney.

A B

C D
Hepatic metastases. A: Transverse sonogram in a neonate with stage IV-S neuroblastoma shows multiple echogenic lesions (arrows)
Fig. 12.11
in the liver. SP  spine. B: Fat-saturated T2-weighted magnetic resonance image shows multiple high-signal-intensity hepatic metas-
tases and the primary tumor (T) in the right adrenal gland. C: Transverse sonogram in another neonate shows the primary tumor (calipers) and mul-
tiple hypoechoic and anechoic metastases within the liver (arrowheads). D: Longitudinal sonogram of a neonate shows diffuse heterogeneity of the
liver (L) and the primary adrenal tumor (arrows).
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470 P E D I AT R I C S O N O G R A P H Y
A B
Ganglioneuroblastoma, 9-year-old boy. A: Longitudinal sonogram shows a well-circumscribed, heterogeneous, suprarenal mass
Fig. 12.12
(calipers) with hyperechoic areas representing calcification. K  right kidney; L liver. B: Computed tomography scan without con-
trast confirms the presence of calcium (arrow) within the tumor.
fistulous communication with the colon (33). Renal atro-
phy may result from infarction due to encasement or com-
pression of the renal vessels by the primary tumor or fol-
low surgical trauma, chemotherapy, or radiation therapy
(34).
Hepatic metastases occur most often in neonates who
have stage IV-S disease. They have a variable appearance
and can be discrete and solitary or multifocal. Discrete
hepatic lesions can appear hyperechoic, hypoechoic, or
anechoic (Fig. 12.11AC). Diffuse metastatic infiltration
produces hepatomegaly with heterogeneity of the hepatic
parenchyma (Fig. 12.11D).
After the presence of an abdominal mass has been con-
firmed by sonography, computed tomography (CT) or
magnetic resonance imaging (MRI) and meta-iodobenzyl-
guanidine (MIBG) imaging are performed to define the full
extent of local and metastatic disease (35).
GANGLIONEUROBLASTOMA AND GANGLIONEUROMA
In older infants and children, other neural crest tumors,
such as ganglioneuroblastoma and ganglioneuroma, may
mimic neuroblastoma. These tumors are part of a spec-
trum of lesions ranging from neuroblastoma, the most
primitive tumor in this spectrum, to ganglioneuroma, the
most differentiated tumor. Ganglioneuroblastoma is a
malignant tumor containing both primitive and differen-
tiated cells. Ganglioneuroma is a benign tumor com-
posed of mature ganglion cells. Ganglioneuroblastoma
and ganglioneuroma tend to occur later in the first
decade or in the second decade of life. They have imag-
ing findings similar to those of neuroblastoma. Sono-
graphically, both tumors are solid, echogenic masses.
They may be homogeneous or heterogeneous and may
contain areas of calcification (Fig. 12.12). The sono-
graphic findings are nonspecific, and the diagnosis is
made histologically by the degree of cellular maturation
and differentiation.
PHEOCHROMOCYTOMA
Pheochromocytoma is a catecholamine-secreting tumor
arising from chromaffin cells of the sympathetic nervous
system. Less than 5% of all pheochromocytomas occur in
children. Most pheochromocytomas originate in the adre-
nal medulla, but up to 30% may arise in extra-adrenal
sites, mainly in the paravertebral sympathetic chain, para-
aortic bodies, and bladder wall. When a catecholamine-
secreting tumor arises in an extra-adrenal location, it is
labeled a paraganglioma (36,37).
Clinical features suggestive of the diagnosis are hyper-
tensive episodes, which may be sustained or paroxysmal;
headache; tachycardia; palpitation; diaphoresis; and pal-
lor. Micturition syncope can occur in patients with blad-
der wall paragangliomas. There is an increased incidence
of pheochromocytomas in patients with multiple
endocrine neoplasia (MEN) type 2 (medullary thyroid
carcinoma and parathyroid disease) and in patients with
tuberous sclerosis, Sturge-Weber syndrome, neurofibro-
matosis, and von Hippel-Lindau disease (37). Multiple or
bilateral tumors are more likely in these syndromes. The
diagnosis of pheochromocytoma is usually established by
biochemical testing, based on detection of elevated levels
of urinary or serum catecholamines or their metabolites.
Pheochromocytomas are usually large (2 cm in
diameter), sharply marginated lesions that are either
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A B

C D
Pheochromocytoma. Twelve-year-old girl with hypertension. A: Transverse sonogram shows a fairly homogeneous mass (arrowheads)
Fig. 12.13
compressing the right kidney (K) posteriorly. L  liver. B: Axial computed tomography (CT) scan performed following intravenous
injection of iodinated contrast reveals a well-circumscribed mass (arrowheads) compressing the right kidney. The mass appears more heteroge-
neous on CT. C: Longitudinal sonogram in another adolescent patient shows a minimally heterogeneous solid mass (M) above the left kidney (LK).
D: T2-weighted coronal magnetic resonance image shows a heterogeneous mass (M) with central necrosis.

heterogeneously or homogeneously solid (Fig. 12.13). Metastases

Smaller tumors commonly have a homogeneous matrix,
while larger tumors are often heterogeneous due to
necrosis, hemorrhage, and calcifications. A rare finding
is inferior vena cava invasion (38). The signs of malig-
nancy include local invasion, lymph node enlargement,
and distant metastases. Metastatic disease is the only
reliable finding of malignancy. The sonographic appear-
ance of pheochromocytoma is not specific and differenti-
ation from other adrenal tumors requires biochemical
studies.
Adrenal metastases are rare in children. Lymphomatous
involvement of the adrenal gland can produce solid, homo-
geneous, hypoechoic or echogenic masses.
Adrenocortical Tumors
Adrenocortical lesions in children are usually hyperfunc-
tioning, and presenting features relate to the specific sub-
stance produced by the tumor. Less commonly, they are
nonfunctioning. Nonfunctioning adenomas present as
abdominal masses.
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472 P E D I AT R I C S O N O G R A P H Y
Adrenal cancer. Six-month-old boy with Cushing syn-
Fig. 12.14
drome. Longitudinal sonogram shows a large, slightly
heterogeneous mass (arrowheads) between the left kidney (K) and the
spleen (S).
ADRENOCORTICAL CANCER
Adrenal carcinoma is a rare, highly malignant neoplasm of
the adrenal cortex, accounting for less than 1% of all pedi-
atric malignancies. Mean patient age at diagnosis is 9
years. Adrenal cancers are usually hormonally active, caus-
ing virilism in girls and pseudoprecocious puberty in boys.
Cushing syndrome, feminization, and hyperaldosteronism
are less common presentations (5,6,3942). Adrenocorti-
cal carcinoma is associated with the Beckwith-Wiedemann
syndrome and hemihypertrophy (20). Biochemical criteria
for diagnosis of a virilizing tumor are elevated levels of uri-
nary 17-ketosteroids and normal to mildly elevated uri-
nary cortisol levels. The tumor may invade the inferior
vena cava and spread to regional lymph nodes. Distant
metastases are to lung, liver, and lymph nodes.
A B
Adrenal adenoma. A: Transverse sonogram in a 2-year-old boy with Cushing syndrome shows a hypoechoic mass (arrowheads) with a focal
Fig. 12.15
shadowing hyperechoic area representing calcification. RK  right kidney; SP  spine. B: Color Doppler sonogram shows central flow.
Adrenal carcinomas are usually large, greater than 5 cm
in diameter, at the time of presentation. The larger lesions are
commonly heterogeneous, with hypoechoic or hyperechoic
areas representing necrosis, hemorrhage, or calcification (Fig.
12.14) (5,6,39,43,44). Calcification is found in up to 40% of
tumors. Small tumors may have a homogeneous echotexture.
Invasion of the inferior vena cava or liver and regional lymph
node enlargement also may be noted (39,40,4446). Doppler
imaging is useful in detecting venous invasion.
ADRENOCORTICAL ADENOMAS
Cushing Syndrome
Cushing syndrome results from overproduction of cortisol
by the adrenal cortex. Most cases in patients under 10 years
of age are ACTH independent, usually due to adrenal carci-
noma or a cortical adenoma. In older children, Cushing syn-
drome is usually a result of excess ACTH production, result-
ing from a pituitary adenoma or adrenal hyperplasia (47,48).
Clinical features of Cushing syndrome include generalized or
truncal obesity, muscle wasting, hirsutism, hypertension, and
abdominal striae. Biochemical abnormalities include ele-
vated 24-hour urinary cortisol and 17-hydroxycorticoids. In
children with Cushing syndrome caused by carcinoma, the
urine 17-ketosteroids as well as the 17-hydroxycorticoids are
increased. The high-dose dexamethasone suppression test
can help in distinguishing pituitary from ectopic causes of
elevated ACTH. Urinary cortisol excretion is suppressed in
children with pituitary ACTH secretion, but not in children
with ectopic ACTH production due to autonomously func-
tioning adrenal tumors.
Cortisol-producing adenomas are usually homogeneous,
round or oval echogenic masses ranging between 2 and 5 cm
in diameter. They are echogenic and may be hypoechoic or
hyperechoic to liver depending on the amount of adipose
tissue in the tumor (Fig. 12.15). Peripheral or central
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vascularity may be observed on color Doppler sonogra-
phy.
Primary pigmented nodular adrenocortical disease is a
rare cause of Cushing syndrome (49). The disorder is asso-
ciated with Carney complex (skin pigmentation, cardiac
and soft tissue myxomas, and Sertoli cell tumors of the
testis). Typically, cortisol levels are elevated, but ACTH
levels are decreased. The adrenal glands contain multiple,
small (2 mm) autonomous cortical-secreting adenomas.
The cortex between the nodules is atrophic, unlike ACTH-
dependent nodular hyperplasia, where the adrenal glands
are diffusely thickened (49).
Primary Aldosteronism
Primary aldosteronism (Conn syndrome) is the result of
overproduction of the mineralocorticoid aldosterone. Most
cases result from an autonomous aldosterone-secreting ade-
noma (aldosteronoma) or adrenal hyperplasia. A rare cause
is adrenal carcinoma. Clinical findings include hyperten-
sion, muscle weakness, and tetany. Biochemical abnormal-
ities are reduced plasma renin levels, hypokalemia, and the
inability to suppress aldosterone excretion with infusions of
normal saline. At sonography, aldosteronomas appear as
small (usually 2 cm in size) round or oval lesions
(37,50,51).
Myelolipoma
Adrenal myelolipoma is a rare nonfunctioning neoplasm
composed of fat and bone marrow elements. Tumors are usu-
ally discovered incidentally during examination for other clin-
ical indications. The echogenicity depends on the relative pro-
portions of the constituents (52,53). Fatty components are
highly echogenic, while myeloid elements are hypoechoic or
isoechoic to normal parenchyma (Fig. 12.16). Cystic changes
may be present if there is associated hemorrhage (53).
Myelolipoma. Transverse sonogram in a young adult shows
Fig. 12.16
a highly echogenic mass in the right suprarenal area. Com-
puted tomography (not shown) revealed a predominance of fat.
473
Adrenal Hemangioendothelioma
Stromal tumors of the adrenal gland are rare, with one of
the most common being hemangioendothelioma (54).
Sonographic findings are a hypoechoic suprarenal mass.
Doppler imaging may show hypervascularity.
Adrenal Hemorrhage
NEONATAL ADRENAL HEMORRHAGE
Spontaneous adrenal hemorrhage in the pediatric age
group occurs primarily in term neonates secondary to birth
trauma or perinatal anoxia, but it can be seen in the setting
of overwhelming septicemia and anticoagulation therapy
(5,6,55). The resulting hemorrhage may be unilateral or
bilateral. The right adrenal gland is more commonly
affected than the left.
Two mechanisms have been proposed to explain neona-
tal adrenal hemorrhage. One mechanism is reflex shunting of
blood away from the splanchnic and visceral bed in response
to perinatal hypoxia or asphyxia, causing hemorrhagic
infarction. The other mechanism is inferior vena caval com-
pression due to prolonged abdominal compression during
delivery, causing elevation of adrenal venous pressures and
venous engorgement with subsequent rupture of vessels.
Clinical findings of neonatal adrenal hemorrhage are a
palpable mass, anemia, and jaundice. Rare complications
include intestinal obstruction due to bowel compression by
the enlarged hemorrhagic adrenal gland (56), hyperten-
sion, and impaired renal function, which is usually sec-
ondary to an associated renal vein thrombosis (57).
Adrenal insufficiency (Addison disease) is rare, even in
bilateral cases.
The typical sonographic appearance is a round, oval, or
triangular suprarenal mass, replacing the entire adrenal
gland. Less commonly, the hemorrhage is limited to a part of
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474 P E D I AT R I C S O N O G R A P H Y

A B
Neonatal adrenal hemorrhage. A: Longitudinal sonogram in a 2-day-old boy with a palpable left-flank mass and jaundice shows a well-
Fig. 12.17
defined suprarenal mass (arrows) that is isoechoic to kidney. LK  left kidney. B: Follow-up sonogram 2 weeks later demonstrates a
hypoechoic mass (calipers). LK  left kidney.

one limb, appearing as a focal mass adjacent to a normal por-
tion of the gland. The echogenicity varies with the age of the
hemorrhage. Acute hemorrhage is isoechoic or hyperechoic
relative to surrounding tissues (Fig. 12.17A). Within several
days the hematoma becomes more hypoechoic and cyst-like
as the clot liquefies (Fig. 12.17B). During the next several
weeks, the mass involutes and eventually disappears, often
leaving a residual focus of calcification (Fig. 12.18). Sponta-
neous adrenal hemorrhage is intracapsular, but the blood
may stretch or disrupt the cortex, resulting in retroperitoneal
or intraperitoneal hemorrhage (58).
The most important differential diagnostic considera-
tion is neuroblastoma. The sonographic differentiation
between neonatal neuroblastoma and adrenal hemorrhage
can be difficult or impossible, especially since neuroblas-
toma can be complicated by hemorrhage. Serial sono-
graphic examinations can help to differentiate between the
two lesions. Adrenal hematomas decrease in size, become
cystic, and eventually disappear. By comparison, neuro-
blastoma tends to retain its echogenicity and to remain sta-
ble or increase in size. Elevated levels of urine cate-
cholamines or their metabolites, which occur in about 90%
of patients with neuroblastoma, also increase diagnostic
specificity. Since neonatal neuroblastoma has a relatively
good prognosis and delayed diagnosis is not harmful, serial
sonography is a useful method of separating the two lesions
if clinical and laboratory data are not diagnostic.
Another lesion that can be confused with neonatal neu-
roblastoma or adrenal hemorrhage is infradiaphragmatic
extralobar pulmonary sequestration. Extralobar pulmonary

A B
Adrenal calcification secondary to antecedent hemorrhage. Transverse (A) and longitudinal (B) sonograms through the right flank of
Fig. 12.18
a 3-week-old infant show a linear area of hyperechogenicity (calipers panel A, arrow panel B), conforming to the expected location of
the adrenal gland. Acoustic shadowing is present. RK  right kidney.
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Chapter 12 A D R E N A L G L A N D S , PA N C R E A S , A N D O T H E R R E T R O P E R I T O N E A L S T R U C T U R E S
Infradiaphragmatic extralobar sequestration. Coronal
Fig. 12.19
sonogram in neonate with a mass on an in utero sono-
gram shows a solid echogenic mass (calipers) that is separate from
the normal adrenal gland (arrowhead). S  spleen.
sequestration occurs primarily on the left side and often is
positioned below the diaphragm in a paraspinal location.
The sequestered lung can have a variable sonographic
appearance, ranging from partially cystic to entirely solid.
Sonographic findings allowing a diagnosis of sequestration
are a feeding vessel arising from the aorta and reverberation
artifacts in the mass due to air-filled bronchi (Fig. 12.19).
POSTTRAUMATIC HEMORRHAGE
In older children, adrenal hemorrhage is usually due to
abdominal trauma, but it also can occur as a complication of
Traumatic adrenal hematoma. Transverse sonogram in a
Fig. 12.20
1-year-old girl with blunt abdominal trauma shows an
echogenic right adrenal mass (arrows).
475
anticoagulant therapy; severe stress; overwhelming sepsis,
especially that caused by Neisseria meningitidis; and liver
transplantation (5962). Most posttraumatic hematomas are
asymptomatic and detected on studies performed for evalua-
tion of other abdominal injury. The right adrenal gland is
affected more often than the left. The hemorrhage is com-
monly associated with hepatic and splenic lacerations (59,60).
Approximately 3% of children with blunt abdominal
trauma have adrenal hemorrhage. The sonographic fea-
tures of adrenal hemorrhage are similar to those seen in the
neonate. Initially, the hemorrhage appears as an echogenic
mass (Fig. 12.20). Serial studies show a decrease in the size
of the hematoma and conversion to a cystic appearance,
with eventual resolution and occasional calcification (63).
Orthotopic liver transplant is another cause of adrenal
hemorrhage. In this procedure, a segment of the recipients
inferior vena cava is excised, requiring ligation and division
of the right adrenal vein, which can cause venous conges-
tion and hematoma or hemorrhagic infarction in the right
adrenal gland (64). The sonographic appearance of post-
traumatic and postsurgical adrenal hematoma is similar.
Adrenal Cysts
Adrenal cysts are usually pseudocysts secondary to prior
adrenal hemorrhage or infection. The most common cause
of infection is echinococcal disease (65). Cysts, which are
characteristically hemorrhagic and located in the capsule or
superficial regions of the cortex, have been described in
Beckwith-Wiedemann syndrome (66,67). At sonography,
adrenal cysts are well-circumscribed, round, anechoic masses
with thin walls and throughsound transmission. Septations,
fluid-fluid levels, and wall calcification may be seen in the
presence of hemorrhage or infection. Very large multilocular
cystic masses, measuring more than 8 cm in diameter, may
develop in Beckwith-Wiedemann syndrome (Fig. 12.21) (66).
Adrenocortical macrocyst. Three-month-old girl with
Fig. 12.21
Beckwith-Wiedemann syndrome. Longitudinal sonogram
shows a large, complex adrenal mass (arrows) with cystic (arrow-
heads) and solid components. K  right kidney; L  liver.
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476 P E D I AT R I C S O N O G R A P H Y
Adrenal abscess. Five-week-old girl with fever and signs
Fig. 12.22
of septicemia and history of traumatic delivery and an
adrenal hematoma. Transverse sonogram shows a left suprarenal
mass (arrowheads) with an echogenic rim and internal debris. Diag-
nosis was confirmed surgically.
Infection
ADRENAL ABSCESS
Adrenal abscess is a rare cause of a suprarenal mass in the
neonate. Most cases are believed to develop as a result of
hematogenous seeding of adrenal hemorrhage. Escherichia
coli is the most common infecting organism. Group B
Streptococcus, Staphylococcus aureus, and Bacteroides
species have also been cultured (68). Adrenal abscess usu-
ally is unilateral, but bilateral cases have been reported.
The clinical signs are generally similar to those seen with
adrenal hemorrhage, along with the additional findings of
fever and leukocytosis.
Sonographically, adrenal abscesses are predominantly
thick-walled, hypoechoic masses (Fig. 12.22). They may
contain echogenic debris that shifts and layers with
changes in patient positioning or hyperechoic foci due to
gas-producing organisms. Distinction between adrenal
abscess and hemorrhage or neuroblastoma requires clinical
correlation and often aspiration or biopsy.
OTHER INFECTIONS
Other organisms that can infect the adrenal gland are her-
pes simplex type I virus, tuberculosis, histoplasmosis,
meningococcus, and Pneumocystis. Sonographic findings of
acute infection include focal or diffuse enlargement of the
glands and a complex mass with hypoechoic and hyper-
echoic areas secondary to necrosis and calcifications, respec-
tively. Chronic findings include atrophy and calcifications
(69,70).
Xanthogranulomatous disease is a rare inflamma-
tory process of the adrenal gland. The sonographic
appearance is a complex, solid, and cystic mass with
poorly defined margins. Color Doppler imaging can
show increased vascularity in the solid part of the mass
(71).
Adrenal Hyperplasia
CONGENITAL ADRENAL HYPERPLASIA
Primary adrenal insufficiency can be congenital or
acquired. The most common inherited cause for adrenal
insufficiency is congenital adrenal hyperplasia (CAH),
also termed adrenogenital syndrome (47). CAH is a
group of autosomal recessive disorders in which there is
an inborn error in one of the enzymes in the adrenal
steroid synthetic pathway, which results in inadequate
production of the normal end-products of the adrenal cor-
tex. This deficiency leads to excessive pituitary ACTH
production, which in turn leads to chronic stimulation of
the adrenal glands, resulting in cortical hyperplasia. The
clinical and biochemical features depend on which hor-
mone is deficient and the biologic properties of the inter-
mediate hormones that are overproduced. These include
glucocorticoid and mineralocorticoid deficiencies as well
as findings of androgen excess.
21-Hydroxylase deficiency is the most common cause
of CAH, accounting for more than 90% of cases (47). The
remaining cases are usually due to errors in production of
11b-hydroxylase and 3b-hydroxysteroid dehydrogenase
(47). The classic forms of CAH present in infancy. 21-
Hydroxylase deficiency presents in infancy with ambigu-
ous genitalia in genetic females and salt-wasting crisis in
boys. 11b-Hydroxylase deficiency presents with ambigu-
ous genitalia in genetic females; affected males are usually
normal in the newborn period. 3b-Hydroxysteroid dehy-
drogenase presents with salt-wasting crisis. The nonclassic
or late-onset forms of CAH present later in childhood or
adolescence with premature adrenarche, hirsutism, and/or
menstrual irregularity (47).
The adrenal glands are enlarged or at the upper limit of
normal in size (Fig. 12.23) (5,6,72,73). Mean adrenal
gland length of 20 mm or greater and mean width of 4 mm
or greater are suggestive of the diagnosis (73). The
enlarged glands retain a triangular configuration and cor-
ticomedullary differentiation (Fig. 12.23). The cortical
thickness increases, and the margins may become irregular
resulting in a wrinkled cerebriform pattern (Fig. 12.24)
(74). Of note, infants with ambiguous genitalia from
causes other than CAH have normal-sized adrenal glands.
In older children with untreated CAH, the adrenal glands
can have a nodular appearance.
LIPOID ADRENAL HYPERPLASIA
Lipoid adrenal hyperplasia is a rare form of CAH resulting
in absent synthesis of all adrenal and gonadal steroids (47).
There is a deficiency in the steroidogenic acute regulatory
protein, which leads to a defect in the conversion of
cholesterol to pregnenolone, which in turn leads to
impaired synthesis of mineralocorticoids, glucocorticoids,
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Chapter 12 A D R E N A L G L A N D S , PA N C R E A S , A N D O T H E R R E T R O P E R I T O N E A L S T R U C T U R E S 477

A B
Congenital adrenal hyperplasia due to 21-hydroxylase deficiency. Newborn female infant with ambiguous genitalia. A, B: Transverse
Fig. 12.23
sonograms through the right and left adrenal glands (arrows), respectively. Both adrenal glands are enlarged but they maintain a nor-
mal triangular or Y-shaped configuration. Corticomedullary differentiation is preserved. Calipers indicate the kidneys.

and sex steroids. Patients present in infancy with salt-
wasting crisis and ambiguous external genitalia. The adre-
nal glands are markedly enlarged as a result of accumula-
tion of lipoid material, composed of cholesterol and
cholesterol esters (75).
Wolman Disease
Wolman disease is an autosomal recessive inborn error of
lipid metabolism due to a deficiency of lysosomal acid
lipase, leading to massive accumulation of cholesterol
esters and triglycerides in most tissues of the body (47,76).
This disorder presents in the first weeks of life with find-
ings of marked hepatosplenomegaly, vomiting, diarrhea,
steatorrhea, and anemia. Pathologically, the adrenal glands
are bilaterally symmetrically enlarged. The normal shape
of the adrenal glands is retained. The adrenal cortex con-
tains lipid-laden cells, with prominent areas of necrosis
and calcification. The adrenal medulla is not involved.
Most patients die by the end of the first year of life.
Sonography shows bilateral, enlarged, triangular-shaped
adrenal glands that are highly echogenic with acoustic
shadowing related to calcifications (Fig. 12.25) (76,77).
Hyperechoic thickened bowel walls and hepatosplenomegaly
with fatty infiltration are other findings (77).

Congenital adrenal hyperplasia due to 21-hydroxylase
Fig. 12.24
deficiency. Newborn male infant with salt-wasting syn-
drome. Longitudinal sonogram shows an enlarged adrenal gland with
a wrinkled cerebriform cortical pattern (arrowheads).
Wolman disease. Longitudinal sonogram in a neonate
Fig. 12.25
with hepatomegaly shows an enlarged right adrenal
gland with highly reflective margins (arrows) associated with posterior
acoustic shadowing (open arrows). RK  right kidney.
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478 P E D I AT R I C S O N O G R A P H Y
PANCREAS
Scanning Technique
The highest-frequency transducer that provides adequate
penetration should be used. This usually is a 5.0- to 7.5-MHz
probe, but in large individuals a lower-frequency transducer
may be needed. Identifying the spine or great vessels ensures
that penetration is adequate.
The sonographic examination is performed with the
patient fasting to minimize gaseous distension of bowel,
which can impair visualization of the pancreas. The pan-
creas is imaged in transverse and sagittal planes with the
patient supine. The neck and body usually are best eluci-
dated with the transducer positioned in the midline below
the xiphoid using the left lobe of the liver as an acoustic
window. The pancreatic head and uncinate process are
often best seen through a right subcostal approach. The
pancreatic tail is visualized best on coronal scans with the
spleen or left kidney as a window. Using the fluid-filled
stomach as an acoustic window may improve demonstra-
tion of the tail of the pancreas.
Portions of the liver should be included on both scans
so that pancreatic and liver echotexture can be compared.
Scans should extend cephalad at least to the celiac axis and
caudad to the level of the portal vein to ensure coverage of
the entire gland.
Normal Anatomy
The pancreas has an oblique orientation, extending from
the second portion of the duodenum to the splenic hilum.
Classically, it is subdivided into a head, neck, body, tail,
and uncinate process. The head lies medial to the duode-
num and to the right of the superior mesenteric vessels,
and the neck and body lie anterior to these vessels. The tail
is situated to the left of the mesenteric vessels and extends
superoposterior to the splenic hilum, where it becomes
intraperitoneal for a short distance. The uncinate process,
a caudal and medial extension of the head, is located pos-
terior to the superior mesenteric vein.
Several vascular structures serve as useful landmarks
to help in the sonographic localization of the pancreas.
The head of the pancreas lies anterior to the inferior vena
cava. The body and tail of the pancreas are situated ante-
rior to the splenic vein and the portal-splenic vein conflu-
ence. The origin of the celiac axis is situated superior to
the pancreas, and the splenic artery also courses along the
superior aspect of the pancreas. The gastroduodenal artery
arises from the common hepatic artery and is in close
proximity to the anterior surface of the pancreatic head or
neck.
Several other anatomic relationships are particularly
important for understanding the spread of disease. The
pancreas lies in the anterior pararenal space, which is con-
tiguous with the renal fascia (Fig. 12.26). The stomach lies
anterior to the pancreas and is separated from it by the
parietal peritoneum and lesser sac. The transverse meso-
colon courses along the ventral surface of the pancreas.
These relationships become important in acute pancreati-
tis, as the retroperitoneal and peritoneal communications
can serve as pathways for the extension of inflammatory
exudate.
The pancreas is composed of exocrine and endocrine
tissues. The exocrine pancreas accounts for about 80% of
the pancreatic tissue and contains acinar and ductal ele-
ments. The endocrine (islet) cells make up about 2% of the
gland. The remainder of the parenchyma is fibrous stroma
containing vessels, lymphatics, and nerves (78).
PANCREATIC ECHOTEXTURE
The normal pediatric pancreas is well marginated and
homogeneous with an echogenicity usually equal to that of
the liver (79). In about 10% of infants and young children,
the pancreas is less echogenic than the liver. The echo pattern
is thought to be secondary to the relatively large amounts
of glandular tissue in the pancreas of young children, with
little fibrosis or fat, which accounts for the increased
echogenicity seen in older individuals. In neonates, the
pancreas can be hyperechoic to liver (Fig. 12.27) (80).
After the neonatal period, marked hyperechogenicity of
Normal extraperitoneal anatomy. A: The
Fig. 12.26
anterior pararenal space (horizontal
lines) lies anterior to the anterior renal fascia and con-
tains the pancreas (Panc), duodenum (D), and ascend-
ing (AC) and descending (DC) colon. The perirenal
space (dotted area) lies between the anterior renal fas-
cia and posterior renal fascia and contains the kidneys.
The posterior pararenal space (cross-hatched lines)
lies behind the posterior renal fascia. (Reprinted with
permission from Meyers MA. The extraperitoneal
spaces: normal and pathologic anatomy. In: Meyers
MA, ed. Dynamic radiology of the abdomen: normal
and pathologic anatomy. 4th ed. New York: Springer-
Verlag, 1994:219342.)
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Chapter 12 A D R E N A L G L A N D S , PA N C R E A S , A N D O T H E R R E T R O P E R I T O N E A L S T R U C T U R E S 479

A B
Normal pancreas. A: Neonate. The pancreas is hyperechoic with respect to liver. Arrows indicate the pancreas. L  liver; A  aorta;
Fig. 12.27
St  stomach; PV  portal vein. B: Seven-year-old boy. The pancreas and liver are isoechoic. The tail is larger than the body and neck,
which is a typical configuration in the older child. Arrows indicate the pancreas. L  liver; PV  portal vein.

the pancreas usually indicates a fatty replacement process, often associated with acute pancreatitis (82). Side branches
such as cystic fibrosis, steroid therapy or chemotherapy, are not seen unless the main duct is dilated.
chronic pancreatitis, or obesity. The common bile duct appears as a round anechoic
structure posteriorly in the head of the pancreas. The main
PANCREATIC DUCT pancreatic duct may or may not be seen joining the com-
The normal pancreatic duct is seen at least partially in up mon bile duct before entering into the duodenum.
to 85% of healthy children (81). It is best seen on trans-
verse views in the central part of the body, where the duct DIMENSIONS
is perpendicular to the sound beam. The mean diameter of The method used to measure the pancreas is illustrated
the pancreatic duct in healthy children is 1.65  0.45 mm in Figure 12.29. The anteroposterior dimension of the
(range 1 to 3 mm). The duct can appear either as a pancreas varies throughout the gland and with the age of
single echogenic linear structure or as a tubular structure
with smooth, parallel echogenic walls and an anechoic
lumen (Fig. 12.28) (82). Pancreatic ducts greater than 1.5
mm in diameter in children between 1 and 6 years of age,
greater than 1.9 mm in children aged 7 to 12 years, or
greater than 2.2 mm in children aged 13 to 18 years are

Diagram of the normal pediatric pancreas (Pan), illustrat-

Normal pancreatic duct. Transverse sonogram. The pan-
Fig. 12.28
creatic duct (calipers) appears as an anechoic tubular
structure with echogenic walls and a diameter of 1.0 mm. Arrows indi-
cate the pancreatic margin. L  liver; PV  portal vein.
Fig. 12.29
ing the points for measurement of the maximum antero-
posterior dimensions. 1, head; 2, body; 3, tail. Ao  aorta; IVC  inferior
vena cava; Sp  spine. (Adapted from Siegel MJ, Martin KW,
Worthington JL. Normal and abnormal pancreas in children: US studies.
Radiology 1987;165:1518.)
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480 P E D I AT R I C S O N O G R A P H Y

Measurement of the Pancreas Correlated with Age
Table 12.2 (Maximum Anteroposterior Dimensions, Mean  SD, cm)
Age Head Body
1 mo 1.0  0.4 0.6  0.2
1 mo1 y 1.5  0.5 0.8  0.3
15 y 1.7  0.3 1.0  0.2
510 y 1.6  0.4 1.0  0.3
1019 y 2.0  0.5 1.1  0.3
From Siegel MJ, Martin KW, Worthington JL. Normal and abnormal pancreas in
children: US studies. Radiology 1987;165:1518.
the individual. The pancreas grows substantially during
the first year of life and more slowly between 1 and 18
years of age. The pancreatic head and tail are usually sim-
ilar in size and are larger than the neck and body (Fig.
12.27B; Table 12.2) (79).
PITFALLS AND ARTIFACTS
The ligamentum teres, which is composed of fat and fibrous
tissue, sometimes produces acoustic shadowing that crosses
the body of the pancreas, mimicking a parenchymal lesion.
Positioning the transducer on either side of the ligament
and scanning at a slight obliquity should help to distinguish
this artifact from a pathologic process.
If the liver is abnormally echogenic due to fatty infiltra-
tion, the pancreas can appear artifactually hypoechoic, sug-
gesting pancreatitis. Failure to visualize the echogenic por-
tal triads, which are silhouetted by the fatty parenchyma,
and poor sound transmission through the liver should sug-
gest hepatic steatosis. Conversely, if the liver is abnormally
hypoechoic due to acute hepatitis, the pancreas may appear
hyperechoic, suggesting fatty replacement or chronic pan-
creatitis. The increased conspicuity of the portal triads, pro-
ducing the starry sky appearance, is the clue to the diag-
nosis of hepatitis.
Embryology
The pancreas develops from two separate anlagen: a
larger dorsal anlage and a smaller ventral anlage (83,84).
By the seventh week of development, there is fusion of
these two primordia. The dorsal anlage gives rise to the
cephalad part of the pancreatic head as well as the neck,
body, and tail. The ventral anlage develops into the cau-
dal part of the head and the uncinate process. In the early
Tail
part of gestation, each anlage has a separate pancreatic
1.0  0.4 duct. These ducts empty separately into the duodenum
1.2  0.4 through two different openings, the major and minor
1.8  0.4 papillae. The duct systems of the two primordia usually
1.8  0.4 fuse in the region of the pancreatic head after the pancre-
2.0  0.4 atic anlagen fuse.
The union of the dorsal and ventral ducts forms the
duct of Wirsung or main pancreatic duct. The ventral duc-
tal system becomes the dominant duct system and drains
more than 70% of the pancreas. The dorsal duct drains
only a small portion of the pancreatic head. The main pan-
creatic duct joins the common bile duct just outside the
ampulla of Vater, after which both ducts enter the medial
side of the second portion of the duodenum at the major
papilla. However, in some individuals, the accessory pan-
creatic duct, called the Duct of Santorini, drains into the
minor papilla (Fig. 12.30) (83,84). It maintains a commu-
nication with the main pancreatic duct.
Congenital Anomalies
PANCREAS DIVISUM
Pancreas divisum, the most common congenital variant of
pancreatic anatomy, results when the ventral and dorsal
pancreatic ducts fail to fuse. The incidence ranges from 4%
to 14% in autopsy series and between 1.3% and 6.7% on
endoscopic retrograde pancreaticography (85). As a result
of nonunion of the ducts, the ventral duct drains separately
into the major papilla, while the dorsal duct drains sepa-
rately into the minor papilla. The major drainage of the
pancreas is via the dorsal duct (Fig. 12.30C). The majority
of individuals are asymptomatic. A small number of patients
may have repeated episodes of pancreatitis (86). In pancreas
divisum, it has been suggested that the duct of Santorini and
the accessory papilla are too small to transmit the volume of
pancreatic secretions that must flow through. The result is a
functional stenosis and pooling of secretions, leading to
pancreatitis (86). In pancreas divisum, it has been suggested
that the duct of Santorini and the accessory papilla are too
small to transmit the volume of pancreatic secretions that

A B C
Pancreatic ductal anatomy, common variations. A: Single-duct drainage (most common pattern). The dorsal and ventral ducts have
Fig. 12.30
fused. The main pancreatic duct drains most of the pancreas through the duct of Wirsung at the major papilla. The duct of Santorini
has not established a communication with the duodenum. B: Communicating ductal drainage. Drainage is through the ventral duct of Wirsung at the
major papilla and also through the dorsal duct of Santorini at the minor papilla. C: Noncommunicating ductal drainage (pancreas divisum). The dor-
sal and ventral ducts have not fused. Thus, the dorsal pancreas drains through the minor papilla and the ventral pancreas drains through the major
papilla. The dorsal duct accounts for most of the drainage. (Adapted from Schulte SJ. Embryology, normal variation, and congenital anomalies of
the pancreas. In: Freeny PC, Stevenson GW, eds. Alimentary tract radiology. St. Louis, LO: Mosby, 1994:10391051.)
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Chapter 12 A D R E N A L G L A N D S , PA N C R E A S , A N D O T H E R R E T R O P E R I T O N E A L S T R U C T U R E S
must flow through. The result is a functional stenosis and
pooling of secretions, leading to pancreatitis.
The overall size of the pancreas may be normal or the
thickness of the pancreatic head may be increased. The
dorsal pancreatic duct may be identified by sonography,
but demonstration of a separate ventral duct is often not
possible. The ductal anatomy is seen best on MRI.
DORSAL PANCREAS AGENESIS
Agenesis of the dorsal pancreatic anlagen results in a con-
genitally short pancreas. It may occur spontaneously or in
association with the polysplenia syndrome. In this anom-
aly, only the pancreatic head develops. The diagnosis can
be made on sonography based on identification of a short
pancreatic head adjacent to the duodenum and absence of
other pancreatic tissue (87). Polysplenia can be an associ-
ated finding (See Fig. 9.6 Chapter 9, Spleen and Peritoneal
Cavity). Because most of the islet cells are located in the
distal pancreas, patients with this anomaly have an increased
risk of diabetes mellitus.
ANNULAR PANCREAS
Annular pancreas is the second most common congenital
anomaly of the pancreas (84). It results from the develop-
ment of a bifid ventral pancreatic bud with encasement of
the duodenum by the separate ventral moieties, producing
a variable degree of duodenal obstruction. Complete
obstruction presents in the neonate as vomiting and
abdominal distention, resulting in a classic double bub-
ble sign on plain abdominal radiographs. With incom-
plete obstruction, the clinical manifestations may be mild
or absent and the diagnosis is made incidentally on imag-
ing studies for other clinical indications or at autopsy.
At sonography, the annular pancreas appears as a cir-
cumferential band of echogenic tissue encircling a fluid-
filled, dilated descending duodenum (88,89).
COMMON PANCREATICOBILIARY CHANNEL
Common pancreaticobiliary channel is another pancreatic
duct anomaly. In this anomaly, the junction of the common
bile duct and pancreatic duct is outside the duodenum
(90). The normal common channel is usually up to
5 mm in length; the abnormal common channel exceeds
10 mm (84). The anomalous ductal arrangement allows
reflux of pancreatic secretions into the common bile duct
and vice versa, predisposing to development of choledochal
cyst; stone formation in the gallbladder; bile ducts or pan-
creatic ducts; inflammatory diseases such as pancreatitis,
cholangitis, and cholecystitis; and gallbladder, bile duct, or
pancreatic duct cancer (90). Sonographic diagnosis of a
common pancreaticobiliary channel is based on demon-
stration of an extraduodenal pancreaticobiliary junction.
ECTOPIC PANCREAS
Ectopic pancreatic tissue is an aberrant rest of pancreatic tis-
sue that lacks anatomic and vascular continuity to the main
pancreas (84). Approximately 70% are found in the stom-
ach, duodenum, and jejunum, with the remainder occurring
481
in the ileum, liver, splenic hilum, biliary tract, mesentery, or
umbilicus (84,91). The tissue is typically submucosal in loca-
tion. Ectopic pancreatic tissue is usually asymptomatic and
an incidental finding on contrast examinations of the gas-
trointestinal tract or endoscopy. Symptoms such as abdomi-
nal pain or bleeding may be related to mucosal ulceration,
pancreatitis (due to functioning ectopic tissue), bowel
obstruction, or intussusception. The characteristic endo-
scopic sonographic findings of ectopic pancreatic tissue are a
hypoechoic mass with a heterogeneous echotexture in the
submucosa or in the submucosa and muscularis propria (92).
Congenital Systemic Diseases
CYSTIC FIBROSIS
Cystic fibrosis (CF) is caused by an autosomal recessive gene
found on the long arm of chromosome 7, which codes for a
polypeptide of 1480 amino acids called the transmembrane
conductance regulator (CFTR) (93). The putative role of CFTR
in the biliary epithelium is to facilitate water and solute move-
ment via chloride secretion and therefore promote bile flow. In
CF, a defect in this regulator gene impairs the transmembrane
chloride ion transport, resulting in abnormally thick luminal
secretions. These secretions, in turn, lead to obstruction of the
pancreatic ducts and ductules and ultimately glandular atro-
phy, fibrosis, and fatty replacement (94, 95). Affected patients
have pancreatic exocrine dysfunction. More than 90% of the
exocrine function needs to be absent before clinical findings
such as abdominal pain, fat intolerance, steatorrhea, and fail-
ure to thrive develop.
The pancreatic manifestations of cystic fibrosis are
diverse and include fatty infiltration (present in most
patients), cyst formation, calcification, and atrophy. Fatty
replacement causes the classic hyperechogenicity of the
pancreas; pancreatic size is normal (Fig. 12.31) (9699).
The pancreas may be enlarged if there is associated pan-
creatitis, occurring in up to 15% of pancreatic-sufficient
patients with CF (93).
Cystic fibrosis. The pancreas (arrowheads) is markedly
Fig. 12.31
hyperechoic, reflecting fatty replacement of the exocrine
pancreatic tissue. P  portal vein.
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482 P E D I AT R I C S O N O G R A P H Y
A B
Cystic fibrosis with pancreatic cysts. A: Longitudinal sonogram in a 16-year-old girl shows a circumscribed anechoic cyst (arrowhead)
Fig. 12.32
in the body anterior to the portal confluence (arrow). L  liver. B: Contrast-enhanced computed tomography scan again demonstrates
the cyst (arrowhead) in the pancreas anterior to the portal confluence (arrow).
The cysts are often microscopic or small, ranging
between 1 and 3 mm in diameter, but occasionally, there is
nearly complete replacement of the pancreatic parenchyma
by multiple macroscopic cysts, a condition referred to as
pancreatic cystosis (Fig. 12.32) (95,98,100,101). The cysts
are true cysts lined by epithelium. They are believed to be
the result of inspissated secretions leading to ductal dilata-
tion. Calcifications are usually coarse and may involve one
part of the pancreas or be widely distributed.
Associated biliary tract abnormalities include a small
gallbladder and gallstones (102,103). Hepatic abnormali-
ties include steatosis, fibrosis, and cirrhosis (104,105).
SHWACHMAN-DIAMOND SYNDROME
Shwachman-Diamond syndrome is the second most com-
mon inherited cause of pancreatic insufficiency (93). It is
an autosomal recessive genetic disorder caused by muta-
tions of the SBDS gene. The hallmarks of this condition
are exocrine pancreatic dysfunction, bone marrow dys-
function (predominantly neutropenia), metaphyseal
dysostosis, and dwarfism (106,107). Clinical manifesta-
tions are steatorrhea, failure to thrive, diarrhea, and short
stature. Histologic studies show fatty replacement of the
acini with preserved ducts (93). The sonographic findings
are a diffusely hyperechoic pancreas (108). The gland
may be large initially, but later becomes normal sized or
small. Unlike cystic fibrosis, pancreatic calcifications and
cyst formation are not features of Shwachman-Diamond
syndrome.
Other causes of pancreatic lipomatosis include Johan-
son-Blizzard syndrome (congenital aplasia of the nasal
alae, deafness, hypothyroidism, dwarfism, and malabsorp-
tion) (93,109), chronic pancreatitis, steroid therapy, Cush-
ing syndrome, obesity, and obstruction of the main pan-
creatic duct. A specific diagnosis is based on a combination
of clinical and biochemical findings.
CONGENITAL SYNDROMES WITH MULTIPLE CYSTS
Von Hippel-Lindau Disease
Von Hippel-Lindau disease is an autosomal dominant
disorder characterized by retinal angiomatosis; cerebel-
lar, medullary, and spinal hemangioblastomas; pheochro-
mocytomas; and cysts in various organs, particularly in
the pancreas, kidney, liver, epididymis, and adrenal
glands. The pancreatic lesions are usually simple cysts,
but serous microcystic adenomas and adenocarcinomas
can occur (110,111). Pancreatic cysts are usually clini-
cally silent and discovered during routine screening
examinations. Rarely, they are associated with epigastric
pain, diabetes mellitus, or steatorrhea (110). Cysts can
also be found in the kidneys, adrenal glands, liver, and
spleen (110). Sonographic findings are those of a simple
cyst.
Autosomal Dominant Polycystic Disease
Autosomal dominant polycystic disease is a hereditary
disorder with 100% penetrance but variable expressiv-
ity. Renal cysts are the major clinical feature, but cysts
can also be seen in the liver, spleen, and pancreas (Fig.
12.33).
Congenital Hyperinsulinism
Congenital hyperinsulinism, previously known as nesid-
ioblastosis, is a rare disorder characterized by islet cell pro-
liferation leading to hyperinsulinemia and hypoglycemia
(112,113). Symptoms begin in the first few hours of life
and are severe and persistent. Two histologic forms are rec-
ognized: a diffuse form (also termed diffuse adenomato-
sis), accounting for two thirds to three fourths of cases,
and a focal form (focal adenomatosis), accounting for the
remaining cases (112,113). The hypoglycemia is usually
resistant to medical therapy. Treatment for the diffuse
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A B
Autosomal dominant polycystic disease. A: Transverse sonogram shows a small cyst (arrowhead) in the pancreatic head. PV  portal
Fig. 12.33
vein. B: Longitudinal sonogram of the kidney shows multiple renal cysts.
form is near-total (95%) pancreatectomy; treatment of the
focal form, is resection of the lesion. Sonography in con-
genital hyperinsulinism may be normal or show an
enlarged pancreas with diffusely increased echogenicity or
a focal heterogeneous mass (Fig. 12.34) (96,112,114).
Pancreatic regeneration after near-total pancreatectomy
has been reported (114).
Tumors
Pancreatic tumors are rare in children, accounting for
0.2% of all pediatric tumors (78,112,115117). They can
be divided histologically into exocrine, endocrine (islet
cell), nonepithelial, and cystic tumors (112).
Focal endocrine adenomatosis of the pancreas. Trans-
Fig. 12.34
verse sonogram in a 1-month-old girl with persistent
hypoglycemia shows focal enlargement of the body of the pancreas
(arrowheads) anterior to the portal vein (arrow).
483
EXOCRINE TUMORS
The common exocrine tumors are pancreatoblastoma,
adenocarcinoma, and solid pseudopapillary tumors
(112).
Pancreaticoblastoma
Pancreaticoblastoma is an infantile type of pancreatic carci-
noma with a distinctive histopathologic appearance resem-
bling that of a fetal pancreas at the eighth week of devel-
opment (78,116121). Mean patient age at diagnosis is 4.5
years, but the tumor can present in the fetus and neonate
as well as older patients (112,118121). Congenital cases
have been associated with Beckwith-Wiedemann syndrome
(120). Pancreaticoblastoma is usually a large, solitary mass
ranging in size from 1.5 to 20 cm (mean 10.6 cm) (119). It
is a low-grade malignancy and usually has a favorable out-
come. Rarely, it can invade adjacent vessels and metasta-
size to liver and to local and distant lymph nodes. The clin-
ical presentation is usually a large abdominal mass, but
symptoms such as abdominal pain, nausea, vomiting, and
jaundice can occur.
Sonography shows a large, well-defined, hypoechoic or
hyperechoic mass relative to normal parenchyma (Fig.
12.35) (118,122124). Large lesions may be heterogeneous
with cystic and solid areas. Pancreatic and biliary duct
dilatation may also be seen (125). Pancreaticoblastoma is
vascular on color Doppler imaging. Regional adenopathy,
hepatic metastases, and ascites, indicating metastatic
disease, may be present (124).
Adenocarcinoma
Pancreatic adenocarcinoma can be of ductal or acinar ori-
gin, with the former being more common (112,126). Mean
patient age at time of presentation is 6 years. Adenocarci-
noma is usually a large mass ranging in size from 2 to 30 cm
(mean 10 cm) and local extension or metastases are com-
mon at the time of diagnosis. Surgical excision provides the
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484 P E D I AT R I C S O N O G R A P H Y

Pancreatic adenocarcinoma. Transverse sonogram

Pancreaticoblastoma. Longitudinal sonogram in a 2-year-
Fig. 12.35
old girl shows a well-circumscribed, homogeneous,
echogenic mass (M) arising in the pancreatic tail.
Fig. 12.36
shows a mass in the pancreatic head (cursors) with
obstruction of the distal pancreatic duct (arrow), which is dilated.

only possibility of cure, but the overall resectability rate is
low. Symptoms include abdominal pain, weight loss, and
jaundice. Sonography usually shows a poorly defined,
homogeneous or heterogeneous, hypoechoic mass (Fig.
12.36). Biliary and pancreatic ductal dilatation may also be
seen. Ancillary findings of malignancy include vascular
encasement and invasion, infiltration of surrounding organs
and tissues, and ascites, best seen on CT or MRI.
Solid Pseudopapillary Tumor
Solid pseudopapillary tumor of the pancreas (previously
known as solid and papillary epithelial neoplasm, solid
cystic papillary tumor, papillary cystic tumor, and Frantz
tumor) is a low-grade malignant tumor seen in adolescent
girls and young women with a mean age of 22 years
(112,127130). The tumor is typically large (mean diame-
ter of 9.0 cm) and well circumscribed and arises in the pan-
creatic tail, but any part of the pancreas can be involved
(112). Histologically, it contains solid sheets of epithelial
cells with an endocrine appearance, pseudopapillae, and
cystic areas. Clinical findings include an upper abdominal
mass, abdominal pain, and, rarely, jaundice. Prognosis fol-
lowing surgical resection is excellent (112,127130).
The typical sonographic appearance is a well-defined
complex mass with solid and cystic components, reflecting the
presence of hemorrhage and cystic degeneration (131,132).
However, the tumor can appear entirely solid (Fig. 12.37) or
nearly completely cystic with a small amount of solid tissue at

A B
Cystic solid papillary epithelial neoplasm. A: Longitudinal sonogram shows a large solid mass (M) in the pancreatic head. B: Computed
Fig. 12.37
tomography scan confirms a low-attenuation solid mass (M), which histologically had epithelial cells, hemorrhage, and cystic degen-
erated areas.
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the periphery. Calcifications, septations, and fluid-debris lev-
els may be present (112,131).
ENDOCRINE TUMORS (ISLET CELL TUMORS)
Endocrine tumors, also known as islet cell tumors, are
believed to arise from neural crest tissue that gives rise to
the cells of the islets of Langerhans. Most tumors are hor-
monally active and produce increased amounts of polypep-
tide hormones, including insulin, gastrin, glucagon, vasoac-
tive intestinal peptide, and somatostatin. Affected patients
present with manifestations related to the dominant hor-
mone that is produced or with findings of metastatic dis-
ease. Islet cell tumors can be sporadic, but they also can be
seen in patients with MEN type 1, von Hippel-Lindau dis-
ease, and other phacomatoses (133135). Most neuroen-
docrine tumors in children are benign.
Functioning Islet Cell Tumors
Insulinomas are the most common type of islet cell tumors
(47% of functioning tumors) (121). Patients present with
symptoms related to hypoglycemia and have elevated serum
insulin levels. Most insulinomas are small (mean size 2 to
2.2 cm), solitary, and benign. Cystic changes and necrosis
are uncommon. At sonography, they generally are homoge-
neous and hypoechoic relative to normal parenchyma,
and they may have a hyperechoic capsule (Fig. 12.38)
(121,136139). Color Doppler sonography shows a hyper-
vascular mass.
Gastrinomas are the second most common islet cell
tumors after the insulinomas (30% of functioning tumors)
(121). Symptoms are due to gastric acid hypersecretion
and include peptic ulcer disease and diarrhea. Gastrinomas
are larger than insulinomas (mean diameter 4.2 cm) and
more likely to have a heterogeneous matrix, with areas of
necrosis and calcification, even if relatively small
(136,137). They also have a higher likelihood of malig-
nancy (139).
Glucagonoma, somatostatinoma, and the VIPomas
(which secrete vasoactive intestinal peptide) are extremely
rare functioning islet cell tumors. They tend to be relatively
large at presentation (5 cm in diameter) and heteroge-
neous with cystic areas and calcification (112). Further-
more, they are more likely to be associated with malignant
behavior. Findings suggesting malignancy include local
invasion, vascular invasion, lymphadenopathy, and
vascular invasion (136). Hepatic metastases tend to be
echogenic.
The sensitivity of preoperative sonography for detect-
ing islet cell tumors, especially insulinomas, is limited by
the small size of the tumors. In adults, intraoperative
sonography appears to be a more sensitive method of
imaging islet cell tumors, increasing the detection rate to
over 95% (138).
Nonfunctioning Islet Cell Tumors
A small subset of islet tumors is hormonally inactive, and
these neoplasms are usually detected because they cause
pain or symptoms related to metastases (136,137). Non-
functioning tumors are typically larger than functioning
tumors at the time of diagnosis (mean diameter about 8 cm).
They share the characteristics noted for the noninsulin-
producing types of hyperfunctioning tumors, including
calcification, cystic changes, and malignant behavior
(Fig. 12.39) (136,137).

A B
Insulinoma. Young adult woman with recurrent hypoglycemic attacks. A: Transverse sonogram shows a small hypoechoic mass
Fig. 12.38
(calipers) measuring 1.7  1.5 cm in the pancreatic head. B: Color Doppler image shows internal vascularity.
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486 P E D I AT R I C S O N O G R A P H Y

A B
Nonfunctioning islet cell tumor. A: Transverse sonogram shows a 4.5-cm solid mass (calipers) in the pancreatic body. The tumor was
Fig. 12.39
vascular on color Doppler imaging. B: Transverse sonogram shows a hyperechoic liver metastasis (arrows).

NONEPITHELIAL NEOPLASMS hemorrhagic. Distinguishing between a septated congenital

Nonepithelial pancreatic tumors arise from the connective,
lymphatic, vascular, and neuronal tissues of the pancreas.
The clinical presentation of these tumors includes a palpa-
ble abdominal mass, pain, and obstructive jaundice.
Lymphangioma
Lymphangioma is a congenital mass due to obstruction of
fetal lymphatics (112). At pathologic examination, it is
multicystic and surrounded by a thin capsule. The cystic
spaces contain serous or chylous fluid and rarely hemor-
rhage. Sonographically, lymphangioma appears as a sep-
tated, predominantly hypoechoic mass (Fig. 12.40). Inter-
nal echoes or debris can be seen if the contents are
cyst (see later) and lymphangioma may require tissue sam-
pling.
Cystic Teratoma
Cystic teratoma develops from pluripotential cells of the
embryonic remnants of the ectoderm (111,140,141). These
tumors are large (8 to 12 cm) and often palpable. Sonog-
raphy shows a predominantly cystic mass with varying
amounts of fat, calcification, bone, and soft tissue
(111,140142).
Lymphoma
Pancreatic lymphoma is rare in children (112,143). When
it occurs, it is more common in non-Hodgkin lymphoma

A B
Lymphangioma of the pancreas. Five-year-old boy with 1-week history of abdominal pain and vomiting. Sonography shows a predom-
Fig. 12.40
inantly cystic mass in the pancreatic body and tail (arrowheads) with multiple thin, enhancing septations. Straight arrow indicates the
inferior vena cava; curved arrow indicates the aorta. L  liver; GB  gallbladder; K  kidney. B: Computed tomography scan confirms the presence
of a multiloculated, water attenuation, pancreatic head mass (arrowheads). No solid components are evident. Arrow indicates the gallbladder.
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A B
High-grade sarcoma of the pancreas in a 10-year-old boy who presented with jaundice, nausea, and vomiting. A: Sonogram shows an
Fig. 12.41
ill-defined, echogenic mass (arrows) in the pancreatic head and a dilated main pancreatic duct (arrowhead). SP  Spine. B: Contrast-
enhanced computed tomography scan shows a heterogeneous mass in the pancreatic head causing mass effect on the gallbladder (arrow). Arrow-
heads indicate the pancreatic body and tail.

than in Hodgkin lymphoma. Sonographic findings include
diffuse hypoechoic, pancreatic enlargement and multiple,
homogenous, hypoechoic or anechoic masses. Anechoic
lesions can mimic a pancreatic cyst, but the finding of
coexisting splenomegaly or widespread lymph node
enlargement helps to establish the diagnosis of lymphoma.
Other Tumors
Rare benign nonepithelial lesions include inflammatory
pseudotumor (144,145), hemangioendothelioma (146),
leiomyoma, lipoma, neurofibroma, and schwannoma.
Rare malignant tumors include primitive neuroectodermal
tumor (PNET), which is now included as part of the Ewing
sarcoma family of tumors (147); rhabdomyosarcoma
(148); malignant schwannoma; fibrosarcoma; liposar-
coma; and malignant fibrous histiocytoma (Fig. 12.41).
These tumors are large, ill-defined, and often heteroge-
neous with cystic or necrotic areas. They may be hypoe-
choic, isoechoic, or hyperechoic to surrounding structures.
of adjacent structures. Typically, they are thin-walled,
unilocular, anechoic masses (Fig. 12.42) (112,149,151,
152). Occasionally, they contain septations or low-level
echoes due to debris or proteinaceous material. Associ-
ated anomalies include polydactyly, polycystic kidneys
and renal tubular ectasia, and anorectal malformations
(149151).
Miscellaneous Cystic Lesions
Other cystic tumors, such a microcystic or serous cystade-
noma, macrocystic or mucinous cystadenoma, and intra-
ductal papillary mucinous neoplasms, are very rare in
children. Microcystic cystadenoma is usually seen in

CYSTIC MASSES
Cystic lesions may be congenital, neoplastic, or inflam-
matory. The most common cystic mass is a pseudocyst
(see subsequent section on pancreatitis). Other cystic
lesions include congenital pancreatic cyst, lymphan-
gioma, solid pseudopapillary tumor, and cysts associated
with hereditary syndromes (see prior discussion).

Congenital Pancreatic Cysts

Congenital pancreatic cysts are thought to be the result
of abnormal segmentation of the primitive ductal system
(112,149,150). They are usually found prenatally or in
children younger than 2 years or age, but they may be
seen at any age (149151). Most involve the pancreatic Congenital pancreatic cyst. Transverse sonogram of a
tail. Clinical findings include an abdominal mass or dis- Fig. 12.42
2-year-old boy shows a large cystic mass (C) in the pan-
tension, vomiting, and jaundice related to compression creatic head. GB  gallbladder; K  right kidney; L  liver.
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488 P E D I AT R I C S O N O G R A P H Y
elderly women and is composed of multiple cysts typically
smaller than 2 cm in diameter. Mucinous cystadenoma is
more common in middle-aged women and often contains
cysts greater than 2 cm in diameter. Intraductal papillary
mucinous tumor is characterized by cystic dilatation of
branch ducts and diffuse dilatation of the main pancreatic
duct.
METASTATIC LESIONS
Secondary involvement of the pancreas can occur by direct
extension from a retroperitoneal tumor, most commonly
sarcoma, or from hematogenous spread.
Acute Pancreatitis
Acute pancreatitis is defined as an acute inflammatory
process of the pancreas with variable involvement of other
local tissues or remote organ systems (153155). Leading
causes of pancreatitis in children include accidental and
nonaccidental abdominal trauma (156,157), medications,
infections (viral, human immunodeficiency virus [HIV],
ascariasis), structural abnormalities that alter drainage of
pancreatic secretions (pancreas divisum, annular pancreas,
duodenal duplication, choledochal cyst) (86,158,159),
hereditary diseases (cystic fibrosis and hereditary pancre-
atitis), and multisystem diseases (Reye syndrome,
Kawasaki disease, inflammatory bowel disease) (154,155).
The cause of acute pancreatitis is unknown in as many as
30% of children (155). Recurrent acute pancreatitis is seen
in about 10% of children after the initial acute episode
(154).
CLASSIFICATION: PATHOLOGIC AND CLINICAL CHARACTERISTICS
The severity of acute pancreatitis is classified as mild or
severe based on histologic and clinical findings
(153155). Histologically, mild pancreatitis is character-
ized by interstitial edema, small foci of acinar cell necro-
sis, and no or minimal peripancreatic inflammation. Clin-
ical signs include abdominal pain and tenderness,
vomiting, and fever. Pancreatic enzyme levels are elevated
in the blood, urine, or both. Mild pancreatitis is usually
a self-limited disease with a rapid response to conserva-
tive therapy, improvement in clinical and laboratory find-
ings within 48 to 72 hours, and no significant complica-
tions.
The severe form of pancreatitis is characterized by
macroscopic areas of pancreatic necrosis and hemorrhage,
ductal disruption, and extensive peripancreatic inflamma-
tory changes (153155). It is associated with major organ
failure (including gastrointestinal bleeding and renal and
pulmonary insufficiency) and low serum calcium levels.
Local complications, such as pseudocyst formation, pancre-
atic abscess, and necrosis, are more common than in the
mild form. Progression from mild to severe pancreatitis is
rare.
The diagnosis of acute pancreatitis is usually based on
clinical and laboratory findings (e.g., elevated amylase and
lipase levels in serum). However, biochemical studies are
initially normal in some patients. In these patients, as well
as in acutely ill patients in whom complications are sus-
pected, sonography can be helpful to substantiate the diag-
nosis, detect complications, and evaluate for biliary tract
disorders or stones as causes of the pancreatitis. CT is con-
sidered the procedure of choice for displaying severe com-
plications of pancreatitis (e.g., necrosis, abscess, hemor-
rhage, and extrapancreatic fluid collections) (160,161).
SONOGRAPHIC FINDINGS OF UNCOMPLICATED ACUTE PANCREATITIS
In most patients with mild pancreatitis, the pancreas
appears normal on sonography. With more severe
disease, a focally or diffusely enlarged pancreas with
irregular margins and hypoechoic parenchyma is seen
(Fig. 12.43) (162). Focal enlargement generally involves
the pancreatic head and rarely the tail. Pancreatic and
common bile duct dilatation are other signs of acute pan-
creatitis.
The pancreas does not have a well-developed fibrous
capsule, and so the inflammatory process may spread
through the thin surrounding connective tissue layer into
adjacent tissues. Approximately 50% of children with
acute pancreatitis have extrapancreatic fluid collections.
Extrapancreatic fluid collections lack a well-defined capsule
and distend an already existing anatomic space (160,161).
Initially, peripancreatic fluid is located in or near the pan-
creas, accumulating in the anterior pararenal space (71%
of cases), lesser sac (57%), lesser omentum (50%), and
transverse mesocolon (50%). As the pancreatitis pro-
gresses, inflammatory fluid can extend into the perihepatic
spaces, subphrenic spaces, small bowel mesentery, and
lesser and greater omentum (161,162). Fluid also dissects
into the lower peritoneal cavity or pelvis and large collec-
tions extend into the mediastinum. Other extrapancreatic
abnormalities include bowel wall thickening, gallbladder
Acute pancreatitis due to blunt abdominal trauma. Trans-
Fig. 12.43
verse sonogram shows an enlarged pancreas (cursors)
with normal echogenicity equal to that of adjacent liver (L).
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Peripancreatic fluid. Transverse sonogram shows ane-

Fig. 12.44 Pancreatic pseudocyst. Transverse sonogram shows a
choic fluid collections in the lesser sac (LS) and also in Fig. 12.45
the pancreatic head (H). well-defined pseudocyst (C) with internal debris anterior
to the pancreatic body (B) and tail (T). There is a communication
(arrow) with a small intrapancreatic fluid collection (arrowhead).

wall thickening with or without pericholecystic fluid, and
splenic involvement (163), which includes intrasplenic
pseudocyst, abscess, hemorrhage, infarction, splenic rup-
ture, and vascular injury.
Acute extrapancreatic fluid collections often have
poorly defined, irregular contours (Fig. 12.44). Most are
hypoechoic, but the fluid can be echogenic as a result of
hemorrhage, infection, or necrotic debris. The fluid may
change in size and shape and usually resolves completely
within a few weeks. The absence of a wall is helpful in dis-
tinguishing them from pseudocysts.
Fluid in the lesser sac (Fig. 12.44) between the pancreas
and the stomach and in the perirenal space is the easiest to
identify with sonography. Mesocolon fluid is the most dif-
ficult to visualize. The anterior subxiphoid approach is
best to visualize fluid collections in the lesser sac and in the
peripancreatic soft tissues. A lateral approach using the
liver or spleen as a window can aid in identifying fluid in
the anterior pararenal space, the perirenal space, and the
interfascial space.
toneum, and mediastinum. At sonography, pseudocysts are
usually well-circumscribed, anechoic or hypoechoic masses
with through-transmission. The fluid often contains septa-
tions or internal echoes due to debris or hemorrhage (Figs.
12.45 and 12.46) (111,156,157, 164).
Complications of pseudocysts include rupture into a
contiguous part of the gastrointestinal tract or into the
peritoneal cavity; slow intraperitoneal leakage causing
ascites, hemorrhage, abscess formation, or obstruction of
adjacent stomach, duodenum, colon, or bile ducts; and dis-
section into the spleen, liver, stomach, or an adjacent
artery. The treatment for most pancreatic pseudocysts is

COMPLICATIONS
Pseudocyst Formation
Pseudocyst formation is the most common complication
of acute pancreatitis. It typically requires several weeks
(4 to 6 weeks) to form (155). These cysts are surrounded
by thick-walled capsules composed of fibrous and gran-
ulation tissues and have nonepithelialized lining (hence,
they are called pseudocysts rather than true cysts).
Unlike acute fluid collections, which resolve sponta-
neously, resolution of a pseudocyst is less likely.
Pseudocysts are usually found close to the pancreas and Pancreatic pseudocyst. Longitudinal sonogram shows a
lesser omental sac, but they can occur in the pararenal Fig. 12.46
septated anechoic pseudocyst (calipers) adjacent to the
space, left lobe of the liver, juxtasplenic area, retroperi- pancreatic tail (T).
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490 P E D I AT R I C S O N O G R A P H Y
A B
Pancreatic necrosis. A: Transverse sonogram shows a fluid collection (C) in the pancreatic tail. Normal pancreatic tissue is not seen.
Fig. 12.47
L  liver. B: Computed tomography scan shows no enhancing pancreatic tissue.
percutaneous catheter drainage (155,160,165). Surgical
drainage is performed when percutaneous drainage fails,
when there is catastrophic bleeding, or when the percuta-
neous access route is considered too hazardous for catheter
placement.
Other Complications
Pancreatic abscess is a walled-off collection of purulent
material, containing little or no pancreatic necrosis (160).
Pancreatic necrosis is defined as a focal or diffuse area of
liquefied, nonviable pancreatic parenchyma associated with
peripancreatic fat necrosis (160). Sonographic features of
pseudocyst, abscess, and necrosis are similar and include a
hypoechoic or anechoic fluid collection containing debris,
septations, or a fluid-debris level (Fig. 12.47). Gas bubbles
may be present, but they are not specific for infection or
necrosis and can also be seen in patients with pancreati-
coenteric fistulas. CT or needle aspiration of the fluid is
usually needed for differentiation and for planning clinical
management. Abscesses may respond to percutaneous
drainage, whereas infected necrosis may require surgical
debridement.
Pseudoaneurysm formation and venous thrombosis
and occlusion are rare complications of pancreatitis in
childhood. Pseudoaneurysm is the result of destruction
of the arterial walls by proteolytic enzymes released in
pancreatitis. The splenic artery and branches of the pan-
creaticoduodenal arteries are the most commonly
involved vessels. Pseudoaneurysms can arise within or
adjacent to the pancreas or within a pseudocyst
(153,166). On gray-scale sonography, pseudoaneurysm
appears as a complex mass and can simulate a pseudocyst.
Doppler imaging is useful to demonstrate the turbulent
arterial flow within the mass, indicative of a pseudo-
aneurysm (167). Thrombosed pseudoaneurysms, however,
can be difficult to diagnose and their appearance may
simulate that of a solid pancreatic mass. Angiography
with embolization is the treatment of choice for
pseudoaneurysm.
Venous obstruction results when a contiguous inflamma-
tory mass or pseudocyst compresses the vein. The splenic
and mesenteric veins are the most commonly involved vessels
(163). Acute thrombosis can cause focal echogenicity in the
lumen of the vein or an abrupt cutoff of the involved vein.
Chronic thrombus can appear hypoechoic or anechoic and
may be associated with perigastric and mesenteric varices.
(See Fig. 9.24, Chapter 9, Spleen and Peritoneal Cavity).
Chronic Pancreatitis
Chronic pancreatitis is an inflammatory process charac-
terized by progressive destruction of the pancreatic
parenchyma resulting from recurrent episodes of acute pan-
creatitis. It is usually idiopathic or associated with heredi-
tary pancreatitis. Other causes include pancreaticobiliary
ductal anomalies (e.g., pancreas divisum and anomalous
insertion of the common bile duct), which impede drainage
of pancreatic secretions; cystic fibrosis; hyperparathy-
roidism; idiopathic fibrosing pancreatitis; and autoimmune
pancreatitis (155,168,169). Children with chronic pancre-
atitis usually present because of recurrent abdominal pain.
Obstructive jaundice can be a presenting feature of fibrosing
pancreatitis.
Hereditary pancreatitis is an autosomal dominant dis-
order, characterized by recurrent episodes of acute pancre-
atitis beginning in childhood and continuing over many
years. Late complications include exocrine and endocrine
pancreatic insufficiency, pseudocyst formation, and adeno-
carcinoma.
Idiopathic fibrosing pancreatitis is a chronic process of
unknown cause. Histologically, the pancreatic parenchyma
is replaced by fibrous tissue. In addition to symptoms of
pancreatitis, fibrosing pancreatitis can cause obstructive
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Chronic pancreatitis. Fifteen-year-old boy with familial
Fig. 12.48
pancreatitis. Transverse sonogram shows calculi (arrows)
in the pancreatic body. A  aorta. Open arrows  gas-filled jejunum.
jaundice if the fibrotic tissue narrows the common bile
duct (168,169). Fibrosing pancreatitis is associated
with inflammatory bowel disease and is not character-
ized by episodes of acute pancreatitis or pseudocyst
formation.
SONOGRAPHIC FINDINGS
The sonographic hallmark of chronic pancreatitis is pancreatic
calcification, which may be intraductal or parenchymal in loca-
tion (Fig. 12.48). Calcifications appear as focal areas of hyper-
echogenicity. Acoustic shadowing may or may not be present.
Other findings include an irregular, tortuous, and dilated
pancreatic duct (Fig. 12.49); glandular atrophy; peripancre-
Chronic pancreatitis. Transverse sonogram shows a
Fig. 12.49
dilated pancreatic duct (arrows) and parenchymal atro-
phy (*).
491
Traumatic pancreatitis. Transverse sonogram shows a
Fig. 12.50
diffusely enlarged pancreas (P) with an echogenicity
equal to liver (L) and fluid in the lesser sac (arrow).
atic inflammatory changes; and biliary duct dilatation (170).
The parenchymal echotexture is commonly heterogeneous
and the echogenicity is often increased secondary to a com-
bination of fatty replacement and/or fibrosis.
Trauma
Pancreatic injuries account for less than 5% of injuries in
children sustaining blunt abdominal trauma. Most are due
to motor vehicle accidents, handlebars of a bicycle, or
child abuse (171). CT is the primary imaging study for the
initial evaluation of suspected pancreatic injury. However,
sonography may be useful in follow-up evaluation.
Traumatic pancreatic injuries include pancreatitis,
hematoma, laceration, and fracture. Sonographic findings
of traumatic pancreatitis are the same as those of nontrau-
matic pancreatitis and include diffuse or focal gland
enlargement and intra- or extrapancreatic fluid collections
(Fig. 12.50). Pancreatic hematoma appears as poorly mar-
ginated intraparenchymal fluid collection. Lacerations and
fractures are linear areas in the parenchyma, usually cours-
ing perpendicular to the long axis of the gland. Obstructive
pancreatitis has been described in conjunction with trau-
matic duodenal hematoma. Sonographically, there is dif-
fuse pancreatic enlargement, pancreatic and extrahepatic
bile duct dilatation, and hematoma of the second part of
the duodenum.
RETROPERITONEAL GREAT VESSELS
Scanning Techniques
Scanning through the anterior abdominal wall in the mid-
line usually allows good visualization of the superior por-
tions of the inferior vena cava and abdominal aorta.
Coronal scans through both flanks can improve demon-
stration of the more inferior segments of these vessels.
The highest-frequency transducer that gives adequate
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492 P E D I AT R I C S O N O G R A P H Y

Normal aorta in a neonate. Coronal sonogram shows the

Fig. 12.51
aorta (A) and both common iliac arteries (arrows). LK 
left kidney.
penetration should be used. Ideally patients should be
scanned after fasting to minimize the amount of air-filled
bowel.
Aorta
ANATOMY
The abdominal aorta begins at the diaphragmatic hiatus
and extends caudally anterior and slightly to the left of the
lumbar vertebral bodies. At the level of the fourth lumbar
vertebra, it bifurcates into the paired common iliac arter-
ies. Sonographically, the aorta is pulsatile and has
echogenic walls and an anechoic lumen (Fig. 12.51).
Pulsed Doppler analysis shows a high-resistance flow pat-
tern with a rapid upstroke and sharp systolic peak fol-
lowed by a rapid drop in velocity and a brief period of
reversed flow in early diastole. During the rest of diastole,
there is low-velocity antegrade flow (Fig. 12.52) (172,
173). The flow pattern in the main aortic branches to the
kidney, liver, and postprandial bowel is usually character-
ized by a lower-resistance pattern and continuous ante-
grade flow.
Aorta, pulsed Doppler examination. The aortic waveform
Fig. 12.52
is characterized by a sharp increase in antegrade flow
velocity during systole, followed by a reversal of flow in early diastole
and then low-velocity antegrade flow in the remainder of diastole.
in cardiovascular malformations. Factors predisposing to
thrombosis associated with the use of umbilical catheters
include calcium in the catheter infusate, placement of the
catheter above the level of the renal arteries, and use of a
small (3.5 French) catheter (1500 g) (174). Patients
may present for evaluation with clinical signs of lower
extremity vascular compromise or hematuria or hyper-
tension if thrombus involves the renal arteries, but in
many patients the thrombi are asymptomatic and inci-
dental sonographic findings. Long-term complications
include renovascular hypertension and leg-growth distur-
bances (175).
Sonograms of infants with suspected clots should
include scans of the entire abdominal aorta and both

UMBILICAL ARTERIAL CATHETER LOCALIZATION

Sonography can reliably localize the position of intra-
abdominal umbilical arterial catheters. The catheter is seen
either as a brightly echogenic linear or parallel-walled
structure within the aortic lumen (Fig. 12.53). The ideal
location of the catheter is either in the thoracic aorta below
the arch vessels or in the abdominal aorta below the origin
of the renal and mesenteric arteries.

THROMBOSIS
Aortic thrombi occur most often in neonates and are
most commonly a complication of an indwelling aortic
catheter (173,174). Less commonly, they are the result of
a clotting disorder or embolism from thrombi originating
Umbilical arterial catheter. Coronal sonogram through
Fig. 12.53
the left flank demonstrates the echogenic catheter
(arrows) with a central anechoic channel in the aortic lumen (A).
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A B
Aortic thrombus. Two infants with history of umbilical arterial catheterization. A: Longitudinal sonogram shows echogenic thrombus
Fig. 12.54
(calipers) nearly filling the aortic lumen (A) just above the bifurcation of the iliac arteries. B: Longitudinal sonogram in another infant
shows an echogenic thrombus (arrows) partially occluding the lumen. The aorta (A) proximal to the thrombus is mildly dilated. S  superior mesen-
teric artery.

kidneys. Thrombi can appear as an echogenic mass par-
tially or completely filling the vascular lumen (Fig. 12.54)
or as a thin, linear, flap-like structure floating within the
aortic lumen (172177). Color and pulsed Doppler imag-
ing can confirm whether the thrombus is completely or
partially occlusive and the formation of collateral vessels.
In contrast to the sharp systolic upstroke and triphasic
high-resistance flow of the normal aorta, collateral vessels
often show low-velocity waveforms with delayed upstroke
and increased diastolic flow due to downstream arteriolar
dilatation. After fibrinolytic therapy, Doppler sonography
can show restoration of flow following recanalization of
the lumen.
AORTIC ANEURYSM
An aneurysm is a permanent dilatation of the aortic wall.
Age-related normal standards for the ascending and
descending thoracic aorta in children have been estab-
lished on CT and can be used for reference when aortic
enlargement is suspected (178).
Aortic aneurysms in infants are most commonly related
to umbilical arterial catheterization. Most are mycotic and
associated with bacteremia, particularly Staphylococcus
aureus infection (179183). They occasionally are congen-
ital (184,185). In older children, aortoiliac aneurysms are
usually associated with connective tissue disorders (Mar-
fan disease or Ehlers-Danlos syndrome), Takayasu aortitis,
infection, or trauma (186,187). In Marfan disease, there
often is an associated aneurysm or dilatation of the tho-
racic aorta. In Kawasaki disease, there may be multiple
sites of aneurysm formation, including the abdominal
aorta; iliac, femoral, and splanchnic arteries; and coronary
arteries. While Takayasu aortitis can lead to aneurysm for-
mation, it more often results in stenoses and vascular
occlusion (188,189).
Gray-scale sonography shows focal or diffuse aortic
dilatation (Fig. 12.55). Color Doppler imaging shows a
swirling flow pattern in the lumen of the aneurysm.
Pulsed interrogation shows high peak systolic frequency
shifts and bidirectional flow. Mural thrombus, which
usually has low to medium echogenicity, may also be
noted.
AORTIC STENOSIS OR OCCLUSIVE DISEASE
Aortic occlusion or stenosis in children is most commonly
secondary to Takayasu arteritis, midaortic dysplastic syn-
drome, William syndrome, and neurofibromatosis
(188191). Takayasu arteritis is a large-vessel vasculitis.
The midaortic syndrome is a congenital disorder charac-
terized by noninflammatory aortitis leading to aortic
hypoplasia. Patients with aortic stenosis present with sys-
temic hypertension and may have an abdominal bruit,
abdominal pain, and/or weakness or absence of the
femoral pulses (190,191). Patients with Takayasu arteritis
also may have angina, claudication, syncope, and visual
impairment (188).
Gray-scale and Doppler sonography show narrowing
of the abdominal aorta (Fig. 12.56). Narrowing of the
major branch vessels, particularly the renal arteries, and
collateral vessel formation may also be noted. Arterial wall
thickening may be present in Takayasu arteritis but not in
the midaortic syndrome. Doppler imaging shows elevated
velocities and aliasing at the site of stenosis and dampened
flow velocities distally.
AORTIC DISSECTION
Aortic dissection is extremely rare in the pediatric age
group. It is most often associated with Marfan syndrome,
but it also can be idiopathic or iatrogenic. Abdominal aor-
tic dissection in Marfan disease is almost always associated
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494 P E D I AT R I C S O N O G R A P H Y

A B

Mycotic aortic pseudoaneurysm. A: Transverse view

Fig. 12.55
of the upper abdomen in a neonate with a pulsatile
mass shows an aneurysm (AN) of the abdominal aorta. B: Color
Doppler sonogram shows swirling flow within the pseudoaneurysm.
C: Pulsed Doppler image in another patient shows elevated peak
C systolic shifts and bidirectional flow.

RA

Aortic stenosis. Longitudinal color

Fig. 12.56
Doppler sonogram shows mild
narrowing of the aorta (arrows) with turbulent
flow (color aliasing) distal to the origin of the
renal artery (RA).
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Aortic dissection. Young adult with Marfan disease and

Fig. 12.57
abdominal pain. Transverse sonogram shows an echogenic
flap (arrow) in a dilated abdominal aorta. LK  left kidney.
with thoracic aortic dissection. The diagnosis is based on
demonstration of an intimal flap (Fig. 12.57).
IDIOPATHIC ARTERIAL CALCIFICATION
Idiopathic arterial calcification of infancy is a rare disease
of unknown cause (192). Histologically, it is characterized
by destruction and dystrophic calcification of the internal
elastic laminae and patchy intimal proliferation and fibro-
sis, which causes luminal narrowing, leading to ischemia.
Calcifications can occur in systemic, pulmonary, and coro-
nary arteries. Most patients present in infancy or early
childhood with cardiac failure and respiratory distress. At
sonography, the walls of the abdominal aorta and its major
branches are markedly hyperechoic with intense acoustic
shadowing (193). Infants who survive the neonatal period
usually die within the first year of life from myocardial
ischemia due to the coronary artery involvement.
Normal inferior vena cava. Longitudinal sonogram at the
Fig. 12.58
level of the liver shows pulsatile flow resulting from right
atrial pulsations. Distally, the cardiac activity has less effect on flow
velocities.
atrial pulsatility (Fig. 12.58). Distally, the waveform can be
monophasic or slightly pulsatile. Right-sided heart failure,
tricuspid insufficiency, and pericardial tamponade increase
the diameter of the inferior vena cava and exaggerate the
normal Doppler waveforms (Fig. 12.59). Conversely, hypo-
volemic shock causes a small flat inferior vena cava and a
more monophasic flow pattern.
CONGENITAL ANOMALIES
The inferior vena cava and azygos-hemiazygos systems are
formed by the successive development and regression of
three paired cardinal veins (Fig. 12.60) (194). Infrahepatic
interruption of the inferior vena cava with azygos or

Inferior Vena Cava

ANATOMY
The inferior vena cava (IVC) arises at the confluence of the
two common iliac veins at the level of the fifth lumbar verte-
bra. It ascends anterior to the vertebral bodies and to the
right of the aorta in front of the right crus to traverse the liver
and drain into the right atrium. The walls of the cava are
thinner and less echogenic than those of the aorta, and its size
varies with changes in respiration and intra-abdominal pres-
sure. With deep inspiration and the Valsalva maneuver,
venous return decreases and the inferior vena cava increases
in diameter. With deep expiration, venous return increases
and the inferior vena cava decreases in caliber.
The inferior vena cava lumen is anechoic. The pulsed Dilated inferior vena cava secondary to right heart fail-
Doppler waveform varies with location (172). The proxi- Fig. 12.59
ure. The inferior vena cava (IVC) is dilated secondary
mal part of the inferior vena cava has a triphasic waveform to passive venous congestion from elevated intracardiac pressures.
similar to that seen in the hepatic veins, reflecting right H  heart.
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496 P E D I AT R I C S O N O G R A P H Y

Embryologic segments contributing to formation of the

Fig. 12.60
inferior vena cava, azygos, and hemiazygos veins. In
infrahepatic interruption of the inferior vena cava, the hepatic and pre-
renal segments fail to unite. Persistence of the midportion of the right
(azygos) or left (hemiazygos) supracardinal vein leads to azygos or
hemiazygos continuation, respectively. (Adapted from Lee JKT, Hiken JN,
Semelka RC. Retoroperitoneum. In: Lee KTL, Sagel SS, Stanley RJ,
et al., eds. Computed body tomography with MRI correction. New York:
Lippincott-Raven, 1998;10231085.)

hemiazygos continuation is an anomaly caused by failure
of fusion of the hepatic and prerenal (subcardinal) veins.
The hepatic veins drain directly into the right atrium. This
anomaly has an increased frequency in patients with con-
genital heart disease and visceral abnormalities, such as the
asplenia and polysplenia syndromes, but it can also be
found as an isolated defect.
The pathognomonic sonographic features of inferior
vena caval interruption include absence of the intrahep-
atic segment of the IVC, drainage of the confluence of
hepatic veins into the right atrium, an enlarged right-sided
azygos or left-sided hemiazygos venous channel, and
a renal artery ventral to the azygos vein (Fig. 12.61)
(195). The left renal vein, which communicates with the

A B
Infrahepatic interruption of the inferior vena cava with hemiazygos continuation. A: Transverse sonogram shows absence of the infe-
Fig. 12.61
rior vena cava at the level of the liver. The hepatic veins drained directly into the right atrium. B: Transverse sonogram in another
patient at the level of the upper pole of the right kidney (K) shows an enlarged hemiazygos vein (V) anterior to the aorta (A).
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hemiazygos system, is enlarged and may show reversed
flow (194).
Other developmental anomalies affecting the inferior
vena cava include retroaortic left renal vein, circumaortic
left renal vein, duplication of the inferior vena cava, and
transposition of the inferior vena cava. In retroaortic left
renal vein, the left renal vein crosses posterior to the aorta
to connect the left kidney to the IVC. Circumaortic renal
vein is characterized by a true vascular ring. The ventral
(preaortic) left renal vein connects to the IVC at the
expected level of the renal veins, while the dorsal (retroaor-
tic) branch connects to the IVC at a more caudal level.
Duplication of the IVC is characterized by a right-sided
IVC above the level of the renal veins and bilateral cava
below the level of the renal veins. The left cava crosses
anterior or posterior to the aorta at the level of the renal
veins to join the right cava. Transposition is characterized
by a single, right-sided inferior vena cava above the level of
the renal veins, a vascular channel crossing either anterior
or posterior to the aorta connecting the renal veins, and a
single left-sided inferior vena cava below the level of the
renal veins.
CAVAL THROMBOSIS AND OCCLUSION
Thrombosis of the inferior vena cava occurs in a variety
of neoplastic and nonneoplastic conditions. The nonneo-
plastic causes are indwelling catheters, clotting disorders,
dehydration, sepsis, nephrotic syndrome, homocystinuria,
phlebitis or periphlebitis, and extension from renal vein or
pelvic venous thrombosis. Neoplastic involvement of the
cava has been associated with renal tumors (Wilms tumor,
renal cell carcinoma, and angiomyolipoma), hepatocellu-
lar carcinoma, adrenocortical carcinoma, pheochromocy-
toma, retroperitoneal sarcomas and germ cell tumors, and
malignant pelvic bone tumors (38,46,196).
Sonographic findings of bland and malignant thrombo-
sis are intraluminal echogenic foci, totally or partially fill-
ing the lumen (Figs. 12.62 and 12.63). Tumor thrombi
often show patchy flow on spectral or color Doppler imag-
ing as a result of neovascularization (197). Bland thrombi
are typically avascular, although on occasion, they show
linear flow as a result of tubular recanalization. Doppler
waveforms in the cava distal to the thrombus are absent in
complete luminal occlusion and dampened if there is par-
tial obstruction or drainage via collateral vessels.
Caval thrombi may completely resolve, leave a linear
flap, or calcify (Fig. 12.64) (198). A calcified thrombus
appears as an elongated, intraluminal hyperechoic mass
with acoustic shadowing.
The differential diagnosis of a membranous filling
defect in the inferior vena cava at its junction with the
right atrium includes a prolapsing Chiari malformation. A
Chiari malformation results from excessive fenestration of
the valves of the inferior vena cava and the coronary sinus,

A B
Inferior vena caval thrombus secondary to umbilical venous catheter. A: Longitudinal sonogram shows echogenic thrombus (calipers)
Fig. 12.62
nearly filling the lumen of the inferior vena cava (C). B: Color Doppler image in another patient shows flow around a nonocclusive
thrombus.
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498 P E D I AT R I C S O N O G R A P H Y
A B
Tumor thrombus. Renal cell carcinoma extending into inferior vena cava. A: Longitudinal sonogram at the level of the liver shows
Fig. 12.63
echogenic thrombus (arrows) distending the lumen of the inferior vena cava (C). B: Longitudinal color Doppler image in another patient
with tumor thrombus (arrows) shows color flow within the thrombus.
producing a network of fine membranes in the right atrium
(199). At echocardiography, the Chiari malformation
appears as an oscillating, long, thin, echogenic membrane
within the right atrium that moves toward the tricuspid
valve during atrial systole and away from it during dias-
tole. However, with tricuspid insufficiency, the malforma-
tion may prolapse into the inferior vena cava during atrial
Calcified thrombus in the inferior vena cava. Longitudinal
Fig. 12.64
sonogram shows highly echogenic caval thrombus
(arrow) with distal acoustic shadowing.
diastole, producing a flap-like intraluminal structure that
mimics a thrombus.
CRURA AND PSOAS MUSCLES
Normal Anatomy
DIAPHRAGMATIC CRURA
The diaphragmatic crura are the linear muscular portions
of the diaphragm that lie adjacent to the aortic hiatus and
attach to the anterolateral surfaces of the upper lumbar
vertebrae. The two crura enclose the retrocrural space,
which contains the aorta, the thoracic duct, lymph nodes,
the azygos and hemiazygos veins, and fatty tissue. The
right crus is larger and longer than the left. It attaches
to the first through third lumbar bodies and adjacent
intervertebral discs. The left crus attaches to the first and
second lumbar vertebrae and corresponding intervertebral
discs.
On transverse scanning, the crura appear as elongated,
hypoechoic structures anterolateral to the upper lumbar
spine (Fig. 12.65). Care should be taken not to mistake the
cephalic portion of the crura for the adrenal glands or the
inferior crus for an enlarged retroperitoneal lymph node.
On longitudinal scans, the crura appear as elongated struc-
tures extending caudally into the abdomen anterior to the
spine.
PSOAS AND QUADRATUS LUMBORUM MUSCLES
The paired psoas muscles originate from the lateral sur-
faces of the last thoracic vertebra and 1st to 4th lumbar
vertebrae and descend in a paravertebral location into the
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A B
Normal diaphragmatic crus. A: Transverse sonogram at the level of the right adrenal gland (arrows). The crura (C) are seen as elon-
Fig. 12.65
gated, hypoechoic structures anterolateral to the upper lumbar spine (LS). B: On a longitudinal scan, the right crus (C) appears as a
linear structure anterior to the spine. V  inferior vena cava.

iliac fossa, where they merge with the iliacus to become the
iliopsoas muscle, which inserts on the lesser trochanter of
the femur. The psoas muscle increases in size as it descends
into the pelvis. On transverse views, the cranial end of the
muscle has a triangular shape, whereas the caudal end is
ovoid or round. On coronal scans, the psoas muscle is an
elongated structure that enlarges caudally (Fig. 12.66).
The quadratus lumborum muscles arise from the ili-
olumbar ligament and adjacent portion of the iliac crest
and insert into the 12th rib and transverse processes of the
upper four lumbar vertebrae. Anterior to the quadratus
lumborum are the kidney and psoas muscle. On transverse
views, the muscles have a flat, quadrilateral shape (Fig.
12.66). On longitudinal views, they are elongated struc-
tures that are wider cranially than they are caudally.
Both the psoas and quadratus lumborum muscles are
hypoechoic structures with internal echogenic striations.
Care should be taken not to mistake the hypoechoic psoas
muscle on longitudinal scans for a dilated ureter or the
quadratus lumborum muscles for a fluid collection. Scan-
ning the contralateral side is useful, because the muscles
are usually symmetric.
Pathology
The psoas muscles are closely apposed to other structures of
the retroperitoneum, such as the lymph nodes, kidneys, pan-
creas, duodenum, ascending and descending colons, and
vertebral bodies. Therefore, disease processes that involve
the retroperitoneum can also involve the psoas muscles.
Psoas abscess can be the result of bacteremia or direct
extension from inflammatory diseases, such as appendicitis,
inflammatory bowel disease, lymphadenitis, renal infection,
vertebral osteomyelitis, and discitis. Abscesses from primary
bacteremia, discitis, or vertebral osteomyelitis are usually
caused by S. aureus, whereas abscesses due to appendiceal
or bowel disease are caused by gram-negative organisms.
Clinical findings include fever, leg or groin swelling, limita-
tion of leg motion, pain, and limp (200). Sonography shows

A B
Normal retroperitoneal muscles. A: Transverse sonograms at the level of the lower poles of the kidneys shows the psoas muscle (PS)
Fig. 12.66
and the flat, quadrilateral shaped quadratus lumborum muscle (arrow). B: Longitudinal sonogram shows the psoas muscle (PS) enlarg-
ing as it courses caudally anterior to the spine (SP).
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500 P E D I AT R I C S O N O G R A P H Y
Psoas abscess. Longitudinal sonogram shows a hypo-
Fig. 12.67
echoic fluid collection (calipers), which arose in the left
psoas muscle.
a well-defined, hypoechoic mass within an enlarged psoas
muscle. The abscess cavity may be homogeneous or contain
internal debris and/or septations (Fig. 12.67).
The common neoplastic diseases involving the psoas
muscles are lymphoma, Wilms tumor, and neuroblastoma.
Neoplastic involvement of the psoas muscle is usually the
result of direct extension, although rhabdomyosarcoma
can arise within the psoas muscle (201). Sonographic fea-
tures of neoplastic invasion are an enlarged psoas muscle
with irregular or poorly defined margins. Hypoechoic
A B
Retroperitoneal lymphadenopathy from lymphoma. A: Longitudinal sonogram shows enlargement of multiple retroperitoneal lymph
Fig. 12.68
nodes (N), which appear as discrete, rounded, hypoechoic structures. B: Color Doppler image shows virtual absence of neovascular-
ity, typical of lymphoma.
areas representing necrosis may be seen. Differentiation
between tumor, abscess, and hematoma can be difficult
based on sonographic findings, and a specific diagnosis
requires clinical correlation. Hematoma, rather than abscess,
is suggested in the clinical setting of a bleeding disorder or
trauma.
RETROPERITONEAL LYMPH NODES
Normal Anatomy
Retroperitoneal lymph nodes are not routinely seen on
sonographic examinations of infants and young children.
Any node, regardless of size, in prepubertal patients
should be regarded as abnormal. On the other hand, small
nodes, less than 10 mm in diameter, may be a normal find-
ing in adolescent patients. Multiple nodes, nodes greater
than 1 cm in diameter, or nodes in the retrocrural area
should be viewed with suspicion, and the sonographic
findings should be correlated with clinical and laboratory
data. Normal retroperitoneal lymph nodes are isoechoic or
hypoechoic to adjacent muscle and are most commonly
found adjacent to the aorta and inferior vena cava. They
typically appear as discrete flat or oval structures.
Pathology
Lymphoma, Wilms tumor, and neuroblastoma are the
common causes of malignant retroperitoneal lym-
phadenopathy in children, but other neoplasms such as
rhabdomyosarcoma and ovarian and testicular malignan-
cies also can involve these nodes.
Abnormal retroperitoneal lymph nodes usually have a
perivascular distribution, surrounding the aorta and inferior
vena cava. The appearance of malignant lymphadenopathy
ranges from one or more enlarged lymph nodes (Fig. 12.68)
to a large, confluent mass in which individual nodes are no
longer visualized. A large mantle of confluent adenopathy
may obscure the contours of adjacent structures and
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Chapter 12 A D R E N A L G L A N D S , PA N C R E A S , A N D O T H E R R E T R O P E R I T O N E A L S T R U C T U R E S 501

Malignant retroperitoneal nerve sheath tumor. Trans-

Fig. 12.69
verse sonogram through the upper abdomen shows an
echogenic paraspinal mass (M) with central necrosis compressing the
inferior vena cava (open arrows). PV  portal vein; SP  spine.

displace the great vessels and bowel anteriorly as well as the
kidneys laterally.
Typically, lymphomatous lymph nodes are hypoechoic
or anechoic and have a homogeneous internal architecture
and poor sound transmission (see Fig. 12.68). Nodal dis-
ease due to metastatic deposits may be hypoechoic, iso-
echoic, or hyperechoic to adjacent muscles and is often
heterogeneous. Lymphomatous nodes are often relatively
avascular on Doppler imaging. Peripheral or central flow
may be noted in sarcomas or metastatic tumor.
Infection can also produce lymph node enlargement.
The sonographic appearance is nonspecific and can mimic
that of neoplasm.
PRIMARY RETROPERITONEAL TUMORS
Primary retroperitoneal tumors can arise in the lymphatic
channels, nerves, and connective tissues of the retroperi-
toneum. Benign primary tumors include mature teratoma
(202,203), hemangioma (204), lymphangioma (205,206),
lipoblastoma, and tumors of neural origin (207,208). The
common malignant retroperitoneal tumors are neurob-
lastoma and rhabdomyosarcoma. Less common tumors
are fibrosarcoma (209), malignant germ cell tumor,
leiomyosarcoma, malignant fibrous histiocytoma, Ewing
sarcoma, and myofibroblastic tumor. The latter tumor
contains an admixture of myofibroblasts and fibroblasts
with a chronic inflammatory infiltrate. It is regarded as a
low-grade sarcoma, since it can progress to a frank sar-
comatous tumor and has a tendency for local recurrence
and small risk of distant metastasis. It shows a predilec-
tion for the lung, abdomen, and pelvis in children and
young adults (210).
Malignant retroperitoneal tumors do not have specific
sonographic characteristics. They usually appear as solid
masses of variable echogenicity, often containing hypo-
echoic or anechoic areas secondary to necrosis (Figs. 12.69
and 12.70) or hemorrhage and hyperechoic areas due to

A B
Inflammatory myofibroblastic tumor. A: Transverse sonogram shows a large, predominantly hypoechoic mass (arrowheads) anterior
Fig. 12.70
to the aorta (arrow). S  spine. B: Corresponding computed tomography image shows the hypoattenuating tumor (arrowheads) abut-
ting the aorta.
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502 P E D I AT R I C S O N O G R A P H Y

A B
Benign retroperitoneal teratoma. A: Longitudinal sonogram through the right abdomen in a neonate shows a complex mass contain-
Fig. 12.71
ing anechoic and solid components. B: Contrast-enhanced computed tomography scan shows a low-attenuation mass with fat, calci-
fications, and septations displacing the right kidney (RK) inferiorly.

calcifications. The heterogeneity helps to differentiate
sarcomas from lymphoma, which typically is homoge-
neous. Vessel displacement or encasement, ascites, inva-
sion of adjacent organs, and hepatic metastases also may
be seen.
Some benign tumors have sonographic characteristics
that can suggest a specific diagnosis. Lipomas and lipoblas-
tomas are likely to be hyperechoic to muscle, related to the
presence of fat. Teratomas appear as complex masses con-
taining an admixture of hypoechoic fluid, hyperechoic fat,
bone or calcifications, and mildly echogenic soft tissue (Figs.
12.71 and 12.72) (202). Hemangiomas appear isoechoic or
slightly hyperechoic to adjacent muscle and may be either
homogeneous or complex; they are typically hypervascular
on Doppler imaging (204). Lymphangiomas are anechoic
and may be unilocular or multilocular, containing echogenic

A B
Benign retroperitoneal teratoma. A: Transverse sonogram in a 1-month-old girl reveals a complex, predominantly anechoic mass
Fig. 12.72
(arrows) containing a complex mural nodule (curved arrow), which, in turn, contains cysts and a shadowing calcification (arrowhead).
B: Coronal T1-weighted image following gadolinium administration shows the nonenhancing, large cystic mass (arrowheads) surrounding the left
kidney (K) and the enhancing mural nodule (curved arrow).
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Chapter 12 A D R E N A L G L A N D S , PA N C R E A S , A N D O T H E R R E T R O P E R I T O N E A L S T R U C T U R E S 503

A B
Retroperitoneal lymphangioma. Longitudinal (A) and transverse (B) sonograms in a 24-year-old male show the right kidney (K) sur-
Fig. 12.73
rounded by a cystic mass with multiple septations (arrowheads).

septations and debris (Figs. 12.73 and 12.74) (205,211).
With the exception of hemangiomas, most benign retroperi-
toneal tumors show little flow on color Doppler sonogra-
phy.
RETROPERITONEAL HEMORRHAGE
Retroperitoneal hemorrhage usually follows blunt abdom-
inal trauma. Less frequently, it is a complication of percu-
taneous renal biopsy, anticoagulant therapy, a bleeding
diathesis, a malpositioned indwelling catheter, or retroperi-
toneal malignancy. Hemorrhage resulting from renal
trauma or biopsy surrounds the kidney before extending
into the retroperitoneum. Hemorrhage associated with
anticoagulant therapy or a bleeding diathesis usually dif-
fusely infiltrates the retroperitoneum.
Fresh blood appears as a hyperechoic or complex fluid
collection containing cystic and echogenic areas. In later
stages, as the hemoglobin is resorbed and the clot lyses, the
clot becomes hypoechoic.

A B
Retroperitoneal lymphangioma. A: Longitudinal sonogram in a neonate shows a large, hypoechoic mass with scattered septations and
Fig. 12.74
internal debris anterior to the right kidney (K) and spine (SP). B: T1-weighted coronal magnetic resonance image shows a fluid-filled
mass filling the abdomen and displacing bowel to the left.
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504 P E D I AT R I C S O N O G R A P H Y
RETROPERITONEAL FIBROSIS
Retroperitoneal fibrosis is most commonly seen in middle-
aged adults, but rare cases have been reported in children
(212214). It is usually idiopathic, although it can be asso-
ciated with ergot-derivative drugs (methysergide); systemic
diseases such as lupus erythematosus, juvenile rheumatoid
arthritis, and sickle cell disease; retroperitoneal hemor-
rhage; and urine leakage. The fibrotic process typically
begins below the aortic bifurcation and then extends cepha-
lad along the anterior surface of the spine, encasing the
blood vessels and ureters, or caudad into the pelvis, encas-
ing or compressing the rectosigmoid colon and bladder.
Sonography shows a smoothly marginated, homoge-
neous, hypoechoic mass anterior to the aorta and inferior
vena cava. Slight anterior displacement of the encased ves-
sels is not uncommon, but marked displacement is atypical
and should suggest the possibility of a primary retroperi-
toneal tumor, such as lymphoma or neuroblastoma.
REFERENCES
1. Scott EM, Thomas A, McGarrigle HHG, et al. Serial adrenal
ultrasonography in normal neonates. J Ultrasound Med 1990;9:
279283.
2. Marchal G, Gelin J, Verbeken E, et al. High-resolution real-time
sonography of the adrenal glands: a routine examination? J
Ultrasound Med 1986;5:6568.
3. Mitty HA. Embryology, anatomy, and anomalies of the adrenal
gland. Semin Roentgenol 1988;23:271279.
4. Yeh HC. Adrenal gland and nonrenal retroperitoneum. Urol
Radiol 1987;9:127140.
5. Paterson A. Adrenal pathology in childhood: a spectrum of dis-
ease. Eur Radiol 2002;12:24912508.
6. Westra SJ, Zaninovic AC, Hall TR, et al. Imaging of the adre-
nal gland in children. Radiographics 1994;14:13231340.
7. Ashley DJB, Mostofi FK. Renal agenesis and dysgenesis. J Urol
1960;83:211230.
8. Moore KL. The developing human: clinically oriented embryol-
ogy. 4th ed. Philadelphia, PA: WB Saunders, 1988.
9. Barwick TD, Malhotra A, Webb JA, et al. Embryology of the
adrenal glands and its relevance to diagnostic imaging. Clin
Radiol 2005;60:953959.
10. Avila NA, Prekumar A, Shawker TS, et al. Testicular adrenal
rest tissue in congenital adrenal hyperplasia: findings at gray-
scale and color Doppler US. Radiology 1996;198:99104.
11. Burton EM, Strange ME, Edmonds DB. Sonography of the cir-
cumrenal and horseshoe adrenal gland in the newborn. Pediatr
Radiol 1993;23:362364.
12. Hoffman CK, Filly RA, Callen PW. The lying down adrenal
sign: a sonographic indicator of renal agenesis or ectopia in
fetuses and neonates. J Ultrasound Med 1992;11:533536.
13. McGahan JP, Myracle MR. Adrenal hypertrophy: possible pit-
fall in the sonographic diagnosis of renal agenesis. J Ultrasound
Med 1986;5:265268.
14. Brodeur GM, Maris JM. Neuroblastoma. In: Pizzo PA, Poplack
DG, eds. Principles and practice of pediatric oncology. 5th ed.
Philadelphia, PA: Lippincott Williams & Wilkins, 2006:933
970.
15. Gurney JG, Davis, Severson RK, et al. Trends in cancer inci-
dence among children in the U.S. Cancer 1996;78:532541.
16. Lonergan GJ, Schwab CM, Suarez ES, et al. Neuroblastoma,
ganglioneuroblastoma, and ganglioneuroma: radiologic-patho-
logic correlation. Radiographics 1992;22:911934.
17. Maris JM, Weiss MJ, Mosse Y, et al. Evidence for a hereditary
neuroblastoma predisposition locus at chromosome 16p12-13.
Cancer Res 2002;62:66516658.
18. Mitchell WG, Davalos-Gonzalez Y, Brumm Vl, et al. Opso-
clonus-ataxia in childhood neuroblastoma: developmental and
neurologic sequelae. Pediatrics 2002;109:8698.
19. Rudnick E, Khakoo Y, Antunes NL, et al. Opsoclonus-
myoclonus-ataxia syndrome in neuroblastoma: clinical outcome
and antineuronal antibodiesa report from the Childrens Can-
cer Group Study. Med Pediatr Oncol 2001;36:612622.
20. Abramson SJ. Adrenal neoplasms in children. Radiol Clin
North Am 1997;35:14151453.
21. Brodeur GM, Seeger RC, Barrett A, et al. International criteria
for diagnosis, staging and response to treatment in patients with
neuroblastoma. J Clin Oncol 1988;6:18741881.
22. Brodeur GM, Pritchard J, Berthold F, et al. Revision of the
international criteria for neuroblastoma diagnosis, staging and
response to treatment. J Clin Oncol 1993;11:14661477.
23. Bordow SB, Norris MD, Haber PS, et al. Prognostic significance
of MYCN oncogene expression in childhood neuroblastoma. J
Clin Oncol 1998;16:32863294.
24. Brodeur GM. Neuroblastoma: biologic insights into a clinical
enigma. Nat Rev Cancer 2003;3:203216.
25. Siegel MJ. Neuroblastoma. In: Husband JE, Reznek RH, eds.
Textbook of imaging in oncology. 3rd ed. London: Informa
Healthcare; 2010, 923940.
26. David R, Lamki N, Fan S, et al. The many faces of neuroblas-
toma. Radiographics 1989;9:859882.
27. Cassady C, Winters WD. Bilateral cystic neuroblastoma: imag-
ing features and differential diagnoses. Pediatr Radiol 1997;27:
758759.
28. Richards ML, Gundersen AE, Williams MS. Cystic neuroblas-
toma of infancy. J Pediatr Surg 1995;30:13541357.
29. Teoh SK, Whitman GJ, Chew FS. Neonatal neuroblastoma.
AJR Am J Roentgenol 1997;168:54.
30. Pfluger T, Czekalla R, Hundt C, et al. MR angiography versus
color Doppler sonography in the evaluation of renal vessels and
the inferior vena cava in abdominal masses of pediatric
patients. AJR Am J Roentgenol 1999;173:103108.
31. Fernbach SK. Ascites produced by peritoneal seeding of neu-
roblastoma. Pediatr Radiol 1993;23:569.
32. Day DL, Johnson R, Cohen MD. Abdominal neuroblastoma
with inferior vena caval tumor thrombus: report of three cases
(one with right atrial extension). Pediatr Radiol 1991;21:
205207.
33. Mohd TbH, Yip CH. Cystic neuroblastoma with colonic fis-
tula. Pediatr Radiol 1988;18:406.
34. Day DL, Johnson RT, Odrezin G, et al. Renal atrophy or infarc-
tion in children with neuroblastoma. Radiology 1991;180:
493495.
35. Siegel MJ, Ishwaran H, Fletcher B, et al. Staging of neuroblas-
toma by imaging: report of the Radiology Diagnostic Oncology
Group. Radiology 2002;223:168175.
36. Reddy VS, ONeill JA Jr, Holcomb GW III, et al. Twenty-five-
year surgical experience with pheochromocytoma in children.
Am Surg 2000;66:10851091; discussion 1092.
37. Cirillo RL Jr, Bennett WF, Vitellas KM, et al. Pathology of the
adrenal gland: imaging features. AJR Am J Roentgenol
1998;170:429435.
38. Hoffman JC, Weiner SN, Koenigsberg M, et al. Pheochromocy-
toma invasion of the inferior vena cava: sonographic evalua-
tion. Radiology 1983;149:793795.
39. Agrons GA. Lonergan GJ, Dickey GE, et al. Adrenocortical
neoplasms in children: radiologic-pathologic correlation. Radi-
ographics 1999;19:98981008.
40. Lack EE. Adrenal cortical neoplasms in childhood. In: Lack EE,
ed. Atlas of tumor pathology: tumors of the adrenal gland and
extra adrenal paraganglia, fasc 19, ser 3. Washington, DC:
Armed Forces Institute of Pathology, 1997:153168.
LWBK505-C12_p461-508.qxd 7/7/10 1:37 PM Page 505 Aptara Inc
Chapter 12 A D R E N A L G L A N D S , PA N C R E A S , A N D O T H E R R E T R O P E R I T O N E A L S T R U C T U R E S
41. Lee PDK, Winter RJ, Green OC. Virilizing adrenocortical
tumors in childhood: eight cases and a review of the literature.
Pediatrics 1985;76:437444.
42. Sabbaga CC, Avilla SG, Schulz C, et al. Adrenocortical carci-
noma in children: clinical aspects and prognosis. J Pediatr Surg
1993;28:841843.
43. Prando A, Wallace S, Marins JLC, et al. Sonographic findings of
adrenal cortical carcinomas in children. Pediatr Radiol 1990;20:
163165.
44. Ribeiro J, Ribeiro RC, Fletcher BD. Imaging findings in pedi-
atric adrenocortical carcinoma. Pediatr Radiol 2000;30:4551.
45. Chiche L, Dousset B, Kieffer E, et al. Adrenocortical carcinoma
extending into the inferior vena cava: presentation of a 15-patient
series and review of the literature. Surgery 2006;139:1527.
46. Godine LB, Berdon WE, Brasch RC, et al. Adrenocortical car-
cinoma with extension into inferior vena cava and right atrium:
report of 3 cases in children. Pediatr Radiol 1990;20:166168;
discussion 169.
47. Henwood MJ, Katz LEL. Disorders of the adrenal gland. In:
Pediatric endocrinology: the requisites in pediatrics. St. Louis,
MO: Elsevier Mosby, 2005:193213.
48. Medina LS, DAlessandro M, Buonomo C. Adrenocortical ade-
noma. Radiographics 1996;16:449451.
49. Davies RP, Lam AH. Adrenocortical neoplasm in children.
J Ultrasound Med 1987;6:325328.
50. Dunnick NR. Adrenal imaging: current status. AJR Am
J Roentgenol 1990;154:927936.
51. Abasiyanik A, Oran B, Kaymakci A, et al. Conn syndrome in a
child, caused by adrenal adenoma. Pediatr Surg 1996;31:430432.
52. Hadjigeorgi C, Lafoyianni S, Pontikis Y, et al. Asymptomatic
myelolipoma of the adrenal. Pediatr Radiol 1992;22:465466.
53. Musante F, Derchi LE, Zappasodi F, et al. Myelolipoma of the adre-
nal gland: sonographic and CT features. AJR Am J Roentgenol
1988;151:961964.
54. Soboleski D, Mehta A, Kamal I, et al. Hemangioendothelioma
of the adrenal gland in a 4-month-old male infant. AJR Am J
Roentgenol 1999;172:235237.
55. Sivit CM, Short BL, Revenis ME, et al. Adrenal hemorrhage in
infants undergoing ECMO: prevalence and clinical significance.
Pediatr Radiol 1993;23:519521.
56. Levine C. Intestinal obstruction in a neonate with adrenal hemor-
rhage and renal vein thrombosis. Pediatr Radiol 1989;19: 477478.
57. Demirci A, Selcuk MB, Yazicioglu I. Bilateral adrenal hemor-
rhage associated with bilateral renal vein and vena cava throm-
bosis. Pediatr Radiol 1991;21:130.
58. Heij HA, Taets van Amerongen AHM, Ekkelkamp S, et al.
Diagnosis and management of neonatal adrenal haemorrhage.
Pediatr Radiol 1989;19:391394.
59. Sivit CJ, Ingram JD, Taylor GA, et al. Posttraumatic adrenal
hemorrhage in children: CT findings in 34 patients. AJR Am J
Roentgenol 1992;158:12991302.
60. Nimkin K, Teeger S, Wallach MT, et al. Adrenal hemorrhage in
abused children: imaging and postmortem findings. AJR Am J
Roentgenol 1994;162:661663.
61. Levin TL, Morton E. Adrenal hemorrhage complicating ACTH
therapy in Crohns disease. Pediatr Radiol 1993;23:457458.
62. Sarnaik AP, Sanfilippo DJ, Slovis TL. Ultrasound diagnosis of
adrenal hemorrhage in meningococcemia. Pediatr Radiol
1988;18:427428.
63. Murphy BJ, Casillas J, Yrizarry JM. Traumatic adrenal hemor-
rhage: radiologic findings. Radiology 1988;169:701703.
64. Bowen AD, Keslar PJ, Newman B, et al. Adrenal hemorrhage
after liver transplantation. Radiology 1990;176:8588.
65. Broadley P, Daneman A, Wesson D, et al. Large adrenal cysts in
teenage girls: diagnosis and management. Pediatr Radiol
1997;27:550552.
66. McCauley RGK, Beckwith JB, Elias ER, et al. Benign hemor-
rhagic adrenocortical macrocysts in Beckwith-Wiedemann syn-
drome. AJR Am J Roentgenol 1991;157:549552.
505
67. Walton GR, Peng BCH, Berdon WE, et al. Cystic adrenal
masses in the neonate associated with hemihypertrophy and the
relation to the Beckwith-Wiedemann syndrome. J Urol 1991;
146:580582.
68. Atkinson GO Jr, Kodroff MB, Gay BB Jr, et al. Adrenal abscess
in the neonate. Radiology 1985;155:101104.
69. Morrison SC, Comisky E, Fletcher BD. Calcification in the
adrenal glands associated with disseminated herpes simplex
infection. Pediatr Radiol 1988;18:240241.
70. Wilson DA, Nguyen DL, Tytle TL, et al. Sonography of the
adrenal glands in chronic disseminated histoplasmosis. J Ultra-
sound Med 1986;5:6973.
71. Trinavarat P, Sasiwimonphan K, Sansopha L, et al. Xan-
thogranulomatous adrenalitis in a neonate: CT and US findings.
Pediatr Radiol 2009;39:286289.
72. Menzel D, Hauffa BP. Changes in size and sonographic charac-
teristics of the adrenal glands during the first year of life and the
sonographic diagnosis of adrenal hyperplasia in infants with 21-
hydroxylase deficiency. J Clin Ultrasound 1990;18:619625.
73. Sivit CJ, Hung W, Taylor GA, et al. Sonography in neonatal con-
genital adrenal hyperplasia. AJR Am J Roentgenol 1991;156:
141143.
74. Avni EF, Rypens F, Smet MH, et al. Sonographic demonstration
of congenital adrenal hyperplasia in the neonate: the cerebri-
form pattern. Pediatr Radiol 1993;23:8890.
75. Ogata T, Ishikawa K, Kohda E, et al. Computed tomography in
the early detection of congenital lipoid adrenal hyperplasia.
Pediatr Radiol 1988;18:360361.
76. Ozmen MN, Aygun N, Kilic I, et al. Wolmans disease: ultra-
sonographic and computed tomographic findings. Pediatr
Radiol 1992;22:541554.
77. Dutton RV. Wolmans disease: ultrasound and CT diagnosis.
Pediatr Radiol 1985;15:144146.
78. Jaffe R. The pancreas. In: Stocker J, Dehner L, eds. Pediatric
pathology. 2nd ed. Philadelphia, PA: Lippincott Williams &
Wilkins, 2002:797834.
79. Siegel MJ, Martin KW, Worthington JL. Normal and abnormal
pancreas in children: US studies. Radiology 1987;165:1518.
80. Cramer WB, Pushpanathan C. Pancreatic echogenicity in pre-
mature and newborn infants. Pediatr Radiol 1990;20:323325.
81. Swobodnik W, Wolf A, Wechsler JG, et al. Ultrasound charac-
teristics of the pancreas in children with cystic fibrosis. J Clin
Ultrasound 1985;13:469474.
82. Chao HC, Lind SJ, Kong MS, et al. Sonographic evaluation of
the pancreatic duct in normal children and children with pan-
creatitis. J Ultrasound Med 2000;19:757763.
83. Shirkhoda A, Gore R. Anomalies and anatomic variants of the
pancreas. In: Gore R, Levein M, eds. Textbook of gastrointesti-
nal radiology. Philadelphia, PA: Saunders, 2000:17541766.
84. Sreedharan R, Mamula P. Congenital anomalies. In: Pediatric
gastroenterology: the requisites in pediatrics. Philadelphia, PA:
Mosby Elsevier, 2008:307313.
85. Delhaye M, Engelholm L, Cremer M. Pancreas divisum: congen-
ital anatomic variant or anomaly? Gastroenterology 1985;89:
951958.
86. Bernard JP, Sahel J, Giovanni M, et al. Pancreas divisum is a
probable cause of acute pancreatitis: a report of 137 cases. Pan-
creas 1990;5:248254.
87. Herman TE, Siegel MJ. Polysplenia syndrome with congenital
short pancreas. AJR Am J Roentgenol 1991;156:799800.
88. Norton KI, Tenreiro R, Rabinowitz JG. Sonographic demon-
stration of annular pancreas and a distal duodenal diaphragm
in a newborn. Pediatr Radiol 1992;22:6667.
89. Orr LA, Powell RW, Melhem RE. Sonographic demonstration
of annular pancreas in the newborn. J Ultrasound Med 1992;
11:373375.
90. Chapuy S, Gorincour G, Roquelaure B, et al. Sonographic diag-
nosis of a common pancreaticobiliary channel in children. Pedi-
atr Radiol 2006;36:13001305.
LWBK505-C12_p461-508.qxd 7/7/10 1:37 PM Page 506 Aptara Inc
506 P E D I AT R I C S O N O G R A P H Y
91. Eklof O, Lassrich A, Stanley P, et al. Ectopic pancreas. Pediatr
Radiol 1973;1:2427.
92. Zinkiewicz K, Juskiewicz W, Zgodzinski W, et al. Ectopic pan-
creas: endoscopic, ultrasound and radiological features. Folia
Morphol 2003;62:205209.
93. Atlas AB, Rosh JR. Cystic fibrosis and congenital anomalies of
the exocrine pancreas. In: Wyllie R, Hyams JS, eds. Pediatric
gastrointestinal and liver disease. Philadelphia, PA: Saunders
Elsevier, 2006:10231041.
94. Ratjen F, Doring G. Cystic fibrosis. Lancet 2003;361:681689.
95. Agrons GA, Corse WR, Markowitz RI, et al. Gastrointestinal
manifestations of cystic fibrosis: radiologic-pathologic correla-
tion. Radiographics 1996;16:871893.
96. Berrocal T, Prieto C, Pastor I, et al. Sonography of pancreatic
disease in infants and children. Radiographic 1995;15:301313.
97. Chaudry G, Navarro OM, Levine DS, et al. Abdominal mani-
festations of cystic fibrosis in children. Pediatr Radiol
2006;36:233240.
98. Haber HP. Cystic fibrosis in children and young adults: findings
on routine abdominal sonography. AJR Am J Roentgenol
2007;189:8999.
99. Nijs E, Callahn MJ, Taylor GA. Disorders of the pediatric pan-
creas: imaging features. Pediatr Radiol 2005;35:358373.
100. Berrocal T, Pajares MP, Zubillaga AF. Pancreatic cystosis in chil-
dren and young adults with cystic fibrosis: sonographic, CT, and
MRI findings. AJR Am J Roentgenol 2005;184:13051309.
101. Hernanz-Schulman M, Teele RL, Perez-Atayde A, et al. Pan-
creatic cystosis in cystic fibrosis. Radiology 1986;158:629631.
102. McHugo JM, McKeown C, Brown MT, et al. Ultrasound find-
ings in children with cystic fibrosis. Br J Radiol 1987;60:
137141.
103. Quillin SP, Siegel MJ, Rothbaum R. Hepatobiliary sonography
in cystic fibrosis. Pediatr Radiol 1993;23:533535.
104. Colombo C, Russo MC, Zazzeron L, Romano G. Liver disease
in cystic fibrosis. J Pediatr Gastroenterol Nutr 2006;43 Suppl
1:S4955.
105. Lenaerts C, Lapierre C, Patriquin H, et al. Surveillance for cys-
tic fibrosis-associated hepatobiliary disease: early ultrasound
changes and predisposing factors. J Pediatr 2003;143:343350.
106. Shwachman H, Diamond LK, Oski FA, et al. The syndrome of
pancreatic insufficiency and bone marrow dysfunction. J Pedi-
atr 1964;65:645663.
107. Cubuk M, Arslan G, Ceken K, et al. Shwachman-Diamond
syndrome. A case report. Acta Radiol 2000;41:627628.
108. Robberecht E, Nachtegaele P, Rattinghe V, et al. Pancreatic
lipomatosis in the Shwachman-Diamond syndrome. Pediatr
Radiol 1985;15:348349.
109. Trellis DR, Clouse RE. Johanson-Blizzard syndrome. Progres-
sion of pancreatic involvement in adulthood. Dis Sci
1991;36:365369.
110. Choyke PL, Glenn GM, Walther MM, et al. von Hippel-Lindau
disease: genetic, clinical, and imaging features. Radiology 1995;
194:629642.
111. Ros PR, Hamrick-Turner JE, Chiechi MV, et al. Cystic masses
of the pancreas. Radiographics 1992;12:673686.
112. Chung EM, Travis MD, Conran RM. Pancreatic tumors in chil-
dren: radiologic-pathologic correlation. Radiographics 2006;26:
12111238.
113. Sempoux C, Guiot Y, Jaubert F, et al. Focal and diffuse forms
of congenital hyperinsulinism: the keys for differential diagno-
sis. Endocr Pathol 2004;15:241246.
114. Berrocal T, Luque AA, Pinilla I, et al. Pancreatic regeneration
after near-total pancreatectomy in children with nesidioblasto-
sis. Pediatr Radiol 2005;35:10661070.
115. Jaksic T, Yaman M, Thorner P, et al. A 20-year review of pedi-
atric pancreatic tumors. J Pediatr Surg 1992;27:13151317.
116. Shorter NA, Glick RD, Klimstra DS, et al. Malignant pancreatic
tumors in childhood and adolescence: the Memorial Sloan-Ketter-
ing experience, 1967 to present. J Pediatr Surg 2002;37:887889.
117. Vane DW, Grosfeld JL, West KW, et al. Pancreatic disorders in
infancy and childhood: experience with 92 cases. J Pediatr Surg
1989;24:771776.
118. Montemarano H, Lonergan GJ, Bulas DI, et al. Pancreatoblas-
toma: imaging findings in 10 patients and review of the litera-
ture. Radiology 2000;214:476482.
119. Klimstra DS, Wenig BM, Adair CF, et al. Pancreatoblastoma. A
clinicopathologic study and review of the literature. Am J Surg
Pathol 1995;19:13711389.
120. Muguerza R, Rodriguez A, Formigo E, et al. Pancreatoblas-
toma associated with incomplete Beckwith-Wiedemann syn-
drome: case report and review of the literature. J Pediatr Surg
2005;40:13411344.
121. Solcia E, Capella C, Klppel G. Atlas of tumor pathology:
tumors of the pancreas. Washington, DC: Armed Forces Insti-
tute of Pathology, 1997.
122. Lee JY, Kim IO, Kim WS, et al. CT and US findings of pancre-
atoblastoma. J Comput Assist Tomogr 1996;20:370374.
123. Lumkin B, Anderson MW, Ablin DS, et al. CT, MRI, and color
Doppler ultrasound correlation of pancreatoblastoma: a case
report. Pediatr Radiol 1993;23:6162.
124. Roebuck DJ, Yuen MK, Wong YC, et al. Imaging features of
pancreatoblastoma. Pediatr Radiol 2001;31:501506.
125. Gupta AK, Mitra DK, Berry M, et al. Sonography and CT of
pancreatoblastoma in children. AJR Am J Roentgenol 2000;174:
16391641.
126. Klimstra DS, Heffess CS, Oertel JE, et al. Acinar cell carcinoma
of the pancreas: a clinical-pathologic study of 28 cases. Am
J Surg Pathol 1992;16:815837.
127. Sun CD, Lee WJ, Choi JS, et al. Solid-pseudopapillary tumours
of the pancreas: 14 years experience. ANZ J Surg 2005;75:
684689.
128. Tipton SG, Smyrk TC, Sarr MG, et al. Malignant potential of
solid pseudopapillary neoplasm of the pancreas. Br J Surg 2006;
93:733737.
129. Wang KS, Albanese C, Dada F, et al. Papillary cystic neoplasm
of the pancreas: a report of three pediatric cases and literature
review. J Pediatr Surg 1998;33:842845.
130. Zhou H, Cheng W, Lam KY, et al. Solid-cystic papillary tumor
of the pancreas in children. Pediatr Surg Int 2001;17:614620.
131. Buetow PC, Buck JL, Pantongrag-Brown L, et al. Solid and
papillary epithelial neoplasm of the pancreas: imaging-patho-
logic correlation on 56 cases. Radiology 1996;199:707711.
132. Lee DH, Yi BH, Lim JW, et al. Sonographic findings of solid
and papillary epithelial neoplasm of the pancreas. J Ultrasound
Med 2001;20:12291232.
133. Davies PF, Shevland JE, Shepherd JJ. Ultrasonography of the
pancreas in patients with multiple endocrine neoplasia type I. J
Ultrasound Med 1993;12:6772.
134. Kloppel G, Heitz PU. Pancreatic endocrine tumors. Pathol Res
Pract 1988;183:155168.
135. Van Nieuwenhove Y, Vandaele S, Op de Beeck B, et al. Neu-
roendocrine tumors of the pancreas. Surg Endosc 2003;17:
16581662.
136. Buetow PC, Parrino TV, Buck JL, et al. Islet cell tumors of the
pancreas: pathologic-imaging correlation among size, necrosis
and cysts, calcification, malignant behavior, and functional sta-
tus. AJR Am J Roentgenol 1995;165:11751179.
137. Buetow PC, Miller DL, Parrino TV, et al. Islet cell tumors of the
pancreas: clinical, radiologic, and pathologic correlation in
diagnosis and localization. Radiographics 1997;17:453472.
138. Gouya H, Vignaux O, Augui J, et al. CT, endoscopic sonography,
and a combined protocol for preoperative evaluation of pancre-
atic insulinomas. AJR Am J Roentgenol 2003;181:987992.
139. Rossi P, Allison DJ, Bezzi M, et al. Endocrine tumors of the
pancreas. Radiol Clin North Am 1989;27:129161.
140. Jacobs JE, Dinsmore BJ. Mature cystic teratoma of the pan-
creas: sonographic and CT findings. AJR Am J Roentgenol
1993;160:523524.
LWBK505-C12_p461-508.qxd 7/7/10 1:37 PM Page 507 Aptara Inc
Chapter 12 A D R E N A L G L A N D S , PA N C R E A S , A N D O T H E R R E T R O P E R I T O N E A L S T R U C T U R E S
141. Mester M, Trajber HJ, Compton CC, et al. Cystic teratomas of
the pancreas. Arch Surg 1990;125:12151218.
142. Yu CW, Liu KL, Lin WC, et al. Mature cystic teratoma of the
pancreas in a child. Pediatr Radiol 2003;33:266268.
143. Lin H, Li SD, Hu XG, et al. Primary pancreatic lymphoma:
report of six cases. World J Gastroenterol 2006;12:50645067.
144. McClain MB, Burton EM, Day DS. Pancreatic pseudotumor in
an 11-year-old child: imaging findings. Pediatr Radiol 2000;30:
610661.
145. Slavotinek JP, Bourne AJ, Sage MR, et al. Inflammatory
pseudotumour of the pancreas in a child. Pediatr Radiol 2000;
30:801803.
146. Tunell WP. Hemangioendothelioma of the pancreas obstructing
the common bile duct and duodenum. J Pediatr Surg 1976;11:
827830.
147. Movahedi-Lankarani S, Hruban RH, Westra WH, et al. Primi-
tive neuroectodermal tumors of the pancreas: a report of seven
cases of a rare neoplasm. Am J Surg Pathol 2002;26:
10401047.
148. Yasuda I, Adachi S, Kasahara S, et al. Pancreatic rhab-
domyosarcoma. Gastrointest Endosc 2004;60:433434.
149. Auringer ST, Ulmer JL, Sumner TE, et al. Congenital cyst of the
pancreas. J Pediatr Surg 1993;28:15701571.
150. Boulanger SC, Borowitz DS, Fisher DF, et al. Congenital pan-
creatic cysts in children. J Pediatr Surg 2003;38:10801082.
151. Kazez A, Akpolat N, Kocakoc E, et al. Congenital true pancre-
atic cyst: a rare case. Diagn Interv Radiol 2006;12:3133.
152. Crowley JJ, McAlister WH. Congenital pancreatic pseudocysts:
a rare cause of abdominal mass in a neonate. Pediatr Radiol
1996;26:210211.
153. Bradley EL III. A clinically based classification system for acute
pancreatitis. Arch Surg 1993;128:586590.
154. Nydegger A, Couper RTL, Oliver MR. Childhood pancreatitis.
J Gastroenterol Hepatol 2006;21:499509.
155. Stringer MD. Pancreatitis and pancreatic trauma. Semin Pedi-
atr Surg 2005;14:239246.
156. Siegel MJ, Herman TE. Pancreatic pseudocyst. In: Siegel BA,
Proto AV, eds. Pediatric disease (fourth series) test and syllabus.
Reston, VA: American College of Radiology, 1993:532555.
157. Siegel MJ, Sivit CJ. Pancreatic emergencies. Radiol Clin North
Am 1997;35:815830.
158. Kawahara H, Takahashi T, Okada A. Characteristics of duode-
nal duplications causing pancreatitis in children and adoles-
cents: a case report and review of the literature. J Pediatr Gas-
troenterol Nutr 2002;35:372376.
159. Hunter CJ, Connelly ME, Ghaffari N, et al. Enteric duplication
cysts of the pancreas: a report of two cases and review of the
literature. Pediatr Surg Int 2008;24:227233.
160. Balthazar EJ, Freeny PC, vanSonnenberg E. Imaging and inter-
vention in acute pancreatitis. Radiology 1994;193:297306.
161. King LR, Siegel MJ, Balfe DM. Acute pancreatitis in children:
CT findings of intra- and extrapancreatic fluid collections.
Radiology 1995;195:196200.
162. Jeffrey RB Jr. Sonography in acute pancreatitis. Radiol Clin
North Am 1989;27:517.
163. Fishman EK, Soyer P, Bliss DF, et al. Splenic involvement in
pancreatitis: spectrum of CT findings. AJR Am J Roentgenol
1995;174:631635.
164. Lee CM, Chang-Chien CS, Lin DY, et al. The real-time ultra-
sonography of pancreatic pseudocyst: comparison of infected
and noninfected pseudocysts. J Clin Ultrasound 1988;16:
393398.
165. Jaffe RB, Arata JA Jr, Matlak ME. Percutaneous drainage of
traumatic pancreatic pseudocysts in children. AJR Am J
Roentgenol 1989;152:591595.
166. Ahmed H, Hagspiel H, McGahren E, et al. Pancreatic pseudo-
aneurysm in a child with hereditary pancreatitis: diagnosis with
multidetector CT angiography. Pediatr Radiol 2004;34:
656659.
507
167. Falkoff GE, Taylor KJW, Morse S. Hepatic artery pseudo-
aneurysm: diagnosis with real-time and pulsed Doppler US.
Radiology 1986;158:5556.
168. Atkinson GO Jr, Wyly JB, Gay BB Jr, et al. Idiopathic fibrosing
pancreatitis: a cause of obstructive jaundice in childhood. Pedi-
atr Radiol 1988;18:2831.
169. Deshpande AV, LaHei ER, Shun A, et al. Idiopathic fibrosing
pancreatitis in childrena single-center experience. J Pediatr
Surg 2006;41:19871991.
170. Bolondi L, Li Bassi S, Gaiani S, et al. Sonography of chronic
pancreatitis. Radiol Clin North Am 1989;27:815833.
171. Jacombs ASW, Wines M, Holland AJA, et al. Pancreatic trauma
in children. J Pediatr Surg 2004;39:9699.
172. Coley BD. Pediatric applications of abdominal vascular
Doppler: part II. Pediatr Radiol 2004;34:772786.
173. Hernanz-Schulman M. Applications of Doppler sonography to
diagnosis of extracranial pediatric disease. Radiology 1993;
189:114.
174. Seibert JJ, Taylor BJ, Williamson SL, et al. Sonographic detec-
tion of neonatal umbilical-artery thrombosis: clinical correla-
tion. AJR Am J Roentgenol 1987;148:965968.
175. Seibert JJ, Northington FJ, Miers JF, et al. Aortic thrombosis
after umbilical artery catheterization in neonates: prevalence of
complications on long-term follow-up. AJR Am J Roentgenol
1991;156:567569.
176. Deeg KH, Wlfel D, Rupprecht T. Diagnosis of neonatal aortic
thrombosis by colour coded Doppler sonography. Pediatr
Radiol 1992;22:6263.
177. Stringer DA, Krysl J, Manson D, et al. The value of Doppler
sonography in the detection of major thrombosis in the neona-
tal abdomen. Pediatr Radiol 1990;21:3033.
178. Fitzgerald SW, Donaldson JS, Poznanski AK. Pediatric thoracic
aorta: normal measurements determined with CT. Radiology
1987;165:667669.
179. Mendeloff J. Aortic aneurysm resulting from umbilical artery
catheterization: case report, literature review, and management
algorithm. J Vasc Surg 2001;33:419424.
180. Lobe TE, Richardson J, Boulden TF, et al. Mycotic thrombo-
aneurysmal disease of the abdominal aorta in preterm infants:
its natural history and its management. J Pediatr Surg 1992;27:
10541060.
181. Kirpekar M, Augenstein H, Abiri M. Sequential development
of multiple aortic aneurysms in a neonate post umbilical arte-
rial catheter insertion. Pediatr Radiol 1989;19:452453.
182. Long D, Long F, Seguin J. Thoracic aortic aneurysm as a late
complication of umbilical arterial catheter. Arch Pediatr Ado-
lesc Med 1999;153:11951196.
183. Wyers M, McAlister. Umbilical artery catheter use complicated by
pseudoaneurysm of the aorta. Pedatr Radiol 2002;32:199201.
184. Cheung SC, Khong PL, Chiu W, et al. Congenital abdominal
aortic aneurysm and renal dysplasia. Pediatr Radiol 2004;34:
827830.
185. Kim JI, Lee W, Kim SJ, et al. Primary congenital abdominal
aortic aneurysm: a rare report with perinatal serial follow up
imaging. Pediatr Radiol 2008;38:12491252.
186. Sarkar R, Cilley RE, Coran AG. Abdominal aneurysms in
childhood: report of a case and review of the literature. Surgery
1991;109:143148.
187. Restrepo R, Ranson M, Chait P, et al. Extracranial aneurysms
in children: practical classification and correlative imaging.
AJR Am J Roentgenol 2003;181:867878.
188. Kerr GS, Hallashan CW, Giordano J, et al. Takayasu arteritis.
Ann Intern Med 1994;120:919929.
189. Gotway MB, Araoz PA, Macedo TA, et al. Imaging findings in
Takayasus arteritis. AJR Am J Roentgenol 2005;184:19451950.
190. Adams WM, John PR. US demonstration and diagnosis of the
midaortic syndrome. Pediatr Radiol 1998;28:461463.
191. Panayiotopoulos YP, Tyrell MR, Koffman G, et al. Mid-aortic
syndrome presenting in childhood. Br J Surg 1996;83:235240.
LWBK505-C12_p461-508.qxd 7/7/10 1:37 PM Page 508 Aptara Inc
508 P E D I AT R I C S O N O G R A P H Y
192. Patel M, Andronikou S, Solomon R, et al. Idiopathic arterial
calcification in childhood. Pediatr Radiol 2004;34:652655.
193. Rosenbaum DM, Blumhagen JD. Sonographic recognition of
idiopathic arterial calcification of infancy. AJR Am J Roentgenol
1986;146:249250.
194. Bass JE, Redwine MD, Kramer LA, et al. Spectrum of congen-
ital anomalies of the inferior vena cava: cross-sectional imaging
findings. Radiographics 2000;20:639652.
195. Geley TE, Unsinn KM, Auckenthaler TM, et al. Azygos con-
tinuation of the inferior vena cava: sonographic demonstration
of the renal artery ventral to the azygos vein as a clue to diag-
nosis. AJR Am J Roentgenol 1999;172:16591662.
196. Nuss R, Hays T, Manco-Johnson M. Childhood thrombosis.
Pediatrics 1995;96:291294.
197. Hubsch P, Schurawitzki H, Susani M, et al. Color Doppler
imaging of the inferior vena cava: identification of tumor
thrombus. J Ultrasound Med 1992;11:639645.
198. Uglietta JP, Woodruff WW, Effmann EL, et al. Duplex Doppler
ultrasound evaluation of calcified inferior vena cava thrombo-
sis. Pediatr Radiol 1989;19:250252.
199. Lewandowski B, Challender J, Dery R. Prolapsing Chiari mal-
formation in tricuspid regurgitation: a moving filling defect in
the inferior vena cava. J Ultrasound Med 1985;4:655658.
200. Dib M, Bedu A, Garel C, et al. Ilio-psoas abscess in neonates:
treatment by ultrasound-guided percutaneous drainage. Pediatr
Radiol 2000;30:677680.
201. Knowles MC, Magid D, Fishman EK, et al. Case report 612:
rhabdomyosarcoma of the right psoas muscle. Skeletal Radiol
1990;19:299301.
202. Davidson AJ, Hartman DS, Goldman SM. Mature teratoma of
the retroperitoneum: radiologic, pathologic, and clinical corre-
lation. Radiology 1989;172:421425.
203. Luo CC, Huang CS, Chu SM, et al. Retroperitoneal teratomas
in infancy and childhood. Pediatr Surg Int 2005;21:536540.
204. Koci TM, Worthen NJ, Phillips JJ, et al. Perirenal hemangioen-
dothelioma in a newborn: sonography and MR findings. J
Comput Assist Tomogr 1989;13:145147.
205. Davidson AJ, Hartman DS. Lymphangioma of the retroperi-
toneum: CT and sonographic characteristic. Radiology
1990;175:507510.
206. Wilson SR, Bohrer S, Losada R, et al. Retroperitoneal lym-
phangioma: an unusual location and presentation. J Pediatr
Surg 2006;41:603605.
207. Fenton LZ, Foreman N, Wyatt-Ashmead J. Diffuse, retroperi-
toneal mesenteric and intrahepatic periportal plexiform neurofi-
broma in a 5-year-old boy. Pediatr Radiol 2001;31:637639.
208. Scherer A, Niehues T, Engelbrecht V, et al. Imaging diagnosis of
retroperitoneal ganglioneuroma in childhood. Pediatr Radiol
2001;31:106110.
209. Wong CH, Dietrich RB, Pais MJ, et al. Pediatric case of the day.
Congenital, undifferentiated retroperitoneal fibrosarcoma.
Radiographics 1994;14:14281430.
210. Gleason BC, Hornick JL. Inflammatory myofibroblastic
tumours: where are we now? J Clin Pathol 2008;61:428437.
211. Iyer R, Eftekhari F, Varma D, et al. Cystic retroperitoneal lym-
phangioma: CT, ultrasound and MR findings. Pediatr Radiol
1993;23:305306.
212. Amis ES Jr. Retroperitoneal fibrosis. AJR Am J Roentgenol
1991;157:321329.
213. Miller OF, Smith LJ, Ferrara EX, et al. Presentation of idio-
pathic retroperitoneal fibrosis in the pediatric population. J
Pediatr Surg 2003;38:16851688.
214. Sherman C, Winchester P, Brill PW, et al. Childhood retroperi-
toneal fibrosis. Pediatr Radiol 1988;18:245247.
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Female Pelvis
Technique Nonneoplastic Ovarian Lesions
Transabdominal Sonography Benign Ovarian Neoplasms
Transvaginal Sonography Malignant Ovarian Neoplasms
Sonohysterography Secondary Neoplasms
Three-dimensional Ultrasonography Doppler Imaging in Ovarian Malignancy
Doppler Imaging Pelvic Inflammatory Disease
Adnexal Torsion
Ovaries
Normal Anatomy Uterus and Vagina
Ovarian Masses Normal Anatomy
ransabdominal sonography remains the imaging study
T of choice for the initial evaluation of gynecologic
abnormalities in the pediatric population (16). Trans-
vaginal and transperineal scanning can be valuable ancil-
lary tools when a more detailed evaluation of gynecologic
structures is required. This chapter reviews the various
techniques for performing pelvic sonography and the sono-
graphic features of the normal and abnormal pelvis in
female infants, children, and adolescents. The roles of gray-
scale and Doppler imaging are emphasized in the evalua-
tion of pelvic masses, pelvic pain, disorders of puberty, and
ambiguous genitalia and clinical and pathologic features of
the common disease processes are reviewed.
TECHNIQUE
Transabdominal Sonography
Transabdominal sonography is performed through a dis-
tended urinary bladder, which serves as an acoustic win-
dow to view the pelvic organs. The distended bladder dis-
places gas-filled bowel loops out of the pelvis, allowing
transmission of sound into deeper structures of the pelvis
and easier visualization of the ovaries and uterus. Ade-
quate bladder filling usually can be achieved with oral
intake of fluid. Bladder catheterization with instillation of
sterile fluid may be needed if the patient is unable to toler-
ate large fluid volumes orally.
Pelvic sonography in infants and young children is usu-
ally performed with a 5- or 7.5-MHz sector or linear array
transducer. A 3.5-MHz transducer may be required in very
large patients.
Scans of the ovaries and uterus are obtained in both sagit-
tal and transverse planes. Angling the transducer obliquely
may improve visualization of the uterus and ovaries. In some
instances, placing the patient in a decubitus position and
scanning directly over the adnexa will improve visualization
of the ovaries.
CHAPTER
MARILYN J. SIEGEL
13
Congenital Uterine Anomalies
Congenital Vaginal Anomalies
Uterine Tumors
Vaginal Tumors
Disorders of Puberty
Precocious Puberty
Amenorrhea
Intersex Disorders
In patients in whom there is a question of a pseudotu-
mor (i.e., fluid or fecal material within the bowel mas-
querading as a gynecologic or other pelvic mass), a water
enema may be useful. With this technique, the rectosig-
moid colon can be easily identified and differentiated from
a mass or pathologic fluid collection.
Transvaginal Sonography
In the pediatric population, the use of endovaginal scanning
has been largely limited to adolescent patients with obstetric
and gynecologic problems. This approach can be useful to
clarify equivocal or confusing findings on transabdominal
sonography, to confirm the presence or absence of a pelvic
mass, to determine the size and internal contents of a mass,
and to delineate the relationship of a mass to adjacent struc-
tures. Contraindications include virginal patients and patients
who do not willingly consent orally to the examination.
The transvaginal examination is performed with the
bladder empty. A coupling gel is applied to the face of the
transducer. The transducer is then covered with a rubber
sheath, and air bubbles that have accumulated between the
protective cover and transducer are expressed. An external
lubricant is placed on the outside of the rubber sheath and
then the transducer is inserted into the vagina with the
patient supine and the knees gently flexed. If possible, the
patient should insert the probe; this helps to minimize anx-
iety and pain. The transducer should be placed halfway, or
at most two thirds of the way, into the vagina. If correctly
inserted, it will not touch the cervix. When properly done,
the transvaginal technique is relatively noninvasive and
painless. Sagittal and coronal images are obtained by gently
rotating and angling the transducer from side to side. Trans-
vaginal sonography is accepted well by most adolescents.
TRANSABDOMINAL VERSUS TRANSVAGINAL SONOGRAPHY
Transabdominal sonography shows the entire pelvis and
gives a global overview of all structures. Its major limitation
is the need to fill the bladder. The advantages of endovaginal
509
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510 P E D I AT R I C S O N O G R A P H Y
A B
Normal ovarian anatomy demonstrated with a transabdominal approach (A) and an endovaginal approach (B). Ovarian margins (arrows)
Fig. 13.1
and cortical follicles appear better defined on the endovaginal scan than on the transabdominal scan.
over transabdominal scanning are the obviation of bladder
filling and improved near-field focusing, which provides bet-
ter image quality and anatomic detail (Fig. 13.1). The major
limitation of this technique is a limited field of view. The
depth of penetration of the ultrasound beam from the trans-
ducer face is approximately 8 to 10 cm. Thus, large or very
laterally positioned masses or superiorly or laterally posi-
tioned ovaries may be incompletely visualized or missed (7).
In general, transabdominal sonography is the initial
examination in a patient who has not had a previous pelvic
sonogram. If the transabdominal examination is normal or
it unequivocally reveals an abnormality, transvaginal
sonography is usually not necessary. Transvaginal imaging
should be done if the transabdominal findings are indeter-
minate or confusing or to better characterize an abnor-
mality (8,9). It also should be performed if endometrial
disorders are suspected. For the follow-up examination of
a known abnormality, it may be appropriate to use trans-
vaginal sonography as the only examination.
Sonohysterography
Sonohysterography has been used primarily in adult women
to assess the endometrial canal and its lining (10). This pro-
cedure requires the insertion of a speculum and the place-
ment of a tiny catheter into the uterine cavity. The catheter
is introduced by means of a long forceps and is inserted to
the level of the fundus. The catheter is filled with saline prior
to insertion to minimize air bubble artifacts. The speculum
is removed and the transvaginal probe, which is covered
with a condom and sterile gel, is inserted into the vagina.
Sterile saline is injected slowly through the catheter under
sonographic guidance and images of the uterine cavity are
obtained in sagittal and coronal planes to demonstrate the
endometrial canal.
The indications for sonohysterography include (a) char-
acterization of an abnormal endometrial interface sus-
pected or detected on conventional gray-scale sonography,
(b) determination of the cause of abnormal uterine bleeding,
and (c) characterization of congenital uterine anomalies
(10). The anechoic, saline-distended endometrial cavity
facilitates differentiation between intracavitary, endome-
trial, and submucosal abnormalities. The usefulness of this
technique in prepubertal children is obviously limited.
However, this technique may hold promise for characteriz-
ing congenital uterine anomalies in adolescent girls.
Three-dimensional Ultrasonography
The newest emerging technology is three-dimensional or
volume sonography. Early clinical experience suggests that
three-dimensional sonography allows a more accurate evalu-
ation of the uterus, endometrial cavity, and adnexa and can
be particularly useful for evaluating the external uterine con-
tour, especially the fundus, for the diagnosis of uterine anom-
alies (11). It also may allow a more accurate evaluation of the
site of origin of a tumor and the extent of tumor invasion.
Doppler Imaging
Color and pulsed Doppler sonography are used to demon-
strate vascular structures in the pelvis and provide infor-
mation about flow characteristics (12). Such information
can be helpful in characterizing gynecologic tumors and in
diagnosing ectopic pregnancy and adnexal torsion. Color
Doppler parameters (velocity scale, gain, sensitivity, and
wall filter) should be optimized to detect low-frequency
shifts of slow-flowing blood (13). Impedance can be quan-
tified by the use of the resistive index.
OVARIES
Normal Anatomy
PREPUBERTAL OVARY
The ovaries descend from the upper abdomen into the
pelvis during fetal life. At birth, they usually lie within the
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Chapter 13 F E M A L E P E L V I S 511

Table 13.1 Ovarian Volume Measurements

Mean Ovarian
Age Volume in cm3 (1 SD)

Premenarchal
1 d3 mo 1.1 (1.0)
412 mo 1.1 (0.7)
1324 mo 0.7 (0.4)
2y 0.8 (0.4)
3y 0.7 (0.2)
4y 0.8 (0.4)
5y 0.9 (02)
6y 1.2 (0.4)
7y 1.3 (0.6)
8y 1.1 (0.5)
9y 2.0 (0.8)
10 y 2.2 (0.7)
11 y 2.5 (1.3)
12 y 3.8 (1.4)
13 y 4.2 (2.3) Normal prepubertal ovary. Longitudinal sonogram of the
Fig. 13.2
Postmenarcheal 9.8 (0.6) right ovary (arrows) in a 2-year-old girl shows multiple
small anechoic follicles, measuring less than 9 mm in diameter.
SD, standard deviation. B  bladder.
From Cohen HL, Shapiro MA, Mandel FS, et al. Normal ovaries in neonates and infants:
a sonographic study of 77 patients 1 day to 24 months old. AJR Am J Roentgenol
1993;160:583586; Cohen HL, Tice HM, Mandel FS. Ovarian volumes measured by US:
in premenarcheal children, likely related to pulsatile secre-
bigger than we think. Radiology 1990;177:189192; and Orsini LF, Salardi S, Pilu G,
et al. Pelvic organs in premenarcheal girls: real-time ultrasonography. AJR Am J
tions of low levels of gonadotrophin-releasing hormones,
Roentgenol 1984;153:113116. which stimulate ovarian maturation before clinical signs of
puberty develop.

superior margin of the broad ligaments. On occasion, POSTMENARCHEAL OVARY

descent is arrested and the ovaries may be found anywhere
from the inferior edge of the kidney down to the broad lig-
ament. Rarely, the ovaries descend below the broad liga-
ments and lie in the inguinal canal (14).
The shape of the ovaries is variable, although the
majority of ovaries are ovoid with their craniocaudal axes
paralleling the broad ligaments (15). Because of the vari-
ability in shape, ovarian volume, which is determined by
the formula for a simple prolate ellipsoid (0.523  width 
thickness  length), is considered the best method for
determining ovarian size. Mean ovarian volume in the first
year of life is approximately 1.0 cm3. Volume is somewhat
less during the second year of life, averaging 0.7 cm3 (16).
The ovaries are relatively stable in size until 7 to 8 years of
age, when an age-related growth spurt starts, related to
approaching menarche (17). Mean ovarian volume in pre-
menarcheal girls 2 to 13 years of age ranges from 0.7 to
4.2 cm3, respectively (15). The normal range of ovarian
volumes versus patient age is shown in Table 13.1.
Premenarcheal ovaries contain numerous small cysts,
representing unstimulated (primordial) follicles. Small folli-
cles or cysts have been reported in 84% of ovaries in infants
younger than 2 years of age and in 68% of ovaries in chil-
dren aged 2 through 12 years. Follicular diameter is less
than 9 mm, with the mean follicle size being 6 to 7 mm
(Fig. 13.2) (1820). In neonates, follicular diameter may
exceed 9 mm, most likely related to maternal stimulation.
Occasionally, large follicles exceeding 9 mm in size are seen
With activation of the hypothalamic-pituitary-ovarian axis
at puberty, the ovaries increase in size and descend deeper
into the pelvis, ultimately lying posterolateral to the uterus,
although not necessarily at the same horizontal level. In
some individuals, descent is incomplete, and the ovaries
remain high in the pelvis, lying dorsal or cephalad to the
uterus. They may be seen posterior to the uterus if liga-
mentous attachments are lax.
Normal ovarian measurements in the menstruating
female are a length of 2.5 to 5.0 cm, width of 1.5 to 3.0 cm,
and thickness of 0.6 to 1.5 (21). Mean ovarian volume is
approximately 9.8 cm3 (Table 13.1) (21,22). Ovarian vol-
ume peaks in the third decade. The ovaries of the pubertal
girl contain multiple cortical cysts, representing both stim-
ulated and unstimulated follicles (Fig. 13.3).
OVARIAN PHYSIOLOGY
The appearance of the ovary, as well as its size and position,
changes with hormonal stimulation. Grossly, the ovary is
composed of two layers: an outer cortical and an inner
medullary layer. The cortex is larger than the medulla and
contains the follicles that undergo maturation. The medulla
is composed of fibrous tissue without follicles. Under the
influence of pituitary gonadotropins, the ovary goes
through three phases during each menstrual cycle: the fol-
licular phase, ovulation, and the luteal phase (23).
The follicular phase begins on the first day of the men-
strual cycle and continues until ovulation, which is usually
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512 P E D I AT R I C S O N O G R A P H Y

A B
Normal postmenarcheal ovary. A: Longitudinal transabdominal sonogram of a 13-year-old girl demonstrates multiple developing folli-
Fig. 13.3
cles within the left ovary (calipers). Ovarian length  5.2 cm. B  bladder. B: Endovaginal sonogram of the right ovary (calipers) in
another adolescent girl on day 9 of the menstrual cycle shows multiple cortical follicles. The largest follicle (F) measures 1.1  1.2 cm and is likely
the follicle destined for ovulation. The remaining follicles have a diameter of approximately 5 mm.

day 14 of a 28-day cycle. In the early follicular phase, in
response to follicle-stimulating hormone, a number of pre-
viously dormant primordial follicles (composed of an oocyte
surrounded by a single layer of epithelium) begin to develop,
forming the antral follicles. Although unstimulated primor-
dial follicles are too small to resolve sonographically, antral
follicles measuring 0.5 to 1.0 cm in diameter can be imaged,
appearing as round or oval anechoic structures surrounded
by ovarian parenchyma. By day 8 or 9, the dominant folli-
cle (termed the graafian follicle) destined for ovulation
emerges and continues to develop under the influence of
estrogen (Fig. 13.3B) (23,24). The other stimulated follicles
that do not progress to ovulation ultimately atrophy. By the
time of ovulation, the diameter of the graafian follicle ranges
from 15 to 30 mm (mean 20 to 23 mm) (23,24).
In the 24 hours just prior to ovulation, a zone of
decreased echogenicity may be noted around the develop-
ing follicle and the wall of the follicle also becomes indis-
tinct. With follicular rupture and extrusion of the ovum
(ovulation), there is a sudden decrease in follicular size

A B
Graafian follicles. A: Transverse transabdominal sonogram of the left ovary on day 13 of the menstrual cycle demonstrates a hypoechoic
Fig. 13.4
follicle (calipers), measuring 2.2  2.0 cm. Arrows indicate ovarian margins. UT  uterus. B: Longitudinal endovaginal sonogram in
another patient on day 12 of the menstrual cycle shows a dominant anechoic follicle measuring 3.0  2.0 cm. UT  uterus.
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Chapter 13 F E M A L E P E L V I S 513

and intrafollicular echoes appear, related to follicular col-

lapse, crenation of the walls, and accumulation of blood
within the follicle. The collapsed blood-filled follicle,
termed a corpus hemorrhagicum, can be present as
early as 1 hour postovulation. Simultaneous with ovula-
tion, a small amount of fluid can be seen in the cul-de-sac
(21,2527).
The luteal phase (days 15 to 28) begins after ovula-
tion. The remaining granulosa cells in the corpus hemor-
rhagicum enlarge and accumulate lipid and lutein, and
vascularization of the granulosa occurs to form the cor-
pus luteum. The corpus luteum remains for 14 days,
after which it rapidly degenerates unless the ovum is fer-
tilized (21,26). The mature corpus luteum follicle usually
ranges between 15 and 30 mm in diameter (21). Eventu-
ally, the follicle atrophies and is replaced by collagen-
rich scar tissue, resulting in the corpus albicans. This
remnant of follicular development is not detectable by
sonography. Corpus luteum cyst. Endovaginal sonogram through the
Graafian or developing follicles and corpus luteum Fig. 13.5
right ovary on day 20 of the menstrual cycle shows a fluid-
cysts can usually be seen at sonography. Preovulatory filled follicle (arrows) with scattered internal echoes and a septation.
developing follicles are typically unilocular, homoge- The follicle measures 2.5 cm in greatest diameter.
neous, and anechoic (Fig. 13.4). Corpus luteum cysts
may be homogeneous and anechoic or complex, con-
taining debris or septations as a result of hemorrhage
(Fig. 13.5). The diameter of a physiologic cyst should
not exceed 3 cm. the adnexal branches of the uterine artery. Color
The differential diagnosis of the normal ovary with Doppler sonography can identify flow within the ovary,
multiple follicles is polycystic ovary disease. The diagnosis although it cannot distinguish between the two blood
of polycystic ovary disease is made on the basis of a com- supplies. On color imaging, intraovarian arteries appear
bination of clinical, biochemical, and sonographic criteria as short, straight branches (12). Color signal can be
(see later discussion). identified in about 80% of prepubertal ovaries and
90% of postmenarcheal ovaries on transabdominal
OVARIAN BLOOD FLOW sonography (Fig. 13.6). Flow is more likely to be
The ovary receives its blood supply from both the main demonstrated on transvaginal than on transabdominal
ovarian artery, which arises directly from the aorta, and examinations.

A B
Normal ovarian vasculature. Transabdominal (A) and transvaginal (B) color Doppler images show flow in the ovarian parenchyma
Fig. 13.6
(arrows) but not in the follicles. Color flow is more apparent on the transvaginal scan than on the transabdominal image.
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514 P E D I AT R I C S O N O G R A P H Y
A B
Doppler waveforms. A: Transverse image in a 16-year-old girl on day 5 of the cycle shows high-impedance waveform (resistive index
Fig. 13.7
[RI]  1.0). B: Transverse sonogram in a 15-year-old girl on day 10 of the menstrual cycle shows a low-impedance waveform with higher
levels of diastolic flow (RI  0.05). Also note monophasic venous flow.
The appearance of the pulsed Doppler waveforms
varies with the phase of the menstrual cycle (Fig. 13.7).
During the early follicular phase (days 0 to 7) and late
luteal phase (days 18 to 28), vascular impedance is high
and end-diastolic velocity is low or absent. The resistive
index (RI) is close to 1.0. During the late follicular and
early luteal phase (days 7 to 17), end-diastolic flow velocity
increases in the ovary destined for ovulation and vascular
impedance decreases. The RI during the late follicular and
early luteal phases is approximately 0.5.
The ovarian veins follow the course of the arteries. They
leave the ovarian hilum and form a plexus of veins, the
pampiniform plexus, in the broad ligament. The vessels
comprising the plexus unite in the abdomen to form a single
vein that ascends on the psoas muscle. The right ovarian
vein drains into the inferior vena cava inferior to the right
renal vein. The left ovarian vein drains directly into the left
renal vein.
Ovarian Masses
Ultrasonography is used initially in the evaluation of most
children with a suspected pelvic mass because it is easy to
perform, can determine the organ or site of origin of the
mass, and can predict a specific diagnosis in many patients
(28, 29). Computed tomography (CT) and magnetic reso-
nance imaging (MRI) are useful adjuncts for definitively
establishing the diagnosis of teratoma and for staging of
pelvic malignancies (30, 31).
Nonneoplastic Ovarian Lesions
The most common benign ovarian mass is the functional
cyst, which can be of follicular, corpus luteal, or theca
luteal origin. Less frequent causes of ovarian cysts include
paraovarian cysts and peritoneal inclusion cysts.
FUNCTIONAL CYSTS: NEONATES
Functional cysts have a bimodal age distribution: neonates
and adolescent girls. Neonatal functional ovarian cysts
result from exaggeration of normal follicular development
secondary to excessive maternal hormonal stimulation in
utero (32,33). The cysts may be incidental findings on pre-
natal or postnatal sonography, or if they achieve a large
size, they may present postnatally as a pelvic or pelvic-
abdominal mass. The most common complication is
adnexal torsion, which has been reported in 50% to 80%
of neonatal cysts (34). Other complications include intes-
tinal obstruction, urinary tract obstruction, and respira-
tory compromise.
The sonographic appearance of a functional cyst is
variable depending on whether or not it is complicated by
torsion or hemorrhage. The simple, uncomplicated cyst
has anechoic contents, a thin wall no septa and distal
acoustic enhancement (Fig. 13.8). The daughter cyst sign is
another finding of an ovarian cyst (35). The sonographic
appearance is that of a follicle within an ovarian cyst (see
Fig. 13.8). Large ovarian cysts can extend into the upper
abdomen (see Fig. 13.8).
Hemorrhagic cysts and cysts associated with adnexal
torsion appear as complex masses containing multiple sep-
tations, low-level echoes, clotted blood, and/or a fluid-
debris level (Fig. 13.9) (36). Other findings of torsion
include thick, echogenic walls and a twisted vascular pedi-
cle (Fig. 13.10) (32,33,37).
Simple uncomplicated cysts less than 4 cm in diameter
usually resolve spontaneously in 3 to 4 months (33,38,39).
Cyst puncture or cystectomy and surgical resection have
been recommended in symptomatic neonates and in
neonates with very large cysts (4 to 5 cm in diameter),
because the likelihood of torsion with loss of the ovary is
high and the likelihood of spontaneous resolution is low
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Chapter 13 F E M A L E P E L V I S 515

Neonatal ovarian cyst. A: Longitudinal sonogram

Fig. 13.8
through the upper abdomen of a 1-day-old neonate
shows an anechoic cyst (arrows) (6.0  3.5 cm) with small
daughter cysts (arrowheads) anterior to the right kidney (RK).
B: The cyst is avascular on color Doppler imaging. C: Follow-up
longitudinal sonogram 6 weeks later shows internal decrease in
size of the cyst (calipers) (measuring 2.8 cm  1.8 cm), which is
now confined to the right hemipelvis. BL  bladder. C

A B
Hemorrhagic ovarian cyst complicated by torsion. Longitudinal (A) and left lateral decubitus (B) sonograms in a newborn girl show a large
Fig. 13.9
ovarian cyst (C), with low-level echoes and a fluid-debris level (arrows), in the left lower quadrant. The fluid level shifts with changes in
patient position. At surgery, the ovary had undergone torsion and contained a hemorrhagic cyst, which acted as the fulcrum for the torsion.
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516 P E D I AT R I C S O N O G R A P H Y

Torsed neonatal ovarian cyst. Transverse sonogram

Fig. 13.10
at the base of an ovarian cyst (C) shows radiating
echogenic lines (arrow) representing the torsed vascular pedicle.

(40). Surgery has also been suggested for neonates with
large cysts that fail to regress after several months of obser-
vation, because of the rare risk of neoplasia (34).
FUNCTIONAL CYSTS: POSTMENARCHEAL GIRLS
In adolescent girls, functional ovarian cysts result when a
graafian follicle continues to grow after failed ovulation or
when a corpus luteum fails to involute after ovulation. The
cysts often are asymptomatic and discovered incidentally
on pelvic sonograms performed for other reasons, but
large cysts may cause acute pain due to associated hemor-
rhage or torsion.
The distinction between a functional cyst and a physi-
ologic follicle is based on size. Functional cysts usually
range between 3 and 5 cm in diameter, although they may
be as large as 20 cm (41). Physiologic cysts or follicles are
smaller than 3 cm in diameter. At histologic examination,
follicular cysts contain clear serous fluid, whereas corpus
luteal cysts can contain serous or hemorrhagic fluid.
Similar to the neonate, the sonographic appearance of
the pathologic ovarian cyst in the adolescent girl is variable,
depending on the presence or absence of hemorrhage. Non-
hemorrhagic cysts are classically anechoic, thin-walled,
unilocular masses, exhibiting posterior acoustic enhance-
ment (Fig. 13.11) (41). The cysts are avascular on Doppler
imaging.
Hemorrhagic ovarian cysts have a wide spectrum of
sonographic findings, reflecting the age of the blood. Fresh
blood is usually hyperechoic, becoming more complex or
heterogeneous and eventually anechoic as the clot lyses.
Most hemorrhagic ovarian cysts (85%) are complex
masses, commonly containing interdigitating septations.
This pattern has been termed a fishnet, cobweb or spider-
web appearance (Fig. 13.12A,B) (42,43). Other findings

A B
Ovarian cyst. A: Transverse sonogram in a 14-year-old girl with lower abdominal pain shows a 6-cm anechoic cyst (C) with impercep-
Fig. 13.11
tible walls and sound transmission in the expected region of the right ovary. The cyst failed to involute on subsequent sonograms.
Operation showed a corpus luteum cyst. BL  bladder; UT  uterus. B: Longitudinal color Doppler sonogram of another patient with an ovarian cyst
shows no flow in the cyst and minimal flow in the adjacent parenchyma.
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Chapter 13 F E M A L E P E L V I S 517

A B

Hemorrhagic ovarian cysts, spectrum of sonographic

Fig. 13.12
appearances. A: Transverse color Doppler sonogram in a
14-year-old girl shows a large complex cyst (C) with multiple septations
creating a reticular or fishnet pattern. The cyst is avascular. B: Trans-
verse sonogram in another girl shows a complex cyst (calipers, 4.2 
3.2 cm) containing low-level echoes. Again note a reticular or fishnet
appearance due to fibrin strands. Follow-up sonogram 5 weeks later
showed spontaneous resolution of this hemorrhagic cyst. C: Longitudi-
nal sonogram of the right adnexa in a third patient demonstrates a cys-
C tic mass (C) with a fluid-debris level (arrows).

include low-level echoes, a fluid-debris level (Fig. 13.12C),
clotted blood, a thick wall (approximately 4 mm), and
acoustic enhancement (42,43). The remaining cysts (15%)
are homogeneous and usually hyperechoic to the uterus
(Fig. 13.13). Hemorrhagic cysts are avascular on color
Doppler sonography. Complications associated with hem-
orrhagic cysts include rupture and torsion. In the presence
of rupture, echogenic fluid is seen in the pelvis and some-
times in the peritoneal cavity.
The presence of a complex cystic mass is nonspecific
and the differential diagnosis includes hemorrhagic cyst,
ovarian teratoma, tubo-ovarian or appendiceal abscess,
and ectopic pregnancy. Ectopic pregnancy and tubo-ovar-
ian or appendiceal abscess can be diagnosed by clinical and
laboratory data. Teratomas and hemorrhagic cysts gener-
ally can be distinguished by serial sonography. Hemor-
rhagic ovarian cysts decrease in size and become anechoic
over time before involuting completely, whereas cystic neo-
plasms will remain unchanged or increase in size.
The natural history of follicular and corpus luteum cysts
in adolescent girls is complete involution over time, usually
within one to two menstrual cycles. The likelihood of spon-
taneous resolution diminishes if the cyst diameter exceeds
5 to 6 cm (41), and percutaneous drainage or surgical
removal may be warranted. If sonography is used to follow
involution, the arbitrary time period between sonographic
studies is 6 weeks or at least after the start of the next men-
strual cycle. Cysts that persist for several cycles may need to
be investigated further with CT, MRI, or percutaneous or
surgical aspiration to exclude a cystic neoplasm (44).
THECA LUTEIN CYSTS
Theca lutein cysts are the largest of the hyperstimulated
follicles. They occur in adolescent girls and adult women
with gestational trophoblastic disease and as a complication
of drug therapy to stimulate ovulation (26). Affected patients
have elevated levels of human chorionic gonadotropins.
Sonographically, both ovaries are enlarged and contain
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518 P E D I AT R I C S O N O G R A P H Y
Hemorrhagic ovarian cyst. Transverse sonogram of the
Fig. 13.13
right adnexal region in a 16-year-old girl shows a hyper-
echoic cyst (arrows) with some acoustic enhancement. UT  uterus;
B  bladder.
multiple cysts, which may resemble a spoke-wheel appear-
ance (Fig. 13.14) (29, 45). Ancillary findings are those related
to the gestational trophoblastic disease and include an
enlarged, thick-walled uterus and dilated parametrial vessels.
The cysts usually regress after the source of gonadotrophin is
removed.
PAROVARIAN CYSTS
Parovarian cysts are of paramesonephric or mesothelial
origin and arise in the broad ligament or fallopian tubes
A B
Paraovarian cyst. Longitudinal (A) and transverse (B) sonograms show a large cyst (C) with imperceptible walls that is adjacent to but
Fig. 13.15
separate from the right ovary (arrows). B  bladder.
Theca lutein cysts. Longitudinal sonogram of an infant born
Fig. 13.14
to a mother with gestational trophoblastic disease shows a
markedly enlarged right ovary (arrows) containing multiple simple cysts.
(41,46). Most are discovered in the third or fourth
decades of life, but they may be found at any age. The
classic sonographic appearance is a round or oval, ane-
choic mass with thin walls and throughsound transmis-
sion (Fig. 13.15) (46). Septations and low-level internal
echoes may be present due to hemorrhage. Parovarian
cysts are easily recognized if a normal ipsilateral ovary is
visualized separate from the cyst. Because parovarian
cysts are not physiologic, they will not show cyclic
changes or regress on follow-up examinations.
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Peritoneal inclusion cyst. Longitudinal sonogram in a
Fig. 13.16
19-year-old woman who had prior surgery in infancy for
necrotizing enterocolitis shows a multiloculated fluid collection
(arrows) in the right lower quadrant. The ovary (arrowheads) is adja-
cent to the multilocular cyst.
PERITONEAL INCLUSION CYSTS
Peritoneal inclusion cysts are found in women who have
pelvic adhesions, usually secondary to prior abdominal sur-
gery or pelvic inflammatory disease, and active ovaries. The
ovaries are the main producers of peritoneal fluid in young
women, and the resultant fluid is normally transported
throughout the peritoneal cavity, where it is absorbed by
the mesentery and ligaments. When there are extensive
peritoneal adhesions, the fluid produced by the ovaries may
be trapped in the pelvis and is the source of the fluid in the
inclusion cysts (4749). Affected patients present with pain,
a palpable pelvic mass, or both findings. Histologically,
there is reactive fibroblastic and mesothelial proliferation.
The sonographic finding is that of a nonspecific, cystic
mass containing septations, representing loculated ascites
(4749). The ovary may be inside the fluid collection or
adjacent to it (Fig. 13.16). The configuration often con-
forms to the contours of the adjacent pelvis structures, but
it may also have a round or ovoid shape (29).
Benign Ovarian Neoplasms
Benign ovarian neoplasms constitute about two thirds of
ovarian masses in children, with malignant neoplasms
constituting the remainder of tumors (50,51). Tumors of
the ovary can arise from germ cells, stroma, or surface
epithelium. Most ovarian tumors in the pediatric age
group occur in the second decade of life (5053).
CYSTIC TERATOMA
Cystic teratoma is by far the most common tumor,
accounting for more than 90% of all benign ovarian neo-
plasms (5053). Approximately 90% of teratomas are
benign and 10% are malignant. Teratomas are composed
of elements from all three germ cell layers (ectoderm,
mesoderm, and endoderm). On the basis of the histologic
examination, they are classified as mature (cystic) (90%
Chapter 13 F E M A L E P E L V I S 519
of teratomas), immature (containing embryonic neural
elements), and malignant (5053). Because ectodermal
elements usually predominate, mature cystic teratomas
are also called dermoid cysts.
Mature cystic teratomas are usually unilateral, but
approximately 10% to 20% are bilateral (50). They vary
from 0.5 to 30 cm in maximum dimension, with most
measuring between 5 and 10 cm. Most affected patients
present with asymptomatic palpable masses, which may be
abdominal in location because of tumor extension outside
of the pelvis. Occasionally, patients present with acute
abdominal or pelvic pain caused by hemorrhage, torsion,
or rupture of the tumor.
The sonographic appearance of teratomas depends on
the relative amounts of sebum, serous fluid, calcium, hair,
and fat. The spectrum includes (a) a complex mass
with echogenic and hypoechoic components (75%) (Fig.
13.17), (b) an anechoic mass (12.5%), and (c) a solid
mass (12.5%) (54,55). The hypoechoic components cor-
respond to sebum. Pure sebum mimics simple fluid on
sonography because it is liquid at body temperature and
it lacks a significant number of interfaces. The echogenic
foci represent soft tissue, hair, fat, or calcification. The
echogenic components can appear as a mural nodule or
nodules projecting from the cyst wall or as multiple lin-
ear hyperechoic strands, representing hair fibers, floating
within the cyst. The latter appearance is termed the der-
moid mesh sign (Fig. 13.17B). In general, benign cystic
teratomas contain less than 50% soft tissue elements
(54).
Acoustic shadowing is another classic sign of cystic ter-
atoma. Acoustic shadowing does not necessarily imply cal-
cified material such as teeth, but may instead represent a
matted mixture of sebum and hair (54,55). Large amounts
of these tissues can completely obscure visualization of the
back wall of the tumor, producing the tip of the iceberg
sign (Fig. 13.18).
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A B

C D
Ovarian teratoma. A: Transverse sonogram of the right adnexal region shows a cystic mass (C) with a solid echogenic mural nodule
Fig. 13.17
(N), which is characteristic of teratoma. B: Transverse sonogram in another patient shows an anechoic mass (calipers) containing two
peripheral echogenic nodules. C: Longitudinal view of the right adnexa of a third patient shows a complex cystic mass (arrows) containing a mural
nodule (N) and echogenic strands (i.e., dermoid mesh sign). D: Computed tomography scan in the same patient shows a low-attenuation mass
(arrows) with a soft tissue mural nodule (N) and septations, which are partially calcified. At histopathologic examination, all three teratomas con-
tained sebum and the nodules contained a combination of hair, fat, and calcification. The echogenic strands in the third patient contained hair.

Ovarian teratoma. Transverse sonogram shows an

Fig. 13.18
echogenic mass (M) in the anterior part of the teratoma
with ill-defined posterior shadowing (arrows), which obscures visuali-
zation of the posterior wall of the tumor (tip of iceberg sign). The
mass contained hair and fat.
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Chapter 13 F E M A L E P E L V I S 521

A less common, but also characteristic finding of

Ovarian teratoma. Longitudinal sonogram in a 15-year-
Fig. 13.19
old girl with pelvic pain demonstrates a cystic mass (M)
superior to the bladder (B). There is a fat-fluid level (arrowhead) and
mural nodule (arrow). Note the echogenic fat components are in a
non-dependent position.
ovarian teratoma is a fluid-fluid level with the more
echogenic solid components (fat and hair) located in a
non-dependent location (Fig. 13.19). This appearance dif-
fers from that seen in hemorrhagic ovarian cysts, where
the echogenic blood or debris is in the dependent position
(see Fig. 13.9).
Although most benign teratomas are complex on
sonography, the spectrum ranges from purely cystic to
completely echogenic (Fig. 13.20) (5456). Anechoic ter-
atomas are almost totally composed of serous fluid or
sebum. Small mural nodules (5 mm in diameter) are
present on pathologic examination, but these are too
small to produce acoustic interfaces (Fig. 13.20A). Pre-
dominantly echogenic tumors contain teeth, cartilage,
hair, and fat and a sparse amount of fluid (Fig. 13.20C)
(54,57). It should be noted that a predominance of
echogenic soft tissue elements can also be seen in malig-
nant tumors.

A B

Atypical teratomas. A: Anechoic teratoma. Transverse

Fig. 13.20
sonogram through the right adnexa of a 13-year-old
girl shows a large cystic mass (calipers). B: Color Doppler image
shows flow in the adjacent ovarian parenchyma but not in the ter-
atoma. The cyst did not involute after several menstrual cycles and
surgery was performed. At pathologic examination, the lesion con-
tained sebum and a 5-mm mural nodule. C: Echogenic teratoma.
Transverse sonogram through the right adnexa of a 14-year-old girl
shows an echogenic mass (arrows) adjacent to the uterus (U).
Surgical exploration confirmed a benign ovarian teratoma con-
C taining predominantly fat and calcification.
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522 P E D I AT R I C S O N O G R A P H Y

A B

C D
Serous cystadenoma. Transverse sonogram of the pelvis (A) and longitudinal sonograms of the upper abdomen (B) show a large
Fig. 13.21
unilocular cyst (C) (20  11 cm). C: Contrast-enhanced computed tomography scan shows a low-attenuation mass (arrows) filling the
pelvis. D: Transverse image of the left ovary of another patient shows a cystic mass (arrows) with echogenic septations and internal debris.

CYSTADENOMA Malignant Ovarian Neoplasms

Cystadenomas are rare in patients under the age of
20 years, accounting for less than 5% of benign ovarian
tumors. The serous type is slightly more frequent than the
mucinous type in childhood. Most cystadenomas are large
lesions, ranging in size from 4 to 20 cm, and present as
pelvic masses (58,59). Histologically, serous cystadenomas
are filled with thin watery fluid. Mucinous cystadenomas
contain thick, viscous fluid.
Sonographically, serous cystadenomas are thin-walled,
unilocular cystic masses (Fig. 13.21). Occasionally, they
contain thin septations and papillary projections (Fig.
13.21D) (41,45). Mucinous cystadenomas usually appear
as multiloculated cystic lesions with thin septations (Fig.
13.22). They can contain low-level internal echoes related
to the presence of mucoid material and papillary projec-
tions (41,45,58). Ascites secondary to tumor rupture is a
rare complication.
Ovarian tumors account for 1% to 2% of all malignant
neoplasms in children younger than 17 years of age
(50,52). Germ cell tumors (teratoma, dysgerminoma,
endodermal sinus tumor, mixed malignant germ cell
tumor, embryonal carcinoma) account for 60% to 90%
of malignant neoplasms; stromal tumors (Sertoli-Leydig
cell, granulosa-theca cell, and undifferentiated neo-
plasms) have a 10% to 13% incidence; and epithelial car-
cinomas account for 5% to 11% of malignant ovarian
lesions (5053). Rare germ cell tumors (1%) include
choriocarcinoma, polyembryoma, and leiomyosarcoma
(60).
GERM CELL TUMORS
Most malignant germ cell tumors are found in postmenar-
cheal girls and present as asymptomatic pelvic or abdominal
masses. They are typically larger than 10 cm in diameter at
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Chapter 13 F E M A L E P E L V I S 523

A B
Mucinous cystadenoma. A: Longitudinal sonogram through the pelvis shows a large cystic mass (arrows) with multiple thin septations
Fig. 13.22
and low-level internal echoes. B: Contrast-enhanced computed tomography scan demonstrates a low-attenuation septated mass
(arrows) filling the pelvis and abdomen.

the time of diagnosis (61). a-Fetoprotein levels can be ele- Malignant teratomas (i.e., teratocarcinomas) contain
vated in patients with immature teratomas and endodermal histologically identifiable malignant elements, such as
sinus tumors, whereas b-human choriogonadotropin levels endodermal sinus tumor, embryonal carcinoma, and chori-
increase in patients with embryonal carcinomas and mixed ocarcinoma, in addition to derivatives of the three germ cell
germ cell tumors (Table 13.2). Intra-abdominal spread layers. By comparison with benign tumors, which are chiefly
usually is to lymph nodes and liver. cystic, malignant teratomas contain more than 50% soft
tissue elements. Sonographic findings are those of a solid
echogenic or cystic-solid mass with irregular walls, thick
septations, and papillary projections (Fig. 13.23). Calcifi-
cations are common and are scattered throughout the
Table 13.2 Clinical Features of Ovarian Tumors parenchyma. Ascites, lymphadenopathy, and hepatic metas-
tases are signs of intra-abdominal spread.
Median Clinical
Tumor Type Age (y) Features Immature teratomas contain immature or fetal tissue,
usually primitive neuroectoderm, and mature tissue ele-
Germ cell ments (53,59,61). They may demonstrate clinically malig-
Dysgerminoma 16 nant behavior and they may be associated with implanta-
Endodermal sinus tumor 18 cAFP; 75% tion of mature glial tissue on the peritoneum (gliomatosis
Teratoma
peritonei). Sonographically, these tumors present as pre-
Mature (solid, cystic) 1015
dominantly solid echogenic masses with fine scattered cal-
Immature 1114 cAFP; 30%
Malignant mixed germ cell tumor 16 cAFP and HCG cifications (Fig. 13.24).
Embryonal carcinoma 14 cHCG Dysgerminoma is composed of undifferentiated germ
Other (polyembryoma, Teens cells and it is histologically identical to the testicular semi-
choriocarcinoma) noma (Fig. 13.25) (62). Endodermal sinus tumor, also
Nongerm cell known as yolk sac tumor, shows selective differentiation
Epithelial (serous, mucinous) 8 toward yolk sac and vitelline structures (Fig. 13.26). Mixed
Sex cordstromal tumors 8 germ cell tumors contain more than one malignant compo-
(granulosa, Sertoli-Leydig, mixed) nent (Fig. 13.27) (52). Sonographically, these tumors can
AFP, -fetoprotein; HCG, human chorionic gonadotropin. appear as a relatively homogeneous echogenic mass or as a
Adapted from Cushing B, Perlman EJ, Marina NM, et al. Germ cell tumors. In: Pizzo PA, complex mass with cystic areas related to hemorrhage
Poplack DG, eds. Principles and practice of pediatric oncology. 5th ed. Philadelphia, and/or necrosis (Figs. 13.25 to 13.27). Highly cystic tumors
PA: Lippincott Williams & Wilkins, 2006:11161138. may contain internal septations, creating a multiloculated
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A B
Malignant ovarian teratoma. A: Transverse sonogram through the lower abdomen of a 9-year-old girl shows a large, predominantly
Fig. 13.23
echogenic mass (arrows) with hypoechoic areas representing necrosis. B: Contrast-enhanced computed tomography scan shows a
mostly soft tissue mass with areas of fat and calcification.

A B
Immature teratoma. A: Longitudinal sonogram through the pelvis demonstrates a large echogenic mass (arrows). B: Contrast-
Fig. 13.24
enhanced computed tomography scan shows a soft tissue mass with small areas of calcification (arrows).

A B
Dysgerminoma. A: Transverse sonogram through the pelvis of an adolescent girl shows a slightly heterogeneous echogenic mass
Fig. 13.25
(arrows) in the right adnexa. B  bladder. B: Computed tomography scan shows a solid soft tissue mass filling the pelvis.
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Endodermal sinus tumor. Transverse sonogram shows a

Fig. 13.26
large solid mass (calipers) with cystic areas represent-
ing hemorrhage and necrosis.

A B

Mixed germ cell tumor. A: Transverse sonogram of the lower

Fig. 13.27
abdomen shows a large heterogeneous mass (arrows) with
hypoechoic areas representing necrosis. B: Transverse color Doppler
image shows flow in the solid parts of the tissue. C: Coronal computed
tomography image shows a solid and cystic mass arising in the pelvis and
extending into the abdomen. At surgery, the tumor arose from the left ovary.
Histologic examination showed germ cell components, including embryonal
C carcinoma, yolk sac tumor, immature teratoma, and dysgerminoma.
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526 P E D I AT R I C S O N O G R A P H Y

A B

C D
Granulosa theca cell tumors. Longitudinal (A) and extended field-of-view transverse (B) sonograms of a 4-year-old girl with premature
Fig. 13.28
thelarche and adrenarche show a heterogeneous pelvic mass (arrows) with large cystic areas. C: Longitudinal sonogram in a 3-year-
old girl shows a heterogeneous left adnexal mass (arrows) with multiple cystic areas posterior to the bladder (B). D: Color Doppler sonogram shows
flow in the periphery of the tumor.

appearance. Color Doppler sonography shows arterial
flow within the solid echogenic components of the tumor
(6264).
SEX CORDSTROMAL TUMORS
Sex cordstromal tumors arise from the sex cords (granu-
losa and Sertoli cells) of the embryonic gonad and are
more common in premenarcheal than pubertal girls. They
are considered to be low-grade malignancies (52,65). The
stromal tumors are commonly symptomatic. Granulosa
theca cell tumors cause isosexual precocity due to exces-
sive production of estrogen, whereas Sertoli-Leydig cell
tumors cause virilization due to androgen production
(51,53).
Granulosa cell and Sertoli-Leydig tumors are usually
heterogeneous masses with cystic areas; thick, irregular
septations; and solid components (Figs. 13.28 and 13.29).
However, they also can appear as predominantly solid or cys-
tic (53,65,66). Metastases, although uncommon, are to the
peritoneal surfaces and liver (67). Doppler sonography can
show peripheral or central flow or a combination of both.
Nonfunctioning stromal tumors include fibromas and
sclerosing stromal tumors (51,53). Fibromas present as
pelvic or abdominal masses or with Meigs syndrome (asso-
ciated pleural effusion and ascites). They can occur in the
basal cell nevus syndrome, an autosomal dominant syn-
drome associated with development of basal cell carcino-
mas and abnormalities of bone, eyes, nervous system, and
reproductive system (68). Sonographic findings are a het-
erogeneous or homogeneous solid mass with marked
acoustic shadowing (68,69). On occasion, they may have a
small cystic component (29).
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Sertoli-Leydig cell tumor. Six-year-old girl with viriliza-
Fig. 13.29
tion. Transverse sonogram shows a heterogeneous mass
with solid and cystic (necrotic) areas.
The sonographic findings of the sclerosing stromal tumor
are a non-specific complex mass with calcifications, cystic
areas, and septations (70). Doppler imaging may show
increased vascularity in the periphery of the mass.
OVARIAN CANCER
Ovarian cancer is exceedingly rare in the pediatric popula-
tion. It presents as an asymptomatic pelvic or abdominal
mass or with findings related to metastatic disease. The
sonographic appearance is that of a solid or complex mass
(Fig. 13.30). Areas of necrosis; thick, irregular septations;
A B
Epithelial cancer. A: Transverse scan of the pelvis shows an echogenic solid mass (arrows) with irregular walls posterior to the blad-
Fig. 13.30
der (BL). B: Computed tomography scan shows a necrotic mass (arrows) with papillary nodules and enhancing walls. The tumor arose
in the right ovary.
Chapter 13 F E M A L E P E L V I S 527
and papillary excrescences are common. Intraperitoneal
seeding (i.e., omental and mesenteric implants) is typical
of epithelial neoplasms. Peritoneal implants appear as
echogenic soft tissue nodules on the lateral peritoneal sur-
faces or in the ligaments and mesenteries of the abdomen.
Omental implants appear as discrete echogenic nodules
or as conglomerate soft tissue masses (omental cake) in
the greater omentum beneath the anterior abdominal
wall.
Secondary Neoplasms
The ovaries may be a sanctuary for leukemia and they also
may be a site for metastatic spread from neuroblastoma,
lymphoma, and colon cancer. Metastatic involvement is
usually asymptomatic and the diagnosis is made at
autopsy. Rarely, the tumors grow large enough to produce
a palpable mass. Sonographically, secondary ovarian neo-
plasms produce unilateral or bilateral ovarian enlarge-
ment. The echogenicity of the enlarged ovary may be
hypoechoic, isoechoic, or hyperechoic to the uterus (71).
Less commonly, metastatic involvement produces a dis-
crete solid or complex intraovarian mass.
Doppler Imaging in Ovarian Malignancy
Malignant tumors tend to have central, low-resistance
Doppler waveforms (resistive index 0.4 or pulsatility
index 1.0). The lack or relative paucity of a muscular
layer in the neoplastic vessels is thought to be the cause of
the decreased vascular resistance (72,73). Benign ovarian
masses tend to show peripheral, high-resistance flow (resis-
tive index or pulsatility index 1.0) (7480). Unfortu-
nately, many nonneoplastic lesions, including tubo-ovarian
abscess, ectopic pregnancy, and functioning corpus
luteum, also have low-resistance flow and some malignant
tumors show high-resistance flow, thereby limiting the
specificity of Doppler imaging (73,81,82). In addition,
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528 P E D I AT R I C S O N O G R A P H Y

Pelvic inflammatory disease, pyosaplinx. Longitudinal

Fig. 13.31
transabdominal sonogram of the right adnexal region
shows a dilated, thick-walled fallopian tube (arrowheads) with internal
echoes and an enlarged right ovary (arrows).

malignant lesions can have only peripheral flow and can appear as a oval or round mass, rather than as an elon-
benign lesions can have central flow (80). gated structure (Fig. 13.32). Fluid-debris levels are often
visualized and rarely air-fluid levels may be seen (83).
Pelvic Inflammatory Disease Ovarian involvement has a spectrum of appearances,
Pelvic inflammatory disease is an infection of the genital including (a) an enlarged, echogenic ovary (see Fig. 13.31);
tract. It affects girls of reproductive age and is usually due (b) an irregular complex adnexal mass containing the
to an ascending sexually transmitted infection. The com- echogenic ovary and dilated fluid-filled fallopian tube mat-
mon causative organisms are Neisseria gonorrhoeae and ted together (tuboovarian complex) (Fig. 13.33); and (c) a
Chlamydia trachomatis (83,84). Clinical symptoms include round or oval, hypoechoic or complex intraovarian mass
fever, pelvic pain and tenderness, and vaginal discharge. containing internal debris, septations, or a fluid-debris
The diagnosis of pelvic inflammatory disease is usually level, representing a tubo-ovarian abscess (Fig. 13.34) (83).
established clinically, but sonography has a role in identi-
fying complications (namely, pyosalpinx and tubo-ovarian
abscess) and in assessing response to treatment. Transab-
dominal sonography is used to image the global extent of
disease. Transvaginal imaging may improve visualization
of dilated fallopian tubes, periovarian inflammation, and
tubo-ovarian abnormalities (8,85,86).
Sexually transmitted infection begins as a vaginal infec-
tion. The pathogens may then ascend to the endometrium,
resulting in endometritis, and to the fallopian tubes, caus-
ing inflammation of the walls or a pyosalpinx (i.e., pus-
filled fallopian tube). Peritoneal spillage can follow with
subsequent infection of the ovaries and parametrium,
resulting in a tubo-ovarian complex, which develops when
inflammatory adhesions fuse the ovary to the fallopian
tube, or in a tubo-ovarian abscess (83).
The sonographic findings vary depending on the stage
of the inflammatory process. Early in the course of infec-
tion, there are minimal if any sonographic abnormalities.
Abnormalities that may be seen include uterine enlargement;
endometrial fluid or thickening, indicating endometritis;
and poor definition of uterine margins, referred to as the
indefinite uterus sign (85). Pyosalpinx: Longitudinal endovaginal sonogram shows a
Pyosalpinx appears as a thick-walled, fluid-filled tubu- Fig. 13.32
markedly dilated left fallopian tube (arrows) with echogenic
lar structure containing low-level echoes representing puru- debris. The fallopian tube has folded on itself, mimicking a solitary
lent debris (Fig. 13.31). When markedly dilated, the tube mass. The left ovary (not shown) was separate from the dilated tube.
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A B
Tubo-ovarian complex. A: Longitudinal sonogram shows a complex adnexal mass resulting from fusion of a dilated fallopian tube
Fig. 13.33
(arrowheads) which contains a fluid-debris level (arrow) to the left ovary (O). BL  bladder. B: Longitudinal sonogram of the right adnexal
region in a second adolescent girl shows another complex mass (calipers) representing the inflamed ovary (O) and fallopian tube (T) matted together.

A B

Tubo-ovarian abscess. A: Longitudinal sonogram shows an

Fig. 13.34
enlarged right ovary containing a round, complex cystic
mass (arrows) with multiple septations. B: Color Doppler sonogram
shows flow in the soft tissues around the abscess. C: Contrast-enhanced
computed tomography (CT) scan shows a low-attenuation mass with an
enhancing rim (arrows) in the right adnexa. The septations are not seen
C well on CT. Also noted is a left pyosalpinx (*).
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530 P E D I AT R I C S O N O G R A P H Y

A B
Tubo-ovarian abscess. A: Transverse image of the right ovary shows an oval, anechoic mass (calipers) with highly reflective echoes,
Fig. 13.35
which were mobile at real-time imaging. B: Contrast-enhanced computed tomography scan shows an air-fluid level in the right ovary
(arrows). U  uterus.

Mobile, hyperechoic foci with acoustic shadowing may be
noted if the abscess cavity contains gas bubbles (Fig. 13.35).
Color flow Doppler findings include increased color
signal in the uterus, adnexa, and pelvic soft tissues. In the
presence of an abscess, flow can be noted in the wall of the
abscess, but not within the abscess cavity itself (see Fig.
13.34B). Pulsed Doppler interrogation shows a low-resis-
tive flow pattern (mean resistive index 0.5).
Perihepatic inflammation (i.e., Fitz-High-Curtis syn-
drome) is a rare complication of pelvic inflammatory dis-
ease, resulting from ascending spread of infection along the
pericolic gutter, leading to localized inflammation of the
anterior surface of the liver and parietal peritoneum.
Patients present with right upper quadrant pain and tender-
ness, mimicking acute cholecystitis. Sonographic findings
include perihepatic and perisplenic fluid and thickening of
the soft tissues between the liver and right kidney (87,88).
Following antibiotic or surgical treatment, pelvic
inflammatory disease can resolve or it can leave chronic
residue, such as a hydrosalpinx and adhesions. A hydro-
salpinx appears as a tubular cystic structure that is sepa-
rate from the ipsilateral ovary (Fig. 13.36). The opposing
walls may be indected, an appearance termed the waist
sign.
Adnexal Torsion
Adnexal torsion involves both the ovary and fallopian tube
(89, 90) and is the result of partial or complete rotation of the

Hydrosalpinx. Longitudinal sonogram demonstrates an

Fig. 13.36
anechoic right adnexal mass (M), which laparoscopi-
cally was confirmed to be a hydrosalpinx.
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Chapter 13 F E M A L E P E L V I S 531

ovary on its vascular pedicle. This causes compromise of
lymphatic, venous, and arterial flow, and ultimately infarc-
tion. Pathologically, the ovarian parenchyma shows a spec-
trum of findings ranging from massive ovarian edema to
ovarian necrosis. The former appearance is more likely
with partial obstruction, while the latter pattern is usually
the result of complete arterial obstruction leading to
infarction. Adnexal torsion is nearly always unilateral.
Bilateral torsion is asynchronous (91).
Adnexal torsion has been reported in all age groups,
but it is more common in adolescents and young women.
The classic presentation is acute onset of lower abdominal
pain, often associated with nausea or vomiting and leuko-
cytosis (90). Some patients have a history of recurrent
pain, reflecting intermittent torsion and detorsion.
Torsion can occur in normal adnexa or in association
with an underlying mass, which acts as a fulcrum. Neonates
and infants are more likely than adolescent girls to have an
underlying lesion. Approximately 65% of neonates but only
10% of postpubertal girls have pathologic lesions (92).
Lesions predisposing to torsion are ovarian cysts in neonates
and either cysts or teratomas in adolescent girls. The most
likely explanation for torsion of a normal adnexum is exces-
sive mobility secondary to lax supporting ligaments. This
allows the adnexa to move with changes in intra-abdominal
pressure or body position, predisposing to twisting.
GRAY-SCALE FINDINGS
The sonographic findings of torsion of the normal adnexa
are an enlarged ovary with multiple small cysts (represent-
ing dilated follicles) and increased acoustic enhancement,
the latter reflecting the pathologic findings of vascular
engorgement and stromal edema (Fig. 13.37) (89,92,93).
The affected ovary is at least five to six times larger than the
normal contralateral ovary (93). The only sign considered
relatively specific for ovarian torsion is the demonstration of
multiple peripherally located cysts. The cystic changes are
attributed to transudation of fluid into follicles secondary to
vascular congestion and have been found in up to 74% of
torsed ovaries. The positive predictive value of multifollicular

A B

Adnexal torsion. A: Transverse sonogram in a 13-year-old

Fig. 13.37
girl shows an enlarged right ovary (O) containing periph-
eral dilated follicles (arrowheads) posterior to the bladder (B). The left
ovary (arrow) is normal. B: Power Doppler image shows an enlarged
ovary with no demonstrable flow. The color signal adjacent to the ovary
is in the soft tissue. C: Endovaginal sonogram of the right adnexal region
in another patient shows an enlarged ovary (arrows) with peripheral
C cysts representing dilated follicles posterior to the uterus (UT).
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532 P E D I AT R I C S O N O G R A P H Y
enlargement is 87.5% and the specificity is 93.3% (94).
Associated masses are usually large (4 cm) and vary in
appearance from cystic to solid (Fig. 13.38) (89).
Other features of adnexal torsion are cul-de-sac fluid
(approximately 90% of cases), an extra-adnexal location
of the ovary (see Fig. 13.37C), a twisted vascular pedicle,
and ipsilateral deviation of the uterus to the side of the tor-
sion (89,92,95,96). Approximately 50% to 70% of torsed
ovaries assume a midline position, either behind the blad-
der or cephalad to the uterus. The twisted vascular pedicle
(containing the fallopian tube, broad ligament, and ovar-
ian branches of the uterine artery and vein) appears as a
round structure on short-axis views and as a tubular struc-
ture on long-axis views with alternating hypoechoic and
hyperechoic rings or layers (see Figure 13.10).
COLOR DOPPLER IMAGING
Doppler sonography commonly shows absence of flow in
the adnexum) (see Fig. 13.37B) (92,9799). However, arte-
A B
Ovarian torsion. A: Flow is noted in the cortex of the torsed left ovary, which contains a cyst (C). B: Pulsed Doppler examination shows
Fig. 13.39
diminished arterial flow. Venous flow is absent.
Adnexal torsion secondary to a hemorrhagic cyst. Lon-
Fig. 13.38
gitudinal sonogram demonstrates a cystic mass (C) with
thick irregular walls (calipers) posterior to the bladder and uterus.
B  bladder; U  uterus. Surgery revealed a hemorrhagic ovarian cyst
with 720 torsion of the fallopian tube.
rial flow can occasionally be noted in torsed adnexa, either
in the ovary or in the twisted vascular pedicle (Fig. 13.39)
(92,97100). Possible explanations for this observation are
(a) venous occlusion that produces symptoms before arte-
rial occlusion occurs and (b) arterial flow from uterine
arteries. Flow when present may be central, peripheral, or a
combination of the two patterns. Gray-scale sonographic
features need to be taken into consideration. If the gray-
scale appearance is typical of ovarian torsion, regardless of
the color flow pattern, one should be able to suggest a
specific diagnosis of torsion.
ISOLATED TUBAL TORSION
Isolated torsion of the fallopian tube is a rare cause of
acute lower quadrant pain mimicking adnexal torsion in
postmenarcheal girls (101). The right tube is more fre-
quently involved than the left tube. Sonography demon-
strates a dilated fallopian tube, which may contain low-
level internal echoes, thickened walls, and thickened
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Torsion of the fallopian tube. Longitudinal sonogram in
Fig. 13.40
an adolescent girl show a dilated left fallopian tube
(calipers) posterior to the bladder (B).
mucosal folds (Fig. 13.40). The ovaries can appear normal
and show flow on Doppler imaging (101).
MASSIVE EDEMA OF THE OVARY
Massive edema is the result of partial or intermittent tor-
sion of the ovarian pedicle, resulting in obstruction of
venous and lymphatic drainage but not arterial perfusion.
It has been reported in individuals 6 to 33 years of age
(mean age 21 years). The involved ovaries are between 5
and 40 cm in diameter with a mean diameter of 12 cm
(102,103). Histologic examination shows marked stromal
edema and normal follicles (104). Typical clinical symp-
toms are intermittent lower abdominal pain, sometimes of
A B
Normal prepubertal uterus. A: Neonatal uterus. Longitudinal sonogram shows a tubular uterus (arrowheads) with no clear-cut sepa-
Fig. 13.41
ration between the cervix and fundus and a thin echogenic endometrial stripe (arrows), as a result of in utero hormonal stimulation.
B: Eight-year-old girl. The uterus (arrowheads) is small and tubular with no differentiation between the fundus and cervix. The endometrial stripe is
absent. B  bladder.
Chapter 13 F E M A L E P E L V I S 533
several months duration. However, the pain can be acute
in onset.
The sonographic findings are a large ovary with hetero-
geneous internal echoes and increased acoustic enhance-
ment. Small cortical follicles may be observed (102,103,
105). Arterial flow is present but it may be diminished.
Differentiation between massive edema and torsion is dif-
ficult and often requires laparotomy.
UTERUS AND VAGINA
Normal Anatomy
PREPUBERTAL UTERUS
The fetal uterus increases in size late in gestation as the
result of maternal hormone stimulation. The normal
neonatal uterus is a tubular structure with the anteropos-
terior diameter of the cervix equal to or slightly greater
than that of the fundus (Fig. 13.41A) (15,106,107). The
length ranges between 2.3 and 4.6 cm (mean 3.4 cm), the
fundal width ranges from 0.8 to 2.1 cm (mean 1.2 cm),
and the cervical width from 0.8 to 2.2 cm (mean 1.4 cm).
The endometrial cavity is visualized in almost all female
neonates (97%) as a thin, highly echogenic line in the cen-
ter of the uterus (Fig. 13.41). This linear echo is caused
either by mucus or secretions within the uterine cavity or
by the endometrium itself. A hypoechoic halo surrounding
the endometrial canal is noted in about 30% of neonatal
uteri. The halo is believed to represent the inner third of
the myometrium, which is hypoechoic related to vascular
engorgement (106).
Immediately after the neonatal period, the uterus
regresses in size because of declining levels of maternal
hormones, maintaining a tubular shape. From infancy
until approximately 7 to 8 years of age, uterine size
shows little change with length, fundal width, and cervi-
cal width remaining relatively stable (Fig. 13.41B and
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534 P E D I AT R I C S O N O G R A P H Y

Table 13.3 Normal Uterine Diameters and Volume

Length (cm), Mean AP Dimension, of Corpus AP Dimension, of Cervix

Age (1 SD) (cm), Mean (1 SD) (cm), Mean (1 SD) Volume (cm3)

2y 3.3 (0.4) 0.7 (0.3) 0.8 (0.2) 2.0 (02)

3y 3.4 (0.4) 0.6 (0.1) 0.8 (0.2) 1.6 (0.08)
4y 3.3 (0.3) 0.6 (0.2) 0.9 (0.2) 2.1 (0.06)
5y 3.3 (0.6) 0.8 (0.3) 0.8 (0.2) 2.4 (0.1)
6y 3.2 (0.4) 0.7 (0.3) 0.8 (0.2) 1.8 (0.2)
7y 3.2 (0.4) 0.8 (0.2) 0.8 (0.3) 2.3 (0.1)
8y 3.6 (0.7) 0.9 (0.3) 0.8 (0.2) 3.1 (0.2)
9y 3.7 (0.4) 1.0 (9.3) 0.9 (0.2) 3.7 (0.2)
10 y 4.0 (0.6) 1.3 (0.5) 1.1 (0.3) 6.5 (0.4)
11 y 4.2 (0.5) 1.3 (0.3) 1.1 (0.3) 6.7 (0.3)
12 y 5.4 (0.8) 1.7 (0.5) 1.4 (0.6) 16.2 (0.9)
13 y 5.4 (1.1) 1.6 (0.5) 1.5 (0.2) 13.2 (0.6)

AP, anteroposterior; SD, standard deviation.

From Orsini LF, Salardi S, Pilu G, et al. Pelvic organs in premenarcheal girls: real-time ultrasonography. AJR Am J Roentgenol
1984;153:113116.

Table 13.3) (15). The endometrial canal is usually not
visualized. After 7 to 8 years of age, the uterus undergoes
an increase in length and width, with the corpus growing
faster than the cervix. The endometrial canal may be
visualized as a thin echogenic line on longitudinal images.
It is in continuity with the vagina, which also appears as
a bright midline echogenic line, reflecting apposed
mucosal linings.
PUBERTAL UTERUS
As puberty approaches, the uterus descends with the
adnexa deeper into the pelvis. The uterine fundus elon-
gates and thickens and ultimately becomes larger than
the cervix, producing the adult pear-shaped uterus
(Fig. 13.42) (107). After puberty, the uterus measures
approximately 5 to 8 cm in length, 1.6 to 3 cm in maxi-
mum anteroposterior diameter, and 3.5 cm in width
(108). The hyperechoic endometrial stripe reappears
(26,27,109,110).
PHYSIOLOGY
The sonographic appearance of the uterus after puberty
changes during the menstrual cycle (Fig. 13.43) (109111).
Histologically, the endometrium is composed of two lay-
ers: a superficial functionalis layer, which thickens and
sheds with each menses, and the basalis layer, which

A B
Normal postmenarcheal uterus. A: Longitudinal sonogram shows a pear-shaped configuration with a fundal diameter (arrow) that is
Fig. 13.42
greater than that of the cervix (open arrow). B  bladder. B: Retroverted uterus. The body of the uterus is directed posteriorly, which
is a normal variant. Again, note the pear-shaped uterine configuration, with the fundus larger than the cervix. Uterine length (calipers marked as 1)
equals 7.5 cm. Anteroposterior diameter (calipers marked as 2) equals 3.0 cm.
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Chapter 13 F E M A L E P E L V I S 535

A
B

C D
Phases of endometrial development. Sonograms in four different patients. A: Menstrual phase. The endometrial canal is seen as a thin
Fig. 13.43
(3-mm) echogenic stripe (cursors). Arrows indicate the vagina with echogenic endometrial lining (*). B: Proliferative phase. The cen-
tral canal is echogenic and surrounded by the hypoechoic functionalis layer (8-mm thickness) (arrowheads). C: Early secretory phase. There is a
thickened echogenic endometrium (arrows), measuring 8 mm. D: Later secretory phase. The echogenic endometrium has reached its maximal thick-
ness, 15 mm (calipers). Note in all four patients the pear-shaped uterus, with a fundal diameter larger than that of the cervix.

remains intact throughout the cycle and contains vessels
that supply the endometrium as it thickens (109,111). In
the menstrual phase (days 1 to 5), the functionalis layer
of the endometrium is shed, leaving only the basal layer
subadjacent to the myometrium. During this phase, the
endometrium appears as a thin (2 to 3 mm thickness)
echogenic line, reflecting blood and sloughed tissue in the
uterine canal (Fig. 13.43A). During the proliferative
phase (days 6 to 14), the endometrium increases in thick-
ness as ovulation approaches. In the first few days of this
phase, the endometrium appears hypoechoic, probably
reflecting the straight and orderly arrangement of glands
within the functionalis layer (Fig. 13.43B). By the time of
ovulation, the endometrium is moderately thick, measur-
ing 4 to 8 mm in diameter, and echogenic, a reflection of
the increased tortuosity of the glandular elements. After
ovulation, the innermost part of the endometrium (the
functional layer) becomes hypoechoic and is surrounded
by a rim of echogenic tissue (the deep basal layer). This
appearance, best appreciated on transverse sonograms,
has been referred to as a ring sign and is probably a
reflection of stromal edema in the functionalis layer. In
the secretory phase (days 15 to 28), the endometrium
reaches maximal echogenicity and thickness, measuring
12 to 15 mm (Fig. 13.43C,D). The increase in endome-
trial echogenicity and thickness reflects distention of the
endometrial glands by mucin and glycogen (109111).
This appearance persists until the onset of menses, when
the cycle repeats itself.
The myometrium in prepubertal girls is homogeneous
and hypoechoic relative to surrounding soft tissues. In
postmenarcheal girls, the myometrium may have a striated
appearance, showing three distinct zones: a hypoechoic
inner junctional zone, a moderately echogenic intermediate
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536 P E D I AT R I C S O N O G R A P H Y
Normal uterine color flow, adolescent uterus. Longitudi-
Fig. 13.44
nal endovaginal image shows moderate color signal in
the myometrium. The endometrium (arrows) is avascular.
zone, and a hypoechoic outer zone (109). The thickness of
the myometrium increases only slightly during the men-
strual cycle.
UTERUS: DOPPLER IMAGING
The uterus is supplied by the uterine arteries, which
are branches of the internal iliac arteries. The normal
endometrium in both prepubertal and postmenarcheal girls
shows little or no flow on color flow Doppler imaging (112).
In prepubertal girls, the myometrium is also avascular. In
postmenarcheal girls, the myometrium exhibits varying
amounts of color signal on Doppler examination (Fig.
13.44) (112).
VAGINA
The normal vagina appears as a midline tubular structure
posterior to the urinary bladder. The prepubertal vagina is
hypoechoic relative to adjacent tissues; differentiation
between the central canal and the adjacent walls is difficult
by sonography. The postmenarcheal vagina is character-
ized by a central echogenic endometrial lining and an outer
hypoechoic wall (see Figure 13.43A).
Congenital Uterine Anomalies
EMBRYOLOGY
The uterus, cervix, and cranial two thirds of the vagina
develop from fusion of the caudal ends of the two mllerian
ducts. The ducts descend into the pelvis from the upper
abdomen, migrate into the midline, and fuse medially at
about the 10th week of fetal life. The unfused cranial ends
develop into the fallopian tubes. The median septum formed
by the fusion of the medial walls of the ducts eventually
involutes and usually disappears by the 20th week of fetal
life, resulting in a single uterine cavity. Developmental
anomalies result when there is failure or incomplete fusion
of the mllerian ducts or incomplete septal regression
(113116).
The caudal one third of the vagina develops from
the sinovaginal bulb. The distal and proximal parts of
the vagina ultimately fuse when a cellular cord between
the two dissolves. Failure of the mllerian ducts to
meet or canalize will result in vaginal hypoplasia or
agenesis or a transverse vaginal septum (discussed
below).
The prevalence of these malformations is 0.1% to 10%
(113,114). The lower prevalence has been reported in
women evaluated with sonography for nonobstetric indi-
cations, while the higher prevalence has been reported in
women who undergo hysterosalpingography for obstetric
problems (114). Renal tract anomalies are associated with
congenital uterine anomalies because of the close embry-
ologic relationship between the paramesonephric and
mesonephric ducts (113).
Ultrasonography and MRI are the studies of choice
to detect and characterize mllerian duct anomalies
(117). Ultrasonography can be limited by the acoustic
window and bowel loops in the pelvis. Instillation of a
saline solution may further improve diagnostic accuracy
(118).
Although a number of systems have been proposed
for classifying mllerian anomalies, one of the most
widely utilized systems is the one adopted by the Ameri-
can Fertility Society (115). This classification, based on
the degree of failure of normal development, has seven
major subgroups: I, segmental agenesis or hypoplasia
(cervical, fundal, tubal, or combined anomalies); II, uni-
cornuate uterus; III, didelphys uterus; IV, bicornuate
uterus; V, septate uterus; VI, arcuate uterus; and VII,
diethylstilbestrol drug-related uterine hypoplasia with
luminal changes. These abnormalities are discussed
below.
CLASS I: UTERINE AGENESIS OR HYPOPLASIA
Uterine agenesis and hypoplasia are the result of arrested
development of the mllerian ducts bilaterally. Uterine
agenesis can be an isolated finding, but more often it is
associated with the Mayer-Rokitansky-Kster-Hauser syn-
drome (Fig. 13.45).
The Mayer-Rokitansky-Kster-Hauser syndrome is
characterized by complete vaginal atresia, with 90% of
patients having associated cervical and uterine agenesis. In
about 10% of cases, a hypoplastic or duplicated uterus is
present (113). This remnant structure can be functional
(containing an endometrial layer) or nonfunctional
(absence of an endometrial layer). Complete uterine agen-
esis presents as primary amenorrhea. If a functional rem-
nant is present, symptoms are cyclic abdominal pain due
to hematometra (114,119). Renal anomalies, usually
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Chapter 13 F E M A L E P E L V I S 537

A B
Mllerian hypoplasia. Left functional uterine remnant in a 15-year-old girl with surgically diagnosed Mayer-Rokitansky-Kster-Hauser
Fig. 13.45
syndrome. A: Longitudinal image shows the left uterine horn containing a 5-mm endometrial stripe (arrow). B: Coronal fast spin echo
T2-weighted magnetic resonance image shows a left-sided functional uterus (short arrow). A rounded soft tissue mass (long arrow) with a signal
intensity similar to that of the myometrium and no endometrial stripe is present on the right, presumed to be a right-sided uterine remnant. The
vagina is atretic. (Reproduced from Junqueira BL, Allen LM, Spitzer RF, et al. Mullerian duct anomalies and mimics in children and adolescents: cor-
relative intraoperative assessment with clinical imaging. Radiographics 2009;29:10851103, with permission.)

agenesis and rarely ectopia or hydronephrosis, occur in
about 50% of patients and skeletal anomalies in about
15% (119). Affected patients will have a normal female
karyotype, external genitalia, and secondary sexual devel-
opment.
The sonographic findings of Mayer-Rokitansky-
Kster-Hauser syndrome are normal ovaries, absence
of the cervix and upper two thirds of the vagina, and
an absent or small uterus with poorly differentiated
zonal anatomy and absence of the midline echoes
(119,120).
Differential diagnoses that need to be considered in
patients with the Mayer-Rokitansky-Kster-Hauser syn-
drome include primary vaginal atresia with a patent
endometrial canal and cervix and congenital disorders of
sexual differentiation, such as Turner syndrome (45XO
karyotype, streak ovaries), true hermaphroditism (see
discussion below), and the testicular feminization syn-
drome (see discussion below). The latter syndrome is
characterized by a male (46XY) karyotype, female exter-
nal genitalia, blind-ending vagina, and absent uterus. The
gonads are testes that produce normal male levels of
testosterone, but there is absence of testosterone recep-
tors. Patients present because of primary amenorrhea or
with inguinal masses containing testes. A uterus cannot
be identified on sonography, but testes may be noted in
the pelvis or the inguinal area.
CLASS II: UNICORNUATE UTERUS
The unicornuate uterus results from failure of develop-
ment of one of the two mllerian ducts. In this anomaly
there is a single-horned uterus, which communicates with
a normal vagina. In most cases, a contralateral rudimen-
tary horn is observed, which can be cavitary (containing
endometrial tissue) or noncavitary (without associated
endometrium). The rudimentary horn may or may not
communicate with the developed contralateral uterine
horn (113). Unicornuate uterus does not require treatment
unless functional endometrial tissue within a noncommu-
nicating horn causes endometriosis-type symptoms or
hematometra (121).
The diagnosis can be suggested on sonography when
there are two horns of different sizes or when the uterus
appears curved, elongated, and laterally located (i.e.,
banana-shaped uterus) (Fig. 13.46). The developed uterine
horn shows normal zonal anatomy.
CLASS III: UTERUS DIDELPHYS
Uterus didelphys is characterized by two vaginas, two cer-
vices, and two uterine corpora, due to complete nonfusion
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538 P E D I AT R I C S O N O G R A P H Y

A B
Unicornuate uterus with a noncommunicating rudimentary horn. A: Transverse sonogram shows a hypoplastic left uterine horn
Fig. 13.46
(arrowhead), which does not communicate with the laterally deviated right uterine horn (arrow). The right uterine horn has a dilated
endometrial canal (E) with low-level echoes representing blood products. B: T1-weighted magnetic resonance image also shows a noncommuni-
cating hypoplastic left horn (arrowhead) and a developed right horn (arrow) with blood in the endometrial cavity (E). Hematometra was secondary
to vaginal atresia.

of the mllerian ducts (Fig. 13.47). The uterine horns are
separate and each one has normal zonal anatomy. No com-
munication between the two cavities is present. A complete
or partial longitudinal vaginal septum is associated with
this anomaly in 75% of cases (112).
These patients are usually asymptomatic unless there is an
associated vaginal septum causing hematocolpos. Uterus
didelphys with an obstructed hemivagina becomes sympto-
matic at menarche, producing cyclic pelvic pain. Renal agene-
sis is common in patients with an obstructing vaginal septum.
Sonography shows two separate normal-sized uterine
bodies, two cervices, and, occasionally, a longitudinal
septum in the upper vagina (Fig. 13.48). The uterine horns
are widely divergent with a deep midline fundal cleft in the
external contour of the uterus (1 cm in length). Each
horn has a fusiform shape, convex lateral margins, and

A B

Mllerian duct fusion anomalies. A: Uterus didelphys:

C D
Fig. 13.47
two uteri, two cervices, two vaginas. B: Uterus duplex
bicollis: two uteri, two cervices, one vagina. C: Uterus duplex unicollis:
two uteri, one cervix, one vagina. D: Septate uterus: single uterus
divided by a septum. (Adapted from Colodny AH. Disorders of the
female genitalia. In: Kelalis PP, King LR, Belman B, eds. Clinical pedi-
atric urology. Philadelphia, PA: WB Saunders, 1985:888903.)
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Chapter 13 F E M A L E P E L V I S 539

A B
Uterus didelphys. A: Transverse image through the pelvis of a 12-year-old girl with cyclic pelvic pain and irregular menses shows two
Fig. 13.48
uterine horns (arrows) with a deep intercornual cleft. An endometrial stripe (arrowhead) is seen in the right uterine horn. B: Longitu-
dinal view through the left lower hemipelvis demonstrates blood in an obstructed left vagina (L). The right vagina was normal. Magnetic resonance
imaging confirmed left hematocolpos, a normal right vagina, two cervices, and two uterine corpora. BL  bladder.

normal zonal anatomy. In each uterus, the endometrial/
myometrial width and ratio are preserved (113). There is
no effective surgical repair for the uterus didelphys.
CLASS IV: BICORNUATE UTERUS
Bicornuate uterus results when there is partial failure of
fusion of the mllerian ducts (Fig. 13.47). This anomaly
is characterized by two symmetric horns that are fused
caudally and communicate with each other, most often at
the level of the uterine isthmus. Bicornuate uteri in which
the septum extends to the external os is referred to as
uterus duplex bicollis (one vagina, two cervices, and two
uterine corpora). Bicornuate uteri in which the septum
extends to the internal os is referred to as uterus duplex
unicollis (one vagina, one cervix, and two uterine corpora)
(Fig. 13.47). Most patients are asymptomatic, although
they have an increased incidence of spontaneous abortions.
Sonographic features of a bicornuate uterus are two sepa-
rate uterine horns and a concave fundal contour with a deep
cleft (1 cm) between the two uterine bodies (Fig. 13.49). The
tissue between the two horns is composed of myometrium.
The endometrial/myometrial ratio and width are normal

A B
Uterus duplex bicollis. A: Transverse sonogram shows two uterine bodies (arrows). Each uterine horn is of similar size. B: Transverse
Fig. 13.49
sonogram shows two separate cervices (arrowheads). B  bladder.
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540 P E D I AT R I C S O N O G R A P H Y
(113). The bicornuate uterus usually does not require
surgical intervention. Historically, it was treated by trans-
abdominal surgical resection of the muscular division
between the two sides of the uterus to fuse the two horns
(metroplasty) (117).
CLASS V: SEPTATE UTERUS
The septate uterus is the most common mllerian anom-
aly. It is characterized by a single uterus, cervix, and
vagina with a septum dividing the uterus into two
compartments. The anomaly results from partial or
complete failure of resorption of the midline septum.
The septum, located in the midline fundal region, is
composed of poorly vascularized fibromuscular tissue
(113). Affected patients are usually asymptomatic,
although they may have an increased incidence of spon-
taneous abortions.
At sonography, there are two closely apposed endome-
trial cavities, which are divided by a septum that is hypo-
echoic to myometrium (Fig. 13.50) (122). The external
uterine contour may be convex, flat, or mildly concave
(1 cm). The treatment of the septate uterus is hystero-
scopic resection of the septum.
CLASS VI: ARCUATE UTERUS
Arcuate uterus is the mildest fusion anomaly, resulting in a
small indentation in the fundal endometrial canal. There is
no division of the uterine horns. Arcuate uterus is the
result of minimal incomplete resorption of the uterovagi-
nal septum. It is asymptomatic.
Sonography shows a normal external fundal contour
and a single endometrial cavity with minimal fundal inden-
tation.
CLASS VII: DIETHYLSTILBESTROL EXPOSURE
Diethylstilbestrol exposure resulted in a hypoplastic uterus
with an irregular T-shaped configuration (wider than it
is long) (113). This drug was used between 1945 and 1971
to prevent miscarriage and its teratogenic effects are no
longer seen in the pediatric population. Other conditions
associated with diethylstilbestrol exposure included adeno-
sis and clear cell carcinoma of the vagina.
Congenital Vaginal Anomalies
Congenital anomalies of the vagina can be classified into
two groups: those in which the vagina is absent and
those in which it is obstructed due to transverse mem-
branes or septa. Primary vaginal atresia is the result
of absent or arrested development of the sinovaginal
bulb or primitive vagina (lower one third of the vagina).
The transverse membrane or septum results when the
cellular cord between the lower one third and proximal
two thirds of the vagina fails to resorb or undergo canal-
ization.
The terminology used to describe vaginal obstruction
varies with the fluid contents. Hydrocolpos refers to dilata-
tion of the vagina by serous fluid or sometimes urine if
there is a urogenital sinus; hydrometrocolpos is distention
of both the uterus and the vagina with serous fluid. Hema-
tocolpos refers to distention of the vagina with blood,
hematometra to distention of the uterus with blood, and
hematometrocolpos to distention of both the uterus and
vagina with blood.
Vaginal obstruction can be encountered in the neona-
tal period or at the time of menarche. There are two
forms of vaginal obstruction in the neonate. In the first
type, vaginal obstruction is caused by vaginal or cervical
atresia, a transverse septum, or an imperforate mem-
brane. In the second, less common type, vaginal obstruc-
tion is the result of a cloacal malformation (single exit
chamber for the vagina, bladder, and rectum) or urogen-
ital sinus (single exit chamber for only the vagina and
bladder) (123). Vaginal obstruction results when the
communication between the vagina and cloaca or uro-
genital sinus is stenotic or the cloaca or sinus itself is
stenotic.
Septate uterus. Transverse sonogram shows a flattened
Fig. 13.50
external uterine contour (arrowheads) and two endome-
trial cavities (E) with an intervening hypoechoic septum (arrows). The
flat outer contour excludes uterus didelphys and bicornuate uterus.
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Neonatal hydrocolpos. Longitudinal sonogram shows a
Fig. 13.51
dilated fluid-filled vagina (V) outlining the cervix (C) pos-
terior to the bladder (B).
In adolescent girls, vaginal obstruction can be the
result of a simple imperforate membrane or a transverse
vaginal septum (124). A less frequent cause includes
Mayer-Rokitansky-Kster-Hauser syndrome (125).
Vaginal obstruction in the neonate usually presents as
a palpable pelvic or abdominal mass, which is the result of
production and excessive accumulation of vaginal and/or
uterine secretions in utero secondary to maternal hormone
stimulation (123). At times, there is an interlabial mass
resulting from eversion of the obstructing vaginal mem-
brane or septum by accumulated secretions. Adolescent
patients present with primary amenorrhea, cyclic lower
abdominal pain, a pelvic mass, or urinary retention (124).
The incidence of congenital anomalies (e.g., imperforate
anus, esophageal or duodenal atresia, congenital heart
disease, and renal abnormalities) is increased in neonates
with vaginal atresia, but not in patients with imperforate
membrane.
Transabdominal sonography usually suffices for diag-
nosis of hydrocolpos or hydrometrocolpos. The addition
of transperineal scanning to transabdominal sonography
may allow a more precise evaluation of the level and extent
of vaginal obstruction (126,127). The translabial exami-
nation is performed with a high-frequency endovaginal
transducer. The transducer is covered with acoustic gel and
a condom, and then it is placed directly against the labia
minora and external urethral orifice. If needed, a standoff
pad can be placed on the perineum. Longitudinal and
coronal images are obtained of the lower urogenital tract,
and the distance from the perineum to the caudal aspect of
the distended vagina is measured.
SONOGRAPHIC FINDINGS
The sonographic findings of hydrocolpos or hematocolpos
are those of a tubular, fluid-filled, midline mass, repre-
Chapter 13 F E M A L E P E L V I S 541
senting the dilated vagina between the bladder and rectum
(Fig. 13.51) (123,124). The uterine cavity may or may not
be dilated. The distended vagina has a thin, almost imper-
ceptible wall, while the uterus has a thicker muscular wall.
Internal echoes reflecting cellular debris or blood or a
fluid-debris or blood level can be demonstrated within the
uterus or vagina (Fig. 13.52). Occasionally, the fallopian
tubes will be filled with blood. If large enough, the
distended vagina and uterus can obstruct the ureters,
causing hydronephrosis. Additional findings include
ascites related to spillage of contents from the fallopian
tubes into the peritoneal cavity and peritoneal calcifica-
tions (128).
Fluid within the vagina occasionally can be seen as a
normal finding in otherwise normal prepubertal girls
(129). This results when urine refluxes from the bladder
into the vagina during micturition. Differentiation of
nonobstructive from obstructive hydrocolpos is made by
rescanning the patient after having her stand erect. During
standing, the urine in the vagina dribbles out.
Uterine Tumors
Uterine tumors in the pediatric population are rare, but
when they are present they nearly always arise in the
myometrium. They are often best seen by transvaginal
sonography.
MYOMETRIAL TUMORS
Adenomyosis
Adenomyosis is a condition characterized histologically by
the presence of ectopic endometrial glands and stroma
within the uterine myometrium (130, 131). It is usually
more extensive in the posterior uterine wall. Adenomyosis
can present as a diffuse or focal form. The more common
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542 P E D I AT R I C S O N O G R A P H Y
A B
C avascular on color Doppler imaging.
diffuse form is characterized by widely distributed adeno-
myosis in the myometrium, whereas the focal or nodular
form is characterized by circumscribed nodules termed
adenomyomas. Symptoms are nonspecific and include
pelvic pain, dysmenorrhea, and menorrhagia.
Sonographic findings of diffuse adenomyosis are an
enlarged, thick-walled uterus with normal external
contours and normal myometrial and endometrial echo-
texture (Fig. 13.53). The uterus is usually diffusely
enlarged, but occasionally, only the posterior wall is
involved. The sonographic findings of focal or nodular
adenomyomas are a hypoechoic or anechoic myometrial
mass, termed an adenomyotic cyst (Fig. 13.54) (130, 131).
Adenomyotic cysts are the most common cause of myome-
trial cysts.
Hematocolpos in a 13-year-old girl with cyclic pain.
Fig. 13.52
Transverse (A) and longitudinal (B) pelvic sonograms
show a markedly distended vagina (V) with low-level echoes repre-
senting blood. B  bladder. R  rectum. C: The distended vagina is
Leiomyoma
Leiomyomas, also known as fibroids, are composed of
uterine smooth muscle cells and connective tissue. They
most commonly involve the myometrium of the uterine
corpus but may also occur in the cervix. According to
their location, they are classified as submucosal (project-
ing into the endometrial canal), intramural (arising in the
substance of the myometrium), or subserosal (beneath
the serosa). Symptoms include dysmenorrhea and men-
orrhagia.
Most leiomyomas are ovoid or spherical in shape. The
echotexture depends on the relative amounts of smooth
muscle and connective tissue. Leiomyomas are usually
hypoechoic, but they may be isoechoic or hyperechoic to
myometrium (Fig. 13.55) (132). They often distort the
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Chapter 13 F E M A L E P E L V I S 543

A B
Diffuse adenomyosis. Longitudinal (A) and transverse (B) sonograms in an adolescent girl with menorrhagia show an enlarged, thick-
Fig. 13.53
walled uterus (arrows). Hypoechoic contents within the endometrial cavity (E) represent blood products.

A B

Focal adenomyosis. A: Transverse sonogram shows a

Fig. 13.54
hypoechoic lesion (calipers) in the fundal myometrium.
B  bladder. B: Color Doppler image shows blood flow at the periphery
of the mass (M) but not within it. UT  normal uterine myometrium.
B  bladder. C: Contrast-enhanced computed tomography scan shows
a low attenuation mass (arrows) in the myometrium of the uterine fun-
C dus displacing the endometrial canal (E) to the left.
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544 P E D I AT R I C S O N O G R A P H Y
external uterine contour, especially subserosal and large
intramural leiomyomas. Cystic areas related to necrosis and
calcifications may occur in older women.
LYMPHOMA
Non-Hodgkin lymphoma is a rare cause of uterine enlarge-
ment (133).
PREGNANCY-RELATED ABNORMALITIES: TROPHOBLASTIC DISEASE
Gestational trophoblastic disease is a proliferative disease
of the trophoblast with biologic behavior varying from the
relatively benign hydatiform mole to the more malignant
invasive mole and choriocarcinoma (134136). Hydati-
form moles constitute 80% of cases of gestational tropho-
blastic disease and include the complete or classic mole
and the partial mole. The complete mole is characterized
by edematous chorionic villi with trophoblastic prolifera-
tion and absence of fetal parts. The partial mole demon-
strates edematous chorionic villi with little or no tro-
phoblastic proliferation and a gestational sac containing
fetal tissue. Clinical findings are vaginal bleeding and ele-
vated serum human chorionic gonadotropins levels.
The sonographic appearance of a complete hydati-
form mole is that of an enlarged-for-dates uterus con-
taining an echogenic mass with multiple small anechoic
spaces (Fig. 13.56). This appearance is best recognized
during the second trimester. In the first trimester, the
appearance of a molar pregnancy is more variable. It
may appear relatively solid with few or no vesicles visu-
alized and resemble a solid adnexal or uterine mass, or it
may be seen as a large, central fluid collection (136).
Doppler interrogation of the uterine artery shows very
high systolic and diastolic Doppler shifts (Fig. 13.56D)
(137).
An incomplete or partial hydatiform mole can have an
appearance similar to that of a complete mole with an
admixture of solid echogenic material and fluid-filled cysts
filling the uterus. The coexistence of a gestational sac with
or without a fetus allows a specific diagnosis of a partial
mole. The fetus is usually triploid and does not survive
Intramural leiomyoma (fibroid). Sagittal transvaginal sono-
Fig. 13.55
gram in a young adult woman shows a well-circumscribed
intramural mass (calipers) that is nearly isoechoic to uterine myometrium
(UT).
(134137). Often the uterus is small for dates, which can
help differentiate this condition from the classic hydati-
form mole, in which the uterus is enlarged.
Invasive mole is seen in about 10% of patients with ges-
tational trophoblastic disease, and the most malignant form
of trophoblastic disease, choriocarcinoma, occurs in about
5% of cases (136). The presence of a bulky intrauterine mass
with extension into the myometrium and parametrium sug-
gests an invasive mole, while the presence of distant metas-
tases in combination with a molar pregnancy is suspicious
for choriocarcinoma.
Vaginal Tumors
RHABDOMYOSARCOMA
Rhabdomyosarcoma is the most common tumor of the
genitourinary tract in children, accounting for 5% to 15%
of all malignant solid tumors in patients younger than
15 years of age (138140). Most often, it arises in the ante-
rior wall of the vagina adjacent to the cervix. The tumor
can arise in the uterus, but more often uterine involvement
is secondary to direct extension from a vaginal tumor.
Rhabdomyosarcoma has a bimodal age distribution, with
the first peak occurring between 2 and 6 years of age
and the second peak between 14 and 18 years of age. The
embryonal and botryoid subtypes are the predominant
histologic subtypes in the genitourinary tract. Common
presenting features are vaginal bleeding and a vaginal, per-
ineal, or vulvar mass. Metastases are to liver, lymph nodes,
lung, and bone.
At sonography, rhabdomyosarcoma appears as a bulky
solid mass enlarging the vagina or uterus (Fig. 13.57)
(138,139). Cystic areas within the mass, representing
necrosis, are common. The tumor can directly extend into
the uterine cavity or it can extrinsically occlude the cervical
os, resulting in uterine enlargement and fluid collections in
the endometrial cavity. Other findings include bladder or
rectal wall invasion and obstruction of the distal ureters
with resultant hydronephrosis. Lymph node metastases can
be detected if the involved nodes are enlarged.
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Chapter 13 F E M A L E P E L V I S 545

A B

C D
Complete hydatiform mole. Twenty-week molar pregnancy. Longitudinal gray-scale (A) and color Doppler (B) sonograms show a large,
Fig. 13.56
echogenic mass with small cystic spaces filling the uterine cavity (arrows). C: Pulsed Doppler image shows high systolic and diastolic
flow. D: Contrast-enhanced computed tomography scan shows a large, thick-walled uterus (arrows) with a central mass.

ADENOCARCINOMA AND SARCOMA
Other rare vaginal and uterine tumors include adenocarci-
noma and leiomyosarcoma (141). The clinical presentation
is vaginal bleeding or a polypoid vaginal mass. The imag-
ing features are similar to those of rhabdomyosarcoma.
VAGINAL AND PARAVAGINAL CYSTS
Vaginal cysts include Gartner and inclusion cysts. Gartner
duct cysts are remnants of Wolffian ducts; they are usually
found in the upper anterolateral walls of the vagina. Inclu-
sion cysts commonly occur at the lower end of the vagina
on the posterior surface; arise from inclusion of mucosa;
and usually result from perineal lacerations or trauma. Para-
vaginal cysts, also referred to as paraurethral cysts, are
found between the urethra and vagina and open into the
urethra. They are considered to be rudimentary homo-
logues of the prostate. Vaginal and paravaginal cysts usu-
ally have an anechoic or hypoechoic appearance. However,
they can be echogenic if the fluid contains proteinaceous
debris or mucoid material (Fig. 13.58) (142).
DISORDERS OF PUBERTY
Puberty is the stage of life when the reproductive system
matures in association with completion of somatic growth
and sexual maturity (143). The normal age of puberty is 8
to 17.9 years.
Precocious Puberty
Precocious puberty is defined as the development of sec-
ondary sexual characteristics (breast tissue, pubic and
axillary hair, external genitalia, and menses) prior to 8
years of age. There are four types of precocious puberty:
central or true isosexual precocity, peripheral or pseudo-
sexual precocity, premature adrenarche, and premature
thelarche.
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546 P E D I AT R I C S O N O G R A P H Y

A B

C D
Vaginal rhabdomyosarcoma. A: Longitudinal and B; transverse sonograms in a 17-year-old girl with menorrhagia demonstrate an
Fig. 13.57
echogenic mass (arrows) enlarging the vagina. The mass occludes the cervical os (*) resulting in accumulation of blood products in
the endometrial (E) canal. Arrowheads = external uterine contour. C: Color Doppler sonography shows flow within and around the tumor. D: Sagittal
CT scan shows a bulky, soft-tissue mass (M) expanding the vagina. The uterus (UT) is displaced superiorly.

True isosexual precocity is characterized by early devel-
opment of secondary sexual characteristics with menses
(i.e., ovulation) and elevated serum gonadotropins levels.
The majority (80%) of cases are the result of idiopathic
activation of the hypothalamic-pituitary-gonadal axis. The
remaining cases are the result of pituitary gland or hypo-
thalamic lesions (144). Peripheral or pseudosexual precocity
is characterized by early development of secondary sexual
characteristics without ovulation and increased estradiol
levels but low gonadotropin levels. The causes of pseudo-
sexual precocity include functioning ovarian cysts; ovarian
neoplasms (granulosa theca cell tumors, arrhenoblastomas,
thecomas, and choriocarcinomas); adrenal adenomas and
carcinomas; neurofibromatosis; McCune-Albright syn-
drome (fibrous dysplasia and cutaneous pigmentation); and
ingestion of estrogen compounds (144). Premature adrenar-
che is characterized by isolated pubic hair development and
increased levels of adrenal androgens. Premature thelarche
is characterized by isolated breast development and occurs
with normal levels of prepubertal hormones (144).
The role of sonography in patients with precocious
puberty is to determine ovarian and uterine size and the
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Chapter 13 F E M A L E P E L V I S 547

A B
Paravaginal/Paraurethral cyst. A: Transverse perineal sonogram shows a sharply delineated echogenic mass (diameter, 0.9 cm)
Fig. 13.58
(arrowheads) with through transmission. B: Sagittal sonogram shows the echogenic paraurethral cyst (c) situated between the ante-
riorly displaced urethra (u) and the vagina (v) posteriorly. Histologic examination confirmed stratified squamous epithelium or urothelium. (Reprinted
from Breysem L, Rayyan M, Bogaert G, et al. High-resolution perineal ultrasound of a paraurethral cyst in a neonate. Eur Radiol 2008;18:27012703,
with permission.)

ratio of corpus length to cervix length. Uterine and bilateral
ovarian enlargement is indicative of central or true preco-
cious puberty. The uterus will have a pear-shaped configu-
ration (i.e., dominance of the corpus over the cervix) and an
echogenic endometrial canal (Fig. 13.59). Unilateral ovarian
enlargement is typical of pseudosexual precocity (Fig.
13.60). A cyst or tumor may be seen in some patients. Small
prepubertal ovaries and uterus should suggest the diagnosis
of isolated premature thelarche or adrenarche. Mean ovar-
ian volume has been reported to be 4.6 cm3 in true isosex-
ual precocity, 4.1 cm3 in pseudosexual precocity, and less
than 1 cm3 in premature adrenarche (19). The presence of
small follicles (9 mm) is not a reliable indicator of preco-
cious puberty and can be found in slightly more than 50%
of healthy girls and girls with precocious puberty (19).
Sonography has also been used to evaluate the effect of
treatment of precocious puberty. With appropriate ther-
apy, ovarian and uterine size decrease and revert to prepu-
bertal volumes and configuration.
Amenorrhea
Primary amenorrhea is defined as the failure of menstrua-
tion by age 16 years. The causes of primary amenorrhea
include hypothalamic and pituitary lesions; androgen-
producing adrenal tumors; cytotoxic drugs or radiation
therapy for the treatment of malignancy (145); and

A B
3
Central (true isosexual) precocity in a 4-year-old girl. A: Longitudinal sonogram shows an enlarged ovary (arrow) (volume 3.8 cm ) contain-
Fig. 13.59
ing small follicles less than or equal to 9 mm in diameter. B: Longitudinal sonogram shows an enlarged uterus that has a thickened endome-
trial stripe and an adult configuration with the fundus (arrow) slightly larger than the cervix (arrowhead). The prepubertal uterus should have a tubular
shape with no differentiation between fundus and cervix. Also notice the echogenic endometrium (*), which suggests hormonal stimulation.
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548 P E D I AT R I C S O N O G R A P H Y
primary abnormalities of the ovary (gonadal dysgenesis,
polycystic ovary disease, or virilizing neoplasm), the uterus
(absence or hypoplasia or testicular feminization syn-
drome), or the vagina (imperforate hymen, atresia, or
stenosis). Several of these disorders are discussed elsewhere
in this chapter.
POLYCYSTIC OVARIAN DISEASE
Polycystic ovarian disease, also known as the Stein-Leven-
thal syndrome, affects 5% to 7% of the female population.
The classic syndrome is characterized by amenorrhea, obe-
sity, and hirsutism, but this is only one form of presenta-
tion and each clinical feature may occur alone or in any
combination (146). The consistent clinical feature is
chronic anovulation. The endocrine profile of affected
patients shows depressed serum levels of follicule-stimulating
Peripheral (pseudosexual) precocity secondary to an
Fig. 13.60
autonomous cyst. Transverse sonogram through the
pelvis of a 3-year-old girl shows a 3-cm cyst (arrowheads) in the right
ovary and uterine enlargement (U). B  bladder.
hormone and elevated levels of luteinizing hormone. The
resultant hormonal imbalance results in excessive andro-
gen production by the ovarian stroma. Pathologically, the
ovaries contain an increased number of immature and
atretic follicles and hyperstimulated ovarian stroma.
Although Stein and Leventhal originally described bilat-
erally enlarged ovaries, subsequent studies have shown that
there can be normal-sized ovaries and unilateral abnormal-
ities. Approximately 70% of patients with polycystic ovary
disease have bilaterally enlarged ovaries on transvaginal
sonography. The median volume is 9.8 cm3 (147). Ovarian
volume is somewhat larger on transabdominal sonography,
with mean volumes ranging between 12 cm3 and 14 cm3. In
approximately 30% of patients, ovarian volume will be
normal. The ovaries also commonly have a spherical rather
than normal ovoid shape (Fig. 13.61).
Polycystic ovary disease. Longitudinal sonogram demon-
Fig. 13.61
strates an enlarged round ovary (volume, 17 cm3) (arrows)
with multiple small follicles less than or equal to 8 mm in diameter and
increased stromal (S) echogenicity.
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Turner syndrome. Longitudinal scan of the pelvis in a
Fig. 13.62
14-year-old girl with a 45XO karyotype shows a prepu-
bertal-size uterus (arrowheads) with a tubular shape and no zonal dif-
ferentiation. The ovaries could not be identified.
The other typical sonographic findings of polycystic
ovary disease are an increased number of small developing
follicles and increased stromal echogenicity (see Fig.
13.61). Approximately 40% to 75% of ovaries on trans-
vaginal sonography have five or more follicles, ranging
between 0.5 and 0.8 cm in diameter, in each ovary
(21,147151). By comparison, healthy individuals (control
population) usually have no more than three developing
follicles, less than 8 mm in size, in each ovary (147151).
The combination of increased ovarian volume and
increased number of follicles yields a sensitivity of 92%
and a specificity of 97% for the diagnosis of polycystic
ovary disease (147). The sonographic sign of increased
stromal echogenicity has a sensitivity of 94% and a speci-
ficity of 90% (147).
Multiple ovarian cysts can also be seen in children with
primary hypothyroidism and cystic fibrosis (152,153). In
addition, bilateral ovarian enlargement with multiple cysts
has been seen in McCune-Albright syndrome (fibrous
dysplasia, patchy cutaneous pigmentation, and sexual
precocity).
GONADAL DYSGENESIS
Gonadal dysgenesis, or Turner syndrome, is characterized
by streak ovaries and a 45XO or 45XO/46XX karyotype.
A small percentage of patients with Turner syndrome have
a Y chromosome in their karyotype and are at increased
risk for developing gonadoblastoma. Pathologically, the
gonads are replaced by streaks of connective tissue and
contain no germ cells. Clinically, both classic and mosaic
Turner syndrome result in primary amenorrhea and sexual
infantilism. Characteristic physical findings include short
stature, webbed neck, low posterior hairline, shield chest,
scoliosis, and cubitus valgus deformities. Other anomalies
include renal duplication, horseshoe kidney, aortic coarc-
tation, bicuspid aortic valve, and lymphatic obstruction.
Ovarian size and morphology vary with the kary-
otype. Patients with classic 45XO karyotypes have either
Chapter 13 F E M A L E P E L V I S 549
absent or streak-like ovaries, which are difficult to iden-
tify at sonography. Uterine size and configuration remain
prepubertal with increasing age (Fig. 13.62). Patients
who are chromosomal mosaics (45XO/46XX) have a
spectrum of findings, ranging from streak ovaries and an
infantile uterus to a normal-appearing uterus and gonads
(154,155). Adnexal enlargement or an asymmetric ovar-
ian mass may be noted in patients with Y-bearing dysge-
netic gonads that develop gonadoblastomas.
Rudimentary or dysplastic gonads may also be seen in
Noonan syndrome (normal karyotype with unusual facies,
congenital heart disease, short stature, chest deformity,
mental retardation, and bleeding diathesis), Kallmann syn-
drome (hypogonadism associated with gonadotropin-
releasing hormone deficiency and anosmia), Perrault syn-
drome (deafness and streak ovaries), and mixed gonadal
dysgenesis (see below).
INTERSEX DISORDERS
Intersex disorders are characterized by ambiguous external
genitalia and gonads (156). The clinical findings include
cryptorchidism, labial fusion, clitoromegaly, epispadius,
and hypospadias. The role of sonography is to identify the
presence or absence of the uterus, which is important in
distinguishing among the causes of hermaphrodism and in
assigning gender (15,156,157).
Patients with intersex states can be classified into four
broad groups: female pseudohermaphrodite, male pseudo-
hermaphrodite, true hermaphrodite, and mixed gonadal dys-
genesis (156,157). Female pseudohermaphrodites have a nor-
mal female karyotype (46XX), ovaries, uterus, and vagina,
but the external genitalia are masculinized. Most cases are the
result of exposure to excessive androgens in utero, usually
secondary to congenital adrenal hyperplasia, maternal inges-
tion of androgens, or maternal virilizing tumors (156).
Male pseudohermaphrodites have an XY karyotype; nor-
mal testes, although they may be undescended; and feminized
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550 P E D I AT R I C S O N O G R A P H Y
True hermaphrodite. A newborn infant with ambiguous
Fig. 13.63
external genitalia and a palpable mass in the right
inguinal area. Longitudinal sonogram through the right inguinal area
demonstrates a minimally heterogeneous ovoid structure (arrows),
proven at biopsy to be an ovotestis. M  femoral muscle.
or incompletely virilized, ambiguous genitalia. This disorder
is due to a deficiency of testicular secretions or an absent
response to androgen stimulation by the target organ (i.e.,
androgen insensitivity or testicular feminization syndrome).
Testes may be found in the inguinal canal or abdomen.
True hermaphrodites account for less than 10% of the
intersex states. They have both ovarian and testicular tis-
sue, a 46XX or 46XY karyotype, ambiguous genitalia, a
hypoplastic uterus, and an ovary on one side with a con-
tralateral testis or an ovary opposite an ovotestis. Histolog-
ically, the ovarian tissue is usually normal. The testicular
tissue is primitive, or if normal initially, may develop degen-
erative changes at puberty. The sonographic appearance of
the ovotestis is that of a heterogeneous ovoid mass that
contains small cysts (Fig. 13.63). The cysts represent
unstimulated primordial follicles (158).
Patients with mixed gonadal dysgenesis have a
45XO/46XY karyotype, ambiguous external genitalia, a
testis on one side, and a streak gonad containing ovarian
stroma without oocytes on the opposite side. A uterus,
which can be bicornuate, is sometimes present.
REFERENCES
1. Cohen HL, Bober SE, Bow SN. Imaging the pediatric pelvis: the
normal and abnormal genital tract and simulators of its dis-
eases. Urol Radiol 1992;14:273283.
2. Garel L, Dubois J, Grignon A, et al. US of the pediatric female
pelvis: a clinical perspective. Radiographics 2001;21:13931407.
3. Siegel MJ. Pediatric gynecologic sonography. Radiology 1991;
179:593600.
4. Siegel MJ, Surratt JT. Pediatric gynecologic imaging. Obstet
Gynecol Clin North Am 1992;19:103127.
5. States LJ, Bellah RD. Imaging of the pediatric female pelvis.
Semin Roentgenol 1996;31:312329.
6. Surratt JT, Siegel MJ. Imaging of pediatric ovarian masses.
Radiographics 1991;11:533548.
7. DiSantis DJ, Scatarige JC, Kemp G, et al. A prospective evalu-
ation of transvaginal sonography for detection of ovarian dis-
ease. AJR Am J Roentgenol 1993;161:9194.
8. Bellah RD, Rosenberg HK. Transvaginal ultrasound in a childrens
hospital: is it worthwhile? Pediatr Radiol 1991;21:570574.
9. Mendelson EB, Bohm-Velez M. Transvaginal ultrasonography
of pelvic neoplasms. Radiol Clin North Am 1992;30:703704.
10. Davis PC, ONeill MJ, Yoder IC, et al. Sonohysterographic
findings of endometrial and subendometrial conditions. Radi-
ographics 2002;22:803816.
11. Bega G, Lev-Toaff S, OKane P, et al. Three-dimensional ultra-
sonography in gynecology. J Ultrasound Med 2003;22:12491269.
12. Quillin SP, Siegel MJ. Transabdominal color Doppler ultra-
sonography of the painful adolescent ovary. J Ultrasound Med
1994;13:549555.
13. Pellerito JS, Troiano RN, Quedens-Case C, et al. Common pit-
falls of endovaginal color Doppler flow imaging. Radiographics
1995;15:3747.
14. Goske MJ, Emmens RW, Rabinowitz R. Inguinal ovaries in
children demonstrated by high resolution real-time ultrasound.
Radiology 1984;151:635636.
15. Orsini LF, Salardi S, Pilu G, et al. Pelvic organs in premenarcheal
girls: real-time ultrasonography. Radiology 1984;153:113116.
16. Cohen HL, Shapiro MA, Mandel FS, et al. Normal ovaries in
neonates and infants: a sonographic study of 77 patients 1 day
to 24 months old. AJR Am J Roentgenol 1993;160:583586.
17. Harter LD, Golendziner E, Flores JAM, et al. Ovarian and uter-
ine sonography in healthy girls between 1 and 13 years old: cor-
relation of findings with age and pubertal statues. AJR Am J
Roentgenol 2002;178:15311536.
18. Cohen HL, Eisenberg P, Mandel F, et al. Ovarian cysts are com-
mon in premenarchal girls: a sonographic study of 101 children
212 years old. AJR Am J Roentgenol 1992;159:8991.
19. King LR, Siegel MJ, Solomon AL. The usefulness of ovarian
volume and cysts in female isosexual precocious puberty.
J Ultrasound Med 1993;12:577581.
20. Stanhope R, Adams J, Jacobs HS, et al. Ovarian ultrasound
assessment in normal children, idiopathic precocious puberty,
and during low dose pulsatile gonadotropin releasing hormone
treatment of hypogonadotrophic hypogonadism. Arch Dis
Child 1985;60:116119.
21. Hall DA. Sonographic appearance of the normal ovary, of poly-
cystic ovary disease and of functional ovarian cysts. Sem Ultra-
sound 1983;4:149165.
22. Cohen HL, Tice HM, Mandel FS. Ovarian volumes measured
by US: bigger than we think. Radiology 1990;177:189192.
23. Fleischer AC, Daniell JF, Rodier J, et al. Sonographic monitor-
ing of ovarian follicular development. J Clin Ultrasound
1981;9:275280.
24. OHerlihy C, de Crespigny LC, Lopata A, et al. Preovulatory
follicular size: a comparison of ultrasound and laparoscopic
measurements. Fertil Steril 1980;34:2426.
25. Picker RH, Smith DH, Tucker MH, et al. Ultrasonic signs of
imminent ovulation. J Clin Ultrasound 1983;11:12.
26. Ritchie WGM. Sonographic evaluation of normal and induced
ovulation. Radiology 1986;161:110.
27. Pupols AZ, Wilson SR. Ultrasonographic interpretation of
physiological changes in the female pelvis. J Can Assoc Radiol
1984;35:3439.
28. Wu A, Siegel MJ. Sonography of pelvic masses in children: diag-
nostic predictability. AJR Am J Roentgenol 1987;148:11991202.
29. Brown DL, Dudiak KM, Laing FC. Adnexal masses: US character-
ization and reporting. Radiology 2010;254:342354.
30. Siegel MJ. Pelvis. In: Siegel MJ, ed. Pediatric body CT. 2nd ed.
Philadelphia, PA: Lippincott Williams & Wilkins, 2008:361391.
LWBK505-C13_p509-553.qxd 7/7/10 1:39 PM Page 551 Aptara Inc
31. Siegel MJ. Magnetic resonance imaging of the adolescent female
pelvis. Magn Reson Imaging Clin N Am 2002;10:303324.
32. Nussbaum AR, Sanders RC, Hartman DS, et al. Neonatal ovarian
cysts: sonographic-pathologic correlation. Radiology 1988;168:
817821.
33. Schmahmann S, Haller JO. Neonatal ovarian cysts: pathogenesis,
diagnosis and management. Pediatr Radiol 1997;27:101105.
34. Brandt ML, Luks FI, Filiatrault D, et al. Surgical indications in
antenatally diagnosed ovarian cysts. J Pediatr Surg 1991;26:
276282.
35. Lee H-J, Woo S-K, Kim J-S, et al. Daughter cyst sign; a sono-
graphic finding of ovarian cyst in neonates, infants, and young
children. AJR Am J Roentgenol 2000;174:10131015.
36. Kiechl-Kohlendorfer U, Maurer K, Unsinn KM, et al. Fluid-
debris level in follicular cysts: a pathognomonic sign of ovarian
torsion. Pediatr Radiol 2006;36:421425.
37. Enriquez G, Duran C, Toran N, et al. Conservative versus sur-
gical treatment for complex neonatal ovarian cysts: outcomes
study. AJR Am J Roentgenol 2005;185:501508.
38. Mller-Leisse C, Bick U, Paulussen K, et al. Ovarian cysts in the
fetus and neonate changes in sonographic pattern in the
follow-up and their management. Pediatr Radiol 1992;22:
395400.
39. Kessler A, Nagar H, Graif M, et al. Percutaneous drainage as
the treatment of choice for neonatal ovarian cysts. Pediatr
Radiol 2006;36:954958.
40. Galinier P, Carfagna L, Juricic M, et al. Fetal ovarian cysts man-
agement and ovarian prognosis: a report of 82 cases. J Pediatr
Surg 2008;43:20042009.
41. Fried AN, Kenney CM III, Stigers KB, et al. Benign pelvic masses:
sonographic spectrum. Radiographics 1996;16:321334.
42. Baltarowich OH, Kurtz AB, Pasto ME, et al. The spectrum of
sonographic findings in hemorrhagic ovarian cysts. AJR Am J
Roentgenol 1987;148:901905.
43. Jain KA. Sonographic spectrum of hemorrhagic ovarian cysts.
J Ultrasound Med 2002;21:879886.
44. Granberg S, Crona N, Enk L, et al. Ultrasound-guided puncture
of cystic tumors in the lower pelvis of young women. J Clin
Ultrasound 1989;17:107111.
45. Sutton CL, McKinney CD, Jones JE, et al. Ovarian masses
revisited: radiologic and pathologic correlation. Radiographics
1992;12:853877.
46. Kim JS, Woo SK, Suh SJ, et al. Sonographic diagnosis of parao-
varian cysts: value of detecting a separate ipsilateral ovary. AJR
Am J Roentgenol 1995;164:14411444.
47. Hoffer FA, Kozakewich H, Colodny A, et al. Peritoneal inclu-
sion cysts: ovarian fluid in peritoneal adhesions. Radiology
1988;169:189191.
48. Kim JS, Lee HJ, Woo SK, et al. Peritoneal inclusion cysts and
their relationship to the ovaries: evaluation with sonography.
Radiology 1997;204:481484.
49. Sohaey R, Gardner TL, Woodward PJ, et al. Sonographic diag-
nosis of peritoneal inclusion cysts. J Ultrasound Med 1995;14:
913917.
50. Breen JL, Bonamo FJ, Maxson WS. Genital tract tumors in chil-
dren. Pediatr Clin North Am 1981;28:355367.
51. Lack EE, Youong RH, Scully RE. Pathology of ovarian neoplasms
in childhood and adolescence. Pathol Annu 1992;27:281356.
52. Cushing B, Perlman EJ, Marina NM, et al. Germ cell tumors.
In: Pizzo PA, Poplack DG, eds. Principles and practice of pedi-
atric oncology. 5th ed. Philadelphia, PA: Lippincott Williams &
Wilkins, 2006:11161138.
53. Scully RE, Young RH, Clement PB. Atlas of tumor pathology:
tumors of the ovary, maldeveloped gonads, fallopian tube, and
broad ligament. Washington, DC: Armed Forces Institute of
Pathology, 1998.
54. Sisler CL, Siegel MJ. Ovarian teratomas: a comparison of the
sonographic appearance in prepubertal and postpubertal girls.
AJR Am J Roentgenol 1990;154:139141.
Chapter 13 F E M A L E P E L V I S 551
55. Sheth S, Fishman EK, Buck JL, et al. The variable sonographic
appearances of ovarian teratomas: correlation with CT. AJR
Am J Roentgenol 1988;151:331334.
56. Patel MD, Feldstein VA, Lipson SD, et al. Cystic teratomas of
the ovary: diagnostic value of sonography. AJR Am J
Roentgenol 1998;171:10611065.
57. Kiser JW, Sutton CL, Abbitt PL. Sonographic evaluation of the
adnexal mass. Postgrad Radiol 1993;13:85101.
58. Buy JN, Ghossain MA, Sciot C, et al. Epithelial tumors of the ovary:
CT findings and correlation with US. Radiology 1991;178:811818.
59. Cushing B, Perlman E, Marina NM, et al. Germ cell tumors. In:
Pizzo PA, Poplack DG, eds. Principles and practice of pediatric
oncology. Philadelphia, PA: Lippincott Williams & Wilkins,
2002:10911113.
60. OSullivan SG, Das Narla L, Ferraro E. Primary ovarian
leiomyosarcoma in an adolescent following radiation for
medulloblastoma. Pediatr Radiol 1998;28:468470.
61. Brammer HM, Buck JL, Hayes WS, et al. Malignant germ cell
tumors of the ovary: radiologic-pathologic correlation. Radi-
ographics 1990;10:715724.
62. Kim SH, Kang SB. Ovarian dysgerminoma: color Doppler
ultrasonographic findings and comparison with CT and MR
imaging findings. J Ultrasound Med 1995;14:843848.
63. Levitin A, Haller KD, Cohen HL, et al. Endodermal sinus
tumor of the ovary: imaging evaluation. AJR Am J Roentgenol
1996;167:791793.
64. Yamaoka T, Togashi K, Koyama T, et al. Yolk sac tumor of the
ovary: radiologic-pathologic correlation in four cases. J Com-
put Assist Tomogr 2000;24:605609.
65. Outwater EK, Wagner BJ, Mannion C, et al. Sex cord-stromal
and steroid cell tumors of the ovary. Radiographics 1998;18:
15231546.
66. Jung SE, Rha SE, Lee JM, et al. CT and MRI findings of sex
cord-stromal tumor of the ovary. AJR Am J Roentgenol
2005;185:207215.
67. Neste MG, Francis IR, Bude RO. Hepatic metastases from
granulosa cell tumor of the ovary: CT and sonographic find-
ings. AJR 1996;166:11221124.
68. Laufer I, Barki Y, Mordechai Y, et al. Ovarian fibroma in a pre-
pubertal girl. Pediatr Radiol 1996;26:4042.
69. Athey PA, Malone RS. Sonography of ovarian fibromas/theco-
mas. J Ultrasound Med 1987;6:431436.
70. Chang Y-W, Hong SS, Jeen Y-M, et al. Bilateral sclerosing stro-
mal tumor of the ovary in a premenarcheal girl. Pediatr Radiol
2009;39:731734.
71. Lane DM, Birdwell RL. Ovarian leukemia detected by pelvic
sonography. Cancer 1986;58:23382342.
72. Fleischer AC, Rodgers WH, Kepple DM, et al. Color Doppler
sonography of benign and malignant ovarian masses. Radi-
ographics 1992;12:879885.
73. Fleischer AC, Rodgers WH, Rao BK, et al. Assessment of ovar-
ian tumor vascularity with transvaginal color Doppler sonogra-
phy. J Ultrasound Med 1991;10:563568.
74. Brown DL, Doubilet PM, Miller FH, et al. Benign and malignant
ovarian masses: selection of the most discriminating gray-scale and
Doppler sonographic features. Radiology 1998;208:103110.
75. Brown DL, Frates MC, Laing FC, et al. Ovarian masses: can
benign and malignant lesions be differentiated with color and
pulsed Doppler US? Radiology 1994;190:333336.
76. Buy J-N, Ghossain MA, Hugol D, et al. Characterization of
adnexal masses: combination of color Doppler and conventional
sonography compared with spectral Doppler analysis alone and
conventional sonography alone. AJR Am J Roentgenol 1996;
166:385393.
77. Carter J, Saltzman A, Hartenbach E, et al. Flow characteristics
in benign and malignant gynecologic tumor using transvaginal
color flow Doppler. Obstet Gynecol 1994;83:125130.
78. Hamper UM, Sheth S, Abbas FM, et al. Transvaginal color
Doppler sonography of adnexal masses: differences in blood
LWBK505-C13_p509-553.qxd 7/7/10 1:39 PM Page 552 Aptara Inc
552 P E D I AT R I C S O N O G R A P H Y
flow impedance in benign and malignant lesions. AJR Am J
Roentgenol 1993;160:12251228.
79. Kurjak A, Zalud I, Alfirevic Z. Evaluation of adnexal masses
with transvaginal color ultrasound. J Ultrasound Med 1991;10:
295297.
80. Stein SM, Lafter-Narin S, Johnson MB, et al. Differentiation of
benign and malignant adnexal masses: relative value of gray-
scale, color Doppler and spectral Doppler sonography. AJR Am
J Roentgenol 1995;164:381386.
81. Jain KA. Prospective evaluation of adnexal masses with
endovaginal gray-scale and duplex and color Doppler US: cor-
relation with pathologic findings. Radiology 1994;191:6367.
82. Levine D, Feldstein VA, Babcook CJ, et al. Sonography of ovar-
ian masses: poor sensitivity of resistive index for identifying
malignant lesions. AJR Am J Roentgenol 1994;162:13551359.
83. Horrow MM, Rodgers SK, Naqvi S. Ultrasound of pelvic
inflammatory disease. Ultrasound Clin 2007;2:297309.
84. Shafer MA, Sweet RL. Pelvic inflammatory disease in adoles-
cent females. Epidemiology, pathogenesis, diagnosis, treatment,
and sequelae. Pediatr Clin North Am 1989;36:513532.
85. Patten RM, Vincent IM, Wolner-Hanssen P, et al. Pelvic inflam-
matory disease: endovaginal sonography with laparoscopic cor-
relation. J Ultrasound Med 1990;9:681689.
86. Bulas DI, Ahlstrom PA, Sivit CJ, et al. Pelvic inflammatory dis-
ease in the adolescent: comparison of transabdominal and trans-
vaginal sonographic evaluation. Radiology 1992;183:435439.
87. Dinerman LM, Elfenbein DS, Cumming WA. Clinical Fitz-
Hugh-Curtis syndrome in an adolescent. Ultrasonographic find-
ings. Clin Pediatr 1990;29:532535.
88. Schoenfeld A, Fisch B, Cohen M, et al. Ultrasound findings in
perihepatitis associated with pelvic inflammatory disease. J Clin
Ultrasound 1992;20:339342.
89. Chang HC, Bhatt S, Dogra VS. Pearls and pitfalls in diagnosis
of ovarian torsion. Radiographics 2008;28:13551368.
90. Meyer JS, Harmon CM, Harty MP, et al. Ovarian torsion: clin-
ical and imaging presentation in children. J Pediatr Surg 1995;
30:14331436.
91. Worthington-Kirsch RL, Raptopoulos V, Cohen IT. Sequential
bilateral torsion of normal ovaries in a child. J Ultrasound Med
1986;5:663664.
92. Stark JE, Siegel MJ. Ovarian torsion in prepubertal and puber-
tal girls: sonographic findings. AJR Am J Roentgenol 1994;163:
14791482.
93. Servaes S, Zurakowski D, Laufer MR, et al. Sonographic find-
ings of ovarian torsion in children. Pediatr Radiol 2007;37:
446451.
94. Graif M, Itzhak Y. Sonographic evaluation of ovarian torsion in
childhood and adolescence. AJR Am J Roentgenol 1988;150:
647649.
95. Helvie MA, Silver TM. Ovarian torsion: sonographic evalua-
tion. J Clin Ultrasound 1989;17:327332.
96. Harmon JC, Binkovitz LA, Stephens J. Uterine position in
adnexal torsion: specificity and sensitivity of ipsilateral devia-
tion of the uterus. Pediatr Radiol 2009;39:354358.
97. Fleischer AC, Stein SM, Cullinan JA, et al. Color Doppler
sonography of adnexal torsion. J Ultrasound Med 1995;14:
523528.
98. Lee EJ, Kwon HC, Joo JH, et al. Diagnosis of ovarian torsion
with color Doppler sonography: depiction of twisted vascular
pedicle. J Ultrasound Med 1998;17:8389.
99. Rosado WM Jr, Trambert MA, Gosink BB, et al. Adnexal tor-
sion: diagnosis by using Doppler sonography. AJR Am J
Roentgenol 1992;159:12511253.
100. Vijayaraghavan SB. Sonographic whirlpool sign in ovarian tor-
sion. J Ultrasound Med 2004;23:16431649.
101. Orazi C, Inserra A, Lucchetti MC, et al. Isolated tubal torsion:
a rare cause of pelvic pain at menarche. Sonographic and MR
findings. Pediatr Radiol 2006;36:13161318.
102. Hall BP, Printz DA, Roth J. Massive ovarian edema: ultrasound
and MR characteristics. J Comput Assist Tomogr 1993;17:
477479.
103. Hill LM, Pelekanos M, Kanbour A. Massive edema of an ovary
previously fixed to the pelvic side wall. J Ultrasound Med
1993;12:629632.
104. Heiss KF, Zwiren GT, Winn K. Massive ovarian edema in the
pediatric patient: a rare solid tumor. J Pediatr Surg 1994;29:
13921394.
105. Lee AR, Kim KH, Lee BH, et al. Massive edema of the ovary:
imaging findings. AJR Am J Roentgenol 1993;161:343344.
106. Nussbaum AR, Sanders RC, Jones MD. Neonatal uterine mor-
phology as seen on real-time US. Radiology 1986;160:
641643.
107. Salardi S, Orsini LF, Cacciari E, et al. Pelvic ultrasonography in
premenarcheal girls: relation to puberty and sex hormone con-
centrations. Arch Dis Child 1985;60:120125.
108. Baltarowich OH. Female pelvic organ measurements. In: Gold-
berg BB, Kurtz AB, eds. Atlas of ultrasound measurements.
Chicago, IL: Year Book Medical Publishers, 1990:190242.
109. Fleischer AC, Kalemeris GC, Entman SS. Sonographic depiction
of the endometrium during normal cycles. Ultrasound Med Biol
1986;12:271277.
110. Mitchell DG, Schonholz L, Hilpert PL, et al. Zones of the
uterus: discrepancy between US and MR images. Radiology
1989;174:827831.
111. Forrest TS, Elyaderani MK, Milenburg MI, et al. Cyclic
endometrial changes: US assessment with histologic correlation.
Radiology 1988;167:233237.
112. Schiller VL, Grant EG. Doppler ultrasonography of the pelvis.
Radiol Clin North Am 1992;30:735742.
113. Junqueira BL, Allen LM, Spitzer RF, et al. Mllerian duct
anomalies and mimics in children and adolescents: correlative
intraoperative assessment with clinical imaging. Radiographics
2009;29:10851103.
114. Troilano RN, McCarthy SM. Mllerian duct anomalies: imag-
ing and clinical issues. Radiology 2004;233:1934.
115. American Fertility Society classification of adnexal adhesions,
distal tubal occlusion, tubal occlusion secondary to tubal liga-
tion, tubal pregnancies, mllerian anomalies, and intrauterine
adhesions. Fertil Steril 1988;49:944955.
116. Golan A, Langer R, Bukovsky I, et al. Congenital anomalies of
the mllerian system. Fertil Steril 1989;51:747755.
117. Fielding JR. MR imaging of mllerian anomalies: impact on
therapy. AJR Am J Roentgenol 1996;167:14911495.
118. Kiechl-Kohlendorfer U, Geley TE, Unsinn KM, et al. Diagnos-
ing neonatal female genital anomalies using saline enhance
sonography. AJR Am J Roentgenol 2001;177:141144.
119. Rosenberg HK, Sherman NH, Tarry WF, et al. Mayer-Rokitansky-
Kuster-Hauser syndrome: US aid to diagnosis. Radiology 1986;
161:815819.
120. Carranza-Lira S, Forbin K, Martinez-Chquer JC. Rokitansky
syndrome and MURCS associationclinical features and basis
for diagnosis. Int J Fertil Womens Med 1999;44:250255.
121. Brody JM, Koelliker SL, Frishman GN. Unicornuate uterus:
imaging appearance, associated anomalies, and clinical implica-
tions. AJR Am J Roentgenol 1998;171:13411347.
122. Reuter KL, Daly DC, Cohen SM. Septate versus bicornuate uteri:
errors in imaging diagnosis. Radiology 1989;172:749752.
123. Blask ARN, Sanders RC, Gearhart JP. Obstructed uterovaginal
anomalies: demonstration with sonography. Part I neonates and
infants. Radiology 1991;179:7983.
124. Blask ARN, Sanders RC, Rock JA. Obstructed uterovaginal
anomalies: demonstration with sonography. Part II teenagers.
Radiology 1991;179:8488.
125. Khatwa UA, Rajegowda B, Rosenberg HK, et al. McKusick-
Kaufman syndrome presenting prenatally as fetal abdominal
mass. J Perinatol 2005;25:146149.
LWBK505-C13_p509-553.qxd 7/7/10 1:39 PM Page 553 Aptara Inc
126. Graham D, Nelson MW. Combined perineal-abdominal sonogra-
phy in the evaluation of vaginal atresia. J Clin Ultrasound 1986;
14:735738.
127. Scanlan KA, Pozniak MA, Fagerholm M, et al. Value of
transperineal sonography in the assessment of vaginal atresia.
AJR Am J Roentgenol 1990;154:545548.
128. Hu MX, Methratta S. An unusual case of neonatal peritoneal
calcifications associated with hydrometrocolpos. Pediatr Radiol
2001;31:742744.
129. Kilicoglu G, Aslan AR, Ozturk M., et al. Vesicovaginal reflux:
recognition and diagnosis using ultrasound. Pediatr Radiol 2010;
40:114117.
130. Chopra S, Lev-Toaff AS, Ors F, et al. Adenomyosis: common
and uncommon manifestations in sonography and magnetic
resonance imaging. J Ultrasound Med 2006;25:617627.
131. Ho M-L, Raptis C, Hulett R, et al. Adenomyotic cyst of the
uterus in an adolescent. Pediatr Radiol 2008;38:12391242.
132. Karasick S, Lev-Toaff AS, Toaff ME. Imaging of uterine leiomy-
omas. AJR Am J Roentgenol 1992;158:799805.
133. Moon LD, Brenner C, Ancliff P, et al. Non-Hodgkin lymphoma
presenting with uterine and renal enlargement in a young girl.
Pediatr Radiol 2004;34:277279.
134. Green CL, Angtuaco TL, Shah HR, et al. Gestational tro-
phoblastic disease: a spectrum of radiologic diagnosis. Radi-
ographics 1996;16:13711384.
135. Jauniaux E. Diagnosis and follow-up of gestational trophoblas-
tic disorders. In: Callen PW, ed. Ultrasonography in obstetrics
and gynecology. 4th ed. Philadelphia, PA: W.B. Saunders, Co,
2000:847856.
136. Wagner BJ, Woodward PJ, Dickey GE. Gestational trophoblas-
tic disease: radiologic-pathologic correlation. Radiographics
1996;16:131148.
137. Carter J, Fowler J, Carlson J, et al. Transvaginal color flow
Doppler sonography in the assessment of gestational tro-
phoblastic disease. J Ultrasound Med 1993;12:595599.
138. Argons GA, Wagner BJ, Lonergan GJ, et al. Genitourinary
rhabdomyosarcoma in children: radiologic-pathologic correla-
tion. Radiographics 1997;17:919937.
139. Tannous WN, Azouz EM, Homsy YL, et al. CT and ultrasound
imaging of pelvic rhabdomyosarcoma in children. A review of
56 patients. Pediatr Radiol 1989;19:530534.
140. Wexler LH, Meyer WH, Helman LJ. Rhabdomyosarcoma and
the undifferentiated sarcomas. In: Pizzo PA, Poplack DG, eds.
Principles and practice of pediatric oncology. Philadelphia, PA:
Lippincott Williams & Wilkins, 2006:9711001.
141. Pappo AS, Furman WL. Management of infrequent cancers
of childhood. In: Pizzo PA, Poplack DG, eds. Principles and
Chapter 13 F E M A L E P E L V I S 553
practice of pediatric oncology. Philadelphia, PA: Lippincott
Williams & Wilkins, 2006:11721201.
142. Breysem L, Rayyan M, Bogaert G, et al. High-resolution per-
ineal ultrasound of a paraurethral cyst in a neonate. Eur Radiol
2008;18:27012703.
143. Lee PA, Kulin HE. Normal pubertal development. In: Pediatric
endocrinology: The requisites. St. Louis, MO: Elsevier Mosby,
2005:6371.
144. Lee PA. Early pubertal development. In: Pediatric endocrinol-
ogy: The requisites. St. Louis, MO: Elsevier Mosby, 2005:
7386.
145. Blask ARN, Nicholson HS, Markle BM, et al. Sonographic
detection of uterine and ovarian abnormalities in female sur-
vivors of Wilms tumor treated with radiotherapy. AJR Am J
Roentgenol 1999;172:759763.
146. Franks S. Polycystic ovary syndrome. New Engl Med 1995;333:
853861.
147. Hann LE, Hall DA, McArdle CR, et al. Polycystic ovarian dis-
ease: sonographic spectrum. Radiology 1984;150:531534.
148. Orsini LF, Venturoli S, Lorusso R, et al. Ultrasonic findings in
polycystic ovarian disease. Fertil Steril 1985;43:709714.
149. Pache TD, Wladimiroff JW, Hop WCJ, et al. How to discrimi-
nate between normal and polycystic ovaries: transvaginal US
study. Radiology 1992;183:421423.
150. Parisi L, Tramonti M, Derchi LE, et al. Polycystic ovarian dis-
ease: ultrasonic evaluation and correlations with clinical and
hormonal data. J Clin Ultrasound 1984;12:2126.
151. Yeh H-C, Futterweit W, Thornton JC. Polycystic ovarian dis-
ease: US features in 104 patients. Radiology 1987;163:
111116.
152. Lindsay AN, Voorhess ML, MacGillivray MH. Multicystic ovaries
in primary hypothyroidism. Obstet Gynecol 1983;61:433437.
153. Shawker TH, Hubbard VS, Reichert CM, et al. Cystic ovaries
in cystic fibrosis: an ultrasound and autopsy study. J Ultrasound
Med 1983;2:439444.
154. Massarano AA, Adams JA, Preece MA, et al. Ovarian ultrasound
appearances in Turner syndrome. J Pediatr 1989;114:568573.
155. Shawker TH, Garra BS, Loriaux DL, et al. Ultrasonography of
Turners syndrome. J Ultrasound Med 1986;5:25129.
156. Chavhan GB, Parra DA, Oudjhane K, et al. Imaging of ambigu-
ous genitalia: classification and diagnostic approach. Radi-
ographics 2008;28:18911904.
157. Horowitz M, Glassberg KI. Ambiguous genitalia: diagnosis,
evaluation, and treatment. Urol Radiol 1992;14:306318.
158. Eberenz W, Rosenberg HK, Moshang T, et al. True hermaphro-
ditism: sonographic demonstration of ovotestes. Radiology
1991;179:429431.
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CHAPTER

14 Male Genital Tract

BRIAN D. COLEY AND MARILYN J. SIEGEL

Techniques Cystic Scrotal Masses Trauma

Spermatoceles and Epididymal Blunt Trauma
Normal Scrotal Anatomy
Cysts Miscellaneous Trauma
Vascular Anatomy
Testicular Cysts
Testicular Appendages Fluid Collections
Lymphatic Malformations
Testicular Size Hydrocele
Sonographic Anatomy The Acute Scrotum Hematocele
Lymphocele
Congenital Anomalies Torsion/Infarction
Testicular Agenesis Intravaginal Torsion Varicocele
Polyorchidism Extravaginal Torsion
Inguinal Hernia
Testicular Ectopia Torsion of Testicular Appendages
Testicular Size Asymmetry Scrotal Calcifications
Inflammatory Disease
Cystic Dysplasia of the Testes Extratesticular Calcifications
Acute Epididymitis/Orchitis
Cryptorchidism Meconium Periorchitis
Chronic Epididymitis/Orchitis
Microlithiasis
Testicular Tumors Primary Orchitis
Primary Testicular Germ Cell Neoplasms Fournier Gangrene Prostate and Seminal Vesicles
Testicular Stromal Tumors Scrotal Abscess Congenital Anomalies
Miscellaneous Testicular Masses Rhabdomyosarcoma
Edema and Vasculitis
Secondary Testicular Neoplasms Urethra and Penis
Idiopathic Scrotal Edema
Paratesticular Tumors Henoch-Schnlein Purpura
Malignant Lesions (Acute Vasculitis)
Benign Lesions

ray-scale sonography is recognized as the primary imag- be examined, so that differences in the size and echogenicity

G ing method for evaluating morphologic abnormalities

of the scrotum, particularly the location and nature of
scrotal masses and fluid collections (18). The addition and
refinement of color Doppler and power Doppler sonography
has allowed for evaluation of both morphology and perfu-
sion, enabling more accurate diagnosis of testicular torsion,
inflammatory disease of the testis, tumor, trauma, and vas-
cular lesions (2,3,5,815). This chapter will review the use of
gray-scale and Doppler sonography in diagnosing a variety
of scrotal abnormalities.
TECHNIQUES
Scrotal sonography is performed with the patient in the
supine position and the scrotum gently elevated and sup-
ported by towels placed between the thighs. A high-
frequency linear array transducer, operating at or above
7.5 MHz, is used to maximize resolution of the scrotal con-
tents. Abundant warm coupling gel is applied to the surface
of the scrotum to ensure adequate contact between the
transducer and the scrotum and to allow pressure on the
scrotum to be kept to a minimum to avoid unnecessary pain.
The scrotum and its contents are scanned in both transverse
and longitudinal planes; coronal scanning can also be help-
ful. Even if symptoms are unilateral, both hemiscrota should
554
of the intrascrotal contents can be recognized.
Color Doppler imaging provides information about tes-
ticular and scrotal perfusion. Several adjustments in the
color Doppler parameters need to be made to detect low-
volume and low-velocity flow in the small testicular vessels.
Color gain settings should be maximized until background
noise becomes barely visible. Pulse repetition frequency and
wall filters should be adjusted to the lowest settings. In very
small testes, power output may need to be increased in
order to detect flow. Color flow in the two hemiscrota
should be compared for symmetry. A transverse image of
both testes with both gray-scale and color Doppler should
be performed to facilitate direct comparison of testicular
echogenicity and perfusion. This may require using a large-
face linear transducer with a trapezoidal field of view or
even a curved linear array transducer in order to visualize
both testes simultaneously. The addition of pulsed Doppler
imaging allows quantitative evaluation of the arterial wave-
forms and measurements of velocity.
NORMAL SCROTAL ANATOMY
The layers of tissue covering the testis, starting from the
superficial layer, are the scrotal skin, dartos muscle, external
spermatic fascia, cremasteric fascia and muscle, internal
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Spermatic cord
Testicular artery
Deferential
artery
Pampiniform
plexus
Ductus deferens
Body of epididymis
Normal anatomy of the scrotum.
Fig. 14.1 Tail of epididymis
See text for details. (Adapted
from Krone KD, Carroll BA. Scrotal ultra-
sound. Radiol Clin North Am 1985;23:121139,
with permission.)
spermatic fascia, and tunica vaginalis. The average thickness
of the scrotal wall in older children measures between 3 and
6 mm. The testes lie in the scrotum with their long axis
upright and tilted forward and slightly lateral. As it
descends into the scrotal sac first, the left testis usually lies
slightly lower than the right.
The testis and epididymis are covered by the tunica
vaginalis, which surrounds the entire testis, except for a
small area posteriorly (Fig. 14.1). The tunica consists of an
outer parietal and inner visceral layer, separated by 1 to 3 mL
of fluid (16). The parietal layer of the tunica vaginalis lines
the wall of the scrotum and attaches to the fascial covering
of the testis. The visceral layer of the tunica vaginalis covers
the fibrous capsule of the testis (called the tunica albu-
ginea), the epididymis, and the lower portion of the sper-
matic cord (17). The tunica albuginea gives rise to numerous
small septa, which converge posteriorly and invaginate
into the testis to form a vertical septum of fibrous tissue,
called the mediastinum testis (17). The mediastinum
testis provides support for the veins, arteries, and ducts as
they enter and exit the testis.
Each testis is composed of approximately 250 to 400
lobules (3,5,18). The lobules are separated from each other
by thin fibrous septa. One to four seminiferous tubules are
present within each lobule. These tubules course centrally
and converge to form larger straight ducts, termed tubuli
recti. The tubuli recti enter the mediastinum testis, where
they form a network of channels known as the rete
testis. The rete testis drains into 10 to 15 efferent duc-
Chapter 14 M A L E G E N I TA L T R A C T 555
Tunica vaginalis
Head of epididymis
Efferent ductule
Tunica albuginea
Septa of tunica
albuginea
Seminiferous
tubules
Mediastinum
tules, which in turn drain into the head of the epididymis
(3,5,18).
The epididymis is a curved tubular structure along the
posterolateral aspect of the testis. It is composed of a head,
body, and tail. The head, also known as the globus major,
is the largest portion of the epididymis and is located over
the superior pole of the testis. It continues into the epi-
didymal body, and then tapers into the epididymal tail, or
globus minor, which lies along the inferior aspect of the
testis. The efferent ductules in the epididymal head con-
verge into a single duct in the region of the body and tail.
This duct continues as the vas deferens in the spermatic
cord (3,17,18).
Vascular Anatomy
The spermatic cord contains various arteries, the pampini-
form plexus of veins, nerves, and lymphatics, as well as
the vas deferens. The testicular (internal spermatic) artery,
which provides the main blood supply for the testis, is a
branch of the abdominal aorta and enters the spermatic
cord at the deep (or internal) inguinal ring. It courses
along the posterior surface of the testis, where it pene-
trates the tunica albuginea to form capsular arteries,
which run just beneath the tunica albuginea (Fig. 14.2)
(3,5,17). The capsular arteries give rise to centripetal
arteries, which enter the testis and course toward the
mediastinum. As they approach the mediastinum, the
centripetal arteries give rise to recurrent branches that run
back away from the mediastinum. Occasionally, a
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556 P E D I AT R I C S O N O G R A P H Y
Testicular a.
Cremasteric a.
Centripetal a.
Deferential a.
Capsular a.
Normal intrascrotal arterial anatomy. The testicular artery
Fig. 14.2
gives rise to the capsular arteries, which are located
beneath the tunica albuginea. The capsular arteries, in turn, give rise
to centripetal arteries, which course through the testis to the medi-
astinum. The cremasteric and deferential arteries supply the epi-
didymis and peritesticular tissues. (Adapted from Patriquin HB.
Leukemic infiltration of the testis. In: Siegel BA, Proto AV, eds. Pedi-
atric disease (fourth series) text and syllabus. Reston, VA: American
College of Radiology, 1993:667688, with permission.)
centripetal artery gives rise to a branch that enters the
mediastinum and flows to the opposite side to supply cap-
sular arteries. These branches are called transtesticular or
transmediastinal arteries.
The deferential artery (which arises from the vesicu-
lar artery) and the cremasteric artery (which arises from
the inferior epigastric artery) accompany the testicular
artery in the spermatic cord. They provide the arterial
supply to the epididymis, vas deferens, and peritesticular
tissues. The deferential and cremasteric arteries converge
with the testicular artery at the mediastinum testis.
Although there are anastomoses between three arteries,
the testicular artery is responsible for most of the blood
supply to the testis. Branches of the pudendal artery sup-
ply the scrotum itself (5).
The pampiniform plexus, the draining veins of the
testis, empties into the testicular (internal spermatic)
veins. The right testicular vein empties into the inferior
vena cava and the left testicular vein drains into the left
renal vein.
Testicular Appendages
There are three major testicular appendages: (a) the appen-
dix testis, a remnant of the mllerian duct, attached to the
upper pole of the testis; (b) the appendix epididymis, a
remnant of the mesonephron, found on the head of the epi-
Appendix
epididymis
Appendix Appendix
testis vas
Testicular appendages: appendix testis, appendix epi-
Fig. 14.3
didymis, and appendix vas (vas aberrans of Haller).
(Adapted from Leape LL. Torsion of the testis. In: Welch RJ, Ravitch
MM, ONeill JA Jr, eds. Pediatric surgery. Chicago: Year Book,
1986:13301334, with permission.)
didymis; and (c) the vas aberrans, a mesonephric remnant,
located at the junction of the body and tail of the epi-
didymis (Fig. 14.3) (2,5,18).
Testicular Size
The neonatal testis measures 1.5 cm in length and 1.0 cm
in width. During the first 3 months of life, testicular length
increases up to 2.0 cm and width to 1.2 cm due to a nor-
mal increase in testosterone levels (19). The testes then
maintain a relatively constant size until the patient is about
6 years of age (20), when they again enlarge. The postpu-
bescent testes measure 3 to 5 cm in length and 2 to 3 cm in
both anteroposterior diameter and width (16). Testicular
volume ranges from less than 1.0 cm3 in neonates to 30 cm3
in postpubertal adolescents. The testis is considered puber-
tal when testicular volume reaches 4 cm3 (5,16).
Sonographic Anatomy
GRAY-SCALE ANATOMY
On gray-scale sonography, the normal infant testis is
ovoid and has a uniform low to medium level of
echogenicity. Testicular echogenicity increases from age 8
years until puberty, at which time the testis appears as a
homogeneous ovoid structure of medium echogenicity.
The change in sonographic appearance correlates with the
histologic development of germ cell elements and tubular
maturation. In older children and adolescents, the medi-
astinum testis is seen as a linear echogenic structure along
the superior-inferior axis of the testis (Fig. 14.4). The
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Chapter 14 M A L E G E N I TA L T R A C T 557

A B
Normal testes. Longitudinal (A) and transverse (B) scans of the left hemiscrotum of a 15-year-old boy show a homogeneous testis with
Fig. 14.4
medium-level echotexture and ovoid shape. Note also the echogenic mediastinum testis (arrows) and fibrous interlobular septa (arrow-
heads) radiating to the mediastinum.

tunica albuginea is seen as a smooth, uninterrupted, thin DOPPLER IMAGING

echogenic line around the testis. Occasionally, a hypoe-
choic linear band can be noted in the normal testis, usually
in the middle third, corresponding to sites of intratesticular
vessels (Fig. 14.5).
The epididymal head is best seen by scanning longitu-
dinally through the superior pole of the testis (21). It is tri-
angular in shape and has an echogenicity similar to that of
the testis (Fig. 14.6). The epididymal body and tail have an
echogenicity equal to or slightly less than that of the testis
(21). The epididymal tail may be difficult to visualize, espe-
cially in younger patients. Occasionally, in the presence of
a hydrocele, the tail can be identified sonographically as a
separate structure.
Identification of intratesticular arteries is related to the veloc-
ity and volume of blood flow and the size of the arteries,
which are dependent on patient age, and the sensitivity of
the equipment to low flow. Improvements in color Doppler
imaging and the addition of power Doppler imaging have
greatly improved vessel detection (Fig. 14.7). Flow is
detectable in 60% to 83% of prepubertal testes less than 1
cm3 in volume with color Doppler imaging, and in 73% to
92% with power Doppler imaging (22,23). Flow within
intratesticular arteries is seen in virtually all testes with vol-
umes greater than 1 cm3 using color and power Doppler
sonography (22,24,25).

A B
Hypoechoic vascular band. Longitudinal gray-scale (A) and color Doppler (B) images of the left testis of a 15-year-old boy show a
Fig. 14.5
hypoechoic linear band (arrows) that demonstrates flow on color Doppler imaging.
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558 P E D I AT R I C S O N O G R A P H Y

Normal epididymis. Longitudinal scan of left hemiscrotum Normal intratesticular vascular anatomy. Longitudinal
Fig. 14.6 Fig. 14.7
reveals a triangular epididymis (E) that is isoechoic to the image of the right testis of a postpubertal patient shows
testis (T). capsular arteries (arrows) and multiple centripetal arteries, which
course toward the mediastinum.

The periphery of the testis contains both capsular
branches of the testicular artery and branches of the cre-
masteric and deferential arteries, so that patency of the tes-
ticular artery is only reliably established by placing the
Doppler sample volume in the center of the testis. The nor-
mal intratesticular arterial waveform depends on the puber-
tal state of the patient. Postpubertal testes show a low-resist-
ance pattern with high levels of diastolic flow throughout
the cardiac cycle, whereas prepubertal testes show higher
resis-tance and often have little to no demonstrable diastolic
flow (Fig. 14.8) (5,26). Maturational changes in the resistive
index (RI) also occur, with the RI in intratesticular arteries
decreasing in puberty, reflecting increased testicular blood
flow (26). In pubertal males, the RI of the intratesticular
arteries ranges from 0.48 to 0.75 (mean 0.62) and the RI of
the capsular arteries ranges from 0.46 to 0.78 (mean 0.66).

A B
Normal intratesticular Doppler waveforms. A: Image from a postpubertal boy. B: Image from a prepubertal boy. The testis of the post-
Fig. 14.8
pubertal boy shows higher-velocity peak systolic and diastolic flow compared to the testis of the prepubertal patient.
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Chapter 14 M A L E G E N I TA L T R A C T 559

Flow to the peritesticular tissues has a high-resistance

waveform with low diastolic flow. The RI of the suprates-
ticular arteries varies between 0.63 and 1.00 (mean 0.84)
(27).
Color Doppler signal in both testes should be com-
pared for asymmetry, which can aid in the detection of dis-
ease. Absence of flow in an asymptomatic testis most likely
reflects insensitivity of the ultrasound equipment for
detecting low flow or faulty technical settings (e.g., low
gain, high wall filter, high pulse repetition frequency, or
low transducer frequency), rather than true disease.

CONGENITAL ANOMALIES
Testicular Agenesis
Bilateral testicular absence or anorchidism occurs in 1 in
20,000 male newborns. Unilateral testicular absence or
monorchidism occurs in 1 in 5000 boys and is usually left
sided (28). Monorchid testes are associated with blind-
ending spermatic vessels and spermatic cords (Fig. 14.9),
suggesting that in utero torsion or a vascular accident is
the cause of the anomaly. True testicular agenesis is asso-
ciated with abnormal development of the external geni-
talia. By comparison, when there is in utero development
and then in utero atrophy of the testis, the external geni-
talia are normal (29).
Polyorchidism
Polyorchidism or testicular duplication is an unusual
anomaly caused by abnormal division or duplication of the
genital ridge, resulting in multiple testes on one side of the
scrotum. Most cases manifest as triorchidism and are more
commonly left sided (4,29,30). The ipsilateral testes usu-
ally share a common epididymis, vas deferens, and tunica
albuginea, although each testis may have a separate epi-
didymis and vas deferens (30). Polyorchidism is usually an
incidental finding, presenting as an asymptomatic scrotal
In utero testicular torsion. Longitudinal sonogram of the
Fig. 14.9
left groin in a newborn with a solitary right testis shows a
blind-ending left spermatic cord (arrowheads) with no identifiable
testicular tissue.
mass, but it may present with pain due to torsion of one of
the duplicated testes, which occurs in up to 15% of cases
(30). The supernumerary testis may have impaired sper-
matogenesis, may fail to descend normally, and may be
associated with an inguinal hernia (30). Polyorchid testes
have an increased risk of malignancy, up to 6%, necessi-
tating at least clinical follow-up (30,31).
Sonographically, the polyorchid testis has homogenous
medium-level echoes, and is often smaller than the normal
contralateral testis. Other than size, duplicated testes have
sonographic features similar to that of the normal testis
(Fig. 14.10). Sonographic mimics of polyorchidism include
testicular lobulation (Fig. 14.11), splenogonadal fusion,
congenital epididymal separation, and other paratesticular
masses (30,32,33).

Polyorchidism. Longitudinal sonogram of a 14-year-old boy with painless swelling shows two normal testes within the left hemiscro-
Fig. 14.10
tum. There was a normal testis present in the right hemiscrotum.
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560 P E D I AT R I C S O N O G R A P H Y
Lobulated testis. Transverse sonogram of an 11-year-old
Fig. 14.11
boy with a left scrotal mass shows a cleft (arrow) in the
midportion of the left testis.
Testicular Ectopia
Testicular ectopia is an anomaly due to an error in testic-
ular descent (34). Both testes are usually located in the
same hemiscrotum, but the crossed testis may be intra-
B right testis (arrow) compared with the normal left testis (T).
abdominal. Approximately 50% of patients have an asso-
ciated inguinal hernia, 30% have persistent mllerian
duct syndrome (presence of a uterus and sometimes other
Mllerian duct derivatives in a male), and 20% have
hypospadias, seminal vesical cyst, or renal abnormalities
(34). Clinically, most patients present before 2 years of age
with a nonpalpable testis and a contralateral scrotal mass,
often with a coexisting hernia (34,35).
Other than location, crossed ectopic testes have sono-
graphic features similar to those of the normal testis.
Because most ectopic testes lie within the scrotal sac,
sonography is sensitive for detection of this anomaly.
Sonography, however, is not as useful to detect the intra-
abdominal crossed ectopic testis.
Testicular Size Asymmetry
Congenital testicular hypoplasia is associated with Klinefel-
ter syndrome and abnormalities involving the hypothalamic-
pituitary-testicular axis (36). Acquired causes of a small
testis, including cryptorchidism, torsion, inflammation,
varicocele, previous inguinal hernia repair, trauma, and radi-
ation therapy, can mimic hypoplasia, but correlation with
clinical history usually allows a specific diagnosis. The testic-
ular echogenicity can be normal, increased, or decreased.
Testicular size asymmetry may also be seen as a normal and
transient finding in peripubertal patients (Fig. 14.12).
Testicular size asymmetry. A: Transverse sonogram
Fig. 14.12
in an asymptomatic 14-year-old boy shows a smaller
and slightly hypoechoic left testis that was one-third the volume of
the normal right testis. B: Transverse sonogram in a 19-year-old
man after right orchiopexy years earlier shows a small hypoechoic
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Chapter 14 M A L E G E N I TA L T R A C T 561

A B

Fig. 14.13 Cystic dysplasia. Longitudinal (A) and transverse (B) sonograms of the left hemiscrotum show multiple cysts in the testis.

Cystic Dysplasia of the Testes weighing less than 2500 grams, and in up to 5.8% of term
infants (2,42,43). Testicular descent continues in the post-
Cystic dysplasia of the testes is a rare condition character-
natal period, so that at the end of the first year of life, only
ized by cystic dilatation of the rete testis and efferent ducts
0.7% to 0.8% of infants have true cryptorchidism. Ml-
and parenchymal atrophy (37,38). Patients typically pres-
lerian inhibiting substance probably mediates abdominal
ent with painless scrotal enlargement. Unlike the similar-
migration of the testis, whereas migration through the
appearing tubular ectasia of the rete testis in adults, which
inguinal canal is mediated by androgens and local neu-
results from obstructive processes (3), cystic dysplasia of
ropeptides (44). The precise role of the gubernaculum in
the testis is thought to be a failure of fusion of the efferent
testicular descent is unclear, as descent can occur even in its
ducts (arising from the mesonephros) and rete testis (aris-
absence. Cryptorchidism or incomplete testicular descent is
ing from the gonadal blastema) (37,38). Ipsilateral renal
believed to be the result of a disturbance of local factors or
agenesis, multicystic dysplastic kidney, and renal dysplasia
of an abnormality of the hypothalamic-pituitary-testicular
are common associated findings.
axis.
At sonography, the dysplastic testis contains multiple
Testicular migration can be arrested anywhere along
small cysts located in the region of the mediastinum
the course of descent from the retroperitoneum into the
testis. These cysts may compress the surrounding testic-
scrotum. Approximately 80% to 90% of undescended
ular parenchyma, resulting in pressure atrophy of the
testes are located in the inguinal canal or just proximal to
parenchyma (Fig. 14.13) (39). The sonographic findings
the internal inguinal ring, and 10% to 20% are located in
are usually characteristic, although the appearance can
the abdomen (2,45). Rarely, the testis is found in the per-
occasionally mimic a cystic neoplasm (such as teratoma)
ineum or at the base of the penis. Bilateral cryptorchidism
or testicular microlithiasis (40). In addition, if the cysts
occurs in 10% to 30% of patients, and associated urologic
are not fluid filled and instead contain mucoid material
abnormalities are found in 20% of affected boys (45,46).
or debris, they can mimic a solid mass. In these cases,
For the 20% of undescended testes that are not palpable
the associated renal anomalies can help to establish the
on physical examination (45), ultrasonography may be
diagnosis of cystic dysplasia, thus allowing tissue-spar-
valuable for diagnosis, particularly in obese children,
ing surgery or observation rather than an orchiectomy
where palpation may be difficult (47). However, it can
(38).
have limited sensitivity in very obese patients and in detec-
tion of intra-abdominal testes.
Cryptorchidism The diagnosis of an undescended testis is important
Testicular descent occurs between 25 weeks and 32 weeks because of the increased risks of infertility and malignancy
gestation in 97% of fetuses (41). At birth, undescended (48). Orchiopexy is the treatment of choice, although the
testes are found in up to 30% of premature male infants increased risk of malignancy and fertility problems persists
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562 P E D I AT R I C S O N O G R A P H Y
even after successful surgery, perhaps because of underly-
ing testicular injury or dysplasia (49,50). The optimal tim-
ing of surgery is still debated, but there is a trend toward
earlier operation between the ages of 6 and 12 months
(51,52).
Preoperative localization of a nonpalpable, unde-
scended testis by radiologic examination is helpful in
directing the surgical approach (45) and shortening anes-
thesia time. The sensitivity of sonography for detecting
an undescended testis is 54% to 88%, but is highly
dependent on location; the specificity is nearly 100%
(45). Because most undescended testes lie within the
inguinal canal, sonography is the examination of choice
to detect a nonpalpable testis, where the sensitivity for
detection is at least 95% (43,45). Sonography, however,
is not as useful to detect the undescended testis located
higher in the pelvis or in the abdomen, and a negative
ultrasound does not exclude the presence of an intra-
abdominal testis (43,45). When the sonogram is equivo-
cal or negative, further evaluation of a suspected intra-
abdominal testis can be performed with magnetic
resonance imaging (MRI) or laparoscopic evaluation
(47,52).
Sonographically, the cryptorchid testis appears as an
elliptical mass with uniform medium-level echoes anywhere
along the path of testicular descent (Fig. 14.14). Atrophy of
the undescended testis is common, and at sonography the
testis is smaller and more hypoechoic than the contralateral
normally located testis (2,18). A small testis can mimic
inguinal lymph nodes or the pars infravaginalis of the
gubernaculum testis. The gubernaculum testis is a cord-like
structure that connects the testis to the scrotum during fetal
development. It generally atrophies when testicular descent
is complete. If testicular descent is incomplete, the guber-
naculum remains as a fibrotic remnant, which can appear
ovoid or round in shape and hypo- or isoechoic to sur-
rounding tissues. Differentiation from a cryptorchid testis is
Cryptorchidism. Longitudinal scan of the right inguinal
Fig. 14.14
canal above the symphysis pubis demonstrates an
incompletely descended testis (arrowheads). The testis has a normal
shape and echotexture.
facilitated if a mediastinum testis can be identified. Even
after surgical repair, cryptorchid testes tend to remain
smaller and more hypoechoic than normal testes (49,50).
Following orchiopexy, the testis may have a lobulated con-
tour (53), and small calcifications may be seen at the suture
site affixing the tunica albuginea to the scrotal wall.
TESTICULAR TUMORS
The role of sonography in the evaluation of scrotal masses
is to confirm the presence of a lesion, determine its site of
origin, and characterize its contents. The sensitivity of
sonography in detecting testicular tumors is nearly 100%
(2,5,54), while the accuracy in distinguishing between
intra- and extratesticular masses is 90% to 100% (5,54).
This distinction is important because most solid intrates-
ticular lesions are malignant, whereas half of extratesticu-
lar lesions are benign (8,55). The negative predictive value
of a normal sonogram in excluding a testicular mass is
almost 100% (56). Sonography also can aid in character-
izing soft tissue masses as cystic or solid, with an accuracy
of 90% to 100%. However, the final diagnosis of whether
a mass is benign or malignant often ultimately requires tis-
sue sampling.
Primary Testicular Germ Cell Neoplasms
With an annual incidence of 0.5 to 2 cases per 100,000
children (1,7), testicular tumors account for approximately
1% of all childhood malignancies and for 2% of solid
malignant tumors in boys (1). Between 70% and 90% of
primary testicular neoplasms in childhood are of germ cell
origin, and the remaining tumors usually are of stromal
origin (discussed below) (1,7,55,57,58). The two most
common germ cell tumors are yolk sac carcinoma and
mature teratoma (1,7,59,60). The remaining germ cell
tumors are immature teratomas, embryonal carcinomas,
teratocarcinomas, and choriocarcinomas (61).
CLINICAL FEATURES
Patients with testicular neoplasms usually present with
painless scrotal or testicular enlargement (1,55,57,61),
with 15% to 20% having an associated hydrocele (1).
Pain, secondary to torsion or hemorrhage into the tumor,
is a rare presenting feature.
Yolk sac tumors occur predominantly in prepubescent
boys (median age 2 years), whereas the embryonal carci-
nomas, teratocarcinomas, and choriocarcinomas occur
in adolescents or young adults (1,4,55). Elevated serum
a-fetoprotein levels are common in yolk sac and embry-
onal cell tumors, while elevated serum levels of b-human
chorionic gonadotropin are seen most often with embry-
onal cell tumors and teratocarcinomas (7,55,58). In 80%
or more of cases, the tumor is localized to the scrotum
(1,61). The remaining patients have lymphatic spread to
regional and retroperitoneal lymph nodes or, rarely,
hematogenous spread to distant sites (55). Embryonal cell
carcinomas, teratocarcinomas, and choriocarcinomas tend
LWBK505-C14_p554-601.qxd 07/09/2010 7:49 PM Page 563 Aptara
to be aggressive tumors and metastasize early via lymphatic
and hematogenous routes.
Teratoma is the principal benign germ cell tumor of the
testis. It is usually found in children younger than 4 years
of age. Approximately 85% of tumors contain well-differ-
entiated elements from all three germinal cell layers.
Poorly differentiated elements occur in about 15% of
tumors. Even with immature elements, the tumor has a
benign course in prepubertal patients (58). Teratomas in
pubertal patients tend to behave more aggressively and
often contain malignant elements, necessitating orchiec-
tomy.
Seminoma is the most common testicular tumor in
adults (58), but it is rare in the pediatric age group. When
it does occur in this population, it is usually found during
later adolescence. It is the neoplasm most associated with
cryptorchid testes.
METASTASES AND CLINICAL STAGING
The most widely utilized system for staging testicular germ
cell tumors is one from the Childrens Cancer Study
Group/Pediatric Oncology Group (Table 14.1). Approxi-
mately 80% to 90% of prepubertal children with malignant
germ cell tumors have stage I disease; the remainder usually
have stage II or III disease or, rarely, stage IV disease with
hematogenous spread to lungs, liver, bone, or brain (1,7,
55,61,62). By comparison, adolescent patients with testic-
ular tumors are more likely to have an advanced-stage
tumor at the time of diagnosis.
TREATMENT OPTIONS
Most children and teenagers with stage I disease are
treated by radical orchiectomy alone. Chemotherapy is
reserved for patients with advanced disease (e.g., metas-
tases) and those whose tumor markers fail to decline after
orchiectomy. Survival rates exceed 90%. If the imaging
characteristics are sufficiently suggestive of teratoma and
tumor markers are negative in a prepubertal patient, tissue-
sparing surgery may be an option (57,58,60).
SONOGRAPHIC FINDINGS
Germ Cell Tumors
The malignant germ cell tumors, such as yolk sac carcinoma,
embryonal carcinoma, and choriocarcinoma, tend to be well
circumscribed and heterogeneous and contain cystic areas
related to hemorrhage or necrosis, and areas of increased
Table 14.1 Childrens Oncology Group Germ Cell Tumor Staging
Stage I: Tumor entirely resected; normal tumor markers
Stage II: Microscopic tumor residual; tumor markers still elevated
Stage III: Visible tumor remains after initial treatment; lymph node
involvement
Stage IV: Distant metastases
Source: www.curesearch.org.
Chapter 14 M A L E G E N I TA L T R A C T 563
echogenicity, with or without shadowing, representing calci-
fications (Figs. 14.15 and 14.16). They also tend to be hyper-
emic on Doppler imaging (2,5,54,57,58,60).
Teratocarcinomas and teratomas are well-defined,
markedly heterogeneous masses containing hypoechoic
areas, corresponding to serous fluid, and very hyper-
echogenic components, causing acoustic shadowing resulting
from focal calcification (Figs. 14.17 and 14.18) (2,5,7).
They also may contain echogenic foci related to fat.
Pure seminomas are more homogeneous than the germ
cell tumors and usually have predominantly uniform low-
level echoes and appear hypoechoic compared with the
normal echogenic testis. Very rarely do they have a hetero-
geneous appearance and contain cystic areas related to
necrosis (Fig. 14.19) (5).
Other Findings
Invasion of the tunica by aggressive tumors may occur,
producing an irregular testicular contour. Reactive hydro-
celes are an associated finding in 20% of testicular tumors
(1). The scrotal skin is rarely thickened with tumors. The
combination of scrotal skin thickening and an intratesticu-
lar mass is more characteristic of an inflammatory process
than a neoplasm.
Tumors smaller than 1.5 cm in diameter tend to be
avascular or hypovascular (Fig. 14.20), while larger tumors
are often hypervascular (see Fig. 14.15) (63). Vessels within
the hypervascular tumors can have a normal course or they
can be displaced and compressed. In some cases, color flow
Doppler sonography can identify a discrete mass when
gray-scale sonography is normal (18,63). Spectral Doppler
findings in testicular tumors are variable, with RIs varying
between 0.48 and 1.0 with a mean of 0.7. In general, the
gray-scale and Doppler patterns of testicular tumors are
not specific and significant overlap occurs. Biopsy is needed
for a specific diagnosis.
Besides being used for initial diagnosis, sonography can
be used after orchiectomy to survey the contralateral testis
for development of a contralateral tumor (64). Although
the frequency of this occurrence is unknown in pediatric
patients, adult patients with testicular cancers are at a
greater risk for developing tumors in the contralateral
testis (65).
Testicular Stromal Tumors
Stromal tumors account for approximately 10% of pedi-
atric testicular neoplasms (1,7,55,58). Sertoli cell and juve-
nile granulosa cell tumors account for about 40% of stro-
mal tumors each, with Leydig cell tumors accounting for
the remaining 20% (1,58).
Sertoli cell tumors usually present as painless masses in
the first year of life (66). Most are hormonally inactive and
produce estrogens that result in gynecomastia (1). Bilateral
tumors may occur in patients with Peutz-Jeghers syndrome
(2). Juvenile granulosa cell tumors are hormonally inactive,
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564 P E D I AT R I C S O N O G R A P H Y
B mal right testis.
Mixed germ cell tumor. Longitudinal sonogram in a
Fig. 14.16
15-year-old boy with painless scrotal swelling shows a
heterogeneous solid and cystic mass (M) with compression of normal
testicular parenchyma (arrowheads). Elements of embryonal carcinoma,
immature teratoma, and yolk sac tumor were found pathologically.
Yolk sac carcinoma. Trans-
Fig. 14.15
verse gray-scale (A) and
color Doppler (B) images of both testes of a
6-month-old with left scrotal swelling show
a heterogeneously enlarged left testis with
marked hyperemia compared with the nor-
Teratocarcinoma. Transverse sonogram in a 6-year-old
Fig. 14.17
boy shows a complex solid and cystic mass (arrows)
within the testis. The echogenic areas represent calcifications.
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Benign teratoma. Longitudinal sonogram in a 3-year-old
Fig. 14.18
boy with a firm testis shows a heterogeneous solid and
cystic mass (M) with areas of increased echogenicity representing
calcifications (arrows).
present in the first 6 months of life, and are associated with
chromosomal mosaicism (67). Leydig cell tumors are
benign tumors, typically found in prepubertal boys with a
mean age of 7 years (4). Approximately 30% of tumors
produce testosterone with resultant precocious virilization;
they have also been associated with Klinefelter syndrome
(1,7,68,69).
Most stromal tumors are benign, although malignant
Sertoli cell tumors have been reported in older children.
Benign stromal tumors can be treated with enucleation or
tissue-sparing surgery (69), with orchiectomy reserved for
malignant tumors.
SONOGRAPHIC FINDINGS
Sertoli cell and Leydig cell tumors are typically small, well-
circumscribed, hypoechoic, homogeneous masses (Fig.
14.21) (54,68,70). Cystic spaces related to hemorrhage
and necrosis are occasionally seen in larger tumors. A
Seminoma. Longitudinal sonogram of a young adult with
Fig. 14.19
6 months of scrotal swelling shows a well-defined hypoe-
choic mass (M) in the upper pole of the right testis.
Chapter 14 M A L E G E N I TA L T R A C T 565
Tumor hyperemia. Longitudinal color Doppler sonogram
Fig. 14.20
in a teenager with a left testicular embryonal cell carci-
noma shows a 1.2-cm hypoechoic mass (M) with minimal color Doppler
vascularity compared to the rest of the testis.
large-cell calcifying subtype of Sertoli cell tumor has dis-
tinct sonographic features that can suggest a specific diag-
nosis. These tumors are often bilateral and multifocal and
almost completely calcified, appearing highly echogenic
on sonography (Fig. 14.22) (71). Juvenile granulosa cell
tumors appear as solid or multiseptated complex cystic
masses with vascular septations (Fig. 14.23) (67,72).
Miscellaneous Testicular Masses
Gonadoblastomas are very uncommon germ cell tumors
and are nearly always found in phenotypic girls with streak
gonads or testes and a male karyotype (7,73). The majority
are small and diagnosed only at the time of surgery to
remove intra-abdominal dysplastic gonads. These tumors
are usually solid and hypoechoic, although multiple cystic
spaces can be observed. Malignant germ cell elements are
found in 10% (1,73). Treatment is removal of the involved
gonad (1).
Leydig cell tumor. Longitudinal sonogram of a prepuber-
Fig. 14.21
tal patient shows a well-circumscribed hypoechoic mass
(arrowheads) in the upper pole of the testis.
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566 P E D I AT R I C S O N O G R A P H Y

Calcifying Sertoli cell tumor. Longitudinal sonogram of a
Fig. 14.22
16-year-old boy shows a densely calcified mass with
posterior shadowing in the superior part of the right testis.
Juvenile granulosa cell tumor. Longitudinal sonogram of
Fig. 14.23
a 3-month-old boy with painless scrotal swelling shows
a well-defined heterogeneous tumor (T) within the right testis with a
thin rim of remaining compressed testicular parenchyma (arrowhead).

Epidermoid cysts are uncommon benign masses, usu-
ally presenting as a painless testicular mass. Their origin is
unclear, but they may represent a form of teratoma with
monodermal development of the ectoderm (74). These
are true cysts surrounded by fibrous tissue and lined by
squamous epithelium. The cyst is filled with white, cheesy
keratin. A characteristic appearance is a well-defined,
hypoechoic mass with a whorled or lamellated appearance
resembling the layers of an onion skin (Fig. 14.24A)
(74,75). Another pattern is a well-defined, mass with an
echogenic capsule that may contain calcification (Fig.
14.24B). However, epidermoid cysts also may have a non-
specific appearance of a hypoechoic mass with internal
echogenicity with or without calcifications and may
resemble teratomas (76). Testis-sparing enucleation is the
treatment of choice.
Other benign testicular masses include true cysts (see
section on cystic testicular masses), lipoma, hemangioma,
neurofibroma, fibroma, hamartoma, and dermoids (55,77).
These benign lesions are usually solid and hypoechoic, but
they can be complex or hyperechoic.
Nonneoplastic lesions that resemble benign solid neo-
plasms include cystic dysplasia (see above), Leydig cell hyper-
plasia, adrenal rests, and hamartomas (7880).
Leydig cell hyperplasia is a rare benign condition char-
acterized by multiple small testicular nodules, frequently
bilateral. Histologic examination shows an increased num-
ber of hyperplastic Leydig cells that are arranged in multi-
focal nodules. Children are usually between the ages of 5
and 9 years and usually present with precocious puberty.
Sonography reveals multiple small bilateral testicular lesions
(6 mm) that can be hypoechoic or hyperechoic (78).

A B
Epidermoid cyst. A: Transverse sonogram shows a hypoechoic mass with a whorled appearance and echogenic capsule. B: Longitudinal
Fig. 14.24
sonogram in another boy shows a well-defined mass (cursors) with linear internal echoes and an echogenic rim.
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Chapter 14 M A L E G E N I TA L T R A C T 567

A B
Adrenal rests. A: Longitudinal sonogram in an adolescent boy with congenital adrenal hyperplasia shows multiple lobular hypoechoic
Fig. 14.25
masses (arrows) along the mediastinum testis (arrowheads). B: Transverse sonogram of a different patient shows large masses
(arrows) within each testis centered around the mediastinum (arrowheads).

Adrenal rests of the testes arise from fetal adrenal cor-
tical cells that migrate with gonadal tissue in utero (79).
These cells can form tumor-like masses in response to
increased levels of adrenocortical hormones, most com-
monly associated with congenital adrenal hyperplasia and
Cushing syndrome. The incidence in patients with con-
genital adrenal hyperplasia varies from 24% to 94%
(81,82). At sonography, adrenal rests appear as round
hypoechoic, intratesticular nodules, most commonly
located near the mediastinum testis (Fig. 14.25). They are
commonly bilateral and may increase or decrease in size
over time (79,82). The clinical setting (abnormal hor-
monal levels associated with adrenal hyperfunction) usu-
ally clarifies the diagnosis and helps to avoid unnecessary
surgery.
Secondary Testicular Neoplasms
Leukemia, lymphoma, and metastases from solid tumors
are causes of secondary testicular neoplasms. Testicular
involvement with leukemia can occur at the time of initial
diagnosis or after the patient is in bone marrow remission.
The testis appears to act as a sanctuary for leukemic cells
during chemotherapy, as a result of a bloodgonad barrier
that prevents high tissue levels of chemotherapeutic agents
(1,5). Silent testicular involvement is present in as many as
25% of boys with newly diagnosed acute lymphoblastic
leukemia. Occult leukemic infiltrates are present at testicu-
lar biopsy in up to 15% of children with leukemia who are
in bone marrow remission and in 60% to 90% of children
at autopsy (5,83); they are rarely clinically symptomatic.
Lymphoma of the testis is almost always due to sec-
ondary involvement by the non-Hodgkin type (5); primary
testicular lymphoma is rare in children. Testicular infiltra-
tion by lymphoma has been documented at autopsy in 5%
to 30% of children and is clinically symptomatic in about
5% of children.
Leukemic and lymphomatous infiltration typically pro-
duces an enlarged, homogeneous, hypoechoic testis (Fig.
14.26). They usually diffusely replace the testes, although
focal hypoechoic masses can occur (Fig. 14.27) (1,5,18).

Leukemia. Transverse sonogram of both testes of an 8-year-old boy with painless scrotal swelling and a history of acute lympho-
Fig. 14.26
cytic leukemia 3 years earlier shows a diffusely enlarged hypoechoic right testis compared with the normal left testis due to
leukemic relapse.
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568 P E D I AT R I C S O N O G R A P H Y
Leukemia. Transverse sonogram of both testes of a 14-month-old boy shows bilateral hypoechoic masses (M) secondary to acute
Fig. 14.27
myelogenous leukemia.
Involvement is usually bilateral, but it can be unilateral.
Color Doppler imaging shows increased flow with a dis-
organized pattern (Fig. 14.28) (18,23,63). Although
uncommon, the epididymis can be involved, appearing
enlarged and hyperemic, mimicking an inflammatory
process (84).
Nonleukemic or nonlymphomatous metastases to the
testes include Wilms tumor, neuroblastoma, Langerhans
cell histiocytosis, sinus histiocytosis, carcinoid, retinoblas-
toma, and rhabdomyosarcoma (2,63,8587). Routes of
dissemination include hematogenous or lymphatic spread
or direct extension from contiguous tumor. At sonography,
metastases can be hypoechoic, hyperechoic, or complex.
They can cause diffuse testicular enlargement or a focal
mass (63). Color Doppler imaging usually demonstrates
hypervascularity (23,63,85).
PARATESTICULAR TUMORS
Malignant Lesions
Paratesticular tumors, both malignant and benign, are rare
and usually arise from the spermatic cord, and less com-
monly in the epididymis, appendix testis, or testicular
tunics (17). About 30% of spermatic cord tumors are
malignant, with embryonal rhabdomyosarcoma being the
most common (6,8,55). Rhabdomyosarcoma has a bimodal
age distribution, with the first peak occurring in children
aged 5 years or younger and the second peak occurring in
adolescence. Affected children usually present with a rap-
idly growing, painless intrascrotal mass (8,55). Up to 40%
of patients have retroperitoneal lymph node involvement
at presentation. Other malignant paratesticular tumors
include metastatic neuroblastoma, lymphoma, leukemia,
leiomyosarcoma, and fibrosarcoma (85).
Leukemia. Longitudinal color
Fig. 14.28
Doppler sonogram of the testis of
an 11-year-old boy shows an enlarged hypo-
echoic testis with markedly increased flow with
irregular-appearing vessels, reflecting tumor
neovascularity.
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Paratesticular leukemia. Longitudinal sonogram of a
Fig. 14.29
child with leukemia shows a hypoechoic mass (M) infe-
rior to the testis (T). An intratesticular focus of leukemia is also pres-
ent (arrow).
Sonography usually shows a well-circumscribed homo-
geneous or heterogeneous solid mass with an echogenicity
that can be isoechoic, hypoechoic, or hyperechoic to the
testes (Fig. 14.29). Hypoechoic areas representing necrosis
or hemorrhage, or hyperechoic foci reflecting calcification
or fat may be noted (2,8,55). Other findings include inva-
sion of the adjacent testis, epididymis and tunica vaginalis
(Fig. 14.30A) (88). The tumor is often hyperemic on color
Doppler imaging (Fig. 14.30B).
Benign Lesions
Benign paratesticular masses are usually fluid-filled masses
such as spermatoceles and cysts of the epididymis or
tunica albuginea. (These are discussed in a subsequent sec-
tion.) Adenomatoid tumors are uncommon in children,
but they may occasionally be seen in an older adolescent
(5). They are most commonly located in the epididymis,
usually in the body, but they may also arise in the sper-
matic cord or testicular tunics (89). Sonography usually
shows a solid, well-circumscribed mass, which may be
isoechoic, hypoechoic, or hyperechoic to the testis (5).
A B
Paratesticular rhabdomyosarcoma. A: Longitudinal sonogram of a young patient with firm scrotal swelling shows a large heteroge-
Fig. 14.30
neous mass (M) filling the scrotum and encasing the testis (T). The normal echogenic tunica albuginea is interrupted inferiorly (arrow),
indicating testicular invasion by the tumor. B: Color Doppler sonogram shows marked tumor vascularity.
Chapter 14 M A L E G E N I TA L T R A C T 569
Epididymal cystadenomas have been described in pedi-
atric patients with von Hippel-Lindau disease, and appear
as complex cystic masses (5). Splenogonadal fusion is a
rare congenital anomaly with ectopic splenic tissue
appearing as a solid mass usually adjacent to the left testis
(Fig. 14.31) (90). The mass may be isolated (discontinu-
ous form) or may be continuous with a cord of splenic tis-
sue that extends into the left upper quadrant (continuous
form) (91).
Other causes of benign paratesticular tumors include
fibromas, leiomyomas, hemangiomas, arteriovenous mal-
formations, lipomas, dermoids, neurofibromas, and
pseudotumor (Fig. 14.32) (3,8). The sonographic appear-
ance of these tumors is similar to that of the adenomatoid
tumor. Solid benign and malignant paratesticular tumors
cannot be differentiated on the basis of sonography, and
tissue sampling is required for diagnosis. Moreover, other
benign lesions, such as hematoma, inguinal hernia,
hydrocele, varicocele, and spermatic cord cyst, may
mimic a paratesticular neoplasm. This is likely to occur
when these lesions are complex and contain internal
debris or septations.
CYSTIC SCROTAL MASSES
Spermatoceles and Epididymal Cysts
Spermatoceles and epididymal cysts may present as pain-
less palpable masses, but are more commonly detected
incidentally. Spermatoceles result from cystic dilatation
of the efferent tubules and are seen only after puberty
(5,92). Most are located near the upper pole of the testis
in the head of the epididymis. Spermatoceles contain
spermatozoa and thick, white fluid.
Epididymal cysts also result from dilatation of efferent
tubules, but they have no age predilection and can be
found anywhere along the epididymis (92,93). Most are an
isolated finding, but they can be associated with cryp-
torchidism, cystic fibrosis, von Hippel-Lindau syndrome,
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570 P E D I AT R I C S O N O G R A P H Y
Splenogonadal fusion. Longitudinal view of the left hemi-
Fig. 14.31
scrotum shows a mass, representing ectopic splenic tissue
(S), superior to the left testis (T).
and prenatal estrogen exposure (93,94). Epididymal cysts
are filled with clear serous fluid and may resolve sponta-
neously (93).
Sonographically, both spermatoceles and epididymal
cysts appear as hypoechoic or anechoic lesions with thin
walls and posterior acoustic enhancement (Fig. 14.33)
(5,92). Loculations and septations are occasionally seen.
Spermatoceles are more likely to contain mobile internal
echoes from spermatozoa and debris (Fig. 14.34). Doppler
evaluation can show internal movement of this material
due to acoustic streaming (95).
Testicular Cysts
Simple testicular cysts are rare tumors in the pediatric
population (96,97). They often present as painless scrotal
enlargement in boys younger than 1 year of age (98). Sim-
ple cysts are composed of a monolayer of flat or cuboidal
epithelium surrounded by a fibrous wall (96). Sonograph-
Paratesticular dermoid. Longitudinal sonogram of a young
Fig. 14.32
child shows the testis (T) displaced into the inguinal
canal by a large inferior paratesticular mass (M) filling the scrotum.
Histology showed a benign dermoid.
Epididymal cyst. Transverse ultrasound of the left testis
Fig. 14.33
shows an anechoic, irregular, cystic mass (calipers) lat-
eral to the testis (T) in the body of the epididymis.
ically, testicular cysts are anechoic masses with smooth,
thin walls and posterior acoustic enhancement (Fig.
14.35) (96,97). In the infant, these cysts can grow and
compromise testicular parenchyma. Early surgery is advo-
cated to preserve functioning testicular tissue (96), and
simple enucleation is curative (98). The major differential
diagnostic consideration is a cystic neoplasm, particularly
a teratoma.
Cysts of the tunica albuginea are located within the
tunica surrounding the testis. Cysts of the tunica vaginalis
arise from the visceral or parietal layer of the tunica vagi-
nalis. The sonographic appearance is that of a small ovoid
anechoic mass within the tunica (Fig. 14.36).
Lymphatic Malformations
Lymphatic malformations (lymphangiomas) are congenital
malformations characterized by dilated lymphatic channels.
Spermatocele. Longitudinal sonogram of a teenager with
Fig. 14.34
a palpable mass shows a large cyst (C) in the head of the
epididymis with mobile internal echogenic material and posterior
acoustic enhancement (arrowheads). T  testis.
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Testicular cyst. Longitudinal sonogram in a 2-year-old
Fig. 14.35
boy with painless scrotal enlargement shows a simple
intratesticular cyst (C) with a surrounding rim of compressed testicu-
lar parenchyma (arrowheads).
They can present as slow-growing painless scrotal masses
or with signs of an acute scrotum if there is hemorrhage or
infection. Sonographically, they usually appear as cystic
masses with echogenic septations (Fig. 14.37) (92,99). The
cystic components are avascular, while the septations can
show flow on color Doppler imaging. The multicystic form
of this malformation can mimic a complex hydrocele or
hematocele. However, the septations in these cystic collec-
tions are avascular, in contrast to the vascular septa in lym-
phangiomas (100). Microcystic lymphatic malformations
with small channels can appear more complex and solid,
and mimic a solid paratesticular lesion (99,100).
THE ACUTE SCROTUM
Causes of acute scrotal swelling and pain in childhood
include spermatic cord torsion, torsion of a testicular
appendage, epididymitis, orchitis, acute vasculitis, idio-
Tunical cyst. Longitudinal sonogram shows a small an-
Fig. 14.36
echoic cystic mass (arrow) within the tunica albuginea of the
upper pole of the testis (T). E  epididymis.
Chapter 14 M A L E G E N I TA L T R A C T 571
Scrotal lymphatic malformation. Transverse image of the
Fig. 14.37
right hemiscrotum in an 11-year-old boy shows a normal
testis (T) and a multiseptated cystic paratesticular mass (arrowheads),
representing the lymphatic malformation. Internal debris is secondary
to hemorrhage.
pathic scrotal edema, strangulated hernia, and trauma.
The first three are the most common causes of acute
scrotal pain and present the greatest diagnostic chal-
lenges. Differentiation between these conditions is
important because spermatic cord torsion requires
prompt surgical intervention to save the testis, whereas
torsion of an appendage and epididymitis can be
treated medically. It is often impossible to differentiate
between testicular torsion and nonsurgical causes of an
acute scrotum on the basis of clinical findings (101).
While it may provide suggestive findings, gray-scale
sonography alone is not sufficient to separate testicular
torsion from other causes of scrotal pain, since it can-
not provide information about blood flow. The combi-
nation of gray-scale and color flow Doppler sonogra-
phy can be helpful by providing information about
morphology as well as testicular perfusion, thereby
expediting surgery in cases of testicular torsion and
preventing unnecessary surgery in other cases (11,15,
102107).
TORSION/INFARCTION
Torsion of the testis results when the testis and spermatic
cord twist one or more times, obstructing blood flow. Two
types of torsion have been described: intravaginal and
extravaginal, with the former being more common (Fig.
14.38).
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572 P E D I AT R I C S O N O G R A P H Y

A B C
Types of testicular torsion. A: Intravaginal torsion. B: Extravaginal torsion. C: Torsion below the epididymis of the testis. (Adapted from
Fig. 14.38
Leape LL. Torsion of the testis. In: Welch KJ, Ravitch MM, ONeill JA Jr, eds. Pediatric surgery. Chicago: Year Book, 1986:13301334,
with permission.)

Intravaginal Torsion bell clapper deformity (Fig. 14.39). Occasionally, intrav-

Intravaginal torsion most commonly occurs when the
tunica vaginalis completely surrounds the testis and inserts
high on the spermatic cord, preventing fixation of the testis
to the scrotum and allowing the testis to rotate freely on its
vascular pedicle (13). This anomaly is referred to as the
aginal torsion occurs because there is a loose mesorchium
that permits twisting of the testis within the tunica vaginalis
without torsion of the epididymis.
Intravaginal torsion can occur in any age group, but
it is most common in adolescents and young adults

Tunica
vaginalis

Dartos
muscle Fig. 14.39 Bell clapper deformity. A:
Sagittal image shows the
tunica vaginalis completely surrounding the
A C testis and epididymis. B: Cross-sectional
image shows the absence of attachment of
the epididymis to the scrotal wall. C: Sagittal
Tunica image demonstrates twisting of the testis
vaginalis within the tunica vaginalis. (Adapted from
Dartos Holder LE, Martire JR, Holmes ER, et al. Tes-
muscle ticular radionuclide angiography and static
imaging: anatomy, scintigraphic interpreta-
tion, and clinical indications. Radiology
B 1977;125:739752, with permission.)
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Chapter 14 M A L E G E N I TA L T R A C T 573

(13,108,109). Patients present with sudden onset of scro-

tal or lower abdominal pain, often accompanied by nau-
sea, vomiting, anorexia, and low-grade fever. Among
children and adolescents presenting with acute scrotal
pain, spermatic cord torsion is present in 5% to 31% of
patients (11,102,104106,109). Nausea and vomiting are
more common in testicular torsion than in other causes of
the acute scrotum, and have a positive predictive value of
over 96% (110). Clinical findings include a tender testis
with a transverse lie and a swollen, erythematous hemis-
crotum.
If the clinical findings are diagnostic of torsion, emer-
gency surgery is indicated. Imaging is best reserved to eval-
uate patients with an acute scrotum in whom clinical find-
ings are indeterminate or to confirm torsion in patients
with symptoms for more than 24 to 36 hours when surgi- Acute intravaginal torsion. Longitudinal sonogram in a
cal salvage of the testis is believed unlikely. Sonography, Fig. 14.40
peripubertal patient with acute scrotal pain shows an
particularly color Doppler sonography, is the imaging enlarged and hypoechoic testis (T), along with a hydrocele (H) and
method of choice to evaluate patients with acute scrotal scrotal skin thickening (*). There is a small hydrocele separating the
pain. testis from the posterior scrotal wall (arrow) where it should be
Torsion needs to be diagnosed promptly because tes- attached. The only attachment of the testis was at its vascular pedicle
ticular salvage depends on immediate surgical detorsion. (arrowheads), indicating a bell clapper deformity.
The treatment for intravaginal testicular torsion is imme-
diate detorsion, fixation of the testis to the scrotal wall,
and contralateral orchiopexy (111). Testicular viability
depends primarily on the length of time the torsion has choic, isoechoic, or hyperechoic paratesticular mass (Fig.
been present. The salvage rate is virtually 100% if sur- 14.44) (5,116).
gery is performed within 6 hours of onset of symptoms,
about 70% if surgery is performed within 6 to 12 hours DOPPLER FINDINGS
of symptoms, and only 20% or less if surgery is delayed In evaluating color flow, it is critical to compare the sym-
for 12 to 24 hours after onset of pain (107). The testis is metry of flow between the two testes. The sensitivity of
usually not salvageable after 24 hours of torsion. The color flow Doppler sonography for detecting acute torsion
necrotic testis is surgically removed, because it can in children is greater than 90%, with a specificity of nearly
adversely affect the contralateral testis if left in situ 100% (11,12,15,102,104,105). The negative predictive
related to a presumed antibody-induced immunologic value is 97.5% to 100% (15,104).
process.

GRAY-SCALE SONOGRAPHIC FINDINGS

The sonographic appearance of intravaginal testicular tor-
sion is related to the duration of the torsion. Within the
first few hours after torsion, the testicular architecture is
usually normal. After 4 to 6 hours, the testis is enlarged
and usually hypoechoic due to edema (Fig. 14.40); rarely
will the torsed testis be hyperechoic (12). After 24 hours
(late torsion), the testis becomes heterogeneous because of
vascular congestion, hemorrhage, and ischemia (Fig. 14.41)
(5,18). Once the testis becomes heterogeneous, it is generally
nonviable (112).
Other findings of intravaginal torsion include a
twisted spermatic cord (Fig. 14.42), transverse lie of the
affected testis due to shortening of the vascular pedicle
as the testis rotates, reactive hydrocele, scrotal wall
thickening, and epididymal enlargement (13,103,108,
113115). Transverse imaging along the length of the Delayed torsion. Longitudinal sonogram of the left testis
spermatic cord can improve detection of a twisted cord Fig. 14.41
in a patient with symptoms for greater than 24 hours
and the associated spiral appearance of the vessels (Fig. reveals an enlarged, heterogeneous testis (T). At operation, the testis
14.43) (115). The epididymis enlarges because of vascular was infarcted. Note also the associated hydrocele with debris (H) and
congestion and/or ischemia and it may appear as a hypoe- scrotal skin thickening (*).
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574 P E D I AT R I C S O N O G R A P H Y

A B
Acute intravaginal torsion, cord twist. A: Extended field-of-view longitudinal sonogram of a boy with an acutely painful scrotum. The
Fig. 14.42
testis (T) is enlarged, and there is twisting of the spermatic cord (arrowheads). B: Corresponding color Doppler image better demon-
strates the cord twist. There is color flow within the cord, but none within the testis (T).

Reduced or absent vascular perfusion in the affected
testis in conjunction with readily detectable flow in the
contralateral testis is diagnostic of acute torsion (Fig. 14.45).
The Doppler findings become more obvious in cases of late
torsion (24 hours). In late torsion, color flow imaging
typically shows marked hyperemia of the scrotal wall and
paratesticular soft tissues with absent testicular flow (Fig.
14.46). The reactive hyperemia is referred to as the rim
sign.
Two pitfalls in diagnosis need to be recognized. In
incomplete or partial spermatic cord torsion (twist
360 degrees), the testis may demonstrate arterial flow,
although the flow will be decreased compared to the
asymptomatic contralateral testis (Fig. 14.47) (2,13,104).
Secondly, in cases of spontaneous detorsion, flow may
increase in the testis, epididymis, and peritesticular soft
tissues secondary to reactive hyperemia (Fig. 14.48)
(13,117). This reactive hyperemia can mimic the hyper-
reactive blood flow that occurs in inflammatory condi-
tions, such as epididymo-orchitis (13,117). Clinical
findings should help differentiate between detorsion and
scrotal inflammation. The combination of acute scrotal
pain that spontaneously resolves and hyperemia on
color Doppler sonography suggests detorsion, whereas
hyperemia and persistent pain indicate an inflammatory
etiology. Although spontaneously or manually reduced
torsion is not a surgical emergency, affected patients are
at risk for subsequent torsion and do benefit from
orchiopexy (107,117).
Pulsed Doppler waveform analysis is generally not
required to establish the diagnosis of torsion, but it can
support the diagnosis by showing absence of detectable
blood flow in the symptomatic testis. Unfortunately, in
small children, the testicular arteries are small and

Intravaginal torsion, epididymal enlargement. Longitudi-

Spermatic cord twist. Transverse color Doppler image in
Fig. 14.43
a patient with acute torsion shows whirling vessels
(arrowheads) within the spermatic cord. (Case courtesy of Dr. Maria
Gloria del Pozo Garcia, Madrid, Spain.)
Fig. 14.44
nal sonogram of an acutely painful left scrotum in an 11-
year-old boy shows an abnormal orientation of the testis (T), which has
a transverse lie, and abnormal paratesticular soft tissue (arrowheads),
representing edematous epididymis and cord structures. A nonviable
torsed testis was found at surgery.
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Chapter 14 M A L E G E N I TA L T R A C T 575

Late torsion. Longitudinal sonogram in a patient with

Acute testicular torsion. Transverse color Doppler sono- Fig. 14.46
Fig. 14.45 several days of scrotal pain shows hyperemic scrotal
gram of both testes in a teenager with acute right scro- soft tissues, with absent flow to the testis, which is hypoechoic and
tal pain shows flow in the normal right testis, but none in the sympto- heterogeneous.
matic left testis.

Partial torsion. Transverse color Doppler sonogram of a

Fig. 14.47
boy with acute left scrotal pain shows normal flow in the
right (Rt) testis. The left (Lt) testis also demonstrates color flow, but it
is less than the asymptomatic right side. Note also the different orien-
tation of the left testis and a small hydrocele (arrow). Surgery showed
a viable left testis with a 360-degree twist of the spermatic cord.

Rt
Lt
A B
Detorsion. A: Transverse color Doppler sonogram in a boy with acute left scrotal pain shows good flow in the right (Rt) testis, but none
Fig. 14.48
in the left (Lt) testis. B: Image after manual detorsion shows marked color Doppler hyperemia in the left testis. The patient had an
immediate and dramatic reduction in pain after detorsion.
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576 P E D I AT R I C S O N O G R A P H Y
identification of flow can be difficult even in normal
testes. In a partially torsed testis, venous congestion leads
to increased intratesticular impedance and a resultant
decrease or even reversal in diastolic arterial blood flow
(Fig. 14.49) (118).
CHRONIC TORSION
If the infarcted testis is not removed surgically, it will begin
to atrophy after 14 days. The testis may remain hypo-
echoic (Fig. 14.50) or it may become hyperechoic if fibrosis
or calcification develops. The epididymis is often enlarged
and echogenic. Hydroceles are also common in chronic
torsion.
Chronic intermittent torsion. Transverse sonogram of a
Fig. 14.50
teenager with 1 year of intermittent right scrotal pain
shows a small hypoechoic right (RT) testis compared to the normal left
(LT) testis.
Partial torsion Doppler waveform. Longitudinal sono-
Fig. 14.49
gram of a patient with acute left scrotal pain shows that
there is demonstrable arterial flow in the left testis. The flow was much
less than the right side (not shown). Additionally, the Doppler wave-
form shows abnormal reversal of diastolic flow indicative of high
intratesticular impedance. A viable partially torsed testis was found at
surgery.
SEGMENTAL TESTICULAR INFARCTION
Infarction of a portion of the testis is an uncommon
event. Segmental infarction has been associated with
spermatic cord torsion, sickle cell disease, polycythemia,
angiitis, and operative complications (119). Patients
often present with symptoms of an acute scrotum.
Sonography shows a solid avascular area with varying
echogenicity that is frequently wedge shaped with the
vertex directed toward the mediastinum. Most segmental
torsion occurs in the upper and middle thirds of the testis
(119).
OTHER CAUSES OF INFARCTION
In addition to torsion of the spermatic cord, other causes
of complete or partial testicular infarction include
epididymitis, orchitis, trauma, polyarteritis nodosa, and
subacute bacterial endocarditis. The appearance is similar
to that seen in intravaginal testicular torsion (Fig. 14.51).
Testicular ischemia can be produced by extrinsic compres-
sion of the cord or testis, and has been described with her-
nias (120), hydroceles (121,122), and epididymitis (18).
Extravaginal Torsion
Extravaginal torsion occurs in neonates at the level of the
spermatic cord, because the cord is poorly fixed in the
inguinal canal (see Fig. 14.38B). It usually occurs in utero
and all of the scrotal contents on the affected side are
strangulated. Affected neonates present with a swollen
red scrotum with a firm enlarged testis (123). While it is
most commonly unilateral, bilateral extravaginal perina-
tal torsion does occur (124). The testis is usually necrotic
at birth so that surgical salvage is unlikely. In utero
extravaginal torsion is generally not considered a surgical
emergency and it is controversial whether surgery is
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Partial testicular infarction. Longitudinal sonogram in a
Fig. 14.51
patient several years after severe epididymo-orchitis
shows an irregular, atrophied inferior pole of the testis (arrowheads).
The superior portion of the testis (T) appears normal and had normal
color Doppler flow.
justified at all. In contrast, when extravaginal torsion
occurs after birth or produces only partial ischemia, the
testis may be viable and, hence, salvageable with surgery
(124,125). Differential diagnostic considerations of a
swollen scrotum in the neonatal period include hydro-
cele, hernia, meconium periorchitis, intraperitoneal
bleeding tracking through the patent processus vaginalis,
and tumor.
Sonographic findings of extravaginal torsion vary
depending on the duration of torsion. Findings in more
recent torsion include an enlarged heterogeneous testis
with hypoechoic and hyperechoic areas (Fig. 14.52)
(14,126). More chronic torsion demonstrates a minimally
enlarged or normal-size hypoechoic testis with peripheral
echogenicity corresponding to calcifications in the tunica
albuginea (Fig. 14.53) (14,126). Scrotal skin thickening
and hydroceles with debris and/or septations are common
associated findings (14). Doppler signals are often absent
in the testis and in the spermatic cord (Fig. 14.54),
although some flow may be seen with power Doppler
Extravaginal torsion. Transverse sonogram of a newborn
Fig. 14.52
with left scrotal swelling shows an enlarged and slightly
heterogeneous left (Lt) testis with associated scrotal skin thickening.
There was no color Doppler flow. The right (Rt) testis is normal.
Chapter 14 M A L E G E N I TA L T R A C T 577
Extravaginal torsion. Transverse color Doppler sonogram
Fig. 14.53
of a newborn with left greater than right scrotal swelling
shows a normal right testis (T) with color Doppler flow and a surrounding
hydrocele. The left testis has a calcified tunica albuginea (arrowhead).
Complex debris is seen between the tunica albuginea and the tunica
vaginalis (arrows), and septated fluid (*) is present between the tunica
vaginalis and the scrotal wall.
imaging (124). The contralateral testis may demonstrate
compensatory hypertrophy, a finding seen in other cases
of congenital monorchism (127).
Torsion of Testicular Appendages
Torsion of the appendix testis or appendix epididymis is
the most common cause of acute scrotal pain in prepu-
bertal males, with an incidence of 26% to 70%
(104,109,128,129). The peak incidence occurs between
7 and 14 years of age (2,109). Affected patients typically
present with acute pain, which usually is localized to the
upper pole of the testis. Unlike testicular torsion, associ-
ated nausea and vomiting is very uncommon (110). The
classic finding on physical examination is a small, firm,
palpable, paratesticular nodule, which often exhibits
bluish discoloration through the overlying skin (blue dot
sign). Clinically, the condition can mimic acute testicular
torsion. Clinical differentiation is important because
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578 P E D I AT R I C S O N O G R A P H Y

A B
Extravaginal torsion. A: Longitudinal sonogram of a newborn with a swollen left scrotum shows the spermatic cord (S) within the
Fig. 14.54
inguinal canal. The cord abruptly narrows at the point of torsion (large arrow). There is a small amount of fluid (small arrow) separat-
ing the tunica vaginalis (arrowhead) from the scrotal wall. E  epididymis; T  testis. B: Corresponding power Doppler image shows flow within the
spermatic cord and scrotal soft tissues, but not in the intrascrotal structures below the level of torsion (arrow).

appendiceal torsion is not a surgical emergency, whereas
testicular torsion is.
The testicular appendages are embryologic remnants of
blind-ending mesonephric tubules, paramesonephric ducts,
and the mllerian duct system (2,130). The appendix testis,
present in 83% to 92% of boys, is attached to the tunica
albuginea on the superior pole of the testis. The appendix
epididymis, present in 20% to 25% of boys, is located on
the epididymal head (128). Both appendices may be pedun-
culated (Fig. 14.55), predisposing them to torsion, although
the appendix testis is the more common one to torse. Atro-
phy of the appendage and resolution of symptoms with
supportive care is the usual outcome. Persistently sympto-
matic appendages may require surgical removal.
Sonographic findings of a twisted appendage are a small
hyperechoic or hypoechoic mass adjacent to the superior
aspect of the testis or epididymis (128,130). Whereas nor-
mal appendages are usually 3 mm or less in size, torsed
appendages are usually 5 mm or greater in size, and often
spherical in shape (128,130). Associated findings include
testicular and epididymal enlargement, reactive hydroceles,
and scrotal skin thickening (Fig. 14.56) (128,130). Color
flow Doppler imaging shows epididymal hyperemia along
with the avascular torsed appendage (Fig. 14.57). The testis
may have normal or increased vascularity (Fig. 14.58)
(128,130). The sensitivity and specificity of sonography for
detection of appendiceal torsion is approximately 90%
(131) and 100%, respectively (128). Infarcted appendages

A B
Normal testicular appendages. A: Longitudinal sonogram of a patient with scrotal swelling due to a hydrocele shows a normal trian-
Fig. 14.55
gular appendage (arrowhead) arising from the superior portion of the testis (T). E  epididymis. B: Longitudinal sonogram shows a
normal pedunculated appendage (arrowhead) with a long stalk (arrow) arising from the superior pole of the testis (T).
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Chapter 14 M A L E G E N I TA L T R A C T 579

A B

Appendiceal torsion. A: Longitudinal sonogram in a patient with 4 days of pain shows an enlarged ovoid echogenic appendage (arrow)
Fig. 14.56
adjacent to the testis (T) and epididymis (E) with associated scrotal skin thickening and a small hydrocele (arrowhead). B: Transverse
sonogram in another patient shows an enlarged round heterogeneous appendage (arrow) next to the testis (T) and epididymis (E) with marked scro-
tal skin thickening and a small reactive hydrocele (arrowhead).

A B
Appendiceal torsion. Longitudinal gray-scale (A) and color Doppler (B) images show an enlarged heterogeneous appendage (arrow-
Fig. 14.57
head) with enlargement of the epididymis (E) and a normal testis (T). There is marked hyperemia in the epididymis and soft tissues
adjacent to the torsed avascular appendage. The testis has normal flow.

Appendiceal torsion. Longitudinal color Doppler sono-

Fig. 14.58
gram shows a torsed avascular appendage (A), marked
surrounding soft tissue hyperemia, and increased flow to the testis (T).
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580 P E D I AT R I C S O N O G R A P H Y
A B
Evolution of appendiceal torsion. A: Transverse sonogram in a patient with prior appendiceal torsion shows a detached calcified
Fig. 14.59
appendage (arrowhead) with posterior acoustic shadowing (arrow) in the scrotal sac. B: Longitudinal sonogram of another patient
with appendiceal torsion 6 months previously showing a small calcified appendage (arrowhead).
eventually shrink in size, may calcify, and may break free to
become scrotoliths (Fig. 14.59).
INFLAMMATORY DISEASE
Acute Epididymitis/Orchitis
Acute epididymitis accounts for 6% to 47% of cases of
acute scrotal pain in children (104,109,129). Epididymitis
is more common in pubertal than in prepubertal boys. In
adolescent boys, it is most often due to sexually transmit-
ted organisms, such as Chlamydia trachomatis and Neis-
seria gonorrhoeae (18). In younger patients, epididymitis
can be secondary to genitourinary abnormalities, such as
an ectopic ureter draining into the vas deferens or seminal
vesicles; bladder outlet obstruction, which leads to reflux
of urine into the ejaculatory ducts; and epididymal inflam-
mation even in the setting of sterile urine (2,132134).
Epididymitis may also be secondary to trauma, and it can
be idiopathic (135). In younger patients, the most com-
mon pathogen is Escherichia coli, although urine cultures
are positive in only 10% to 25% of cases of epididymitis
(136).
Patients with epididymitis typically have a more grad-
ual onset of pain and fewer constitutional symptoms
compared with patients who have testicular or appendiceal
torsion (101). Findings on physical examination range
from only mild scrotal tenderness to severe scrotal edema,
pain, and tenderness with fever and pyuria.
SONOGRAPHIC FINDINGS
Sonographic findings of acute epididymitis are a focally or
diffusely enlarged epididymis, with the epididymal head being
most commonly involved (2,18). More diffuse and severe
swelling is seen in children with urinary tract anomalies
and recurrent cases of epididymitis (134). The echogenic-
ity can be decreased or increased and is often heteroge-
neous due to edema or hemorrhage (Fig. 14.60) (18,107).
Adjacent scrotal skin thickening and a reactive hydrocele,
which can be anechoic or complex, are also common
findings (2,17).
Spread of inflammation to the testis occurs in 20% to
40% of postpubertal males with acute epididymitis, produc-
ing epididymo-orchitis (5,137). Conversely, 85% of boys
with orchitis have signs of epididymitis as well (15). The
testis initially is enlarged and hypoechoic compared with the
asymptomatic side, becoming more heterogeneous over time
(Fig. 14.61) (138). Focal orchitis is not as common as diffuse
orchitis, but it can occur. Focal lesions appear as poorly
defined, hypoechoic areas in the periphery of the testicular
parenchyma, in close proximity to the inflamed epididymis
(Fig. 14.62). The sonographic appearance can be difficult to
differentiate from tumor, but the clinical scenario usually
clarifies the diagnosis. In 10% to 40% of patients with orchi-
tis, the testis is normal on gray-scale sonography (5).
Color flow Doppler imaging shows increased blood flow
in the inflamed epididymis and/or the testis compared with
the asymptomatic side (Figs. 14.61 and 14.63) (2,23,134). In
Acute epididymitis. Longitudinal sonogram of a teenager
Fig. 14.60
shows an enlarged, slightly heterogeneous epididymis
(E) that is hyperechoic relative to the testis (T). There is a reactive
hydrocele present (H).
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Chapter 14 M A L E G E N I TA L T R A C T 581

A B
Acute diffuse epididymo-orchitis. A: Transverse gray-scale sonogram of both testes in a patient with right (Rt) epididymitis shows an
Fig. 14.61
enlarged heterogeneous right testis with scrotal skin thickening and a small hydrocele. B: Color Doppler image shows increased right
(Rt) testicular flow, indicating orchitis. The left testis (Lt) is normal.

Focal epididymo-orchitis. Longitudinal sonogram of a

Fig. 14.62
patient with epididymitis shows a focal area of testicular
hypoechogenicity (arrowheads) in the inferior pole of the testis (T)
adjacent to the swollen and inflamed epididymis (E).

A B
Acute epididymitis. Transverse gray-scale (A) and color Doppler (B) sonograms of the left testis in a teenager with epididymitis shows
Fig. 14.63
heterogeneous enlargement of the body of the epididymis (E) with marked hyperemia on color Doppler imaging. The testis (T) is nor-
mal. Note the scrotal skin thickening (*) adjacent to the epididymis and the small reactive hydrocele (arrowhead).
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582 P E D I AT R I C S O N O G R A P H Y

A B
Epididymitis and testicular abscess. A: Longitudinal sonogram of a teenager with gonococcal infection shows an enlarged
Fig. 14.64
epididymis (E) and complex hydrocele (*). There is a complex fluid collection indicating an abscess (A) within the testis (T).
B: Color Doppler image shows the hypoechoic avascular abscess (A) displacing surrounding intratesticular vessels.

the majority of patients (80%), the color Doppler findings are
associated with gray-scale findings typical of scrotal inflam-
matory disease. In 20% of patients with epididymitis, the
gray-scale appearance of the epididymis will be normal (5).
Pulsed Doppler interrogation shows elevated diastolic
flow and a low resistive index (0.7) in the epididymal
arteries and detectable venous flow. Elevated diastolic
flow with decreased vascular resistance in the testicular
arteries (RI 0.5) also is seen in orchitis (5,139).
COMPLICATIONS
Complications of epididymo-orchitis include scrotal and tes-
ticular abscess, testicular ischemia and infarction, and sec-
ondary testicular atrophy (138). The sonographic findings of
testicular abscess are a hypoechoic or complex mass with
low-level echoes, fluid-debris level, and increased through-
transmission. Intensely hyperechoic areas with dirty shad-
owing due to gas bubbles may be observed. Color Doppler
imaging shows a complex intratesticular fluid collection with
peripheral hypervascularity and no internal vessels (Fig.
14.64) (17). Testicular abscess also can be secondary to
missed testicular torsion, trauma, and systemic infections.
The appearance of the abscess in those conditions is identi-
cal to that seen in epididymo-orchitis. A pyocele can occur if
the abscess breaks through the tunica vaginalis (137).
Testicular ischemia occurs when an enlarged epididymis
or edematous spermatic cord compresses spermatic vessels.
While the testicular artery may be compressed, compromise
of the draining pampiniform venous plexus and lymphatics
is probably more important in producing testicular vascu-
lar compromise (140). The sonographic findings of
ischemia are the same as those described for intravaginal
torsion, including an enlarged, heterogeneous testis with
decreased or absent color flow (Fig. 14.65). The associated

A B
Epididymitis and testicular ischemia. A: Longitudinal scan of the left epididymis and testis shows markedly increased epididymal flow
Fig. 14.65
(E), with minimal intratesticular flow (arrows). B: Longitudinal image of the right testis for comparison shows normal flow.
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Chapter 14 M A L E G E N I TA L T R A C T 583

Chronic epididymitis. Longitudinal sonogram of an ado-

Fig. 14.66
lescent with chronic recurrent epididymitis shows a nor-
mal testis (T) and an enlarged heterogeneous epididymis (E) contain-
ing multiple foci of increased echogenicity (arrowheads) representing
calcifications.

findings are the increased blood flow in the proximal
spermatic cord and the dartos secondary to edema and
inflammation. Spectral Doppler waveforms show dias-
tolic flow reversal resulting from edema. Infarction may
involve the entire testis, or it may be focal or multifo-
cal, appearing as hyperechoic or hypoechoic lesions
(5,138).
Chronic Epididymitis/Orchitis
Chronic epididymo-orchitis results in an enlarged and het-
erogeneous epididymis. The testicular tunica is thickened,
appearing as an echogenic rim around the testis. Small
echogenic areas with acoustic shadowing, representing cal-
cifications, can be observed in the epididymis and tunica
albuginea (Fig. 14.66) (5). Color Doppler may show epi-
didymal hyperemia or appear normal (2). Ultimately, the
testis usually atrophies and becomes diffusely or focally
hypoechoic.
bles (5,144). The testis and epididymis usually appear nor-
mal (5,144).
Scrotal Abscess (Pyocele)
Infected scrotal fluid collections may result from several
causes, including secondary infection of hydroceles or scrotal
hematomas, spread from epididymitis or a testicular abscess,
and extension of intraperitoneal infection (peritonitis) into the
scrotal sac via a patent process vaginalis (5). Appendicitis is the
most common cause of associated peritonitis (145), but
abscess can also be found with necrotizing enterocolitis and
other intra-abdominal infections. Sonography shows a com-
plex scrotal fluid collection with scrotal skin thickening and
hyperemic soft tissues (Fig. 14.67) (92,146). The testis and epi-
didymis may be difficult to see due to displacement, but when
visualized, they are often swollen and hyperemic (92,146).

Primary Orchitis
Isolated orchitis is less common than epididymo-orchitis
and is usually viral in origin. Mumps may be a cause of
orchitis in underdeveloped countries. The inflamed testis
is enlarged and hypoechoic and shows increased blood
flow on color Doppler imaging (5,141). An enlarged,
hyperemic epididymis may be seen in one third of patients
(141). Testicular atrophy may result and later fertility may
be reduced (142).

Fournier Gangrene
Fournier gangrene is a necrotizing fasciitis of the scrotum
and perineum (143). Although more commonly a disease
of older adults, in the pediatric population it primarily
affects neonates and infants, who present with edema and
erythema of the scrotum and the inferior surface of the
penis (143). Pathologically, there is scrotal wall edema and
obliterative endarteritis of branches of the internal puden-
dal artery. The testis and spermatic cord are spared since
the testicular artery is not involved by the arteritis. Sono- Scrotal abscess (pyocele). Transverse sonogram through
graphically, the scrotal skin and soft tissues are thickened Fig. 14.67
the left hemiscrotum in an infant with bowel perforation
and heterogeneous, containing hypoechoic and hypere- shows a complex, septated fluid collection indicating a pyocele (P).
choic areas, reflecting the presence of edema and gas bub- Aspiration was positive for infection. Cursors indicate the testis.
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584 P E D I AT R I C S O N O G R A P H Y
Idiopathic scrotal edema. Transverse sonogram of a
Fig. 14.68
7-year-old boy shows diffuse thickening of the scrotal
tissues with hypoechoic areas related to edema. The right testis (T) is
normal.
EDEMA AND VASCULITIS
Idiopathic Scrotal Edema
Acute idiopathic scrotal edema is an uncommon cause of
scrotal enlargement and may involve one or both hemis-
crota (147). The cause is unknown, but it may be second-
ary to an allergic reaction (147). Affected patients are typ-
ically younger than 10 years of age, with most being
between the ages of 4 and 7 years. On physical examina-
tion, the affected scrotum is painful and diffusely edema-
tous and erythematous (147). The underlying scrotal con-
tents are normal to palpation. At sonography, there is
thickening and edema of the scrotal soft tissues with a
normal testis and epididymis (Fig. 14.68) (23,147,148).
Color Doppler imaging shows increased flow in the scro-
A B
Henoch-Schnlein purpura. A: Longitudinal sonogram of a 5-year-old boy shows an enlarged epididymis (E) and normal testis (T) with
Fig. 14.69
associated scrotal skin thickening and a hydrocele. B: Color Doppler image shows increased flow in the epididymis (E) with scattered
testicular (T) signal, which is normal for a prepubertal boy.
tal skin; testicular flow remains normal (148). Acute scro-
tal edema resolves spontaneously within several days
without sequelae, although it may recur in up to 21% of
patients (147).
Henoch-Schnlein Purpura (Acute Vasculitis)
Henoch-Schnlein purpura is a small-vessel vasculitis
that usually affects children younger than 10 years of
age. It is generally preceded by an infection, most com-
monly due to Group A b-hemolytic Streptococcus (149).
The skin, gastrointestinal tract, joints, and kidneys are
affected most often, but the scrotum can be involved in
15% to 38% of cases and genital involvement can pre-
cede other organ involvement (149,150). Gray-scale
sonographic findings include normal testes, unilateral or
bilateral epididymal enlargement with a heterogeneous
echo pattern, a reactive hydrocele, and scrotal wall
thickening. Color flow Doppler imaging shows normal
intratesticular arterial flow with epididymal hyperemia
(Fig. 14.69) (150). The sonographic appearance of epi-
didymal enlargement due to vasculitis is indistinguish-
able from that of acute infectious epididymitis, but the
diagnosis is possible when there is coexisting vasculitis in
other organ systems.
TRAUMA
Blunt Trauma
Testicular trauma can be the result of child abuse, motor
vehicle accidents, athletic injuries, or a straddle injury
from compression of the scrotum against the pubic rami.
The peak age range is from 10 to 30 years, and approxi-
mately 50% of injuries are from athletic activity (5,9).
Physical examination of the scrotum is often limited by
pain and swelling, so sonography can be useful to evaluate
the presence or absence of testicular and extratesticular
hematoma, hematocele, fracture, or rupture.
Testicular hematoma produces an enlarged testis with
focal areas of increased or decreased parenchymal echogenic-
ity depending on the age of the hematoma. Acutely, the
hematoma is heterogeneous and is usually predominantly
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A B
Testicular hematoma. A: Transverse sonogram of a 17-year-old boy after scrotal trauma shows an enlarged and heterogeneous testis
Fig. 14.70
(T) with a focal area of mixed hypoechogenicity (arrowheads). There is also scrotal skin thickening and a small hematocele (arrow).
B: Corresponding color Doppler image shows hyperemia in the scrotal soft tissues and flow in part of the testis (T), but no flow in the intratesticular
hematoma.
hyperechoic to surrounding testicular parenchyma (9,151).
As the blood liquefies, the hematoma becomes septated
and complex with more anechoic areas (9,151). Scrotal
wall thickening is an associated finding. Color flow Doppler
sonography shows a normally perfused testis except for focal
areas of absent vascularity in the area of the hematoma (Fig.
14.70) (9,23,151). The hematoma may resolve completely or
leave a focal area of atrophy. Extratesticular hematomas can
involve the scrotal wall or epididymis. The sonographic
appearance of the blood is similar to that for testicular
hematomas (Fig. 14.71) (5,9,23,151).
Epididymal hematoma. Longitudinal scan of the right
Fig. 14.71
hemiscrotum in a 10-year-old boy after trauma shows an
enlarged, heterogeneous epididymis (arrowheads). The testis (T) is
normal. There is a tiny associated hematocele (arrow).
Chapter 14 M A L E G E N I TA L T R A C T 585
A hematocele is a collection of blood between the lay-
ers of the tunica vaginalis. Acutely, the scrotal blood is het-
erogeneous and predominantly echogenic, becoming more
complex over time. Hematoceles often contain septations
and have thick walls (Fig. 14.72) (9). Large hematoceles
can displace the testis from its normal position so that it
lies in a more peripheral position in the scrotum or in some
cases in the inguinal canal. Compression of the underlying
testis by a large hematocele can lead to diminished or
absent blood flow and testicular ischemia (9). Chronic
hematoceles can show scrotal wall thickening and internal
calcifications (17).
Testicular fracture appears as a linear hypoechoic band
traversing the testicular parenchyma. The testicular con-
tour is smooth and well defined and the tunica albuginea
is intact. An associated hematocele is common (Fig.
14.73). The presence of normal Doppler signals implies
viable testicular tissue, and these injuries can be treated
conservatively. The absence of testicular Doppler signals
indicates ischemia and is an indication for immediate sur-
gery (9,152).
Testicular rupture results from disruption of the tunica
albuginea and leads to extrusion of testicular contents into
the scrotal sac. The sonographic findings of testicular rup-
ture include interruption of the hyperechoic tunica albu-
ginea and the presence of a heterogeneous testis with irreg-
ular, poorly defined borders (Fig. 14.74) (9,152). The
heterogeneity represents parenchymal disruption and hem-
orrhage. Associated findings include scrotal wall thicken-
ing and hematocele (9). Spectral and color Doppler signals
are diminished or absent. The accuracy of sonography in
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586 P E D I AT R I C S O N O G R A P H Y

A B

Hematoceles. A: Longitudinal sonogram of a 5-year-

Fig. 14.72
old boy with an acute splenic laceration shows an
echogenic hematocele (H) from acute intraperitoneal blood track-
ing through a patent processus vaginalis. The testis (T) and epi-
didymis (E) are normal. B: Transverse sonogram of an 8-month-old
boy 1 week after hernia repair shows a septated hematocele with
thick walls just inferior to the testis (T). C: Longitudinal sonogram of
a 12-year-old boy 2 weeks after hydrocele surgery shows another
septated hematocele inferior to the testis (T). The blood in panels B
and C is relatively hypoechoic, reflecting lysis of blood products
and resorption of hemoglobin. Note in Panel C, normal, thin hypo-
C echoic bands that are sometimes seen in the testis.

Testicular fracture. Longitudinal gray-scale images of

Fig. 14.73
the left scrotum of a 9-year-old boy after trauma shows a
heterogeneous testis with curvilinear hypoechoic areas representing
fractures (arrowheads). The tunica albuginea is intact. There is an
associated hematocele (H). Doppler interrogation showed perfusion of
the fragmented testis.
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Chapter 14 M A L E G E N I TA L T R A C T 587

Testicular rupture. Longitudinal sonogram through the left

Fig. 14.74
testis of an 11-year-old boy who was kicked in the scro-
tum shows a heterogeneous testis (cursors). The normal echogenic
tunica albuginea (arrowhead) is interrupted superiorly (arrow). There is
an associated hydrocele. A salvageable testis with tunical disruption
was found at surgery.

diagnosing rupture ranges between 56% and 94%
(152,153). The diagnosis of rupture is particularly impor-
tant because it requires immediate surgical intervention.
Approximately 90% of ruptured testes can be salvaged if
surgery is performed expeditiously (152), whereas less
than 50% are salvaged if treatment is delayed (9). Com-
plications of delayed diagnosis include ischemic necrosis of
the testis, abscess formation, and loss of spermatogenesis
(107,152).
Miscellaneous Trauma
Penetrating trauma is usually due to gunshot or stab
injuries (9) and is much less common in children than in
adults. The role of sonography is the same as in blunt
trauma: to identify the extent of injury, whether or not the
tunica albuginea is intact, and whether there is blood flow
to the testis. Testicular rupture is not uncommon, and the
salvage rate is much less with penetrating injuries (approx-
imately 35%) (154) than with blunt trauma.
Testicular foreign bodies and scrotal urinomas, second-
ary to rupture of the bulbous urethra or bladder, can be
evaluated by sonography. Sonographically, urinomas
appear as anechoic extratesticular fluid collections indis-
tinguishable from a hydrocele (see below). Chronic repeti-
tive microtrauma, occurring with activities such as moun-
tain biking and horseback riding, has been shown to lead
to an increased incidence of hydroceles, epididymal cysts,
and scrotal and testicular calcifications in adolescents and
young adults (155,156).
testis (2,17), have a narrow proximal communication to
the abdominal cavity, and may fluctuate in size (Fig. 14.75).
Hydroceles can present as a loculated or encysted fluid col-
lection around the spermatic cord if the processus vaginalis
closes above the testis and below the internal ring (Fig.
14.76) (92). Rarely (0.4% to 3.1% of cases), the hydrocele
communicates with the peritoneal cavity and presents as
both a scrotal and an intra-abdominal mass (157). This
occurs when the processus vaginalis is closed at the internal
ring and scrotal pressure exceeds abdominal pressure,
allowing fluid to flow back into the abdominal cavity (Fig.
14.77) (157). Clinically, loculated hydroceles and
abdominoscrotal hydroceles can resemble inguinal hernias.
In older children and adolescents, hydroceles are usually
acquired and the result of testicular torsion, trauma, inflam-
matory processes, and tumors (2). Occasionally, patients
with ventriculoperitoneal shunts develop hydroceles
because cerebrospinal fluid or the shunt itself tracks into the
scrotum via a patent process vaginalis (Fig. 14.78) (158).
Most hydroceles are thin-walled anechoic fluid collec-
tions (92), but in some cases, scattered low-level echoes due
to cholesterol crystals, hemorrhage, infection, or calculi can

FLUID COLLECTIONS
Hydrocele
A hydrocele is an abnormal collection of fluid between the
visceral and parietal layers of the tunica vaginalis. It is the
most common cause of a painless scrotal swelling in child-
hood (3). In neonates and infants, virtually all hydroceles
are congenital and associated with a patent process vagi-
nalis, which allows peritoneal fluid to enter the scrotal sac
(2,5,7,92). The majority of hydroceles are isolated to the Typical hydrocele. Longitudinal scan in an infant shows
Fig. 14.75
scrotum, surround the anterior and lateral aspect of the anechoic fluid lateral to the testis (T).
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588 P E D I AT R I C S O N O G R A P H Y

Loculated hydrocele. Longitudinal sonogram of a 1-year-old boy showing a loculated hydrocele (cursors) within the right spermatic
Fig. 14.76
cord. Note the normal testis (T) inferiorly.

Abdominoscrotal
Fig. 14.77
hydrocele. Longitu-
dinal extended field-of-view
sonogram of the right groin in a
2-year-old boy with an enlarged
scrotum. The abdominoscrotal
hydrocele extends superiorly into
the abdomen. Note the normal
testis (T).

Hydrocele from ventriculoperitoneal shunt. Composite longitudinal image of the right inguinal canal and scrotum shows a ventricu-
Fig. 14.78
loperitoneal shunt (arrowheads) passing through the inguinal canal and ending just above the testis (T). There was a moderate hydro-
cele (H) present, a small portion of which is visible.
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Hydrocele with cholesterol crystals. Transverse sono-
Fig. 14.79
gram through the right scrotum in a 4-year-old boy
shows a large hydrocele with internal debris, representing cholesterol
crystals. T  testis.
be observed in the fluid (Fig. 14.79) (2,5,17). Septae also
may be noted, presumably reflecting prior hemorrhage or
infection. Chronic hydroceles can be associated with scro-
tal wall thickening (Fig. 14.80) or scrotoliths (Fig. 14.81).
Hydroceles are avascular on Doppler sonography, although
there can be color assignment to the fluid when transducer
motion causes fluid motion or the acoustic pressure from
Chronic hydrocele. Longitudinal sonogram superior to
Fig. 14.80
the testis in a 14-year-old boy shows a thickened scrotal
wall (arrowheads).
Chapter 14 M A L E G E N I TA L T R A C T 589
Chronic hydrocele with scrotolith. Longitudinal sono-
Fig. 14.81
gram in a patient with a chronic hydrocele shows an
echogenic scrotolith (cursors) with posterior acoustic shadowing
(arrow). T  testis.
the ultrasound beam creates flow patterns (acoustic stream-
ing) in the hydrocele (Fig. 14.82) (159).
The testis on the side of a hydrocele may have a larger
volume than the contralateral testis and may demonstrate
a higher resistive index on Doppler imaging, due to venous
congestion and alterations in arterial impedance (121,122,
160). After hydrocelectomy, the ipsilateral testicular volume
Hydrocele and false color Doppler flow. Longitudinal
Fig. 14.82
color Doppler sonogram in a patient with a hydrocele
shows false assignment of color flow (arrowhead) due to motion of
fluid in the hydrocele. T  testis.
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590 P E D I AT R I C S O N O G R A P H Y
Scrotal lymphocele. Transverse scan in a patient with a
Fig. 14.83
right lower quadrant renal allograft shows septated fluid
collections surrounding the testes (T) and in the soft tissues of the
scrotum.
may decrease to normal and does not necessarily indicate
that there has been an operative complication or develop-
ment of atrophy (121,160).
Hematocele
Hematoceles are collections of blood in the tunica vaginalis.
Most are the result of trauma or surgery (9), but other
causes include malignant tumors and bleeding disorders
(92,161). The sonographic findings of hematocele have
been described above.
Lymphocele
Scrotal lymphoceles are usually associated with ipsilateral
renal transplantation and result from lymphatic disruption
with leakage of lymph fluid into the tunica vaginalis or from
direct extension of a periallograft lymphocele through the
inguinal canal into the scrotum. Sonographically, lympho-
celes appear as septated fluid collections surrounding the
testis (Fig. 14.83).
VARICOCELE
A varicocele is a dilatation of the veins in the pampini-
form plexus of the spermatic cord. The majority are idio-
pathic, resulting from incompetent valves in the testicu-
lar veins that allow retrograde blood flow into the
pampiniform plexus (7,162). Most are found in adoles-
cents and young adults, are usually unilateral, and are
more common on the left than the right. Secondary
varicoceles, uncommon in young patients, result from
increased intra-abdominal pressure (163), or from com-
pression of the spermatic vein by a retroperitoneal mass.
Left renal vein entrapment as it crosses between the
superior mesenteric artery and aorta (nutcracker
anatomy) may be a predisposing factor in varicocele for-
mation (164) and is a risk factor in varicocele recurrence
after treatment (165). A retroaortic left renal vein also
has an increased association with varicocele formation
(166).
On physical examination, large varicoceles can be
visualized as multiple serpiginous structures (bag of
worms) in the hemiscrotum. Small varicoceles are
detected only by palpation with the patient erect or per-
forming the Valsalva maneuver (162). Varicoceles are
associated with asynchronous testicular growth, testicu-
lar atrophy, and reduced sperm quality and altered micro-
circulation, which may lead to infertility (167169).
Sonographic measurements of testicular volume appear
to be more precise than clinical or orchidometer evalua-
tion of size (167,168,170). Normalization of testicular
size can occur in adolescents after varicocele repair
(171,172).
Sonographically, varicoceles appear as tortuous, an-
echoic serpiginous structures adjacent to the testis. Indi-
vidual varices can range between 2 and 7 mm in diame-
ter, in contrast to the diameter of a normal vein, which is
0.5 to 2 mm. Varicoceles increase in size with the patient
in an erect position or performing the Valsalva maneuver.
Augmentation of venous flow during the Valsalva maneu-
ver can be seen on color flow and power Doppler sonog-
raphy (Fig. 14.84) (23). Chronic varicoceles may develop
areas of intense echogenicity with acoustic shadowing,
reflecting calcifications or phleboliths. An unusual vari-
ant is an intratesticular varicocele, which is typically
found in the mediastinum testis but may be subcapsular,
and it is usually associated with an extratesticular varic-
ocele (173).
INGUINAL HERNIA
Indirect hernias are more common in children than direct
hernias and are almost always associated with a patent
processus vaginalis. As the right processus vaginalis closes
after the left, hernias are more commonly right sided. The
incidence is as high as 4.4% and increased in premature
infants and in patients with increased intra-abdominal
pressure (positive-pressure ventilation, ventriculoperi-
toneal shunts) (174). The majority of hernias are clinically
obvious, but sonography can be useful in patients who
present with scrotal enlargement of unknown cause
(4,174,175). The hernia may contain small bowel, colon,
or omentum (4).
Approximately 5% to 20% of patients with a clini-
cally apparent unilateral inguinal hernia will have a
contralateral patent processus vaginalis. While repairing
the asymptomatic side is controversial, sonography can
reliably demonstrate these clinically inapparent defects
(174,176). Hernia repair is required to prevent possible
bowel incarceration or strangulation, and there is some evi-
dence that inguinal hernias can adversely effect testicular
blood flow and function through pressure on the spermatic
vessels (120).
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Chapter 14 M A L E G E N I TA L T R A C T 591

B
Varicocele. A: Longitudinal composite image of the left testis shows multiple tortuous tubular structures (arrowheads) superior and
Fig. 14.84
inferior to the normal testis (T). B: Color Doppler image of the pampiniform plexus superior to the testis shows flow within some of the
dilated veins with the patient breathing quietly (Rest), with dramatic increased flow during the Valsalva maneuver.

Sonography, particularly with use of the Valsalva
maneuver (Fig. 14.85), can aid in establishing a diagnosis
of a hernia by demonstrating peristalsing fluid- or air-
filled loops of bowel in the scrotum and a normal testis
and epididymis (Fig. 14.86). Identification of peristalsis
favors viable bowel, while absence of peristalsis and
blood flow in the herniated bowel suggests ischemic
changes (Fig. 14.87) (4,5,176). When omentum also
extends into the inguinal canal, the hernia will appear as
a complex echogenic mass (Fig. 14.88) (3,4). A canal
width greater than 4 mm at the level of the internal ring
is a reliable indication of hernia (sensitivity 95%) (177).
The sonographic findings of hernia overlap with those of
complex hydroceles, hematoceles, scrotal abscesses, and
urinomas, but differentiation is possible when peristalsis
is identified on real-time examination.
SCROTAL CALCIFICATIONS
Extratesticular Calcifications
Scrotal calcifications can occur in an extratesticular loca-
tion, usually between the layers of the tunica vaginalis, or
within the parenchyma of the testis. Extratesticular calcifi-
cations are the result of calcified loose bodies, meconium
peritonitis, phleboliths, or calcified hematomas. Loose

A B
Valsalva maneuver accentuating visualization of hernia. A: Longitudinal image at the level of the right internal inguinal ring (arrow)
Fig. 14.85
shows no hernia. There is a small hydrocele (*). B: Longitudinal image with Valsalva maneuver shows extension of omentum (O) into
a hernia sac (arrowhead) and widening of the internal ring to 1 cm (calipers).
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592 P E D I AT R I C S O N O G R A P H Y

Inguinal hernia. Longitudinal sonogram

Fig. 14.86
shows bowel (B) herniating into the scro-
tum superior to the testis (T).

A B
Strangulated inguinal hernia. A: Longitudinal sonogram of the right groin of a 3-month-old boy shows bowel (B) extending through the
Fig. 14.87
internal ring (arrows) into the scrotum superior to the testis (T). This hernia was not clinically reducible. B: Corresponding color
Doppler image shows flow within bowel and mesentery above the internal ring (arrows), but no flow in the herniated bowel (B), indicating ischemia
and strangulation. The bowel was still viable at surgery.

Inguinal hernia with omentum. Transverse image through

Fig. 14.88
the right hemiscrotum in a 12-year-old boy shows herni-
ated echogenic omentum (O), adjacent to the testis (T).
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Scrotolith. Longitudinal image of the right testis (T)
Fig. 14.89
shows a calcified paratesticular scrotolith (arrowhead)
with posterior acoustic shadowing (arrow).
bodies are located between the membranes of the tunica
vaginalis and are believed to result from previous torsion
of the appendix testis or epididymis, or from inflammation
of the tunica vaginalis (178,179). Scrotal calculi can be sin-
gle or multiple and typically range in size from 1 to 10 mm
(155,178). On sonography, they appear as round or ovoid,
mobile, hyperechoic foci with distal acoustic shadowing
(Fig. 14.89) (178,179).
Meconium Periorchitis
Meconium periorchitis is the result of in utero bowel per-
foration. Sterile intestinal contents leak into the peritoneal
cavity and can enter the scrotum via a patent process
vaginalis. The leaked meconium results in an inflamma-
tory process with a foreign-body giant-cell reaction that
subsequently calcifies (8). There may be scrotal discol-
oration, and the testis may not be palpable as a separate
structure on physical examination (8,180,181).
On sonography, meconium periorchitis appears as a
complex, highly echogenic mass with areas of acoustic
shadowing (Fig. 14.90) (4,8,180,181). In the presence
of extensive calcifications, the underlying testis can
sometimes be difficult to identify. Meconium peritonitis
can mimic a teratoma, but the presence of peritoneal
Chapter 14 M A L E G E N I TA L T R A C T 593
calcifications supports the diagnosis of meconium depo-
sition. The calcifications gradually resolve over time
(182).
Microlithiasis
Testicular microlithiasis is a condition in which calcifica-
tions form in the lumen of the seminiferous tubules. The
microliths are composed of cellular debris with a calcific
core and surrounding lamellated collagen, resulting from a
failure of Sertoli cell phagocytosis (183). The prevalence
varies between 0.6% and 18.1% (184,185). Microlithiasis
can occur in otherwise healthy individuals, but it also has
been reported in patients with cryptorchidism, pseudoxan-
thoma elasticum, cystic fibrosis, fragile X syndrome,
Down syndrome, and Klinefelter syndrome (94,186188).
Microlithiasis has been associated with testicular
malignancy, cryptorchidism, infertility, and testicular atro-
phy, and conversely all of these conditions are indepen-
dently associated with an increased risk of malignancy
(189,190). The testicular malignancy may arise de novo
or be preexisting (191195). Because of this risk, it is rec-
ommended that patients with microlithiasis have sono-
graphic examinations at least at yearly intervals. Patients
with few microliths (five or less within a testis) may have
Meconium periorchitis. Longitudinal scan of the
Fig. 14.90
left scrotum in an infant with intra-abdominal
calcifications on plain radiography demonstrates multiple
echogenic foci (arrowheads) with posterior acoustic shadow-
ing (arrow) around and inferior to the testis (T).
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594 P E D I AT R I C S O N O G R A P H Y
A B
Microlithiasis. A: Longitudinal sonogram of the right testis of an asymptomatic adolescent boy shows a few scattered calcifications.
Fig. 14.91
B: Transverse sonogram of an 11-year-old boy shows more pronounced diffuse testicular calcifications in both testes. There is an area
of sparing within the left testis (T), but no tumor.
a lower risk of malignancy than do patients with a larger
number of microliths (196). Microlithiasis has also been
associated with mediastinal germ cell tumors in the absence
of a testicular primary (197).
The sonographic pattern is characteristic, consisting of
diffuse, 1- to 3-mm hyperechoic foci throughout the testic-
ular parenchyma with or without acoustic shadowing (Fig.
14.91) (187,198,199). While usually bilateral and diffusely
distributed throughout the testis, microliths may be unilat-
eral or focally distributed (198,199). The number of
microliths present has no correlation with patient age. The
natural history of testicular microlithiasis in children is not
well known, but there have been reports of serial sono-
grams showing a reduced number or resolution of calcifi-
cations (184,200).
PROSTATE AND SEMINAL VESICLES
Congenital Anomalies
The prostate and seminal vesicles can be examined via
either an anterior abdominal approach using the distended
urinary bladder as an acoustic window or with transrectal
transducers. Prostatic abnormalities are rare in the pedi-
atric population. Most are congenital and include prosta-
tic utricles, mllerian duct cysts, and seminal vesicle cysts
(201,202). Congenital cystic lesions are usually asympto-
matic, but they can produce signs and symptoms of cysti-
tis, epididymitis, or prostatitis.
Prostatic utricles and mllerian duct cysts originate
from remnants of mllerian duct structures. Prostatic utri-
cles are usually found in young infants and children and
occur in association with hypospadias (14% to 47% of all
cases), intersex problems, cryptorchidism, and renal dysge-
nesis (203). Mllerian duct cysts have no associated abnor-
malities. Seminal vesicle cysts are remnants of the
mesonephric (wolffian) duct. They may be isolated findings
or associated with autosomal dominant polycystic kidney
disease and renal anomalies, particularly ipsilateral renal
agenesis (201).
Prostatic utricles and mllerian duct cysts appear as
midline cystic masses posterior to the bladder; they taper
inferiorly toward the prostate (Fig. 14.92). Seminal vesicle
cysts are posterior to the bladder and generally located lat-
erally (Fig. 14.93).
Rhabdomyosarcoma
Rhabdomyosarcoma is the most common prostatic malig-
nancy in children. It grows rapidly and can extend outside
the capsule of the prostate, invading the bladder neck, pos-
terior urethra, and adjacent soft tissues. Patients present
with findings of hematuria and urinary tract obstruction.
Sites of distant metastases are the lungs, bone, liver, and
bone marrow.
The sonographic findings of prostatic rhabdomyosar-
coma are a solid or complex, hypoechoic or hyperechoic
mass deforming or displacing the bladder. Extension into
the bladder can produce localized wall thickening or an
intravesical mass (Fig. 14.94). The tumor also may obstruct
the ureters, leading to hydronephrosis.
URETHRA AND PENIS
The posterior urethra can be imaged through the bladder,
through the perineum, or transrectally. The sonographic
study of the anterior urethra requires urethral distension,
most often with retrograde instillation of saline or anes-
thetic gel, and a linear array transducer placed directly on
the penis (204). The penis and bulbous urethra are scanned
in longitudinal and transverse planes. Contrast-enhanced
cystosonography may improve detection of urethral
lesions, although this is not widely available yet (205).
Fibroepithelial polyp of the prostatic urethra is the
most common benign urethral lesion in boys. It arises from
the verumontanum and often presents with signs and
symptoms of obstruction (206). Sonography shows a
pedunculated mass, which may demonstrate color flow
(207).
Posterior urethral valve is the most common congenital
urethral lesion. It is readily seen when the posterior urethra
dilates during voiding and appears as an echogenic band in
the lumen of the urethra (Fig. 14.95) (207,208). Other
lesions that can be detected by sonourethrography include
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A B
Prostatic utricle in a male infant with severe penoscrotal hypospadias. A: Longitudinal sonogram shows a large anechoic utricle (U)
Fig. 14.92
posterior to the bladder (B). The neck of the utricle extends inferiorly below the level of the symphysis pubis (arrow). B: Transverse
sonogram shows that the utricle (U) is midline. B  bladder.

Seminal vesicle cyst. Transverse sonogram through the

Fig. 14.93
pelvis of a 17-year-old boy with an absent right kidney shows
multiple tubular cystic structures (arrowheads) along the right lateral-
posterior wall of the bladder (B).

Prostatic rhabdomyosarcoma. Longitudinal midline sono-

Fig. 14.94
gram of an 18-month-old boy with difficulty voiding shows a
lobulated heterogeneous mass (M) arising from the inferior aspect of the
prostate and extending into the bladder (B). The mass had internal flow on
color Doppler imaging. Low-level intraluminal bladder echoes represent
hemorrhage.
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596 P E D I AT R I C S O N O G R A P H Y

A B
Posterior urethral valve. Prevoiding (A) and postvoiding (B) longitudinal transperineal sonograms in a 10-year-old boy show a dilated
Fig. 14.95
posterior urethra (U) proximal to the level of the valve (arrows). There is marked dilatation of the prostatic urethra during voiding.

Urethral foreign body. Longitudinal sonogram

Fig. 14.96
over the ventral aspect of the penis of a 16-
year-old boy with dysuria shows an echogenic bobby pin
within the urethra. A part of the pin has eroded through the
urethra into the surrounding corpus spongiosum (arrow).

Penile hematoma. Longitudinal sonogram

Fig. 14.97
over the dorsum of the penis in a 9-year-old
boy after trauma shows a heterogeneous hematoma (H).
There was no communication with the underlying corpora
cavernosa (C). The hematoma was avascular on color
Doppler imaging (not shown). U  urethra.
LWBK505-C14_p554-601.qxd 07/09/2010 7:51 PM Page 597 Aptara
strictures, calculi, anterior valves, foreign bodies (Fig.
14.96), bladder neck dyssynergia, diverticula, hematomas,
and postoperative complications (207210).
Epidermoid cyst, postcircumcision granuloma, juvenile
xanthogranuloma, and hemangiomas are rare benign ure-
thral tumors (211,212). Malignant penile lesions in chil-
dren are also rare.
Traumatic penile injuries can result in cavernosal artery
or tunica albuginea rupture, hematoma, and urethral
injury (Fig. 14.97) (213,214). If there is cavernosal artery
rupture, high-flow priapism may result (213215).
REFERENCES
1. Agarwal P, Palmer J. Testicular and paratesticular neoplasms in
prepubertal males. J Urol 2006;176:875881.
2. Aso C, Enriquez G, Fite M, et al. Gray-scale and color Doppler
sonography of scrotal disorders in children: an update. Radi-
ographics 2005;25:11971214.
3. Bhatt S, Rubens DJ, Dogra VS. Sonography of benign intrascro-
tal lesions. Ultrasound Q 2006;22:121136.
4. Coley BD. Sonography of pediatric scrotal swelling. Semin
Ultrasound CT MR 2007;28:297306.
5. Dogra V, Gottlieb R, Oka M, et al. Sonography of the scrotum.
Radiology 2003;227:1836.
6. Frush DP, Sheldon CA. Diagnostic imaging for pediatric scrotal
disorders. Radiographics 1998;18:969985.
7. Skoog SJ. Benign and malignant pediatric scrotal masses. Pedi-
atr Clin North Am 1997;44:12291250.
8. Sung T, Riedlinger W, Diamond D, et al. Solid extratesticular
masses in children: radiographic and pathologic correlation.
AJR Am J Roentgenol 2006;186:483490.
9. Deurdulian C, Mittelstaedt CA, Chong WK, et al. US of acute
scrotal trauma: optimal technique, imaging findings, and man-
agement. Radiographics 2007;27:357369.
10. Gronski M, Hollman AS. The acute paediatric scrotum: the role
of colour Doppler ultrasound. Eur J Radiol 1998;26:183
193.
11. Karmazyn B, Steinberg R, Kornreich L, et al. Clinical and
sonographic criteria of acute scrotum in children: a retro-
spective study of 172 boys. Pediatr Radiol 2005;35:302
310.
12. Paltiel HJ. Sonography of pediatric scrotal emergencies. Ultra-
sound Q 2000;16:5372.
13. Prando D. Torsion of the spermatic cord: sonographic diagno-
sis. Ultrasound Q 2002;18:4157.
14. Traubici J, Daneman A, Navarro O, et al. Testicular torsion in
neonates and infants: sonographic features in 30 patients. AJR
Am J Roentgenol 2003;180:11431145.
15. Weber DM, Rosslein R, Fliegel C. Color Doppler sonography
in the diagnosis of acute scrotum in boys. Eur J Pediatr Surg
2000;10:235241.
16. Ragheb D, Higgins J. Ultrasonography of the scrotum: tech-
nique, anatomy, and pathologic entities. J Ultrasound Med 2002;
21:171185.
17. Garriga V, Serrano A, Marin A, et al. US of the tunica vaginalis
testis: anatomic relationships and pathologic conditions. Radi-
ographics 2009;29:20172032.
18. Akin EA, Khati NJ, Hill MC. Ultrasound of the scrotum. Ultra-
sound Q 2004;20:181200.
19. Cassorla FG, Golden SM, Johnsonbaugh RD, et al. Testicular
volume during early infancy. J Pediatr 1981;99:742743.
20. Kuijper EA, van Kooten J, Verbeke JI, et al. Ultrasonographi-
cally measured testicular volumes in 0- to 6-year-old boys. Hum
Reprod 2008;23:792796.
Chapter 14 M A L E G E N I TA L T R A C T 597
21. Puttemans T, Delvigne A, Murillo D. Normal and variant
appearances of the adult epididymis and vas deferens on high-
resolution sonography. J Clin Ultrasound 2006;34:385392.
22. Bader TR, Kammerhuber F, Herneth AM. Testicular blood flow
in boys as assessed at color Doppler and power Doppler sonog-
raphy. Radiology 1997;202:559564.
23. Luker GD, Siegel MJ. Color Doppler sonography of the scro-
tum in children. AJR Am J Roentgenol 1994;163:649655.
24. Barth RA, Shortliffe LD. Normal pediatric testis: comparison of
power Doppler and color Doppler US in the detection of blood
flow. Radiology 1997;204:389393.
25. Luker GD, Siegel MJ. Scrotal US in pediatric patients: compar-
ison of power and standard color Doppler US. Radiology
1996;198:381385.
26. Paltiel HJ, Rupich RC, Babcock D. Maturational changes in
arterial impedance of the normal testis in boys: Doppler
sonographic study. AJR Am J Roentgenol 1994;163:1189
1193.
27. Horstman WG, Middleton WD, Melson GL, et al. Color
Doppler US of the scrotum. Radiographics 1991;11:941957.
28. McAlister WH, Sisler CL. Scrotal sonography in infants and
children. Curr Probl Diagn Radiol 1990;6:201242.
29. Rousso I, Iliopoulos D, Athanasiadou F, et al. Congenital bilat-
eral anorchia: hormonal, molecular and imaging study of a
case. Genet Mol Res 2006;5:638642.
30. Amodio J, Maybody M, Slowotsky C, et al. Polyorchidism:
report of 3 cases and review of the literature. J Ultrasound Med
2004;23:951957.
31. Danrad R, Askhker L, Smith W. Polyorchidism: imaging may
denote reproductive potential of accessory testicle. Pediatr
Radiol 2004;34:492492.
32. Kao E, Gerscovich E. Benign testicular lobulation: sonographic
findings. J Ultrasound Med 2003;22:299301.
33. Zuppa AA, Nanni L, Di Gregorio F, et al. Complete epididymal
separation presenting as polyorchidism. J Clin Ultrasound 2006;
34:258260.
34. Marjanovic ZO, Perovic SV, Slavkovic A, et al. Transverse tes-
ticular ectopia with and without persistent Mullerian duct syn-
drome. Int Urol Nephrol 2007;39:11671171.
35. Malik MA, Iqbal Z, Chaudri KM, et al. Crossed testicular
ectopia. Urology 2008;71:984.e5984e6.
36. Zeger MP, Zinn AR, Lahlou N, et al. Effect of ascertainment
and genetic features on the phenotype of Klinefelter syndrome.
J Pediatr 2008;152:716722.
37. Bonnet JP, Aigrain Y, Ferkadji L. Cystic dysplasia of the testis
with ipsilateral renal agenesis. A case report and review of the
literature. Eur J Pediatr Surg 1997;7:5759.
38. Wojcik LJ, Hansen K, Diamond DA, et al. Cystic dysplasia of
the rete testis: a benign congenital lesion associated with ipsi-
lateral urological anomalies. J Urol 1997;158:600604.
39. Keetch DW, McAlister WH, Manley CB, et al. Cystic dysplasia
of the testis. Sonographic features with pathologic correlation.
Pediatr Radiol 1991;21:501503.
40. Levin TL, Kogan SJ. Cystic dysplasia of the testis: sonographic
diagnosis and differentiation from testicular microlithiasis.
Pediatr Radiol 1998;28:955957.
41. Achiron R, Pinhas-Hamiel O, Zalel Y, et al. Development of
fetal male gender: prenatal sonographic measurement of the
scrotum and evaluation of testicular descent. Ultrasound
Obstet Gynecol 1998;11:242245.
42. Fait G, Yaron Y, Shenhar D, et al. Sonographic detection of
undescended testes in the third trimester. J Ultrasound Med
2002;21:1518.
43. Nijs SM, Eijsbouts SW, Madern GC, et al. Nonpalpable testes:
is there a relationship between ultrasonographic and operative
findings? Pediatr Radiol 2007;37:374379.
44. Hutson JM, Baker M, Terada M, et al. Hormonal control of
testicular descent and the cause of cryptorchidism. Reprod Fer-
til Dev 1994;6:151156.
LWBK505-C14_p554-601.qxd 07/09/2010 7:51 PM Page 598 Aptara
598 P E D I AT R I C S O N O G R A P H Y
45. Cain MP, Garra B, Gibbons MD. Scrotal-inguinal ultrasonog-
raphy: a technique for identifying the nonpalpable inguinal
testis without laparoscopy. J Urol 1996;156:791794.
46. Pappis CH, Argianas SA, Athanasiades E. Unsuspected urolog-
ical anomalies in asymptomatic cryptorchid boys. Pediatr
Radiol 1988;18:5153.
47. Esposito C, Caldamone AA, Settimi A, et al. Management of
boys with nonpalpable testis. Nat Clin Pract Urol 2008;5:
252260.
48. Wood HM, Elder JS. Cryptorchidism and testicular cancer: sep-
arating fact from fiction. J Urol 2009;181:452461.
49. Riebel T, Herrmann C, Wit J, et al. Ultrasonographic late
results after surgically treated cryptorchidism. Pediatr Radiol
2000;30:151155.
50. Taskinen S, Lehtinen A, Hovatta O, et al. Ultrasonography and
colour Doppler flow in the testes of adult patients after treat-
ment of cryptorchidism. Br J Urol 1996;78:248251.
51. Ritzen EM. Undescended testes: a concensus on management.
Eur J Endocrinol 2008;159(suppl 1):S87S90.
52. Thorup J, Haugen S, Kollin C, et al. Surgical treatment of unde-
scended testes. Acta Paediatr 2007;96:631637.
53. Kanatarci F, Mihmanli I, Yilmaz M, et al. Orchiopexy: a cause
of benign testicular lobulation. J Ultrasound Med 2003;22:
14171419.
54. Woodard P, Sohaey R, ODonoghue M, et al. Tumors and
tumorlike lesions of the testis: radiologic-pathologic correla-
tion. Radiographics 2002;22:189216.
55. Ciftci A, Bingol-Kologlu M, Senocak M, et al. Testicular tumors
in children. J Pediatr Surg 2001;36:17961801.
56. Kennedy PT, Elliott JM, Rice PF, et al. Ultrasonography of
intratesticular lesions: its role in clinical management. Ulster
Med J 1999;68:5458.
57. Metcalfe P, Farivar-Mohseni H, Farhat W, et al. Pediatric tes-
ticular tumors: contemporary incidence and efficacy of testicu-
lar preserving surgery. J Urol 2003;170:24122416.
58. Ross J, Rybicki L, Kay R. Clinical behavior and contemporary
management algorithm for prepubertal testis tumors: a sum-
mary of the prepubertal testis tumor registry. J Urol 2002;168:
16751679.
59. Pohl H, Shukla A, Metcalf P, et al. Prepubertal testis tumors:
actual prevalence rate of histological types. J Urol 2004;172:
23702372.
60. Shukla A, Woodard C, Carr M, et al. Experience with testis
sparing surgery for testicular teratoma. J Urol 2004;171:
161163.
61. De Backer A, Madern GC, Wolffenbuttel KP, et al. Testicular
germ cell tumors in children: management and outcome in a
series of 20 patients. J Pediatr Urol 2006;2:197201.
62. Wu H, Snyder H. Pediatric urologic oncology: bladder,
prostate, testis. Urol Clin North Am 2004;31:619627.
63. Luker GD, Siegel MJ. Pediatric testicular tumors: evaluation
with gray-scale and color Doppler US. Radiology 1994;191:
561564.
64. Bach AM, Sheinfeld J, Hann LE. Abnormal testis at US in
patients after orchiectomy for testicular neoplasm. Radiology
2000;215:432436.
65. Fossa SD, Chen J, Schonfeld SJ, et al. Risk of contralateral can-
cer: a population-based study of 29,515 U.S. men. J Natl Can-
cer Inst 2005;97:10561066.
66. Thomas J, Ross J, Kay R. Stromal testis tumors in children: a
report from the prepubertal testis tumor registry. J Urol
2001;166:23382340.
67. Yikilmaz A, Lee EY. MRI findings of bilateral juvenile granu-
losa cell tumors of the testis in a newborn presenting as
intraabdominal masses. Pediatr Radiol 2007;37:1031
1034.
68. Maizlin ZV, Belenky A, Kunichezky M, et al. Leydig cell tumor
of the testis: gray scale and color Doppler sonographic appear-
ance. J Ultrasound Med 2004;23:959964.
69. Merlini E, Seymandi PL, Betta PG, et al. Testis sparing enucle-
ation of a Leydig-cell tumour in a boy. Pediatr Med Chir
2003;25:6365.
70. Ricci Z, Stein M, Koenigsberg M, et al. Unusual sonographic
appearance of a Leydig cell tumor of the testis. Pediatr Radiol
2004;34:177178.
71. Shin SL, Outwater EK. Benign large cell calcifying Sertoli cell
tumor of the testis in a prepubescent patient. AJR Am J
Roentgenol 2007;189:W65W66.
72. Moore W, Li S, Rifkin MD. Juvenile granulosal cell tumor of
the testicle. Ultrasound Q 2003;19:3941.
73. Papaioannou G, Sebire NJ, McHugh K. Imaging of the unusual
pediatric blastomas. Cancer Imaging 2009;9:111.
74. Docal I, Crespo C, Pardo A, et al. Epidermoid cyst of the testis:
a case report. Pediatr Radiol 2001;31:365367.
75. Cittadini G, Gauglio C, Pretolesi F, et al. Bilateral epidermoid
cysts of the testis: sonographic and MRI findings. J Clin Ultra-
sound 2004;32:370372.
76. Maizlin Z, Belenky A, Baniel J, et al. Epidermoid cyst and
teratoma of the testis: sonographic and histologic similarities.
J Ultrasound Med 2005;24:14031409.
77. Rubenstein R, Dogra V, Seftel A, et al. Benign intrascrotal
lesions. J Urol 2004;141:17651772.
78. Carucci L, Tirkes A, Pretorius E, et al. Testicular Leydigs cell
hyperplasia: MR imaging and sonographic findings. AJR Am J
Roentgenol 2003;180:501503.
79. Dogra V, Nathan J, Bhatt S. Sonographic appearance of testic-
ular adrenal rest tissue in congenital adrenal hyperplasia.
J Ultrasound Med 2004;23:979981.
80. Walker RN, Murphy TJ, Wilkerson ML. Testicular hamar-
tomas in a patient with Bannayan-Riley-Ruvalcaba syndrome.
J Ultrasound Med 2008;27:12451248.
81. Claahsen-van der Grinten HL, Sweep FCGJ, Blickman JG, et al.
Prevalence of testicular adrenal rest tumors in male children
with congenital adrenal hyperplasia due to 21-hydroxylase defi-
ciency. Eur J Endocrinol 2007;157:339344.
82. Stikkelbroeck NM, Suliman HM, Otten BJ, et al. Testicular
adrenal rests in postpubertal males with congenital adrenal
hyperplasia: sonographic and MR features. Eur Radiol 2003;13:
15971603.
83. Askin FB, Land VJ, Sullivan M, et al. Occult testicular
leukemia: testicular biopsy at three years continuous complete
remission of childhood leukemia: a southwest oncology group
study. Cancer 1981;47:470475.
84. Ishigami K, Yousef-Zahra D, Abu-Yousef M. Enlargement and
hypervascularity of both the epididymis and testis do not
exclude involvement with lymphoma or leukemia. J Clin Ultra-
sound 2004;32:365369.
85. Karaosmanoglu D, Karcaaltincaba M, Balli O, Haliloglu M.
Sonographic findings of testicular involvement of neuroblas-
toma: an unusual clinical association. J Ultrasound Med 2008;
26:17851787.
86. Stroosma OB, Delaere KP. Carcinoid tumours of the testis. BJU
Int 2008;101:11011105.
87. Trobs RB, Friedrich T, Lotz I, et al. Wilms tumour metastasis
to the testis: long-term survival. Pediatr Surg Int 2002;18:
541542.
88. Rypens F, Garel L, Franc-Guimond J, Sartelet H. Paratesticular
rhabdomyosarcoma presenting as thickening of the tunica vagi-
nalis. Pediatr Radiol 2009;39:10101012.
89. Kolgesiz A, Kantarci F, Kadioglu A, et al. Adenomatoid tumor
of the tunica vaginalis testis: a special maneuver in diagnosis by
ultrasonography. J Ultrasound Med 2003;22:303305.
90. Cirillo RL Jr, Coley BD, Binkovitz LA, et al. Sonographic
findings in splenogonadal fusion. Pediatr Radiol 1999;29:
7375.
91. Varma DR, Sirineni GR, Rao MV, et al. Sonographic and CT
features of splenogonadal fusion. Pediatr Radiol 2007;37:
916919.
LWBK505-C14_p554-601.qxd 07/09/2010 7:51 PM Page 599 Aptara
92. Chung SE, Frush DP, Fordham LA. Sonographic appearances of
extratesticular fluid and fluid-containing scrotal masses in
infants and children: clues to diagnosis. AJR Am J Roentgenol
1999;173:741745.
93. Homayoon K, Suhre C, Steinhardt G. Epididymal cysts in chil-
dren: natural history. J Urol 2004;171:12741276.
94. Blau H, Freud E, Mussaffi H, et al. Urogenital abnormalities in
male children with cystic fibrosis. Arch Dis Child 2002;87:
135138.
95. Sista AK, Filly RA. Color Doppler sonography in evaluation of
spermatoceles: the falling snow sign. J Ultrasound Med
2008;27:141143.
96. Garcia CJ, Zuniga S, Rosenberg H, et al. Simple intratesticular
cysts in children: preoperative sonographic diagnosis and histo-
logical correlation. Pediatr Radiol 1999;29:851855.
97. Garrett JE, Cartwright PC, Snow BW, et al. Cystic testicular
lesions in the pediatric population. J Urol 2000;163:928936.
98. Ceylan H, Karaca I, Sari I, et al. Simple testicular cyst: a rare
cause of scrotal swelling in infancy. Int J Urol 2004;11: 352354.
99. Weidman E, Cendron M, Schned A, et al. Scrotal lymphan-
gioma: an uncommon cause for a scrotal mass. J Ultrasound
Med 2002;21:669672.
100. Loberant N, Chernihovski A, Goldfeld M, et al. Role of
Doppler sonography in the diagnosis of cystic lymphangioma of
the scrotum. J Clin Ultrasound 2002;30:384387.
101. Kass EJ, Lundak B. The acute scrotum. Pediatr Clin North Am
1997;44:12511266.
102. Baker L, Sigman D, Mathews R, et al. An analysis of clinical
outcomes using color Doppler testicular ultrasound for testicu-
lar torsion. Pediatrics 2000;105:604607.
103. Kalfa N, Veyrac C, Baud C, et al. Ultrasonography of the sper-
matic cord in children with testicular torsion: impact on the
surgical strategy. J Urol 2004;172:16921695.
104. Lam W, Yap T, Jacobsen A, et al. Colour Doppler ultrasonog-
raphy replacing surgical exploration for acute scrotum: myth or
reality? Pediatr Radiol 2005;35:597600.
105. Pepe P, Panella P, Pennisi M, et al. Does color Doppler sonog-
raphy improve the clinical assessment of patients with acute
scrotum? Eur J Radiol 2006;60:120124.
106. Schalamon J, Ainoedhofer H, Schleef J, et al. Management of
acute scrotum in children impact of Doppler ultrasound. J
Pediatr Surg 2006;41:13771380.
107. Siegel MJ. The acute scrotum. Radiol Clin North Am 1997;35:
959976.
108. Arce JD, Cortes M, Vargas JC. Sonographic diagnosis of acute
spermatic cord torsion: rotation of the cord, a key to the diag-
nosis. Pediatr Radiol 2002;32:485491.
109. McAndrew HF, Pemberton R, Kikiros CS, et al. The incidence
and investigation of acute scrotal problems in children. Pediatr
Surg Int 2002;18:435437.
110. Jefferson RH, Perez LM, Joseph DB. Critical analysis of the
clinical presentation of acute scrotum: a 9-year experience at a
single institution. J Urol 1997;158:11981200.
111. Bolln C, Driver CP, Youngson G. Operative management of tes-
ticular torsion: current practice within the UK and Ireland. J
Pediatr Urol 2006;2:190193.
112. Kaye JD, Shapiro EY, Levitt SB, et al. Parenchymal echo texture
predicts testicular salvage after torsion: potential impact on the
need for emergent exploration. J Urol 2008;180(suppl 4):
17331736.
113. Baud C, Veyrac C, Couture A, et al. Spiral twist of the sper-
matic cord: a reliable sign of testicular torsion. Pediatr Radiol
1998;28:950954.
114. Dogra VS, Rubens DJ, Gottlieb RH, et al. Torsion and beyond:
new twists in spectral Doppler evaluation of the scrotum. J
Ultrasound Med 2004;23:10771085.
115. Vijayaraghavan SB. Sonographic differential diagnosis of acute
scrotum: real-time whirlpool sign, a key sign of torsion. J Ultra-
sound Med 2006;25:563574.
Chapter 14 M A L E G E N I TA L T R A C T 599
116. Blask ARN, Rushton HG. Sonographic appearance of the epi-
didymis in pediatric testicular torsion. AJR Am J Roentgenol
2006;187:16271635.
117. Garel L, Dubois J, Azzie G, et al. Preoperative manual detor-
sion of the spermatic cord with Doppler ultrasound monitoring
in patients with intravaginal acute testicular torsion. Pediatr
Radiol 2000;30:4144.
118. Dogra V, Sessions A, Mevorach R, et al. Reversal of diastolic
plateau in partial testicular torsion. J Clin Ultrasound 2001;29:
105108.
119. Fernandez-Perez GC, Tardaguila FM, Velasco M, et al. Radio-
logical findings of segmental testicular infarction. AJR Am J
Roentgenol 2005;184:15871593.
120. Turgut AT, Olcucuoglu E, Turan C, et al. Preoperative ultrasono-
graphic evaluation of testicular volume and blood flow in patients
with inguinal hernias. J Ultrasound Med 2007;26: 16571666.
121. Mihmanli I, Kantarci F, Kulaksizoglu H, et al. Testicular size
and vascular resistance before and after hydrocelectomy. AJR
Am J Roentgenol 2004;183:13791385.
122. Turgut AT, Unsal A, Ozden E, et al. Unilateral idiopathic hydro-
cele has a substantial effect on the ipsilateral testicular geometry
and resistivity indices. J Ultrasound Med 2006;25:837843.
123. Chiang MC, Chen HW, Fu RH, et al. Clinical features of tes-
ticular torsion and epididymo-orchitis in infants younger than
3 months. J Pediatr Surg 2007;42:15741577.
124. Zinn HL, Cohen HL, Horowitz M. Testicular torsion in
neonates: importance of power Doppler imaging. J Ultrasound
Med 1998;17:385388.
125. Ahmed SJ, Kaplan GW, DeCambre ME. Perinatal testicular tor-
sion: preoperative radiological findings and the argument for
urgent surgical exploration. J Pediatr Surg 2008;43:15631565.
126. van der Sluijs JW, den Hollander JC, Lequin MH, et al. Prenatal
testicular torsion: diagnosis and natural course. An ultrasono-
graphic study. Eur Radiol 2004;14:250255.
127. Koff SA. Does compensatory testicular enlargement predict
monorchism? J Urol 1991;146:632633.
128. Baldisserotto M, de Souza L, Pertence A, et al. Color Doppler
sonography of normal and torsed testicular appendages in chil-
dren. AJR Am J Roentgenol 2005;184:12871292.
129. Corbett HJ, Simpson ET. Management of the acute scrotum in
children. ANZ J Surg 2002;72:226228.
130. Yang DM, Lim JW, Kim JE, et al. Torsed appendix testis: gray
scale and color Doppler sonographic findings compared with
normal appendix testis. J Ultrasound Med 2005;24:8491.
131. Hesser U, Rosenborg M, Gierup J, et al. Gray-scale sonography
in torsion of the testicular appendages. Pediatr Radiol
1993;23:529532.
132. Bukowski TP, Lewis AG, Reeves D, et al. Epididymitis in older
boys: dysfunctional voiding as an etiology. J Urol 1995;154:
762765.
133. Hudnall TW, Meservy C. Vas deferens ectopia: an uncommon
finding. Pediatr Radiol 2004;34:179.
134. Karmazyn B, KaeferM, Kauffman S, et al. Ultrasonography and
clinical findings in children with epididymitis, with and without
associated lower urinary tract abnormalities. Pediatr Radiol
2009;39(10):10541058.
135. Gordon LM, Stein SM, Ralls PW. Traumatic epididymitis: eval-
uation with color Doppler sonography. AJR Am J Roentgenol
1996;166:13231325.
136. Lau P, Anderson PA, Giacomantonio JM, et al. Acute epididymi-
tis in boys: are antibiotics indicated? Br J Urol 1997;79: 797800.
137. Kim W, Rosen MA, Langer JE, et al. US-MR imaging correla-
tion in pathologic conditions of the scrotum. Radiographics
2007;27:12391253.
138. Cook JL, Dewbury K. The changes seen on high-resolution
ultrasound in orchitis. Clin Radiol 2000;55:1318.
139. Jee WH, Choe BY, Byun JY, et al. Resistive index of the
intrascrotal artery in scrotal inflammatory disease. Acta Radiol
1997;38:10261030.
LWBK505-C14_p554-601.qxd 07/09/2010 7:51 PM Page 600 Aptara
600 P E D I AT R I C S O N O G R A P H Y
140. Sue SR, Pelucio M, Gibbs M. Testicular infarction in a patient
with epididymitis. Acad Emerg Med 1998;5:11281130.
141. Tarantino L, Giorgio A, de Stefano G, et al. Echo color Doppler
findings in postpubertal mumps epididymo-orchitis. J Ultra-
sound Med 2001;20:11891195.
142. Masarani M, Wazait H, Dinneen M. Mumps orchitis. J R Soc
Med 2006;99:573575.
143. Ameh EA, Dauda MM, Sabiu L, et al. Fourniers gangrene in
neonates and infants. Eur J Pediatr Surg 2004;14:418421.
144. Morrison D, Blaivas M, Lyon M. Emergency diagnosis of
Fourniers gangrene with bedside ultrasound. Am J Emerg Med
2005;23:544547.
145. Bingol-Kologlu M, Fedakar M, Yagmurlu A, et al. An excep-
tional complication following appendectomy: acute inguinal
and scrotal suppuration. Int Urol Nephrol 2006;38:663665.
146. Srinivasan AS, Darge K. Neonatal scrotal abscess: a differential
diagnostic challenge for the acute scrotum. Pediatr Radiol
2009;39:91.
147. Klin B, Lotan G, Efrati Y, et al. Acute idiopathic scrotal edema
in children revisited. J Pediatr Surg 2002;37:12001202.
148. Lee A, Park SJ, Lee HK, et al. Acute idiopathic scrotal edema:
ultrasonographic findings at an emergency unit. Eur Radiol
2009;19:20752080.
149. Tizard EJ, Hamilton-Ayres MJJ. Henoch Schonlein purpura.
Arch Dis Child Ed Pract 2008;93:18.
150. Ben-Sira L, Laor T. Severe scrotal pain in boys with Henoch-
Schonlein purpura: incidence and sonography. Pediatr Radiol
2000;30:125128.
151. Megremis S, Michalakou M, Mattheakis M, et al. An unusual
well-circumscribed intratesticular traumatic hematoma: diag-
nosis and follow-up by sonography. J Ultrasound Med 2005;
24:547550.
152. Buckley JC, McAninch JW. Use of ultrasonography for the
diagnosis of testicular injuries in blunt scrotal trauma. J Urol
2006;175:175178.
153. Herbener TE. Ultrasound in the assessment of the acute scro-
tum. J Clin Ultrasound 1996;24:405421.
154. Cline KJ, Mata JA, Venable DD, et al. Penetrating trauma to
the male external genitalia. J Trauma 1998;44:492494.
155. Frauscher F, Klauser A, Stenzl A, et al. US findings in the scrotum
of extreme mountain bikers. Radiology 2001;219:427431.
156. Turgut AT, Kosar U, Kosar P, et al. Scrotal findings in equestrians.
J Ultrasound Med 2005;24:911917.
157. Fenton L, McCabe K. Giant unilateral abdominoscrotal hydro-
cele. Pediatr Radiol 2002;32:882884.
158. Coley BD, Kosnik EJ. Abdominal complications of ventricu-
loperitoneal shunts in children. Semin Ultrasound CT MR
2006;27:152160.
159. Gerscovich E, Kurzrock E. Acoustic streaming versus venous
pseudoaneurysm in a scrotal mass. J Clin Ultrasound 2002;30:
569570.
160. Adaletli I, Kurugoglu S, Kantarci F, et al. Testicular volume
before and after hydrocelectomy in children. J Ultrasound Med
2006;25:11311136.
161. Miele V, Galluzzo M, Patti G, et al. Scrotal hematoma due to
neonatal adrenal hemorrhage: the value of ultrasonography in
avoiding unnecessary surgery. Pediatr Radiol 1997;27:
672674.
162. Nagar H, Mabjeesh NJ. Decision-making in pediatric varico-
cele surgery: use of color Doppler ultrasound. Pediatr Surg Int
2000;16:7576.
163. Turgut AT, Ozden E, Kosar P, et al. Chronic constipation as
causative factor for development of varicocele in men: a
prospective ultrasonographic study. J Ultrasound Med 2007;26:
510.
164. Kim WS, Cheon JE, Kim IO, et al. Hemodynamic investigation
of the left renal vein in pediatric varicocele: Doppler US, venog-
raphy, and pressure measurements. Radiology 2006;241:
228234.
165. Pallwein L, Pinggera G, Schuster AH, et al. The influence of left
renal vein entrapment on outcome after surgical varicocele
repair. J Ultrasound Med 2004;23:595601.
166. Karazincir S, Balci A, Gorur S, et al. Incidence of the retroaor-
tic left renal vein in patients with varicocele. J Ultrasound Med
2007;26:601604.
167. Kolon TF, Clement MR, Cartwright L, et al. Transient asyn-
chronous testicular growth in adolescent males with a varico-
cele. J Urol 2008;180:11111114.
168. Preston MA, Carnat T, Flood T, et al. Conservative manage-
ment of adolescent varicoceles: a retrospective review. Urology
2008;72:7780.
169. Zampieri N, Zuin V, Corroppolo M, et al. Relationship
between varicocele grade, vein reflux and testicular growth
arrest. Pediatr Surg Int 2008;24:727730.
170. Paltiel H, Diamond D, Di Canzio J, et al. Testicular volume:
comparison of orchidometer and US measurements in dogs.
Radiology 2001;222:114119.
171. Cayan S, Akbay E, Bozlu M, et al. The effect of varicocele
repair on testicular volume in children and adolescents with
varicocele. J Urol 2002;168:731734.
172. Decastro GJ, Shabsigh A, Poon SA, et al. Adolescent varico-
celectomy: is the potential for catch-up growth related to age
and/or Tanner stage? J Urol 2009;181:322327.
173. Tetreau R, Julian P, Lyonnet D, et al. Intratesticular varicocele:
an easy diagnosis but unclear physiopathologic characteristics.
J Ultrasound Med 2007;26:17671773.
174. Graf JL, Caty MG, Martin DJ, et al. Pediatric hernias. Semin
Ultrasound CT MR 2002;23:197200.
175. Robinson P, Hensor E, Lansdown M, et al. Inguinofemoral her-
nia: accuracy of sonography in patients with indeterminate clin-
ical features. AJR Am J Roentgenol 2006;187:11681178.
176. Hata S, Takahashi Y, Nakamura T, et al. Preoperative sono-
graphic evaluation is a useful method of detecting contralateral
patent processus vaginalis in pediatric patients with unilateral
inguinal hernia. J Pediatr Surg 2004;39:13961399.
177. Chen KC, Chu CC, Chou TY, et al. Ultrasonography for
inguinal hernias in boys. J Pediatr Surg 1998;33:1784
1787.
178. Artas H, Orhan I. Scrotal calculi. J Ultrasound Med 2007;26:
17751779.
179. Bushby L, Miller F, Rosairo S, et al. Scrotal calcifications: ultra-
sound appearances, distribution and aetiology. Br J Radiol
2002;75:283288.
180. Herman TE, Siegel MJ. Meconium periorchitis. J Perinatol
2004;24:188190.
181. Williams H, Abernethy L, Losty P, et al. Meconium periorchi-
tis: a rare cause of a paratesticular mass. Pediatr Radiol 2004;
34:421423.
182. Varkonyi I, Fliegel C, Rosslein R, et al. Meconium periorchitis:
case report and literature review. Eur J Pediatr Surg 2000;10:
404407.
183. Drut R, Drut RM. Testicular microlithiasis: histologic and
immunohistochemical findings in 11 pediatric cases. Pediatr
Dev Pathol 2002;5:544550.
184. Coley BD. Resolving testicular microlithiasis in a 12-year-old
boy. J Ultrasound Med 2005;24:14451448.
185. Peterson AC, Bauman JM, Light DE, et al. The prevalence of
testicular microlithiasis in an asymptomatic population of men
18 to 35 years old. J Urol 2001;166:20612064.
186. Bercovich RS, Januario JA, Terry SF, et al. Testicular microlithi-
asis in association with pseudoxanthoma elasticum. Radiology
2005;237:550554.
187. DellAcqua A, Toma P, Oddone M, et al. Testicular microlithi-
asis: US findings in six pediatric cases and literature review. Eur
Radiol 1999;9:940944.
188. Pourbagher MA, Pourbagher A, Erol I. Fragile X syndrome
associated with testicular microlithiasis in siblings. J Ultra-
sound Med 2005;24:17271729.
LWBK505-C14_p554-601.qxd 07/09/2010 7:51 PM Page 601 Aptara
189. Aizenstein RI, DiDomenico D, Wilbur AC, et al. Testicular
microlithiasis: association with male infertility. J Clin Ultra-
sound 1998;26:195198.
190. Kaveggia FF, Strassman MJ, Apfelbach GL, et al. Diffuse testic-
ular microlithiasis associated with intratubular germ cell neo-
plasia and seminoma. Urology 1996;48:794796.
191. Bach AM, Hann LE, Shi W, et al. Is there an increased incidence
of contralateral testicular cancer in patients with intratesticular
microlithiasis? AJR Am J Roentgenol 2003;180:497500.
192. Cast JEI, Nelson WM, Early AS, et al. Testicular microlithia-
sis: prevalence and tumor risk in a population referred for
scrotal sonography. AJR Am J Roentgenol 2000;175:1703
1706.
193. Kim B, Winter TC, Ryu J. Testicular microlithiasis: clinical sig-
nificance and review of the literature. Eur Radiol 2003;13:
25672576.
194. Lam DL, Gerscovich EO, Kuo MC, et al. Testicular microlithiasis:
our experience of 10 years. J Ultrasound Med 2007;26:867873.
195. Miller FNAC, Sidhu PS. Does testicular microlithiasis matter?
A review. Clin Radiol 2002;57:883890.
196. Bennett HF, Middleton WD, Bullock AD, et al. Testicular
microlithiasis: US follow-up. Radiology 2001;218:359
363.
197. Howard RG, Roebuck DJ, Metreweli C. The association of
mediastinal germ cell tumour and testicular microlithiasis.
Pediatr Radiol 1998;28:998.
198. Backus ML, Mack LA, Middleton WD, et al. Testicular
microlithiasis: imaging appearances and pathologic correlation.
Radiology 1994;192:781785.
199. Furness PD III, Husmann DA, Brock JW III, et al. Multi-insti-
tutional study of testicular microlithiasis in childhood: a benign
or premalignant condition? J Urol 1998;160:11511154.
200. Leenen AS, Riebel TW. Testicular microlithiasis in children:
sonographic features and clinical implications. Pediatr Radiol
2002;32:575579.
201. Arora SS, Breiman RS, Webb EM, et al. CT and MRI of con-
genital anomalies of the seminal vesicles. AJR Am J Roentgenol
2007;189:130135.
Chapter 14 M A L E G E N I TA L T R A C T 601
202. Lopatina OA, Berry TT, Spottswood SE. Giant prostatic utricle
(utriculus masculinis): diagnostic imaging and surgical implica-
tions. Pediatr Radiol 2004;34:156159.
203. Milla SS, Chow JS, Lebowitz RL. Imaging of hypospadias: pre-
and postoperative appearances. Pediatr Radiol 2008;38:202208.
204. Berman L, Bearcroft P, Spector S. Ultrasound of the male ante-
rior urethra. Ultrasound Q 2002;18:123133.
205. Duran C, Valera A, Alguersuari A, et al. Voiding urosonogra-
phy: the study of the urethra is no longer a limitation of the
technique. Pediatr Radiol 2009;39:124131.
206. Demircan M, Ceran C, Karaman A, et al. Urethral polyps in
children: a review of the literature and report of two cases. Int
J Urol 2006;13:841843.
207. Spyropoulos C, Konidaris D, Papnicolau A, et al. Posterior ure-
thral polyp in a boy, diagnosed by colour Doppler ultrasonog-
raphy. BJU Int 1999;84:881882.
208. Good CD, Vinnicombe SJ, Minty IL, et al. Posterior urethral
valves in male infants and newborns: detection with US of the
urethra before and during voiding. Radiology 1996;198:387391.
209. Bates DG, Coley BD. Ultrasound diagnosis of the anterior ure-
thral valve. Pediatr Radiol 2001;31:634636.
210. Bertolotto M, Serafini G, Savoca G, et al. Color Doppler US of
the postoperative penis: anatomy and surgical complications.
Radiographics 2005;25:731748.
211. Bradford RK, Choudhary AK. Imaging findings of juvenile xan-
thogranuloma of the penis. Pediatr Radiol 2009;39:176179.
212. Kocakoc E, Kazez A, Dagli AF, et al. Postcircumcision granu-
loma: a rare cause of a penile mass in a boy. J Ultrasound Med
2006;25:16111613.
213. Bertolotto M, Mucelli RP. Nonpenetrating penile traumas:
sonographic and Doppler features. AJR Am J Roentgenol
2004;183:10851089.
214. Bhatt S, Kocakoc E, Rubens DJ, et al. Sonographic evaluation
of penile trauma. J Ultrasound Med 2005;24:9931000.
215. Volgger H, Pfefferkorn S, Hobisch A. Posttraumatic high-flow
priapism in children: noninvasive treatment by color Doppler
ultrasound-guided perineal compression. Urology 2007;70:
590.e3590.e5.
LWBK505-C15_p602-646.qxd 09/07/2010 07:11 PM Page 602 Aptara

CHAPTER

15 Musculoskeletal System and

Vascular Imaging
MARILYN J. SIEGEL

General Techniques Soft Tissue Masses Myositis Ossificans

Imaging Approach Rhabdomyolysis
General Sonographic Anatomy
Congenital Vascular Lesions Fractures
Skin and Subcutaneous Tissue
Benign Nonvascular Masses Foreign Bodies
Skeletal Muscle
Malignant Tumors Tendon and Muscle Injuries
Tendons and Ligaments
Nerves Infection Other Musculoskeletal
Bursae Hip Joint Effusion Conditions
Bone and Cartilage Cellulitis Muscular Dystrophy
Doppler Imaging Necrotizing Fasciitis Limb Enlargement
Abscess Miscellaneous Problems
Normal Anatomy of Major Joints
Pyomyositis
Hip Peripheral Veins
Gas Gangrene
Knee Anatomy
Osteomyelitis
Ankle and Foot Sonographic Techniques
Infectious Tenosynovitis
Shoulder Normal Sonographic Appearance
Septic Bursitis
Elbow Venous Thrombosis
Wrist and Hand Noninfectious Tendon-Joint
Peripheral Arteries
Inflammation
Congenital Anomalies Anatomy
Tendonitis and Tenosynovitis
Developmental Dysplasia of the Hip Sonographic Techniques
Synovitis
Proximal Femoral Focal Deficiency Normal Sonographic Appearance
Tibial Hemimelia Trauma Occlusion and Stenosis
Congenital Knee Anomalies Hematoma Pseudoaneurysm
Congenital Hindfoot Anomalies Fat Necrosis Arteriovenous Fistula

ith the widespread availability and advances in GENERAL TECHNIQUES

W technology, the use of sonography to assess mus-
culoskeletal abnormalities has grown extensively.
The advantages of sonography in musculoskeletal imag-
Optimizing musculoskeletal sonography involves precise
positioning of the patient and the selection of imaging
parameters that maximize resolution. Patients should be
ing are its ability to easily depict soft tissue, cartilagi-
positioned so that the area of interest is in an advantageous
nous, and vascular structures. The capability of
position for interrogation while the patients comfort is
displaying these nonossified components, especially car-
maintained. Resolution is optimized with the use of a lin-
tilage, has allowed sonography to become a primary
ear or curvilinear array, high-frequency, 7.5- to 15-MHz
diagnostic procedure in the evaluation of musculoskele-
transducer. Higher-frequency transducers allow excellent
tal abnormalities (14). Ultrasonography is often the
resolution in the near field. For deep lesions, it may be nec-
initial study of choice for evaluating soft tissue tumors
essary to use a low-frequency transducer to increase tissue
and foreign bodies. It also is used to assess the neonatal
penetration.
hip and to confirm joint effusions, particularly in the
The extended field-of-view software is used to show
hip.
large continuous areas of anatomy and thus the full
This chapter will present the current uses of sonogra-
extent of lesions while maintaining spatial resolution
phy in the evaluation of joint, soft tissue, and peripheral
and anatomic detail. The split-screen function can be
vascular disorders in infants and children. Techniques and
used for side-by-side comparisons of the affected and
anatomy related to performing and interpreting the sono-
normal contralateral extremity, which can help confirm
graphic studies will also be emphasized.
the presence of an abnormality on the symptomatic side.

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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G 603

Color, power, and pulsed Doppler techniques are used to
characterize the vascularity of soft tissue masses and inflam-
matory lesions. Doppler imaging also can increase lesion
detectability by showing increased blood flow in the abnor-
mal areas when gray-scale images are indeterminate. Color
gain should be adjusted to a level just below that at which
all color noise barely disappears from the soft tissues.
GENERAL SONOGRAPHIC ANATOMY
Skin and Subcutaneous Tissue
The epidermis and dermis combined form the skin. The
subcutaneous tissue (hypodermis) is subadjacent to the
dermis and consists of loose fibrous connective tissue and
fat cells. The thickness of this layer varies with body habi-
tus and the region of the body. The epidermis and dermis
appear as a single hyperechoic layer. The subcutaneous tis-
sue layer appears hypoechoic relative to the dermis. The
fibrous septa within the hypodermis are hyperechoic rela-
tive to the fat lobules (Fig. 15.1).
Skeletal Muscle
The skeletal muscles are hypoechoic to adjacent bone and
fat and are surrounded by an echogenic sheath of dense
connective tissue fascia, termed the epimysium. The
muscles are composed of fascicles that are separated by
bands of fibroadipose tissue, termed the perimysium.
On longitudinal sections, the perimysial septa appear as
parallel echogenic lines against the hypoechoic back-
ground of the muscle. On transverse scans, the septa are
shorter and appear as punctate or short echogenic foci
(Fig. 15.1). The mean number of perimysial septa in
healthy individuals is 10.4 (range 8 to 13) (5). Measure-
ments of muscle and soft tissue thickness have been estab-
lished for some areas of the body (5), although they gen-
erally are not necessary for diagnosis of an abnormality.
Tendons and Ligaments
Tendons connect muscle to bone. The normal tendon is
composed of densely packed collagen fibers, which are
arranged in parallel bundles and are separated by fibrous
septa. Normal tendons are hyperechoic relative to adjacent
muscle. In the longitudinal plane, they have a tubular shape
and exhibit a fibrillar pattern of parallel hyperechoic lines
(Fig. 15.2). In the transverse plane, they appear as a hyper-
echoic round or ovoid structure containing bright dots
rather than fibrillar echoes (6). Ligaments have sonographic
findings similar to tendons, but they connect bone to bone.
The display of the echogenic fibrillar texture requires that
the beam be perpendicular to the axis of the tendon. Arti-
factual hypoechogenicity, which can mimic a tear or mass,
will result if the ultrasound beam is oblique to the tendon
fascicles. This artifact, which is the result of the anisotropic
structure of the tendon, tends to occur at the sites of attach-
ment of tendons to bone (Fig. 15.2B) (7). At insertion sites,
tendons have a curved rather than straight course and thus
do not parallel the transducer surface. Changing the angula-
tion of the transducer can minimize the curvature of the ten-
don and minimize or eliminate the artifact.
Tendons are surrounded by either peritenon or syn-
ovial sheaths (6). The peritenon, a layer of looser connec-
tive tissue, surrounds tendons, which have a rectilinear
course, whereas a synovial sheath surrounds curvilinear
tendons. The peritenon appears as a thin hyperechoic line

A B
Normal skin, soft tissues and muscle. Longitudinal (A) and transverse (B) scans of the anterior aspect of the right thigh show the epi-
Fig. 15.1
dermis and dermis as a thin echogenic layer (arrowheads). The subcutaneous fat (S) is hypoechoic to the dermis. Linear and curvilin-
ear echogenic septa course within the subcutaneous layer. Subadjacent to the subcutaneous layer is the relatively hypoechoic rectus femoris (RF)
and vastus intermedius (VI) muscles which are surrounded by thick echogenic sheath of connective tissue (epimysium) (open arrows). The muscles
contain thin hyperreflective fibrous septa (i.e., perimysial septa), which appear as parallel lines on longitudinal views and short foci on transverse
views (open arrowheads). F  femur.
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604 P E D I AT R I C S O N O G R A P H Y

A B
Normal tendon. A: Patellar tendon in an adolescent patient. Longitudinal anterior sonogram shows the patellar tendon (arrowheads)
Fig. 15.2
extending from the inferior pole of the patella (P) to the tibial tuberosity (Tib). The tendon has a typical fibrillar echotexture and is sur-
rounded by echogenic peritenon (arrows). The ossified patella and tibia are highly reflective, showing posterior shadowing. There is edema of the
superficial soft tissues (*). B: Achilles tendon in a 5-year-old child. The insertion of the tendon (arrows) onto the calcaneus (C) is hypoechoic owing
to anisotropy produced when the beam is not perpendicular to the tendon. This artifact tends to occur when the insertion site has a curved rather
than linear course. Note again the fibrillar tendon pattern (arrowheads). T  distal tibia.

surrounding the tendon margin (Fig. 15.2A). The synovial
sheath is a double-layered tubular structure. The two layers
of the sheath are separated by a small amount of fluid (6).
Nerves
Large peripheral nerves may be seen on sonography. They
appear as linear echogenic structures and are less echogenic
than tendons and ligaments.
Bursae
Bursae are synovial-lined structures located around joint
capsules, ligaments, and tendinous insertions. Smaller bur-
sae contain minimal amounts of fluid and are rarely visu-
alized at sonography. Large bursae containing more fluid,
such as the hip joint and infrapatellar bursa, can be seen as
hypoechoic fluid-filled structures. The diameter of normal
bursae should not exceed 2 to 3 mm (8).
Bone and Cartilage
The cortex of the bone appears as a highly echogenic struc-
ture with a smooth surface and distal acoustic shadowing.
The articular cartilage appears as a smooth anechoic layer, 1
to 2 mm thick, paralleling the cortical surface. The nonossi-
fied cartilaginous epiphyses are hypoechoic relative to adja-
cent soft tissue, and usually contain fine-speckled echoes (Fig.
15.3). Ossification centers within cartilage are hyperechoic.

A B
Normal cartilage and bone. A: Neonate shoulder. Longitudinal sonogram of the proximal humerus shows the hypoechoic cartilaginous
Fig. 15.3
epiphysis (E) with scattered internal echoes. The cortical bone (arrows) produces a bright reflective surface. M  metaphysis. G  gle-
noid fossa. B: Shoulder, older child. Longitudinal sonogram shows an ossified humeral head epiphysis (E) with surrounding hypoechoic articular car-
tilage (C). Again, notice the strong linear reflections of ossified cortical bone (arrows). M  metaphysis.
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A B
Normal hip. Neonate. A: Longitudinal view of the right hip reveals the hypoechoic cartilaginous femoral head (F) seated in the center
Fig. 15.4
of the highly echogenic ossified acetabulum (arrows). The fibrocartilaginous labrum (arrowhead) is hyperechoic to unossified cartilage.
B: Longitudinal view of the right hip in a 6-month-old infant. The echogenic area (arrowhead) represents the ossification center for the proximal
femoral epiphysis. The remainder of the epiphysis (E) is unossified, thus appearing hypoechoic relative to the ossified acetabulum (arrows).

Doppler Imaging The extensor mechanism of the knee includes the quadri-
Normal soft tissues, including muscle, tendons, and ceps muscle and the quadriceps and patellar tendons.
peribursal tissues, can exhibit sparsely scattered small ves- Because the tendons have a slightly concave surface when the
sels (9). Color gain should be adjusted to a level just below knee is extended, they should be examined with the knee
that at which all color noise barely disappears from areas partially flexed, which straightens the tendons and eliminates
deep to the cortical bone. the false hypoechogenicity associated with an oblique ultra-
sound beam. The patellar tendon extends from the inferior
pole of the patella to the tibial tuberosity (see Fig. 15.2A).
NORMAL ANATOMY OF MAJOR JOINTS The quadriceps tendon arises from the distal muscles of the
Hip anterior thigh and inserts on the patella (10).
At birth, the femoral head is cartilaginous and hypoechoic
to bone. The ossified parts of the acetabulum appear as
highly reflective linear or curvilinear structures. The fibro-
cartilaginous labrum, which extends laterally to cover the
femoral head, is hyperechoic to the cartilaginous head
(Fig. 15.4). The femoral head ossification center develops
between the second and eight months of life (Fig. 15.4B).

Knee
The cartilaginous epiphyses, articular hyaline cartilage,
and extensor tendons are well suited for examination by
high-frequency transducers. The cartilage of the distal
femur and proximal tibia is best evaluated with the knee
in flexion and the transducer directed into the intercondy-
lar notch. Cartilaginous structures have well-defined
echogenic margins and a hypoechoic echotexture relative
to muscle and bone (Fig. 15.5). The thickness of the carti-
lage is greatest in infants and decreases with age, reaching
a thickness of 1 to 3 mm in the mature knee. The thick- Normal knee. Neonate. Longitudinal view of right knee
ness of the cartilage of the lateral femoral condyle is Fig. 15.5
shows the cartilaginous epiphysis (E), which is hypo-
greater than that of the medial femoral condyle. echoic to the ossified distal femoral cortex (arrows).
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606 P E D I AT R I C S O N O G R A P H Y
The prepatellar bursa lies anterior to the lower part of
the patella and upper part of the patellar tendon. The
infrapatellar bursa lies between the anterior aspect of the
tibia and the inferior part of the patellar tendon (10).
Ankle and Foot
The Achilles tendon is composed of fibers from the soleus
and gastrocnemius muscles. It inserts on the posterior
aspect of the calcaneus. The tendon is best imaged with the
patient in the prone position and the foot in plantar- and
dorsiflexion. The normal Achilles tendon in adolescents
and adults is 4 to 6 mm thick and 5 to 6 cm long. Similar
to tendons in other sites, the Achilles tendon has a fibrillar
appearance and well-defined echogenic margins (see Fig.
15.2B). Sonography can also identify the tendons of the
peroneus longus and brevis muscles laterally, the tendon of
the tibialis posterior muscle medially, and the extensor ten-
dons at the anterior aspect of ankle joint.
Shoulder
In neonates and young infants, the cartilaginous humeral
head appears as a round hypoechoic structure with bright
internal echoes lying within the glenoid fossa (see Fig.
15.3A). Cortical bone appears as a thin, hyperechoic, curvi-
linear reflection relative to cartilage (see Fig. 15.3B) (11).
The rotator cuff covers the humeral head, extending from
the acromion to its insertion on the greater tuberosity (12). It
is composed of four tendons and their associated muscles: the
subscapularis, supraspinatus, infraspinatus, and teres minor.
The rotator cuff is hyperechoic relative to the subadjacent
articular cartilage and more superficial deltoid muscle (Fig.
15.6). The subdeltoid bursa is a thin hypoechoic band imme-
diately overlying the rotator cuff and beneath the deep sur-
Normal rotator cuff. Longitudinal sonogram. The ossified
Fig. 15.6
humeral head (#1) and the greater tuberosity (#2) are seen
as strong convex curvilinear reflections separated by the anatomic
neck of the humerus (#3), which appears as a concave reflection.
Immediately overlying the humeral head is the articular cartilage,
which appears hypoechoic to anechoic (#4). The next tissue layer is
the rotator cuff (#5), which is an echogenic band of tissue that tapers
as it inserts laterally on the greater tuberosity. Superficial to the rota-
tor cuff is the subdeltoid bursa (#6). The overlying deltoid muscle (#7)
is seen superficial to the bursa.
Normal elbow. Longitudinal view of the left elbow in a
Fig. 15.7
3-year-old boy shows the ossified cortex (arrowheads) of
the capitellum (C) and the radial head (R). The unossified cartilage of the
humeral and radial epiphyses (arrows) is hypoechoic to bone and soft
tissues.
face of the deltoid muscle. Vessels are not routinely visible
with Doppler imaging in patients with normal rotator cuffs,
but they may be seen in patients with inflamed cuffs.
The biceps tendon separates the subscapularis and
supraspinatus tendons. It appears as a hyperechoic oval
structure within the biceps groove. The biceps groove is a
concave echogenic structure adjacent to the humeral head
(12). Biceps tendon and rotator cuff abnormalities are
common in adults and have been well described in the lit-
erature (12). Since they are rare in children, they will not
be reviewed further in this chapter.
Elbow
The developing epiphysis appears as a hypoechoic structure
with bright speckled internal echoes. Posterior shadowing is
absent. The capitellum, the first epiphysis to ossify, is usually
visible by age 2 years (Fig. 15.7). The medial epicondylar
epiphysis begins to ossify at 4 years, the radial head at
5 years, the trochlear epiphysis at 8 years, the olecranon epi-
physis at about 9 years, and the lateral epicondylar epiph-
ysis at 10 years (13,14). The tendons of the biceps and tri-
ceps muscles and the flexor and extensor tendons of the
forearm, which insert on the distal humerus, may be identi-
fied when high-frequency transducers are used.
Wrist and Hand
The four compartments of the wrist (radial, ulnar, volar, and
dorsal) are well shown by sonography. These compartments
enclose the phalanges, carpal bones, radius, and ulna and the
extensor and flexor tendons of the wrist, hand, and fingers.
The extensor tendons of the fingers are located in separate
compartments over the dorsum of the wrist, while the flexor
tendons course in a tighter bundle through the carpal tunnel
(Fig. 15.8). The echogenic flexor tendons are surrounded by
hypoechoic bursa and are best seen when the wrist is flexed.
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G
Normal hand. Transverse scan of the palmar surface
Fig. 15.8
shows normal echogenic flexor tendons (arrows) with a
small amount of surrounding fluid. M  ossified metacarpal bones.
CONGENITAL ANOMALIES
Developmental Dysplasia of the Hip
Developmental dysplasia of the hip (DDH), formerly
called congenital hip dislocation, is a spectrum of abnor-
malities ranging from mild acetabular dysplasia and
reducible subluxation to irreducible subluxation or dislo-
cation of the femoral head. Most dislocations are evident
at birth, but some infants do not develop or at least mani-
fest DDH until later in infancy (15). For this reason, the
terminology has changed from congenital dysplasia of the
hip to developmental dysplasia of the hip.
The incidence of DDH is approximately 1.5 in 1000.
Female infants are affected more often than male infants (4:1
or 5:1) (16,17). DDH is believed to be due to abnormal liga-
mentous laxity (rather than a structural abnormality), which
is accentuated by excessive levels of circulating maternal
estrogens. Heritable factors and faulty intrauterine position
also contribute to development of DDH. There is an
increased risk of DDH in infants with a family history of this
condition. The risk is 6% if a sibling has the condition, 12%
if one parent is affected, and 36% if both parents have the
condition (18). DDH is also six times more frequent after
breech delivery than after vertex delivery. The extreme flexion
associated with a breech delivery produces a shortened, con-
tracted iliopsoas muscle, which tends to promote dislocation.
Infants with torticollis, foot deformities (metatarsus adductus
or calcaneovalgus), and neuromuscular problems (spina
bifida, arthrogryposis) are also at increased risk for DDH.
The femoral head and the acetabulum must articulate
with each other for normal hip development. If the hip
subluxes or dislocates, the acetabulum becomes shallow
and steep rather than cup shaped, because it lacks the stim-
ulus of the femoral head for development. Eventually, in
chronic subluxation or dislocation, the joint capsule is
stretched, the acetabulum fills with fibrofatty tissue (pul-
vinar), and the labrum inverts. The dislocated femoral head
also presses on the chondro-osseous pelvis, producing a
false acetabulum (pseudoacetabulum).
607
CLINICAL DIAGNOSIS AND IMAGING
The diagnosis of DDH is suspected clinically when physical
examination reveals asymmetric skin folds, limited abduction
of the hip, or an abnormal Barlow or Ortolani maneuver. The
Barlow maneuver attempts to dislocate the femoral head. In
this maneuver, the hip is flexed and adducted and the knee is
pushed posteriorly and superiorly, as in the functioning of a
piston. The exit of the femoral head over the posterior
labrum produces a palpable vibration or clunk that can be
felt by the examiner (18). The Ortolani maneuver assesses the
reduction of a dislocated hip. The hip is flexed 90 degrees and
abducted into a frogleg position. This causes the femoral head
to move back into the acetabulum. As the femoral head passes
over the posterior labrum, it produces a palpable clunk.
Early diagnosis and treatment of DDH are important for
normal hip development. Sonography has now become the
study of choice for evaluating suspected hip dysplasia. Radi-
ography had been the traditional method for the diagnosis of
the dysplastic hip, but in the neonate, radiographs are not very
sensitive because the femoral epiphysis is unossified. The posi-
tion of the unossified epiphysis must be inferred from the ori-
entation of the femoral metaphysis. When the femoral head
ossifies, usually between 2 and 8 months of age, the relation-
ship of the proximal femur to the acetabulum and the extent
of acetabular coverage can be assessed by plain radiography.
Sonography is superior to conventional radiography in
evaluating hip disorders in neonates and young infants
because it can demonstrate the cartilaginous and soft tissue
components of the hip joint, particularly the femoral head
and labrum, which are not visible on radiography. The
sensitivity and specificity of sonography for the diagnosis
of DDH is virtually 100%. Sonography becomes less
reliable once the femoral head ossifies, because the ossified
nucleus impairs visualization of parts of the acetabulum.
Sonographic evaluation of the hip is usually practical up to
6 months of age. Its use can be extended beyond this time
period if there is delayed ossification of the femoral head.
DYNAMIC IMAGING TECHNIQUE
There are two sonographic methods of evaluating the hip:
the dynamic stress technique and the static Graf technique.
Both approaches are based on identification of femoral
and acetabular landmarks.
The dynamic technique, in addition to evaluating
anatomic relationships, includes a dynamic assessment of the
hip (1,16,1922). It has now become the most widely used
technique in North America. The sonographic examination
is performed with a real-time linear array transducer. The
highest-frequency transducer that provides adequate pene-
tration of the soft tissues should be used. A 7.5-MHz or
higher-frequency transducer usually suffices in infants up to
3 months of age; a 5-MHz transducer may be needed in
older infants. Scanning is performed with the infant supine
and the transducer positioned over the lateral or posterolat-
eral aspect of the hip. Coronal and transverse images of the
hip are obtained in both extension (neutral position) and flex-
ion (Fig. 15.9). With the hip flexed, the femur is adducted and
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608 P E D I AT R I C S O N O G R A P H Y

the Barlow maneuver is performed. When the left hip is
examined, the transducer is held in the right hand and the
left hand is used to manipulate the infants leg. When the
right hip is examined, the transducer is held in the left hand
and the infants leg is manipulated with the right hand.
As described earlier, at birth, the femoral head is a
hypoechoic structure with scattered internal echoes (see
Fig. 15.4A). The acetabulum covering the femoral head
contains both bone and cartilage. Bony ossification cen-
ters are present in the ilium, ischium, and pubis; these are
separated by the triradiate cartilage. The ossified portions
of the acetabulum are echogenic and cast an acoustic
shadow. A cartilaginous rim (the labrum) extends later-
ally from the acetabulum to partially cover the femoral
head (23).
On coronal extension and flexion views, the proximal
femoral epiphysis is contained within the acetabulum and
approximately half of the diameter of the femoral head lies
on either side of the ilium (Fig. 15.10A,B). The labrum,
which contains predominantly hyaline cartilage, appears
as a triangular structure, lying superolateral to the femoral
head. It is hyperechoic to cartilage.

A B

C D
Dynamic sonographic technique: positioning of the hip and transducer. A: Coronal extension (neutral) view. The hip is extended and the
Fig. 15.9
transducer is in a coronal plane with respect to the acetabulum. B: Coronal flexion view. The hip is flexed 90 degrees and the trans-
ducer is in a coronal plane with respect to the acetabulum. C: Transverse extension (neutral) view. The hip is extended and the transducer is directed
so that the transverse plane of interest passes through the femoral head into the acetabulum at the center of the triradiate cartilage. D: Transverse
flexion view. The hip is in 90 degrees of flexion and the transducer is in a transverse plane relative to the acetabulum.
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A B

C D

Normal sonographic anatomy of the hip evaluated by the

Fig. 15.10
dynamic imaging technique. A: Coronal extension. B: Coro-
nal flexion. C: Transverse extension. D: Transverse flexion. E: Transverse
flexion with Barlow maneuver. F  femoral head; IL  ilium; arrowhead
 ischium; open arrow  pubic bone anteriorly; M  femoral metaph-
ysis; G  gluteus minimus; GM  gluteus medius; curved arrow  back
E wall of acetabulum; straight arrow  labrum; *  triradiate cartilage.
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610 P E D I AT R I C S O N O G R A P H Y

A B
Subluxed hip. A: Coronal flexion view of the left hip. The femoral head (F) is positioned laterally in relationship to the medial wall of the
Fig. 15.11
acetabulum (curved arrow), but maintains contact with the lateral border of the bony acetabulum (arrowhead) and the labrum (arrow).
Note also the echogenic pulvinar (P) deep to the femoral head. IL  ilium. B: Transverse extension view. The femoral head (F) is positioned laterally
in relationship to the ossified pubic bone (Pub) and ischium (I). P  pulvinar.

On the transverse extension view, the femoral head is
seated in the center of a V-shaped acetabulum formed by
the ischium posteriorly, the pubic bone anteriorly, and the
triradiate cartilage centrally (Fig. 15.10C). The triradiate
cartilage, which is hypoechoic to bone, allows sound trans-
mission. On the transverse flexion view, the ischium is still
visible, but the pubis is obscured by the femoral shaft (Fig.
15.10D). With the Barlow maneuver, the normal femoral
head remains seated in the acetabulum (Fig. 15.10E).
Pathology
The diagnosis of hip dysplasia is based on an abnormal
position of the femoral head at rest or with stress, a shal-
low acetabulum, or a combination of these findings.
The position and stability of the femoral head at rest
and with stress is reported as normal, subluxed, or dis-
located. The normal hip is seated in the center of the
acetabulum at rest and with stress maneuvers. The sub-
luxed femoral head is positioned laterally, but it remains
partially contained by the acetabulum (Fig. 15.11). The
dislocated femoral head is displaced laterally, posteri-
orly, and superiorly to the acetabulum and the pulvinar
or labrum may be interposed between the femoral head
and acetabulum. The dislocated hip has no contact with
or coverage by the acetabulum (Fig. 15.12). It may be
reducible, returning back into the acetabulum with
abduction (Ortolani) maneuvers (Fig. 15.13). In sublux-
ation and dislocation, the acetabulum is shallow. The

A B
Dislocated hip. A: Coronal flexion view. The femoral head (F) is displaced superiorly and laterally out of the acetabulum (arrowhead)
Fig. 15.12
onto the ilium (IL). There is infolding of the labrum (arrow) and increased pulvinar (P). The acetabulum is shallow, reflecting dysplasia.
B: Transverse flexion image shows posterior dislocation of the femoral head (F) over the ischium (arrowhead). P  -pulvinar.
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G
A B
Dislocated hip, which is reseated with Ortolani maneuver. A: Coronal/flexion view. The femoral head (F) is displaced superiorly and lat-
Fig. 15.13
erally out of a shallow acetabulum (arrowhead) onto the ilium. B: Transverse/flexion view with Ortolani maneuver shows the femoral
head (F) reseated in the acetabulum (arrowhead).
sonographic finding of the shallow acetabulum is a
steeply angled roof.
It is important to recognize that transient instability of
the hips in newborn infants is common. Up to a 6-mm dis-
placement of the femoral head can be seen with stress
maneuvers on the first day of life. This transient laxity usu-
ally diminishes in the first few days of life. In infants who
are 2 to 4 weeks of age, the femoral head should be stable
and not move laterally or posteriorly when stress maneu-
vers are performed. Unless there is obvious clinical evi-
dence of dislocation, sonographic evaluation of the hip
should be delayed until 2 weeks of age. This helps to avoid
multiple unnecessary examinations or treatment in cases of
transient laxity or instability.
Other abnormalities associated with DDH include
increased amounts of intra-articular fibrofatty tissue
(termed pulvinar) (see Figs. 15.11 and 15.12), thickened
acetabular cartilage, a tight iliopsoas tendon, and synovial
hyperplasia. Delayed ossification of the femoral head is
also a sequela of long-standing developmental dysplasia.
GRAF TECHNIQUE
The Graf technique is based on a single direct coronal sono-
gram of the hip obtained with a linear array transducer and
with the infant in the lateral decubitus position and the femur
extended. This plane must demonstrate the midportion of the
acetabulum with the straight iliac line seen superiorly. The tip
of the labrum should also be displayed. The depth of the bony
acetabulum is measured, related to fixed points on the bony
and cartilaginous components of the acetabulum.
Three lines and two angles (alpha and beta) are drawn
around the acetabulum (Fig 15.14) (24,25). The alpha
angle is the angle between one line drawn along the
straight edge of the iliac bone and a second line along the
bony acetabular roof. The beta angle is formed by a line
611
through the straight edge of the iliac bone and a line
through the echogenic fibrocartilaginous labrum. The nor-
mal alpha angle is 60 or greater and the normal beta
angle is 55 or less. The smaller the alpha angle and the
larger the beta angle, the more likely that dysplasia is
present.
Four basic hip types are described in the Graf classifi-
cation based on the  and  angles and the development
of the acetabulum (Fig. 15.15). Type 1 is characterized by
an  angle greater than 60 degrees and a  angle greater
than 55 degrees; the acetabulum is normal. Type 2 has an
 angle of 44 to 59 degrees and a  angle of 55 to
77 degrees; the acetabulum may be normal or mildly
underdeveloped. In types 3 and 4 hips, the  angle is less
than 43 degrees and the  angle is 77 degrees or more. In
the type 3 hip, the acetabulum is underdeveloped but par-
tially covers the femoral head. In the type 4 hip, the
acetabulum is markedly underdeveloped and the femoral
head is dislocated.
Type 1 hips tend to occur in infants younger than
2 weeks of age. They are considered normal and require
no treatment and no follow-up. Type 2 hips are consid-
ered physiologically immature and close observation is
needed as there is a small risk of subluxation or disloca-
tion. Types 3 and 4 hips are dislocated and require imme-
diate treatment.
POSTTREATMENT IMAGING AND SEQUELAE
Hip dysplasia in the neonate is usually treated with a flex-
ion-abduction external rotation harness (such as the Pavlik
harness) or splint. These devices direct the femoral head
toward the triradiate cartilage, thereby stimulating acetabular
development. The infant is maintained in this position for
several weeks until the hip joint capsule tightens and the
acetabulum matures.
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A B
Sonographic anatomy of the hip as evaluated by the Graf technique. Schematic representation of the coronal view of the hip (A) and coro-
Fig. 15.14
nal sonogram (B) delineate the femoral head, bony acetabulum and labrum. A horizontal baseline is drawn along the ilium (1), along with
lines along the labrum (2) and bony acetabulum (3). The alpha angle measures the acetabulum and is equal to greater than 60 in infants with seated
hips and less than 50 in patients with dysplasia. The beta angle increases proportionally with the degree of hip dysplasia and displacement. (Panel A
adapted from Graf R. Classification of hip joint dysplasia by means of sonography. Arch Orthop Trauma Surg 1984;102;248255, with permission.)

A B

C D

Four hip types by the Graf technique. A: Type 1, normal, a angle greater than 60 degrees. B: Type 2, slightly shallow acetabulum.
Fig. 15.15
C: Type 3, shallow acetabulum, femoral head minimally covered and displaced laterally, labrum everted. Notice the increased fibro-
fatty tissue, or pulvinar, deep in the acetabulum (*), and the superior displacement of the labrum (arrow). D: Type 4, dysplastic acetabulum, lat-
eral and cephalad displacement of the femoral head (F) and the labrum (*) interposed between the femoral head and acetabulum.
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G
Serial sonography provides a useful means to assess the
relationship of the femoral head to the acetabulum when
the child is in a splint or harness (26). Sonographic images
are acquired only in transverse/flexion and transverse/coro-
nal views. Neutral views and stress maneuvers are not per-
formed since they would require removal of the harness or
abduction splint. If the dislocation is reduced, the femoral
head should be in the center of the acetabulum. Positioning
of the femoral head laterally, superiorly, or posteriorly indi-
cates unsatisfactory reduction. The acetabulumtofemoral
head relationship usually becomes normal within 6 to
8 weeks of treatment (27). Reduction performed before
4 years of age results in a normal relationship of the acetab-
ulum and femur in more than 95% of patients (28).
Treatment with a harness or other abduction device has a
very low complication rate, and avascular necrosis occurs in
less than 1% of patients. Color Doppler imaging may be help-
ful to assess the integrity of the blood supply to the proximal
femoral epiphysis. Epiphyseal flow can be identified in the
normal femoral epiphysis. Diminished or absent flow may be
seen in neonates at risk for avascular necrosis (29). The long-
term sequela of untreated DDH is early degenerative arthritis.
SCREENING
The use of sonography to screen all newborn infants for
hip dysplasia remains controversial. With screening sonog-
raphy, the incidence of DDH in newborns with normal
clinical examinations is 0.2 to 0.6 per 1000 (30). Although
screening of all neonates could potentially eliminate
missed diagnoses of DDH, it is not considered practical in
the United States because of the cost, equipment, and man-
power that would be required (1,19,20).
The differential diagnosis of developmental dysplasia
includes hip subluxation due to neuromuscular disease,
septic arthritis, epiphyseal fracture, proximal femoral focal
deficiency, and coxa vara. Clinical history and imaging
studies usually allow a specific diagnosis. The sonographic
appearances of these conditions are described elsewhere in
this chapter.
THREE-DIMENSIONAL SONOGRAPHY
Three-dimensional sonography allows imaging in sagittal
and craniocaudal projections. Because three-dimensional
sonography can present a global view of the hip, it appears
Classification of proximal femoral focal
Fig. 15.16
deficiency. The four major types are
based on the presence or absence of the femoral head
and neck and the extent of femoral dysplasia. See text
for more detailed description. (Adapted from Levinson
ED, Ozonoff MB, Royen PM. Proximal focal femoral
deficiency (PFFD). Radiology 1977;125:197203.) A B
613
to be superior to conventional sonography in demonstrat-
ing the position of the femoral head with respect to the
acetabulum (31). However, the three-dimensional tech-
nique is limited by technical factors, such as slow data
acquisition and reconstruction, and therefore, it is not
practical yet for routine use.
Proximal Femoral Focal Deficiency
Proximal femoral focal deficiency (PFFD) is a congenital
abnormality in which there is a variable degree of under-
development of the proximal femur as a result of an error
in formation of subtrochanteric bone. The defect ranges in
severity from mild femoral shortening with varus defor-
mity of the femoral neck to nearly total absence of the
femur. The cause is unknown, but it is thought to be due
to an in utero vascular accident. Most cases are unilateral.
PFFD is usually an isolated anomaly, but it can be associ-
ated with caudal regression syndrome and also can be seen
in infants of diabetic mothers. The diagnosis is usually
made in the neonatal period when the infant is noted to
have a short lower extremity. Occasionally, the diagnosis is
made later when the patient begins to walk, because the
discrepancy in leg length produces a limp.
Four classes of PFFD are recognized, based on the
degree of shortening of the femur and the presence or
absence of the femoral head and neck (Fig. 15.16)
(3234). In type A PFFD, the mildest form, a short seg-
ment of the proximal femur is absent. The femoral head is
seated in a normal acetabulum, and there is a cartilagi-
nous or bony connection between the head and the
remainder of the femur, producing a coxa vara deformity.
In type B PFFD, there is also an absent segment of the
femur below the femoral head. The femoral head is pres-
ent and seated within the acetabulum, which is slightly
dysplastic. There is no connection between the head and
distal shaft (Fig. 15.17). In type C PFFD, the femoral head
is absent, the distal femoral segment is short, and the
acetabulum is dysplastic (Fig. 15.18). In the most severe
form, type D PFFD, the acetabulum and femoral head are
absent and the distal femoral segment is markedly short
and dysplastic. Ipsilateral fibular agenesis is present in
about 70% of all cases.
The treatment of PFFD varies with the severity of the
anomaly. Types A and B PFDD may require a valgus
C D
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614 P E D I AT R I C S O N O G R A P H Y

A C

Proximal focal femoral deficiency, type B. A: Frontal

Fig. 15.17
radiograph shows a short right femur without an
identifiable proximal epiphysis. B: Oblique sonogram shows a
cartilaginous proximal femoral epiphysis (e) within the right
acetabulum, but no connection of the femoral neck (arrowhead)
to the distal femur. C: Gradient echo magnetic resonance image
shows the epiphysis (e) and the disconnection (arrow) with the
B femoral shaft.

Proximal focal femoral deficiency, type C. The femoral head

Fig. 15.18
is absent. The femur (F) is shortened and the acetabulum
(arrow) is underdeveloped. IL  ilium.
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G 615

osteotomy to correct the coxa vara deformity. Types C and
D require more extensive surgery, ranging from leg-length-
ening techniques to amputation of the foot and arthrode-
sis of the knee, which provides a stump for a prosthesis.
The differential diagnosis of PPFD includes develop-
mental hip dysplasia and other conditions that cause short-
ening of the femur, including a variety of skeletal dys-
plasias. In patients with developmental hip dysplasia, the
femoral head is developed but is not centered in the acetab-
ulum. In patients with skeletal dysplasias, there is shorten-
ing of multiple bones (not just the femur).
Tibial Hemimelia
Tibial hemimelia is a rare anomaly characterized by partial
or complete absence of the tibia. Four types have been
described (35). In type 1A, the tibia is absent and the distal
femur hypoplastic. In type 1B, a rudimentary tibia articulates
with a relatively normal femur. In type 2, the proximal tibia
is well developed but the distal tibia is absent. In type 3, the
tibia is an amorphous structure with poor development dis-
tally and proximally. In type 4, the proximal end of the tibia
is normal and the distal end is shortened with diastasis of the
ankle joint. Associated anomalies include hypoplasia of the
distal femur, hypoplasia of the fibula, varus deformity of
the foot and absence of the medial rays of the foot.
Sonography has been used to determine the size and
position of the cartilaginous tibial anlage, the presence or
absence of the patellar tendon, and the relationship of the
rudimentary tibia to the articular surface of the femoral
condyle (Fig. 15.19) (36). This information is helpful in

Tibial hemimelia. A: Anteroposterior radiograph of

Fig. 15.19
the left lower limb shows a hypoplastic and dislo-
cated fibula as well as a clubfoot. Transverse (B) and longitudinal
(C) sonograms show a well-formed fibular epiphysis (E) and small
cartilaginous proximal tibial anlage (TIB). The ossified proximal
C fibula (FIB) casts an acoustic shadow (arrowheads).
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616 P E D I AT R I C S O N O G R A P H Y

planning treatment, which ranges from amputation in
severe cases to fusion of the fibula to the tibial anlage in
milder cases.
Congenital Knee Anomalies
Sonography is an excellent method of assessing the rela-
tionship of the femur and tibia at rest and with motion in
the neonate.
GENU RECURVATUM
Genu recurvatum or hyperextension of the knee is a rare
anomaly. It has been generally classified as simple hyperex-
tension or recurvatum; hyperextension with anterior sub-
luxation of the tibia on the femur; and hyperextension with
dislocation of the tibia on the femur. It can be sporadic and
it can be associated with syndromic abnormalities, such as
Down syndrome, Larsen syndrome, and arthrogryposis.
The knee anomalies are usually clinically apparent at birth.
Early manipulation combined with splinting and casting is
the primary treatment in the neonatal period. Sonography
can depict the articular relationships of the cartilaginous
knee (Fig. 15.20).
CONGENITAL ANOMALIES OF THE PATELLA
Congenital anomalies of the patella include absence,
hypoplasia, and dislocation (37). In absence or hypoplasia
of the patella, patients present with flattening of the ante-
rior aspect of the knee. In congenital dislocation, the
patella is displaced laterally on the lateral femoral condyle.
Infants present with flexion deformity of the knee and lat-
eral rotation of the tibia. The patella ossifies between 3 and
4 years of age, so routine radiographs do not show the dis-
location. Sonography can show the presence, size, and
relationship of the patella to adjacent joint structures (Fig.
15.21) (37).
Congenital Hindfoot Anomalies
Images of the hindfoot are acquired with a 7.5-MHz lin-
ear transducer and stand-off pad. A midline sagittal view
with the transducer placed on the posterior-superior part
of the heel allows assessment of the distal tibiacalcaneus
relationship. Sagittal and transverse views with the trans-
ducer placed medially and anteriorly over the junction of
the ankle and foot allow evaluation of the medial malleo-
lus, talus, navicular, first metatarsal, and medial cuneiform
(Fig. 15.22A). Sagittal and transverse views with the
transducer positioned laterally and anteriorly allow eval-
uation of the calcaneocuboid relationship. Scans are
obtained in neutral position and with abduction of
the foot.
In clubfoot or talipes equinovarus, the navicular bone
is displaced medially. On anteromedial views of the
anklefoot junction with abduction maneuvers, the dis-
tance between the cartilaginous medial malleolar epiphysis
and the cartilaginous navicular is shorter in the clubfoot
than in the normal foot due to this medial displacement

A B
Bilateral genu recurvatum with dislocations. A: Longitudinal scan through the lateral aspect of the left popliteal fossa with the leg
Fig. 15.20
extended in neutral position shows normal alignment of the tibia (T) and femur (F). E  unossified hypoechoic epiphyses. B: Longitu-
dinal scan with the leg hyperextended beyond 90 degrees shows the tibia (T) dislocated anteriorly and superiorly relative to the femur (F).
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A B
Congenital patellar hypoplasia. A: Longitudinal sonogram through the lateral aspect of the right knee in a 3-month-old boy shows a
Fig. 15.21
small cartilaginous patella (P). B: Longitudinal anterior sonogram through the normal left knee shows a larger, well-formed, midline
patella (P). Arrows indicate the patellar tendon. F  femoral metaphysis; EF  cartilaginous femoral epiphysis; ET  tibial epiphysis; T  tibial meta-
physis.

(Fig. 15.22). On the posterior, midline sagittal view of the
heel with the foot in plantarflexion, the distance between
the ossified tibia and the superior surface of the ossified
calcaneus decreases in the normal foot but not in clubfoot.
The Achilles tendon is often shortened in clubfoot defor-
mity (38).
Congenital vertical talus (also known as congenital
rocker-bottom foot) is a fixed foot deformity characterized
by talonavicular dislocation. The talus is plantar flexed
and does not articulate with the navicular bone (39).
SOFT TISSUE MASSES
Imaging Approach
The most common benign soft tissue masses in children
are the congenital vascular tumors, neurofibroma, lipoma,

A B

Clubfoot. Three sagittal images with the transducer

Fig. 15.22
placed over the medial and anterior aspect over the
anklefoot junction. A: Normal foot, neutral position. Sonogram showing
normal relationships between the cartilaginous medial malleolus (Mal),
cartilaginous navicular (Nav), ossified talus (Tal), and ossified first
metatarsal (1 MT). B: Normal foot, abduction. The distance (white line)
between the cartilaginous medial malleolus (Mal) and cartilaginous nav-
icular (Nav) is 1.65 cm. In neutral position, the distance was about 1 cm.
C: Clubfoot, abduction. The distance (white line) between the medial
malleolus (Mal) and navicular (Nav) is 0.77 cm. In neutral position, the dis-
C tance was about 0.45 cm. Tal  ossified talus.
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618 P E D I AT R I C S O N O G R A P H Y
ganglion cyst, hematoma, and abscess. The most frequent
malignant mass is rhabdomyosarcoma. Sonography is
usually the first imaging examination for evaluation of
superficial soft tissue masses in children. It allows deter-
mination of lesion size and internal matrix (i.e., cystic or
solid), and occasionally it can suggest a specific diagnosis
(40,41). Magnetic resonance imaging (MRI) has become
the examination of choice in large lesions to define the
extent of the mass and its relationship to muscle, fat, and
bone (42).
Congenital Vascular Lesions
The nomenclature and classification of vascular neoplasms
is complex because of the multiplicity of clinicopathologic
findings and the overlapping histologic features. A simpli-
fied classification divides these tumors into hemangiomas
and vascular malformations (43,44). Hemangiomas are
endothelial-lined neoplasms that have characteristic prolif-
erating and involuting stages. Vascular malformations are
composed of dysplastic vessels that show no cellular pro-
liferation or regression. They are subcategorized by their
flow (high- or slow-flow malformations) and by the pre-
dominant vascular channel (arteriovenous, venous, capil-
lary, or lymphatic malformations).
A B
C resistance arterial flow.
HEMANGIOMAS
Hemangioma is the most common vascular tumor of
infancy. It is a benign, slow-growing lesion that may also
contain nonvascular elements such as fat, fibrous tissue,
and smooth muscle. It can arise within superficial or deep
soft tissues. Hemangiomas usually appear in the first
decade of life, often in the first week of life, and are located
in the head and neck (60%), the trunk (25%), and the
extremities (15%) (44). They typically present as subcuta-
neous bluish or reddish soft tissue masses. Histologically,
they have a characteristic early proliferating phase
(approximately the first 3 to 9 months of age) and a late
involuting stages (18 months to 10 years of age) (44).
Gray-scale sonography shows a homogeneous or het-
erogeneous mass, which is hypoechoic or isoechoic to adja-
cent soft tissues (Fig. 15.23). Foci of very bright echogenic-
ity may be observed secondary to vessel thrombosis, fatty
tissue, or calcification. Hemangiomas are usually hypervas-
cular masses. Doppler sonography shows multiple vascular
channels with high-velocity arterial flow. Mean Doppler
shift is often 2 kHz (44). Venous flow is monophasic since
arteriovenous shunting is absent (44,45). Lesion size and
the number of vascular channels decrease during the invo-
lution phase.
Hemangioma. A: Longitudinal sonogram in a 3-month-old
Fig. 15.23
girl with swelling behind the ear shows a well-defined,
subcutaneous mass (arrows), which is isoechoic to soft tissues.
B: Color Doppler sonogram shows hypervascularity and a large feed-
ing artery (arrows). C: Pulsed Doppler sonogram documents low-
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G
VASCULAR MALFORMATIONS
High-flow Malformations
Arteriovenous malformations and fistulas are high-flow
vascular lesions. Histologically, arteriovenous malforma-
tions are characterized by a network of multiple abnormal
vascular channels (termed a nidus) interposed between
enlarged feeding arteries and draining veins. The arteri-
ovenous fistula is a form of arteriovenous malformation,
which has a single communication interposed between a
feeding artery and a draining vein. The normal capillary
bed is absent in both lesions. Clinical findings include a
pulsatile mass with a bruit or thrill.
Gray-scale sonography shows hypoechoic channels.
Color Doppler imaging shows high-velocity systolic arte-
rial flow and arterialized venous waveforms (Fig. 15.24)
(44).
Slow Flow Malformations
Venous malformations are slow-flow lesions characterized
by dilated venous spaces and a normal arterial component.
They may involve skin, muscle, or both tissues. Clinically,
they present as soft, compressible masses usually of bluish
color, although the overlying skin may be normal. Gray-scale
sonography shows multiple anechoic or hypoechoic chan-
nels, which may contain highly reflective foci with poste-
rior acoustic shadowing, representing phleboliths (44,46).
Doppler evaluation demonstrates either low-velocity
monophasic flow or no flow at all (Fig. 15.25) (44,46). Aver-
age flow velocity is 0.22 kHz (46). The diameter of the veins
may increase following the Valsalva maneuver.
Capillary malformations (i.e., port wine stain) are
characterized by a collection of small vascular channels in
A B
Arteriovenous malformation. A: Longitudinal color Doppler scan demonstrates numerous enlarged vessels coursing through thickened
Fig. 15.24
subcutaneous tissues. B: Longitudinal pulsed Doppler image shows high-velocity systolic arterial flow. (Case courtesy of Brian Coley, MD.)
619
the dermis. Imaging studies are usually normal, although
increased thickness of the subcutaneous fat and promi-
nent venous channels may be seen in some patients.
Lymphatic malformations, also termed cystic hygro-
mas, are congenital lesions composed of dilated lym-
phatic channels that fail to communicate with peripheral
draining channels (47). They usually present as painless,
soft masses, most often before the second year of life. Sud-
den enlargement suggests bleeding. About 75% are found
in the neck, 20% in the axilla, and the remainder in the
mediastinum, retroperitoneum, bone, and abdominal
organs. Smaller lesions tend to be well marginated, while
larger lesions often are infiltrative and ill-defined. On gray-
scale sonography, they appear as thin-walled, multilocular
masses with hypoechoic spaces and echogenic septations
(Fig. 15.26) (44). Doppler sonography can show flow in
the septations, but not in the fluid-filled locules.
Limb overgrowth and vascular lesions may be observed
in the following syndromes:
1. Klippel-Trenaunay syndrome (capillary port wine stain,
varicosities, and lymphangiomas)
2. Parkes-Weber syndrome (capillary port wine stain, vari-
cosities, and arteriovenous fistulas)
3. Proteus syndrome (port wine stains; lymphangiomas
and lipohemangiomas; lipomas; epidermal nevi; partial
gigantism with cerebroid gyriform hypertrophy of the
hands and/or feet; asymmetric macrocephaly; and intra-
abdominal lipomatosis)
4. Maffucci syndrome (venous malformations, lymphan-
giomas, enchondromas, and exostoses)
5. Blue rubber bleb nevus syndrome (cavernous heman-
giomas in skin and gastrointestinal tract)
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620 P E D I AT R I C S O N O G R A P H Y

A B

Venous malformation. A: Longitudinal view of the left index

Fig. 15.25
finger reveals a subcutaneous network of anechoic chan-
nels (arrows). B: Longitudinal color Doppler image shows flow within the
channels. Venous waveform was documented on Doppler imaging (not
shown). C: Pulsed Doppler image in another patient with a venous mal-
formation shows low-velocity monophasic flow. (Panels A and B courtesy
C of Brian Coley, MD.)

Cystic hygroma. Longitudinal scan of the axilla shows an

Fig. 15.26
ill-defined, complex mass with hypoechoic spaces and
echogenic septations. There was no flow on Doppler interrogation.
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G 621

A B
Lymph nodes. A: Longitudinal view of the right forearm shows two ovoid, hypoechoic nodes. B: Color Doppler image shows central
Fig. 15.27
and peripheral (arrows) vascularity. Biopsy showed non-Hodgkin lymphoma.

Benign Nonvascular Masses occur sporadically or in association with neurofibromato-

LYMPHADENOPATHY
Lymph nodes can enlarge secondary to infectious or neo-
plastic conditions. On gray-scale imaging, infected and
neoplastic nodes are hypoechoic to muscle and homoge-
neous (Fig. 15.27). On color Doppler interrogation, infected
nodes tend to have highly vascular centers, whereas malig-
nant nodes more often show eccentric peripheral or com-
bined peripheral and central vascularity (Fig. 15.27B),
although they can show only central flow.
NEUROFIBROMAS
Neurofibromas are the most common neural tumors in
children. They arise within peripheral nerve fibers and may
sis type 1 (NF1). Those lesions associated with NF1 may
be solitary, multiple, or plexiform, although only the plex-
iform neurofibromas are considered evidence for the diag-
nosis of neurofibromatosis. Malignant degeneration is
rare, but can occur.
Schwannoma is the second most common benign nerve
sheath tumor, although it does not occur frequently in
childhood. It grows at the periphery of the nerve, which is
compressed and displaced. Schwannomas rarely if ever
become malignant.
Tumors of neural sheath origin usually appear as round
or oval, smoothly marginated masses with a characteristic
location in the neurovascular bundle. They are hypoechoic
relative to surrounding tissues (Fig. 15.28), and they may

A B
Nerve sheath tumors. A: Neurofibroma. Transverse view of the dorsum of the right hand shows multiple homogeneous, hypoechoic
Fig. 15.28
masses (arrows). B: Schwannoma. Longitudinal sonogram of the anterior calf of another patient demonstrates a hypoechoic mass
anterior to the tibia (T).
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622 P E D I AT R I C S O N O G R A P H Y
be homogeneous or heterogeneous with highly echogenic
foci reflecting the presence of calcifications (4852).
Distinction between benign and malignant tumors is diffi-
cult, but irregular or infiltrating tumor border, internal het-
erogeneity, or asymmetrically large soft tissue masses
should raise a suspicion of malignancy.
FATTY TUMORS
Almost all lipomatous tumors in children are simple
lipomas or lipoblastomas. Simple lipomas are composed
of mature adipose tissue. They are most common in the
subcutaneous tissues of the extremities. On sonography,
they appear as well-defined, homogeneous masses with
an echotexture equal or greater than that of adjacent
soft tissue (Fig. 15.29) (53,54). Occasionally, they con-
tain thin septations. They are avascular on Doppler
imaging.
Lipoblastoma contains multiple lobules of immature
fatty tissue separated by fibrous septa. It occurs almost
exclusively in young children, usually under 3 years of age.
Most arise in the superficial soft tissues or subcutaneous
tissues of the extremities, although they can occur in the
neck or trunk. They may be well circumscribed, or diffuse
and infiltrative, a condition referred to as diffuse lipoblas-
tomatosis. On sonography, lipoblastoma appears as a
complex echogenic mass. Lipoblastoma and liposarcoma
are indistinguishable on imaging studies, but the latter
tumor is exceedingly rare in children, with an incidence of
less than 1%.
CYSTIC MASSES
Ganglion Cysts
Ganglion cysts are nonsynovial cystic masses containing a
myxoid or clear gelatinous matrix and a fibrous lining.
They arise close to tendon sheaths and structures that con-
Lipoma. Longitudinal sonogram of the proximal thigh
Fig. 15.29
shows a well-defined, homogeneous subcutaneous
mass (calipers) with echogenicity similar to adjacent soft tissue. There
was no appreciable vascularity with color Doppler imaging. F  femur.
Ganglion cyst. Transverse sonogram demonstrates an
Fig. 15.30
ovoid anechoic mass (calipers) adjacent to the volar sur-
face of the distal radius (Rad) and ulnar (Ul).
tain synovial lining. The most common location is along
the dorsal surface of the hand and wrist (particularly near
the scapholunate joint), although the cysts can occur any-
where in the soft tissues. Most do not communicate with
the joint space (55). At sonography, ganglion cysts appear
as fluid-filled structures with well-defined walls and poste-
rior acoustic enhancement (Fig. 15.30). They may contain
low-level echoes from debris or septations and be com-
pressible during real-time imaging.
Popliteal Cysts
Popliteal cysts, also known as Baker cysts, are abnormal
fluid collections in the gastrocnemius-semimembranous
bursa. Most popliteal cysts are isolated abnormalities that
occur in the absence of other intra-articular disease. Occa-
sionally, they are associated with juvenile rheumatoid
arthritis. Patients present with an asymptomatic mass
behind the knee or with knee pain and impaired knee
mobility. Less frequently, these cysts dissect into the calf or
rupture, causing a swollen painful extremity.
Popliteal cysts are seen best with the patient in the prone
position, the knee extended, and the transducer placed pos-
teromedially on the popliteal fossa. They appear as hypoe-
choic fluid collections posterior to the joint (Fig. 15.31)
(56). Extension of fluid superiorly into the thigh or inferi-
orly into the calf may be noted when there is cyst rupture
(Fig. 15.31C). Internal echoes, representing debris, can be
seen when the cysts are inflamed or bleed. A characteristic
diagnostic feature is the presence of a curved beak-like
extension or neck that extends between the medial gastroc-
nemius and the semimembranosus tendon (Fig. 15.31B).
Differential diagnostic considerations include a meniscal
cyst (see next section) and a popliteal artery aneurysm.
Aneurysms are anechoic or hypoechoic masses on gray-scale
imaging and show turbulent flow on Doppler imaging.
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A B

Popliteal cyst. A: Prone longitudinal scan shows an oval

Fig. 15.31
cystic mass (calipers) in the soft tissues posterior to the
knee joint. T  tibia. B: Transverse view shows a characteristic beak-like
extension (arrow) coursing toward the joint space. C: Longitudinal sono-
gram in another patient shows inferior dissection of the cyst into the calf
C (arrows). P  cyst in the popliteal fossa.

Meniscal Cysts
Meniscal cysts form adjacent to a meniscal tear. They can
occur medially or laterally along the joint line. The pres-
ence of a periarticular cystic mass associated with a hypo-
echoic defect in the substance of the meniscus allows a diag-
nosis of meniscal cyst (57,58).
show a fascial defect or focal thinning and elevation of the
fascia at the site of muscle protrusion (Fig. 15.32). The
herniation may be easier to detect when the muscle is con-
tracted. The herniated muscle is often less echogenic than
normal muscle, possibly due to anisotropy or atrophy.

MISCELLANEOUS BENIGN MASSES

Accessory muscles can be found at the ankle and wrist
(59) and can present as a soft tissue mass or be an inci-
dental finding on routine sonography. The mass has sono-
graphic characteristics similar to those of normal muscle.
Dynamic imaging may show shortening and elongation of
the muscle during flexion and extension, confirming the
diagnosis.
Muscle hernias are protrusion of muscle into the sub-
cutaneous fat through a defect in the fascia (60). Most
occur in the lower leg and affect the tibialis anterior mus-
cle, although other muscles can be involved. Sports activ-
ities, trauma, chronic compartment syndrome, and weak-
ness in the overlying fascia due to perforating vessels have
been postulated as causative factors. Patients are usually
adolescents or young adults who present with a soft tissue Herniated muscle. Transverse sonogram of the anterior
mass that enlarges when the affected muscle is contracted Fig. 15.32
calf shows a fascial defect (calipers, measuring 6 mm) in
or the patient is erect and decreases in size when the mus- the tibialis anterior muscle with anterior protrusion of muscular tissue
cle is relaxed or the patient is supine. Sonography can (arrow). The hernia was reducible.
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624 P E D I AT R I C S O N O G R A P H Y

A B
Rhabdomyosarcoma. Longitudinal gray-scale (A) and color Doppler (B) sonograms of the left thigh of a 15-year-old boy show a het-
Fig. 15.33
erogeneous echogenic mass with irregular margins, anechoic areas reflecting necrosis, and absent vascularity.

Hematoma and fat necrosis are other causes of soft tis- tissues (cellulitis and abscess), and muscles (pyomyositis).
sue masses (61). These are discussed later (see discussion In advanced osseous infection (osteomyelitis), it can be
on Trauma). used as an ancillary study to show local complications.

Malignant Tumors Hip Joint Effusion

Rhabdomyosarcoma is the most common malignant soft TRANSIENT (TOXIC) SYNOVITIS
tissue tumor in children (62,63). Approximately two thirds Toxic synovitis (also called transient synovitis) is the most
of rhabdomyosarcomas are diagnosed in children younger common cause of a painful hip and joint effusion in a child
than 6 years of age, with a smaller peak occurring in ado- (28). It typically affects children between 5 and 10 years of
lescence. The head and neck, genitourinary tract, and age, who present with hip or knee pain and a limp. There
extremities are the most common locations. The two is usually a low-grade fever with only mild leukocytosis. The
major histologic subtypes are embryonal and alveolar. exact cause is unknown, but viral infection, allergic reaction,
Tumors arising in the head and neck are nearly always
embryonal, whereas extremity rhabdomyosarcomas are
more frequently of the alveolar subtype.
Other rare sarcomas include synovial sarcoma, fibrosar-
coma, neurofibrosarcoma, malignant fibrous histiocytoma,
leiomyosarcoma, alveolar part sarcoma, and liposarcoma.
Malignant soft tissue tumors can be homogeneous or het-
erogeneous, containing hypoechoic areas due to necrosis or
hemorrhage and hyperechoic areas related to calcification.
The margins may be well circumscribed or poorly defined
and infiltrative. The echogenicity is variable and the tumor
may be hypoechoic, isoechoic, or hyperechoic to adjacent
soft tissues (Figs. 15.33 to 15.35). Increased vascularity may
be noted on color Doppler sonography. The imaging features
of rhabdomyosarcoma and the other sarcomas are nonspe-
cific, and some benign processes, such as acute hematomas,
abscesses, and benign neoplasms, can have appearances sim-
ilar to malignant neoplasms. Tissue sampling is needed for a
specific histologic diagnosis.

INFECTION Ewing sarcoma. Transverse scan along the posterior

Sonography has become a primary imaging study for the Fig. 15.34
joint line of the right knee in an 18-year-old boy shows a
diagnosis of infection of the joint space (effusions), soft predominantly hypoechoic mass (calipers).
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A B
Cutaneous lymphoma. A: Transverse scan of the right midthigh shows a heterogeneous septated mass with poorly defined borders and
Fig. 15.35
subcutaneous skin thickening. B: Color Doppler scan shows increased vascularity in the tumor. (Case courtesy of Brian Coley, MD.)

and trauma have been considered as possible etiologies. The sensitivity of sonography for detecting joint effusion is
Symptoms usually improve within 24 to 48 hours with rest, 90% to 100% (65,66).
and there are usually no complications. A rare sequela is
avascular necrosis (1% to 2% of patients). NORMAL ANATOMY
The femoral head, neck, and shaft are highly echogenic
SEPTIC ARTHRITIS and produce acoustic shadowing. The joint capsule is
Septic arthritis can arise as a hematogenous infection due to composed of anterior and posterior layers, which are
seeding of a joint as a result of sepsis; by direct implanta- separated by either a linear echogenic reflection, repre-
tion in association with a penetrating injury of a joint; or senting the apposed synovial linings, or by a small
by contiguous extension from a focus of osteomyelitis (64). amount of fluid (67). The anterior surface of the joint
Group B Streptococcus is the most common organism in capsule parallels the anterior cortex of the femoral neck
neonates, while Staphylococcus aureus is the common and has a concave configuration (Fig. 15.36). The width
organism in infants and older children. Patients present
with fever, irritability, and lack of movement of the affected
extremity. On physical examination, the hip is held in flex-
ion, abduction, and external rotation. Treatment is urgent
arthrotomy and open drainage. Complications of acute
septic arthritis include osteomyelitis, epiphyseal separation,
joint destruction, fibrous or bony ankylosis, contracture,
and osteonecrosis of the femoral head.

TECHNIQUE
Radiographs are usually normal in patients with toxic syn-
ovitis and early in the course of septic arthritis. As the amount
of joint fluid and pressure within the hip joint increase, the
joint space can be widened and the femur can be displaced
laterally. Normal radiographs do not exclude joint effusion.
Because of its greater sensitivity, sonography is the method of
choice for detecting fluid in the hip joint. Effusions, as small
as 1 mL, have been detected in cadaver studies (65).
The patient is positioned supine with the hip in a neu-
tral position. Scanning is performed from an anterior
approach with the transducer in a sagittal plane parallel to
the long axis of the femoral neck. On occasion, transverse Normal hip capsule. Sonogram obtained from an anterior
views can demonstrate fluid in recesses not seen on the Fig. 15.36
approach shows the joint capsule (arrows) of the left hip
sagittal images. Comparison views are obtained of the paralleling the femoral neck (FN). The capsule has a concave anterior
opposite hip; the split-screen function is particularly useful margin and the anterior and posterior layers are separated by a small
to compare the two hips for the presence of joint effusion. amount of fluid. Capsule-to-bone distance is 3.0 mm.
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626 P E D I AT R I C S O N O G R A P H Y
Septic arthritis. Sagittal sonogram of the right (RT) and left (LT) hips shows fluid distending the joint capsule of the right hip. The cap-
Fig. 15.37
sule has a convex anterior margin (arrows). The left hip is normal. The capsule-to-bone width measured 9 mm on the right (calipers 1)
and 3 mm on the left (calipers 2).
of the capsule, measured from the anterior surface of the
capsule to the anterior surface of the femoral neck, is
normally less than 3 mm. The joint capsules should be
symmetric bilaterally and the difference in width should
not exceed 2 mm. The iliopsoas muscle lies superficial to
the joint capsule.
Doppler sonography can show flow in the anterior
ascending cervical artery, which lies in or near the anterior
layer of the joint capsule (68). The mean resistive index
(RI) is 0.58.
SONOGRAPHIC FINDINGS OF EFFUSION
When an effusion is present, the anterior recess of the cap-
sule becomes distended and bulges anteriorly. The margin
of the capsule appears convex rather than concave, and the
capsule-to-bone distance of the affected hip is greater than
3 mm (Fig. 15.37). The difference in the width of the two
hip capsules is greater than 2 mm. The width of the abnor-
mal joint capsule usually exceeds 5 mm (mean 9.91 mm;
standard deviation [SD] 1.7 mm) (6567). The echogenic-
ity of the fluid is variable and fluid can appear anechoic,
hypoechoic, or hyperechoic.
In patients with toxic synovitis and septic arthritis,
Doppler sonography can show high-resistance wave-
forms in the anterior ascending cervical artery (mean
RI  0.92) (6870). Flow returns to normal in 4 to
6 weeks. Color Doppler sonography shows increased
color signal in the capsule and soft tissues in about 25%
of patients with septic arthritis. Color signal is absent in
the remaining patients. It also is absent in patients with
toxic synovitis.
The capsular-to-bone difference and the echogenicity
of the fluid do not permit distinction of septic arthritis
from a sterile joint effusion (66). If septic hip is sus-
pected clinically, the hip must be aspirated regardless of
the findings on sonography. Aspiration of pus from the
hip confirms the diagnosis. If the results of aspiration
yield sterile fluid, the diagnosis of transient synovitis is
made by exclusion. When fluid is identified, sonography
can be used to guide percutaneous aspiration (Fig.
15.38) (67).
Other entities to consider in a child with a painful hip
are septic arthritis, Legg-Calve-Perthes disease, slipped
capital femoral epiphysis, osteoid osteoma, fracture, and
juvenile rheumatoid arthritis.
Cellulitis
Cellulitis is an acute infection of the subcutaneous tissues.
The most common organisms are S. aureus and Strepto-
coccus pyogenes. In neonates, group B streptococci or
rarely Escherichia coli are the causal organisms. Clinical
findings are cutaneous edema, warmth, erythema, and ten-
derness of the affected extremity. Treatment is antimicro-
bial therapy.
The diagnosis of cellulitis is usually made clinically,
but sonography can be used to show the extent of involve-
ment and complications, such as abscess formation. The
sonographic findings of cellulitis are increased thickness
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G 627

A B
Ultrasound-guided hip aspiration. A: Sagittal sonogram of the hip shows fluid distending the joint capsule (calipers). B: Longitudinal
Fig. 15.38
image during sonographically guided aspiration shows the needle (arrows) positioned in the joint capsule (*). The fluid has been aspi-
rated. E  femoral epiphysis; M  metaphysis.

and echogenicity of the subcutaneous tissues and small Necrotizing Fasciitis

irregular round or oval fluid collections (Fig. 15.39)
(64,71,72). In some cases, a reticular appearance may be
seen with anechoic or hypoechoic striations traversing the
subcutaneous tissues. These striations are the result of
edema and inflammatory exudate dissecting in the tissue
spaces. Doppler imaging shows hyperemia of the affected
tissue.
The sonographic appearance of cellulitis is nonspe-
cific, and it can also result from noninfectious causes,
such as insect and spider bites. Sonography can be
used to guide aspiration of inflammatory fluid in the
subcutaneous tissues to obtain a specimen for microbio-
logic analysis.
Necrotizing fasciitis is a rare infection of the superficial
fascia characterized by local tissue destruction and sys-
temic toxicity. It typically spares muscle. The common
causative organism is group A Streptococcus (72). It usu-
ally occurs in immunocompromised patients, but it may
also occur in healthy individuals. The abdominal wall,
extremities, and perineum are the most common sites of
involvement. Clinical findings include cutaneous erythema
and edema, which rapidly progress to frank tissue gan-
grene and tissue sloughing. Treatment requires surgical
debridement of devitalized tissue along with antimicrobial
therapy.

A B
Cellulitis. A, B: Longitudinal sonograms of the lower extremities of two different patients show diffuse thickening and increased
Fig. 15.39
echogenicity of the subcutaneous tissues, which contain small, poorly defined fluid collections, representing localized edema and
inflammatory exudate (arrows). The fascial planes (arrowheads) between the subcutaneous tissues and subadjacent muscle are preserved. (Case
courtesy of Brian Coley, MD.)
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628 P E D I AT R I C S O N O G R A P H Y
Fasciitis. Longitudinal sonogram of the right thigh shows
Fig. 15.40
thickened and echogenic subcutaneous tissue with
hypoechoic fluid collections (arrows) and poorly defined fascial planes
(arrowheads) between subcutaneous tissue and subadjacent muscle.
Sonographic findings are similar to those of cellulitis
(thickened subcutaneous tissues and fluid collections),
but in addition, the fascial boundaries between soft
tissues and subadjacent muscle are poorly defined or
absent (Fig. 15.40).
Abscess
Abscesses are walled-off, suppurative fluid collections.
They usually are hypoechoic or anechoic subcutaneous
masses with increased through-transmission and mass
A B
Soft tissue abscess. A: Transverse sonogram of the thigh shows a large subcutaneous hypoechoic mass (arrows) with echogenic debris and
Fig. 15.41
through-transmission. B: Color Doppler image shows flow in the wall of the abscess. Percutaneous aspiration yielded purulent material.
effect, but they may be hyperechoic or isoechoic to sur-
rounding tissues (64). The margins may be well circum-
scribed or poorly defined. Septations, internal echoes rep-
resenting debris or gas, and a thick echogenic rim are other
common features (Fig. 15.41) (64,72). Gas-forming organ-
isms may produce highly reflective echoes with acoustic
shadowing. Color Doppler imaging can demonstrate
hyperemia in the wall of the abscess and absence of flow in
the center of the abscess (Fig. 15.41B).
The sonographic appearance of an abscess is nonspe-
cific and may be confused with that of hemorrhage or neo-
plasm unless soft tissue gas is present. In the absence of
percutaneous or open surgical interventions, the presence
of gas is indicative of an inflammatory process. Sonogra-
phy can also be used to guide percutaneous drainage pro-
cedures and document response to therapy.
Pyomyositis
Pyomyositis is a primary muscle infection that is com-
monly associated with abscess formation. It is prevalent in
tropical countries and also can be seen in immunocom-
promised patients and occasionally after local trauma.
The skeletal muscles of the thighs, calves, and buttocks
are most often affected. The skin and subcutaneous tissue
are uninvolved or only mildly involved. The causative
agent is usually S. aureus (90% of cases). The clinical
presentation is nonspecific and includes pain, muscle
aches, and deep soft tissue induration without substantial
erythema.
Two sonographic appearances have been described and
correspond to the two stages of the disease (71). The first
stage is characterized by phlegmon and localized muscle
edema. The sonographic findings are those of thickened
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G
A B
C taneous edema.
echogenic muscle with disorganized echotexture and non-
specific, ill-defined hypoechoic areas in one or more muscle
groups, along the fascial planes, or in both locations (Fig.
15.42). The later stage is characterized by abscess forma-
tion, which appears as an intramuscular fluid collection
with increased peripheral vascularity (64,71,73).
Gas Gangrene
Gas gangrene is the result of extensive tissue damage with
gas formation in devitalized tissues. The common causative
organism is Clostridium perfringens. Clostridial infections
cause muscle necrosis and spare the fascia. The sono-
graphic findings are linear collections of gas that are dis-
persed throughout the muscles.
Osteomyelitis
Acute osteomyelitis in the pediatric population is most
often secondary to hematogenous spread and associated
629
Pyomyositis. A: Longitudinal split-image scan of both
Fig. 15.42
thighs of a 10-year-old girl with acute right (RT) thigh
swelling following trauma demonstrates thickened subcutaneous
tissue (SC) and edematous echogenic muscle (M). F  femur. The
normal left (LT) side is presented for comparison. B: Longitudinal
view of the left thigh in another patient shows a thickened
echogenic muscle (arrows) with loss of visualization of the normal
perimysial lines. C: Axial T2-weighted fat-suppressed image shows
increased signal intensity within the muscles (arrows) and subcu-
with a known focus of infection or with a predisposing
condition, such as a skin or upper respiratory infection or
immune disorder. Less often it is the result of a direct pen-
etrating injury or extension from adjacent structures.
In children over 1 year of age, osteomyelitis initially
affects the metaphyses of bones. From this site, the inflam-
matory process can extend throughout the medullary
cavity, into the subperiosteal space with elevation of the
periosteum, and into the soft tissues. S. aureus is the most
common offending organism in this age group. Clinical
findings include rapid onset of pain, tenderness, limping or
refusal to bear weight, and signs of systemic toxicity,
including fever and leukocytosis.
In patients under 1 year of age, some of the nutrient ves-
sels penetrate the physis and allow extension of infection into
the epiphyses and joints. Osteomyelitis and septic arthritis
often coexist in this younger age group. Neonates are also
more prone to multifocal disease than are older children. The
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630 P E D I AT R I C S O N O G R A P H Y

A B

Acute osteomyelitis with subperiosteal abscess. A: Longitu-

Fig. 15.43
dinal sonogram shows a hypoechoic fluid collection
(arrows) containing debris anterior to the femoral metaphysis (M). The
femoral cortex is thickened and irregular (arrowheads), representing new
bone formation. B: Power Doppler sonogram shows hyperemia in the wall
of the abscess and in adjacent soft tissues. M  femoral metaphysis. C:
Two-week follow-up frontal and lateral views of the left femur shows
extensive destruction with periosteal reaction. (Case courtesy of Brian
C Coley, MD.)

organisms that commonly cause multifocal osteomyelitis in
neonates are -hemolytic Streptococcus and E. coli.
MRI is the imaging study of choice in patients with sus-
pected osteomyelitis because it can demonstrate soft tissue
and osseous abnormalities. Conventional radiography,
conventional tomography (CT), and bone scintigraphy can
also be useful in the diagnosis of acute osteomyelitis.
Sonography has a limited role in the primary diagnosis,
but it can be used to identify fluid collections and guide
fluid aspiration to obtain specimens for microbiologic
examination (64,7478).
The earliest sonographic sign of osteomyelitis is non-
specific soft tissue swelling adjacent to the involved bone
(64). Later findings include a fluid collection (abscess)
immediately adjacent to the affected bone, which is often
subperiosteal in location in young children; periosteal
reaction; and cortical destruction (Figs. 15.43 and
15.44). Abscesses are hypoechoic, heterogeneous fluid
collections with internal debris or septations and usually
parallel the periosteum for several centimeters (79). Sub-
periosteal abscesses result in elevation of the periosteal
layer with exudate and hemorrhage. Periosteal reaction
appears as increased cortical thickening. Color Doppler
sonography can show hyperemia in the wall of the
abscess, in adjacent tissues, and at the site of cortical dis-
ruption (74,75).
In chronic osteomyelitis, sonography may be useful in
demonstrating soft tissue abscesses and sinus tracts, which
are characteristic of this process.
Infectious Tenosynovitis
Acute suppurative tenosynovitis is usually caused by S.
aureus or S. pyogenes and most often involves the tendon
sheaths of the digital flexor muscles (64). It is usually the
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A B

Osteomyelitis with subperiosteal abscess. A: Longitudinal sonogram of the lateral aspect of the distal fibula shows a hypoechoic sub-
Fig. 15.44
periosteal abscess (A) adjacent to an area of cortical destruction (arrow). B: Color Doppler image shows hyperemia at the site of
cortical destruction (arrow) and in the adjacent soft tissues. A  subperiosteal abscess. Percutaneous aspiration of the abscess yielded purulent
material, which grew Staphylococcus aureus.

result of a penetrating injury (human or animal bite, punc-
ture wound) and it also may be associated with the pres-
ence of a foreign body.
Sonography shows fluid (pus) within the tendon
sheath, which is enlarged and may have irregular margins.
The tendon itself may be normal or enlarged if there is
associated tendonitis. Doppler imaging can show hyper-
emia in the walls of the fluid collection or tendon sheath
(6,64). A foreign body may be recognized within or adja-
cent to the synovial sheath. The sonographic findings of
infectious and noninfectious tenosynovitis (see discussion
below) are similar and differentiation requires fluid aspira-
tion and analysis (64) (Fig. 15.45).
The diagnosis of tenosynovitis can be made sono-
graphically when the tendon sheath is enlarged and con-
tains fluid, even a minimal amount, since fluid is not
seen around normal tendons (Fig. 15.45). The tendon is
enlarged when there is associated tendonitis. Color flow
Doppler may show hyperemia in the tendon sheath, ten-
don, and/or surrounding soft tissues (Fig. 15.45B). Similar
findings can be seen in infectious tenosynovitis and a spe-
cific diagnosis requires clinical correlation and often fluid
aspiration.
Chronic tendonitis shows similar findings to acute
tenosynovitis. However, the tendon may also contain tiny
calcifications.

Septic Bursitis Synovitis

Septic bursitis in children most often involves the prepatel-
lar bursa. The common pathogen is S. aureus. Sonography
demonstrates a fluid collection, which may contain debris or
septa, in the expected location of a bursa. The walls of the
bursa may or may not be thickened. Color Doppler imaging
may show hyperemia in the periphery of the fluid collection.
Sonography cannot differentiate between infectious and
noninfectious bursitis. Aspiration is required for this dis-
tinction and can be performed with sonographic guidance.
NONINFECTIOUS TENDON-JOINT INFLAMMATION
Tendonitis and Tenosynovitis
The common cause of inflammatory tendonitis and tenosyn-
ovitis in the pediatric population is juvenile rheumatoid
arthritis, although these conditions can be seen with overuse
or connective tissue disease as well as infection (discussed
above). Overuse syndrome causes cumulative microtrauma
to the tendon and tendon sheath, leading to secondary
inflammation and tenosynovitis.
Synovitis is an inflammation of the synovium. Most
often it affects large joints, but it can occur in small
joints and bursae surrounding tendons and ligaments.
Synovitis is associated with juvenile rheumatoid arthri-
tis, hemophilia, chronic infection, and pigmented villon-
odular synovitis. Clinical findings are pain and tender-
ness in the affected joint. Sonography shows a
hypoechoic effusion and synovial thickening. Synovial
thickening appears as irregularity of the synovial lining
or as a nodular mass projecting into the joint space (Fig.
15.46). Color flow can show hyperemia of the synovium
and adjacent periarticular tissues (80). Other findings in
long-standing arthritis include erosions of the articular
cartilage and tenosynovitis.
TRAUMA
Plain radiographs are the initial imaging study in the eval-
uation of trauma, but sonography can be a useful ancillary
study when radiographs are nondiagnostic and symptoms
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632 P E D I AT R I C S O N O G R A P H Y

A B

C D
Acute inflammatory tenosynovitis. A: Longitudinal scan of the wrist of a young adult with juvenile rheumatoid arthritis shows fluid in
Fig. 15.45
the extensor tendon sheath (arrows) and thickened synovial tissues (arrowheads). The tendon (T) is normal. R  radius, L  lunate,
C  capitate. B: Color Doppler image shows hyperemia. Longitudinal (C) and transverse (D) sonograms of the ankle in a young child show an
enlarged anterior tibial tendon (T) and a small amount of fluid (arrows) in the sheath of the tendon. Tib  tibia, Tal  talus. Ultrasound guided aspi-
ration yielded 0.5 mL of fluid.

persist. Sonography has been used in the diagnosis of soft

tissue injury including muscle and tendon abnormalities,
growth plate fractures, some fractures of superficial bones,
and foreign bodies.

Synovitis. Longitudinal anterior sonogram of the right
Fig. 15.46
elbow in an 8-year-old girl with juvenile rheumatoid
arthritis shows a hypoechoic fluid collection (arrows) with thickened
synovium (arrowheads). H  distal humerus condyle.
Hematoma
Blunt or penetrating trauma is the most common cause of
soft tissue hematoma. Other causes include bleeding diathe-
sis and anticoagulant therapy. The sonographic appearance
of a hematoma varies with the age of the blood. An acute
hematoma contains large amounts of fibrin, and thus, sonog-
raphy obtained within a few hours of injury shows a homog-
enous mass with increased echogenicity (Fig. 15.47A). Over
the next several days, clot retraction and organization occur,
and the hematoma develops a complex echotexture. The
subacute hematoma appears heterogeneous and contains
internal echoes and/or septations (Fig. 15.47B). Within a few
weeks, the hematoma liquefies. The chronic hematoma may
appear as a completely anechoic mass or it may contain fine
echogenic strands and/or debris (Fig. 15.48). In some cases,
a fluid level can be seen due to a hematocrit effect. Color
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A B

Hematoma. A: Acute hematoma. Longitudinal scan of the anterior knee of an 8-year-old boy following trauma demonstrates an
Fig. 15.47
echogenic mass (arrows) in the subcutaneous soft tissues. C  articular cartilages of the distal femur (F) and proximal tibia (T).
B: Subacute hematoma. Extended field-of-view longitudinal sonogram of the anterior thigh of another patient 4 days following blunt trauma demon-
strates a predominantly hypoechoic mass (arrows) with low-level internal echoes in the rectus femoris muscle.

Doppler sonography may show increased vascularity around
acute and subacute hematomas.
Fat Necrosis
Fat necrosis is usually limited to the subcutaneous soft tis-
sues. It commonly occurs in areas overlying bony promi-
nences, such as the anterior tibial and gluteal regions.
Patients present with a subacute or chronic palpable lump
Chronic hematoma. Transverse sonogram of the anterior
Fig. 15.48
right thigh shows a predominantly anechoic mass (arrows)
with fine septations in the soft tissue. F  femur.
or deformity. Most do not recall a specific traumatic
event. On sonography, fat necrosis appears hypoechoic,
has a linear rather than mass-like configuration, and is
restricted to the subcutaneous soft tissues. A sequela of fat
necrosis is tissue atrophy, usually limited to the area of fat
necrosis.
Myositis Ossificans
Myositis ossificans is the formation of heterotopic ossifi-
cation in skeletal muscle. It tends to occur in adolescents
and young adults and is usually secondary to direct
trauma. The common locations of traumatic myositis ossi-
ficans are the thigh, buttocks, and elbow. Involvement of
the shoulder and calf is less common. Histologically,
myositis ossificans shows three distinct zones: a central
zone containing proliferating fibroblasts, a middle zone
containing osteoblasts and foci of immature bone, and a
peripheral layer containing mature trabeculae. Bone mat-
uration proceeds in a centrifugal pattern, beginning
peripherally and progressing centrally (81,82). The diag-
nosis is usually based on clinical and imaging findings.
Biopsy is less reliable and may result in an erroneous diag-
nosis of sarcoma.
The clinical findings are usually a firm palpable mass
and history of trauma, although this history is not always
elicited. The early sonographic finding, occurring within
7 to 14 days, is an elongated hypoechoic intramuscular
mass, which may show a central echogenic core or a
zonal pattern characterized by hypoechoic inner and
outer layers separated by an echogenic zone. Serial
sonograms within 2 to 4 weeks will usually show char-
acteristic peripheral and/or internal calcifications with
acoustic shadowing (81,82). Occasionally, sonography
demonstrates a well-circumscribed mass with a fluid-
fluid level.
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634 P E D I AT R I C S O N O G R A P H Y

A B

Separation of proximal humeral epiphysis. Longitudinal dual-image view shows a normally positioned right humeral head (RH). The left
Fig. 15.49
humeral head is not visualized. M  metaphysis. B: Longitudinal sonogram more posteriorly shows the left humeral head (LH) dis-
placed posteriorly and inferiorly, along the humeral metaphysis (M).

Rhabdomyolysis ographs. These include sternoclavicular dislocation, poste-

Rhabdomyolysis is the necrosis of skeletal muscle fibers
with the release of enzymes and myoglobin into the blood
and extracellular fluid. The prevailing causes in children
are crush injuries and child abuse. Sonographic findings
are nonspecific and consist of foci of increased or
decreased echogenicity and locally disorganized fascicular
architecture (83,84).
Fractures
Sonography has been used to detect subtle fractures or dis-
locations, suspected but not well seen on plain radi-
rior humeral head dislocation associated with Erb palsy
(85), clavicle fractures, nondisplaced fractures of the
greater tuberosity of the humerus (86), physeal plate frac-
tures (Fig. 15.49) (87), elbow fractures (88,89), rib frac-
tures (90), and metaphyseal corner fractures associated
with nonaccidental trauma (91).
Normal bone has a smooth echogenic contour. Frac-
tures appear as discontinuity of the echogenic cortex
(Fig. 15.50). The adjacent muscles and soft tissues may
be thickened and hyperemic owing to edema and hem-
orrhage. Hyperemia also can be noted at the fracture
site.

A B

Fracture. A: Longitudinal sonogram through the proximal thigh of a neonate demonstrates focal discontinuity (arrow) of the femoral
Fig. 15.50
cortex. B: Color Doppler image shows hypervascularity in soft tissues and at the fracture site.
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G 635

A B

Foreign body. A: Longitudinal scan of the volar aspect of the right foot shows an echogenic linear band (arrows) with acoustic shad-
Fig. 15.51
owing. A wooden splinter was removed at operation. B: Longitudinal view in another patient shows a hyperechoic linear focus (arrow-
heads) with acoustic shadowing. The anterior hypoechoic area represents edema (E).

Foreign Bodies intramuscular fluid collections (hematoma) (Fig. 15.52).

The common soft tissue foreign bodies in children are The injury does not extend to the surface of the muscle.
wood, glass, and metal slivers. The latter two elements are The appearance is nonspecific and infection can have a
radio-opaque and therefore usually visible to some degree similar appearance. Differentiation usually is based on
on plain radiographs, whereas wood is usually nonopaque clinical history.
and nearly always imperceptible on conventional imaging Sonographic findings of muscle tear are discontinuity
(9294). When a radiolucent foreign body is suspected, of muscle fibers with the defect extending to the surface of
sonography can be used to identify the foreign body. the muscle and retraction of the muscle ends. The site of
Foreign bodies, regardless of composition, appear as the tear is filled with hypoechoic blood. Dynamic scanning
linear echogenic foci with posterior acoustic shadowing or
reverberating comet-tail artifacts (Fig. 15.51). Associ-
ated edema or inflammatory change appears as a poorly
circumscribed hypoechoic or hyperechoic area. In addition
to confirming the presence of a retained foreign body, sonog-
raphy has proven useful in preoperative and, occasionally,
intraoperative localization, thereby decreasing the extent
of soft tissue dissection (95).
Abscesses and granulomas can develop in chronic cases.
Abscesses appear as well-defined fluid collections with
peripheral hyperemia on color Doppler imaging. Granulomas
appear as hypoechoic masses surrounding the foreign body.

Tendon and Muscle Injuries

MUSCLE INJURIES
Muscles injuries are classified as strains, tears, and
hematomas (96). Strains result from overuse, overstretch-
ing, or strenuous activity. The clinical findings include stiff-
ness, soreness, and pain. Muscle tears are usually caused by
an intense contraction against firm resistance leading to dis-
ruption of fibers. The clinical findings are a painful mass Rectus femoris muscle strain. Longitudinal view of the
that enlarges or appears when the affected muscle contracts Fig. 15.52
thigh shows thickening and increased echogenicity of
and decreases in size or disappears when the muscle relaxes. the rectus femoris muscles (RF), which contains small hypoechoic
Sonographic findings of muscle strain include diffuse fluid collections (hematomas) (arrows). The normal fibrillar architec-
hyperechogenicity in the substance of the muscle and small ture is absent. The vastus intermedius (VI) muscle is normal.
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636 P E D I AT R I C S O N O G R A P H Y

Complete Achilles
Fig. 15.53
tendon tear. Longi-
tudinal extended field-of-view
scan demonstrates a complete
gap (arrows) in the normal contin-
uous echogenicity of the Achilles
tendon. The fibrillar appearance
of the Achilles tendon is lost as a
result of retraction and shortening
of the tendon. The retracted prox-
imal tendon (open arrows) end
appears nodular.

during contraction may increase the size of the retracted tions, idiopathic hemihypertrophy, Beckwith-Wiedemann
fibers (96). Strains and tears can show increased flow on syndrome, and deep venous thrombosis. Sonography, with
color Doppler imaging. Doppler imaging, can separate the vascular abnormalities
from the soft tissue enlargement associated with hemihy-
TENDON TEARS pertrophy and Beckwith-Wiedemann syndrome. Sonogra-
Tears of the tendon are classified as partial or complete (full phy has been used to measure limb lengths, but it is not as
thickness). In the complete tear, there is total discontinuity accurate as conventional radiographic techniques.
of the tendon and the two ends of the tendon are retracted,
becoming thick and nodular (Fig. 15.53). The gap between Miscellaneous Problems
the tendon fragments is filled by hypoechoic blood. The
Miscellaneous uses of sonography include (a) demonstra-
free ends may move freely in the interspersed pool of fluid,
tion of fragmentation and lateral uncoverage of the femoral
an appearance termed the bell clapper sign.
head in Legg-Calve-Perthes disease (100,101), (b) identifi-
Partial rupture produces a focal hypoechoic defect in
cation of slipped femoral capital epiphysis (Fig. 15.54), (c)
the substance of the tendon or its attachment (6). The
defect in the fascicles is filled with blood and edema. The
tendon is deformed or focally thin at the site of injury.
Because of the presence of some intact fibers, retraction is
minimal or absent in a partial tear. Color flow Doppler usu-
ally does not show flow in the area of the tear, which is use-
ful to confirm the diagnosis and exclude focal tendinitis.

OTHER MUSCULOSKELETAL CONDITIONS

Muscular Dystrophy
In neuromuscular disorders, such as the muscular dys-
trophies and Werdnig-Hoffman spinal muscular atrophy,
the muscle fascicles are replaced by fat and connective
tissue and the number of perimysial septa increases
(mean 13 to 14, range 9 to 20) (97). Gray-scale sonog-
raphy shows increased muscular echogenicity and distal
sound attenuation (98). Muscle thickness is either nor-
mal or increased in the muscular dystrophies, whereas it
is usually decreased in spinal muscular atrophy (99).

Slipped capital femoral epiphysis. Longitudinal scan along

Limb Enlargement
Enlargement of an extremity can involve only the soft tis-
sues or both bone and soft tissues. The common causes of
limb enlargement are hemangiomas, vascular malforma-
Fig. 15.54
the axis of the femoral neck shows the proximal femoral
epiphysis (E) displaced posteriorly relative to the femoral neck (FN). Long
arrow indicates physis; short arrows indicate echogenic joint fluid pre-
sumed to be blood. (Case courtesy of James Donaldson, MD, Chicago.)
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G
visualization of the fragmented tibial tubercle in Osgood-
Schlatter disease and patella in Sinding-Larsen disease
(102,103), and (d) evaluation of abnormal tendon move-
ment in the snapping iliopsoas tendon (104,105). In snap-
ping iliopsoas tendon, the tendon shows abrupt displace-
ment over the acetabulum or femoral head, accompanied
by an audible snapping sound, when the hip is extended
(104,105). For comparison, the normal iliopsoas tendon
moves smoothly from side to side over the acetabulum or
femoral head.
PERIPHERAL VEINS
Anatomy
LOWER EXTREMITIES
The venous drainage of the lower extremity is divided into
deep and superficial systems, which both drain into the
common femoral vein (Fig. 15.55) (106,107). The veins
are accompanied by the artery of the same name. The deep
veins of the foot drain into the anterior and posterior tibial
veins. The posterior tibial vein joins the peroneal vein
before anastomosing with the anterior tibial vein to form
the popliteal vein. The popliteal vein lies deep to the gas-
trocnemius and the semimembranosus muscles. It becomes
Diagram showing the major veins of the leg. See text for
Fig. 15.55
detailed description.
637
the femoral vein (also known as the superficial femoral
vein) after it leaves the adductor canal in the lower third of
the distal thigh. The femoral vein ascends deep to the sar-
torius muscle, bounded by the vastus medialis and adduc-
tor longus muscles. It joins the deep (profunda) femoral
vein approximately 8 to 10 cm below the inguinal liga-
ment, becoming the common femoral vein. The common
femoral vein continues as the external iliac vein above the
inguinal ligament.
The superficial venous system includes the lesser and
greater saphenous veins. The lesser saphenous vein drains
the subcutaneous tissues from the medial malleolus and
then ascends posteriorly to its anastomosis with the
popliteal vein. The greater saphenous vein drains the
medial calf and then ascends to join the common femoral
vein in the proximal thigh below the inguinal ligament.
The deep and superficial veins are connected at different
levels in the calf by perforating veins that drain from the
skin to the deep veins.
UPPER EXTREMITIES
The veins of the upper extremity are subdivided, like those
of the lower extremity, into deep and superficial veins
(Fig. 15.56) (108). The deep veins draining the palm of the
Diagram showing the major veins of the upper extremity.
Fig. 15.56
See text for description.
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638 P E D I AT R I C S O N O G R A P H Y
hand form the radial and ulnar veins, which lie laterally
and medially on each side of the forearm, respectively. The
brachial veins are formed when the radial and ulnar veins
join at the antecubital fossa. The brachial veins ascend the
arm medially on the ulna side and join the basilic vein to
form the larger axillary vein. The radial side of the forearm
is drained by the cephalic vein, which travels upward to
join the axillary vein at the level of the axilla. The axillary
vein joins the subclavian vein after passing under the first
rib. The subclavian vein joins with the internal jugular vein
to form the brachiocephalic vein. The left brachiocephalic
vein crosses behind the sternum to reach the right brachio-
cephalic vein, forming the superior vena cava.
The superficial veins arise from a superficial dorsal arch
of the hand. They drain into the ulnar, radial, median,
cephalic, and basilic veins of the forearm. These veins coa-
lesce to form the cephalic vein, which courses laterally, and
the basilic vein, which courses medially. The superficial
veins join with the brachial veins in the upper arm, becom-
ing the axillary vein.
Sonographic Techniques
LOWER EXTREMITIES
Vascular imaging requires high-frequency, usually 5- to
10-MHz array transducers. The lower extremity veins are
imaged with the patient supine or semierect (head elevated
to about 30 degrees). The leg should be slightly abducted
and externally rotated and the knee slightly flexed. The
examination starts just below the level of the inguinal lig-
ament. The common femoral vein is identified and the
transducer is moved distally to identify the femoral (super-
ficial femoral) vein, the deep femoral (profunda femoris)
vein, and the junction of the saphenous vein with the com-
mon femoral vein. The superficial veins are easily visual-
ized by sonography in most patients. The deep veins in the
proximal and midthigh are more difficult to identify
because of the thickness of the overlying muscles. Use of a
Normal venous compressibility. Transverse color Doppler images of the right femoral vein (arrow) without (left panel) and with (right panel)
Fig. 15.57
compression with the ultrasound transducer. With compression, the normal vein collapses and disappears and only the artery remains.
lower-frequency curved array or sector transducer may
improve visualization of the deep venous system.
The popliteal vein is examined with the patient prone
and a pillow placed under the ankle to slightly flex the
knee or with the patient in a decubitus position (with the
side to be evaluated up). The posterior tibial and the per-
oneal veins are imaged using a medial or posteromedial
approach. The anterior tibial veins are imaged from an
anterolateral approach.
It is important to use light pressure with the transducer
so that the veins are not inadvertently compressed. Each
venous segment is scanned in both transverse and longitu-
dinal planes with gray-scale and Doppler imaging.
UPPER EXTREMITIES
The patient is examined in the supine position with the arm
to be examined slightly abducted and rotated externally.
The patients head is turned away from the transducer to
help visualize more proximal parts of the subclavian and
brachiocephalic veins. The axillary veins are examined with
the transducer in the axilla and the patients arm elevated.
The position of the transducer for examination of the sub-
clavian vein varies depending on whether the distal portion
or medial portion of the vein is studied. An infraclavicular
approach is used to image the lateral portion of the subcla-
vian vein, while a supraclavicular approach is used to study
the medial segment of the subclavian vein and the caudal
segment of the internal jugular vein (109).
Normal Sonographic Appearance
GRAY-SCALE FINDINGS
The lumen of the normal vein is anechoic and the walls are
thinner than those of the adjacent artery. The veins of the
lower extremities are usually compressible when pressure is
applied with the transducer. On gray-scale images, the
normal vein collapses completely and the walls coapt
(Fig. 15.57). Compressibility is best assessed on transverse
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G 639

views of the vein. On longitudinal views, the transducer

may roll off the vein.

DOPPLER FLOW PATTERNS: LEG VEINS

Color Doppler interrogation should show flow through-
out the lumen of the interrogated vein. Pulsed Doppler
studies demonstrate low-velocity flow that varies during
the respiratory cycle (110). During inspiration, venous
flow decreases. During expiration, flow increases. Fluctu-
ations with respiration indicate venous patency proximal
to the point of Doppler interrogation. In adults, the max-
imum flow velocity in the femoral veins is 12 to 30 cm/sec
(111).
Valsalva and augmentation techniques are used to
increase the likelihood of thrombus detection. In response
to the Valsalva maneuver, the normal vein shows transient
flow reversal, followed by cessation of flow, and then a
rapid increase in forward flow with release of the Valsalva
maneuver. The Valsalva response determines vein patency
proximal to the point of Doppler interrogation. Normal Doppler waveform, upper extremity. Pulsed
Fig. 15.59
Doppler examination of the brachiocephalic vein shows
Venous flow should increase or augment when the distal
a triphasic waveform related to pressure changes in the right atrium.
extremity is compressed. Flow augmentation (i.e., increased
antegrade flow) can be demonstrated by having the exam-
iner or an assistant squeeze the calf or by having the patient
plantar flex the foot. Flow augmentation indicates vessel
patency distal to the point of Doppler interrogation (Fig.
15.58). Typically, central vessels, such as the brachiocephalic and
subclavian veins, demonstrate a pulsatile waveform related
DOPPLER FLOW PATTERNS: ARM VEINS to cardiac and respiratory cycles (Fig. 15.59). A triphasic
waveform may be seen in the veins closest to the heart
The overlying clavicle makes it difficult to apply compres-
(111). Pulsations are usually absent beyond the axillary
sion to the subclavian vein. Therefore, detection of throm-
vein. In children, maximum flow velocity in the superior
bus depends on standard gray-scale and Doppler analysis.
vena cava is 60 to 80 cm/sec (112).

Augmentation maneuver. Longitudinal Doppler sono-
Fig. 15.58
gram of the common femoral vein shows increased ante-
grade flow (arrow) with calf compression.
Venous Thrombosis
Deep venous thrombosis (DVT) in children is most com-
monly due to stasis secondary to immobilization and central
venous catheterization (113). Less common causes
include hypercoagulable states such as protein S and pro-
tein C deficiency, fractures or local trauma, and decreased
flow from more central obstruction in the superior or
inferior vena cava. Clinical findings include pain, ery-
thema, and swelling in the affected limb. A negative
D-dimer test virtually excludes DVT. A positive D-dimer
test is nonspecific and may be caused by low levels of
fibrin associated with infection, inflammation, vasculitis,
trauma, or surgery. The prevalence of deep venous
thrombosis in children in the intensive care unit is
approximately 4% (113).
ACUTE THROMBOSIS
The gray-scale findings of acute deep venous thrombosis
are (a) an enlarged vein, (b) an echogenic filling defect
within the normally anechoic lumen, and (c) noncom-
pressibility of the lower extremity veins (106,107). It needs
to be recognized that in some healthy patients, artifactual
echoes can be present within the venous lumen. Addition-
ally, venous thrombosis can occasionally appear anechoic.
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640 P E D I AT R I C S O N O G R A P H Y
A B
Acute deep venous thrombosis. Transverse (A) and longitudinal color Doppler (B) images with compression show absent flow in a dis-
Fig. 15.60
tended femoral vein (arrow) and absent coaptation of the walls. Flow is present in the femoral artery (arrowhead).
In these cases, the gray-scale appearance alone is not reli-
able. However, when gray-scale imaging is combined with
compression maneuvers and Doppler studies, the diagnosis
of thrombosis should be possible.
Color flow imaging shows no flow with a completely
occlusive thrombus (Fig. 15.60). The Doppler waveform
is altered and there can be loss of the normal cardiac-
and respiratory-related pulsations distal to the site of
thrombosis. Absent flow augmentation in the lower
extremities can indicate the presence of a distal obstruc-
tion between the site of Doppler interrogation and the
site of mechanical compression. However, the normal
response to the augmentation maneuver often is lost only
when there is extensive venous occlusion. Failure of the
vein to increase during the Valsalva maneuver can indi-
cate an obstruction proximal to the site of Doppler inter-
rogation. Nonocclusive thrombi may not alter the flow
pattern.
The sensitivity and specificity of color Doppler imaging
in detecting lower extremity venous thrombosis are approx-
imately 95% and nearly 100%, respectively (114116).
Detection rates are higher for thrombus above the knee than
for thrombus in the calf. In the upper extremities, the sensi-
tivity and specificity of color flow Doppler imaging are
80% to 100%, with the highest accuracies occurring in the
axillary vein and lateral part of the subclavian vein (117).
CHRONIC THROMBOSIS
Chronic venous thrombosis is characterized by thickened
or irregular walls, a narrowed or irregular lumen, and col-
lateral vessel formation. The clot is usually hypoechoic.
Differentiation between hypoechoic thrombus and normal-
flowing blood requires pulsed or color Doppler imaging.
PERIPHERAL ARTERIES
Anatomy
LOWER EXTREMITY
The common femoral artery starts at the level of the
inguinal ligament and travels approximately 2 to 4 cm
before bifurcating into the deep (profunda femoris) artery
and the superficial femoral artery (Fig. 15.61). The deep
femoral artery supplies branches to the muscles and tis-
sues in the proximal two thirds of the thigh. The superfi-
cial femoral artery supplies muscles and tissues in the
distal third of the thigh. At the level of the adductor canal,
the superficial femoral artery becomes the popliteal artery.
The popliteal artery branches into the anterior tibial
artery and common tibioperoneal trunk. The tibioper-
oneal trunk then branches into the posterior tibial and
peroneal arteries. At the level of the ankle, the peroneal
artery ends as small branches. The posterior tibial artery
branches into the lateral and medial plantar arteries, and
the anterior tibial artery continues as the dorsalis pedis
artery. The dorsalis pedis artery joins the lateral plantar
artery of the posterior tibial artery to form the plantar arch.
UPPER EXTREMITY
The subclavian artery crosses the upper chest after giving
rise to the vertebral artery, the costoclavicular trunk, and
the internal mammary artery (Fig. 15.62). It becomes the
axillary artery at the level of the first rib. The axillary artery
continues as the brachial artery just below the margin of
the teres major muscle. It terminates in the antecubital
fossa, where it bifurcates into ulnar and radial arteries. The
ulnar and radial arteries continue to the level of the wrist,
where the two arteries anastomose. The ulnar artery
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G 641

continues as the superficial arch, which supplies branches

to the digits.

Sonographic Technique
The sonographic technique for interrogating the periph-
eral arteries is similar to that used for the venous system.

Normal Sonographic Appearance

GRAY-SCALE FINDINGS
The lumen of the normal artery is anechoic and the walls
are thicker than those of the adjacent veins. The arteries
will not collapse when pressure is applied with the trans-
ducer.

DOPPLER IMAGING: NORMAL ARTERIES

The central arteries of the upper and lower extremities
show a triphasic flow pattern with forward acceleration
of blood flow during systole, reversal of flow during early
diastole, and low-amplitude antegrade flow during late
diastole (Fig. 15.63) (110). The antegrade diastolic flow
increases with exercise and warmth and decreases with
vasoconstriction.

Occlusion and Stenosis

The sonographic finding of arterial occlusion is absence of
Diagram showing the major arteries of the lower extrem- Doppler signal or color flow. A stenosis of more than 50%
Fig. 15.61
ity. See text for description. is associated with increased peak systolic velocity at the
point of maximal narrowing. Doppler findings in arterial
segments distal to the site of stenosis (i.e., downhill find-
ings) are decreased peak systolic velocity (the parvus
effect), delayed time to reach peak systolic velocity (the
tardus effect), monophasic rather than triphasic Doppler
waveforms, and increased diastolic flow velocities.

Normal arterial waveforms. Left femoral artery. Pulsed

Fig. 15.63
Doppler examination shows a high-resistance triphasic
waveform, which is typical of a peripheral artery at rest. The classic
Diagram showing the major arteries of the upper extrem- triphasic waveform is characterized by a narrow antegrade systolic peak,
Fig. 15.62
ity. See text for description. a brief early retrograde diastolic peak, and a late antegrade diastolic peak.
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642 P E D I AT R I C S O N O G R A P H Y

A pitfall in distinguishing between an occlusion and a
stenosis is erroneous sampling of a collateral branch, thereby
leading to a false-positive diagnosis of a high-grade stenosis
when the arterial segment is in fact occluded. The sensitivity
and specificity for the diagnosis of high-grade arterial steno-
sis (i.e., 50%) and occlusion are approximately 90% to
95%.
Pseudoaneurysm
A pseudoaneurysm is a localized hematoma that maintains
a communication with an artery. Pseudoaneurysms are
usually complications of femoral artery catheterization or
other penetrating injuries (118,119). Initially, the hematoma
is walled off by adjacent structures, but over time a fibrous
capsule develops.
Gray-scale findings are a hypoechoic or complex fluid
collection in the region of an artery (118) (Fig. 15.64). Color
Doppler imaging shows a swirling flow pattern with flow
going into the pseudoaneursym in half of the lumen and flow
going out of the pseudoaneurysm in the other half of the
lumen (yin-yang sign). Another color Doppler finding is
perivascular tissue vibration (random mixture of red and blue
pixels). A characteristic pulsed Doppler finding is the to and
fro waveform within the neck of the pseudoaneurysm. This

A C

B D

Pseudoaneurysm. Patient with a history of a femoral artery catheterization. A: Longitudinal scan of the groin shows a hypoechoic mass
Fig. 15.64
(calipers). B: Color Doppler image shows a swirling flow pattern (yin-yang sign) in the lumen of the pseudoaneurysm. C: Pulsed Doppler
image shows the characteristic to-and-fro waveform (systolic flow into the pseudoaneurysm and diastolic flow out of the pseudoaneurysm). D: Doppler
sonogram of the aneurysm neck in another patient shows the to-and-fro waveform and also perivascular soft tissue vibrations (arrow) in the color insert.
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Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G
reflects antegrade flow into the pseudoaneurysm during sys-
tole, which is displayed above the baseline, and retrograde
flow out of the pseudoaneurysm during diastole, which is
displayed below the baseline (Fig. 15.64).
Arteriovenous Fistula
An arteriovenous fistula is a direct connection between an
artery and vein without an intervening capillary network.
Arteriovenous fistulas can be congenital or result from a
penetrating arterial or venous injury, such as a femoral
puncture. Tramatic fistulas are rarely seen on gray-scale
imaging and are best recognized on Doppler sonography.
Color Doppler analysis demonstrates communication
between an artery and vein, turbulent flow in the region of
the fistula, and perivascular tissue vibrations. Pulsed
Doppler analysis of the artery at the site of the fistulous
connection shows high diastolic flow throughout the car-
diac cycle. This pandiastolic flow pattern is in contradis-
tinction to the high-resistance flow of normal peripheral
arteries. The draining vein can show an arterialized wave-
form (Fig. 15.65) (120,121).
A 17. Rosendahl K, Markestad T, Lie RT. Developmental dysplasia of
B of the hip: the role of sonography. AJR Am J Roentgenol
Arteriovenous fistula. A: Color Doppler image of the
Fig. 15.65
upper arm shows turbulent flow (arrows) in the fistula
between the axillary artery (A) and vein (V). B: Pulsed Doppler image
shows increased systolic and diastolic flow velocities and an arterial-
ized venous waveform. (Case courtesy of Brian Coley, MD.)
643
REFERENCES
1. Harcke HT, Grissom LE. Infant hip sonography: current con-
cepts. Semin Ultrasound CT MR 1994;15:256263.
2. Lin J, Fessell DP, Jacobson JA, et al. An illustrated tutorial of
musculoskeletal sonography: Part I, introduction and general
principles. AJR Am J Roentgenol 2000;175:637645.
3. Lin J, Jacobson JA, Fessell DP, et al. An illustrated tutorial of
musculoskeletal sonography: Part 2, upper extremity. AJR Am
J Roentgenol 2000;175:10791071.
4. Lin J, Fessell DP, Jacobson JA, et al. An illustrated tutorial of
musculoskeletal sonography: Part 3, lower extremity. AJR Am
J Roentgenol 2000;175:13131321.
5. Heckmatt JZ, Pier N, Dubowitz V. Measurement of quadriceps
muscle thickness and subcutaneous tissue thickness in normal
children by real-time ultrasound imaging. J Clin Ultrasound
1988;16:171176.
6. Martinoli C, Bianchi S, Dahmane M, et al. Ultrasound of ten-
dons and nerves. Eur Radiol 2002;12:4455.
7. Fornage BD. The hypoechoic normal tendon a pitfall. J Ultra-
sound Med 1987;6:1922.
8. Adler RS. Ultrasound of the knee, ankle, and foot. In: Bluth EI,
Arger PH, Benson CB, et al., eds. Ultrasound: a practical
approach to clinical problems. 2nd ed. New York: Thieme,
2008:648656.
9. Newman JS, Adler RS, Bude RO, et al. Detection of soft-tissue
hyperemia: value of power Doppler sonography. AJR Am J
Roentgenol 1994;163:385389.
10. Carr JC, Hanly S, Griffin J, et al. Sonography of the patellar
tendon and adjacent structures in pediatric and adult patients.
AJR Am J Roentgenol 2001;176:15351539.
11. Grissom LE, Harcke HT. Infant shoulder sonography: tech-
nique, anatomy, and pathology. Pediatr Radiol 2001;31:
863868.
12. Middleton WD, Teefey SA, Yamaguchi K. Shoulder pain. In:
Bluth EI, Arger PH, Benson CB, et al., eds. Ultrasound: a prac-
tical approach to clinical problems. New York: Thieme,
2008:627637.
13. Barr LL, Babcock DS. Sonography of the normal elbow. AJR
Am J Roentgenol 1991;157:793798.
14. Markowitz RI, Davidson RS, Harty MP, et al. Sonography of
the elbow in infants and children. AJR Am J Roentgenol 1992;
159:829833.
15. Klisic PJ. Congenital dislocation of the hip: a misleading term.
J Bone Joint Surg 1984;71B:136.
16. Rosenberg HK, Smergel E. Neonatal hip dislocation. In: Bluth,
Arger PH, Benson CB, et al., eds. Ultrasound: a practical
approach to clinical problems. New York: Thieme, 2008:
528545.
the hip: prevalence based on ultrasound diagnosis. Pediatr
Radiol 1996;26:635639.
18. Gerscovich EO. A radiologists guide to the imaging in the
diagnosis and treatment of developmental dysplasia of the hip.
II. Ultrasonography: anatomy, technique, acetabular angle
measurements, acetabular coverage of femoral head, acetabu-
lar cartilage thickness, three-dimensional technique, screening
of newborns, study of older children. Skel Radiol 1997;26:
447456.
19. Harcke TH. Screening newborns for developmental dysplasia
1994;162:395397.
20. Harcke HT. The role of ultrasound in the diagnosis and man-
agement of developmental dysplasia of the hip. Pediatr Radiol
1995;25:225227.
21. Harcke HT, Grissom LE. Performing dynamic sonography of
the infant hip. AJR Am J Roentgenol 1990;155:837844.
LWBK505-C15_p602-646.qxd 09/07/2010 07:12 PM Page 644 Aptara
644 P E D I AT R I C S O N O G R A P H Y
22. Karmazyn B, Gunderman RB, Coley BD, et al. ACR appropri-
ateness criteria on the developmental dysplasia of the hip
child. J Am Coll Radiol 2009;6:551557.
23. Yousefzadeh DK, Ramilo JL. Normal hip in children: correla-
tion of US with anatomic and cryomicrotome sections. Radiol-
ogy 1987;165:647655.
24. Graf R. Classification of hip joint dysplasia by means of sonog-
raphy. Arch Orthop Trauma Surg 1984;102:248255.
25. Graf R. Fundamentals of sonographic diagnosis of infant hip
dysplasia. J Pediatr Orthop 1984;4:735740.
26. Grissom LE, Harcke HT, Kumar SJ, et al. Ultrasound evalua-
tion of hip position in the Pavlik harness. J Ultrasound Med
1988;7:16.
27. Rosendahl K, Toma P. Ultrasound in the diagnosis of develop-
mental dysplasia of the hip in newborns. The European
approach. A review of methods, accuracy and clinical validity.
Eur Radiol 2007;17:19601967.
28. Donaldson JS, Siegel MJ. Proximal femoral focal deficiency. In:
Siegel BA, Proto AV, eds. Pediatric disease (fourth series) test
and syllabus. Reston, VA: American College of Radiology,
1993:722752.
29. Bearcroft PW, Berman LH, Robinson AHN, et al. Vascularity of
the neonatal femoral head: in vivo demonstration with power
Doppler US. Radiology 1996;200:209211.
30. Stover B, Bragelmann R, Walther A, et al. Development of late
congenital hip dysplasia: significance of ultrasound screening.
Pediatr Radiol 1993;23:1922.
31. Gerscovich E, Greenspan A, Cronan MS, et al. Three-dimen-
sional sonographic evaluation of developmental dysplasia of
the hip: preliminary findings. Radiology 1994;190:407410.
32. Hillmann JS, Mesgarzadeh M, Revesz G, et al. Proximal
femoral focal deficiency: radiologic analysis of 49 cases. Radi-
ology 1987;165:769773.
33. Levinson ED, Ozonoff MB, Royen PM. Proximal focal femoral
deficiency (PFFD). Radiology 1977;125:197203.
34. Jeanty P, Kleinman G. Proximal femoral focal deficiency.
J Ultrasound Med 1989;8:639642.
35. Schoenecker PL, Capelli AM, Millar EA, et al. Congenital lon-
gitudinal deficiency of the tibia. J Bone Joint Surg 1989;71-
A:278287.
36. Grissom LE, Harcke HT, Kumar SJ. Sonography in the man-
agement of tibial hemimelia. Clin Orthop 1990;251: 266270.
37. Koplewitz BZ, Babyn PS, Cole WG. Congenital dislocation of
the patella. AJR Am J Roentgenol 2005;184:16401646.
38. Chami M, Daoud A, Maestro M, et al. Ultrasound contribution
in the analysis of the newborn and infant normal and clubfoot:
a preliminary study. Pediatr Radiol 1996;26:298302.
39. Schlesinger AE, Deeney VFX, Caskey PF. Sonography of the
nonossified tarsal navicular cartilage in an infant with congeni-
tal vertical talus. Pediatr Radiol 1989;20:134135.
40. Bianchi S, Santa DD. Gauser T, et al. Sonography of masses of
the wrist and hand. AJR Am J Roentgenol 2008;191:17671775.
41. Latifi H, Siegel MJ. Color Doppler US of soft tissue masses.
J Ultrasound Med 1994;13:165169.
42. Siegel MJ. MRI of pediatric soft tissues masses. MR Clin North
Am 2002;39:701720.
43. Paltiel HJ, Burrows APE, Kozakewich HPW, et al. Soft-tissue
vascular anomalies: utility of US for diagnosis. Radiology
2000;214:747754.
44. Dubois J, Garel L. Imaging and therapeutic approach of heman-
giomas and vascular malformations in the pediatric age group.
Pediatr Radiol 1999;29:879893.
45. Dubois J, Patriquin HB, Garel L, et al. Soft-tissue hemangiomas
in infants and children: diagnosis using Doppler sonography.
AJR Am J Roentgenol 1998;171:247252.
46. Trop I, Dubois J, Guibaud L, et al. Soft-tissue venous malfor-
mations in pediatric and young adult patients: diagnosis with
Doppler US. Radiology 1999;212:841845.
47. Siegel MJ, Glazer HS, St. Amour TE, et al. Lymphangiomas in
children: MR imaging. Radiology 1989;170:467470.
48. Beggs I. Sonographic appearances of nerve tumors. J Clin Ultra-
sound 1999;27:363368.
49. Lin J, Martel W. Cross-sectional imaging of peripheral nerve
sheath tumors: characteristic signs on CT, MR imaging and
sonography. AJR Am J Roentgenol 2001;176:7582.
50. Martinoli C, Bianchi S, Derchi LE. Tendon and nerve sonogra-
phy. Radiol Clin North Am 1999;37:691711.
51. Murphey MD, Smith WS, Smith SE, et al. Imaging of muscu-
loskeletal neurogenic tumours: radiologicpathologic correla-
tion. Radiographics 1999;19:12531280.
52. Stuart RM, Koh ESC, Breidahl WH. Sonography of periph-
eral nerve pathology. AJR Am J Roentgenol 2004;182:
123129.
53. Beggs I. Ultrasound of soft tissue masses. Imaging 2002;14:
202207.
54. Fornage BD, Tassin GB. Sonographic appearance of superficial
soft tissue lipomas. J Clin Ultrasound 1991;19:216220.
55. Paivansalo M, Jalovaara P. Ultrasound findings in ganglions of
the wrist. Eur J Radiol 1991;13:178180.
56. Ward EE, Jacobson JA, Fessell DP, et al. Sonographic detection
of Bakers cysts: comparison with MR imaging. AJR Am J
Roentgenol 2001;176:373380.
57. Rutten MJ, Collins JM, van Kampen A, et al. Meniscal cysts:
detection with high-resolution sonography. AJR Am J Roentgenol
1998;171:491496.
58. Seymour R, Lloyd DC. Sonographic appearances of meniscal
cysts. J Clin Ultrasound 1998;26:1520.
59. Lopez Milena G, Ruiz Santiago F, Chamorro Santos C, et al.
Forearm soft tissue mass caused by an accessory muscle. Eur
Radiol 2001;11:14871489.
60. Beggs I. Sonography of muscle hernias. AJR Am J Roentgenol
2003;180:395399.
61. Vasireddy S, Long SD, Sacheti B, et al. MRI and US findings of
subcutaneous fat necrosis of the newborn. Pediatr Radiol 2009;
39:7376.
62. Wexler LH, Meyer WH, Helman LJ. Rhabdomyosarcoma and
the undifferentiated sarcomas. In: Pizzo PA, Poplack DG, eds.
Principles and practice of pediatric oncology. Philadelphia, PA:
Lippincott Williams & Wilkins, 2006:9711001.
63. McCarville MB, Spunt SL, Pappo AS. Rhabdomyosarcoma in
pediatric patients: the good, the bad, and the usual. AJR Am J
Roentgenol 2001;176:15631569.
64. Bureau NJ, Chhem RK, Cardinal E. Musculoskeletal infections:
US manifestations. Radiographics 1999;19:15851592.
65. Miralles M, Gonzalez G, Pulpeiro JR, et al. Sonography of the
painful hip in children: 500 consecutive cases. AJR Am J
Roentgenol 1989;152:579582.
66. Zawin JK, Hoffer FA, Rand FF, et al. Joint effusion in children
with an irritable hip: US diagnosis and aspiration. Radiology
1993;187:459463.
67. Rohrschneider WK, Fuchs G, Troger J. Ultrasonographic eval-
uation of the anterior recess in the normal hip: a prospective
study in 166 asymptomatic children. Pediatr Radiol 1996;26:
629634.
68. Robben SG, Lequin MH, Diepstraten AFM, et al. Doppler
sonography of the anterior ascending cervical arteries of the
hip: evaluation of healthy and painful hips in children. AJR Am
J Roentgenol 2000;174:16291634.
69. Strouse PJ, DiPietro MA, Adler RS. Pediatric hip effusions: eval-
uation with power Doppler sonography. Radiology 1998;206:
731735.
70. Strouse PJ, DiPietro MA, Teo E-LHJ, et al. Power Doppler eval-
uation of joint effusions: investigation in a rabbit model. Pedi-
atr Radiol 1999;29:617623.
71. Loyer EM, DuBrow RA, David CL, et al. Imaging of super-
ficial soft-tissue infections: sonographic findings in cases of
LWBK505-C15_p602-646.qxd 09/07/2010 07:12 PM Page 645 Aptara
Chapter 15 M U S C U L O S K E L E TA L S Y S T E M A N D V A S C U L A R I M A G I N G
cellulitis and abscess. AJR Am J Roentgenol 1996;166:
149152.
72. Chao H-S, Lin S-J, Huang Y-C, et al. Sonographic evalua-
tion of cellulitis in children. J Ultrasound Med 2000;19:
743749.
73. Gottlieb RH, Meyers SP, Hall C, et al. Pyomyositis: diagnostic
value of color Doppler sonography. Pediatr Radiol 1995;25:
S109S111.
74. Azam Q, Ahmad I, Abbas M, et al. Ultrasound and colour
Doppler sonography in acute osteomyelitis in children. Acta
Orthop Belg 2005;71:590596.
75. Chao HC, Lin SJ, Huang YC, et al. Color Doppler ultrasono-
graphic evaluation of osteomyelitis in children. J Ultrasound
Med 1999;18:729734.
76. Mah ET, LeQuesne GW, Gent RJ, et al. Ultrasonic features of
acute osteomyelitis in children. J Bone Joint Surg Br 1994;76:
969997.
77. Riebel TW, Nasir R, Nazarenko O. The value of sonography
in the detection of osteomyelitis. Pediatr Radiol 1996;26:
291297.
78. Wright NB, Abbott GT, Carty HM. Ultrasound in children with
osteomyelitis. Clin Radiol 1995;50:623627.
79. Kaiser S, Rosenberg M. Early detection of subperiosteal
abscesses by ultrasonography. A means for further successful
treatment in pediatric osteomyelitis. Pediatr Radiol 1994;24:
336339.
80. Newman JS, Laing TJ, McCarthy CJ, et al. Power Doppler
sonography in synovitis: assessment of therapeutic response:
preliminary observations. Radiology 1996;198:582584.
81. Fornage BD, Eftekhari F. Sonographic diagnosis of myositis
ossificans. J Ultrasound Med 1989;8:463466.
82. Gindele A, Schwamborn D, Tsironis K, et al. Myositis ossifi-
cans traumatica in young children: report of three cases
and a review of the literature. Pediatr Radiol 2000;30:
451459.
83. Fornage BD, Nerot C. Sonographic diagnosis of rhabdomyoly-
sis. J Clin Ultrasound 1986;14:389392.
84. Lamminen AE, Hekali PE, Tiula E, et al. Acute rhabdomyoly-
sis: evaluation with magnetic resonance imaging compared with
computed tomography and ultrasonography. Br J Radiol 1989;
62:326331.
85. Hunter JD, Franklin K, Hughes PM. The ultrasound diagnosis
of posterior shoulder dislocation associated with Erbs palsy.
Pediatr Radiol 1998;28:510511.
86. Patten RM, Mack LA, Wang KY, et al. Nondisplaced fractures
of the greater tuberosity of the humerus: sonographic detection.
Radiology 1992;182:201204.
87. Diaz MJ, Hedlund GL. Sonographic diagnosis of traumatic sep-
aration of the proximal femoral epiphysis in the neonate. Pedi-
atr Radiol 1991;21:238240.
88. Harada M, Takahara J, Sasaki J, et al. Using sonography for the
early detection of elbow injuries among young baseball players.
Pediatr Radiol 2008;38:982988.
89. Zuazo I, Bonnefoy O, Tauzin C, et al. Acute elbow trauma in
children: role of ultrasonography. Pediatr Radiol 2008;38:
982988.
90. Kelloff J, Hulett R, Spivey M. Acute rib fracture diagnosis in an
infant by US: a matter of child protection. Pediatr Radiol 2009;
39:7072.
91. Markowitz RI, Hubbard AM, Harty MP, et al. Sonography of
the knee in normal and abused infants. Pediatr Radiol 1993;23:
264267.
92. Boyce TD, Fessell DP, Jacobson JA, et al. US of soft tissue for-
eign bodies and associated complications with surgical correla-
tion. Radiographics 2001;21:12511256.
93. Horton LK, Jacobson JA, Powell A, et al. Sonography and radi-
ography of soft-tissue foreign bodies. AJR Am J Roentgenol
2001;176:11551159.
645
94. Peterson JJ, Bancroft LW, Kransdorf MJ. Wooden foreign bod-
ies: imaging appearance. AJR Am J Roentgenol 2002;178:
557562.
95. Shiels WE, Babcock DS, Wilson JL, et al. Localization and
guided removal of soft-tissue foreign bodies with sonography.
AJR Am J Roentgenol 1990;155:12771281.
96. Lee JC, Healy J. Sonography of lower limb muscle injury. AJR
Am J Roentgenol 2004;182:341261.
97. Dock W, Happak W, Grabenwoger F, et al. Neuromuscular dis-
eases: evaluation with high-frequency sonography. Radiology
1990;177:825828.
98. Lamminen A, Jaaskelainen J, Rapola J, et al. High-frequency
ultrasonography of skeletal muscle in children with neuromus-
cular disease. J Ultrasound Med 1988;7:505509.
99. Heckmatt JZ, Pier N, Dubowitz V. Assessment of quadriceps
femoris muscle atrophy and hypertrophy in neuromuscular dis-
ease in children. J Clin Ultrasound 1988;16:177181.
100. Robben SG, Meradji M, Diepstraten AFM, et al. US of the
painful hip in childhood: diagnostic value of cartilage thicken-
ing and muscle atrophy in the detection of Perthes disease.
Radiology 1988;208:3542.
101. Doria AS, Guarniero R, Molnar LJ. Three-dimensional (3D)
contrast-enhanced power Doppler imaging in Legg-Calve-
Perthes disease. Pediatr Radiol 2000;3:871874.
102. Blankstein A, Cohen I, Heim M, et al. Ultrasonography as a
diagnostic modality in Osgood-Schlatter disease. A clinical
study and review of the literature. Arch Orthop Trauma Surg
2001;121:536539.
103. De Flaviis L, Nessi R, Scaglione P, et al. Ultrasonic diagnosis of
Osgood-Schlatter and Sinding-Larsen-Johansson diseases of the
knee. Skeletal Radiol 1989;18:193197.
104. Hashimoto BE, Green TM, Wiitala L. Ultrasonographic diag-
nosis of hip snapping related to iliopsoas tendon. J Ultrasound
Med 1997;16:433435.
105. Pelsser V, Cardinal E, Hobden R, et al. Extraarticular snapping
hip: sonographic findings. AJR Am J Roentgenol 2001;176:
6773.
106. Bluth EI. Leg swelling with pain or edema. In: Bluth EI, Arger
PH, Benson CB, et al., eds. Ultrasound: a practical approach
to clinical problems. 2nd ed. New York: Thieme, 2008:
572587.
107. Lin EP, Shweta H, Dogra VS. Lower extremity venous Doppler.
J Clin Ultrasound 2008;3:147158.
108. Madrazo BL, Amendola M. Sonography of upper extremity
deep venous thrombosis. J Clin Ultrasound 2008;3:139146.
109. Longley DG, Finlay DE, Letourneau JG. Sonography of the
upper extremity and jugular veins. AJR Am J Roentgenol 1993;
160:957962.
110. Chayhan GB, Parra DA, Mann A, et al. Normal Doppler spec-
tral waveforms of major pediatric vessels: specific pattern.
Radiographics 2008;28:691706.
111. Alimoglu E, Erden A, Gursel K, et al. Correlation of right
atrium pressure and blood flow velocities in common femoral
vein obtained by duplex Doppler sonography. J Clin Ultra-
sound 2001;29:8791.
112. Ayabakan C, Ozkutlu S. Normal patterns of flow in the supe-
rior caval, hepatic and pulmonary veins as measured using
Doppler echocardiography during childhood. Cardiol Young
2003;13:143151.
113. DeAngelis GA, McIlhenny J, Willson DF, et al. Prevalence of
deep venous thrombosis in the lower extremities of children in
the intensive care unit. Pediatr Radiol 1996;26:821824.
114. Cronan JJ. Venous thromboembolic disease: the role of US.
Radiology 1993;186:619630.
115. Gottlieb RH, Widjaja J, Tian L, et al. Calf sonography for
detecting deep venous thrombosis in symptomatic patients:
experience and review of the literature. J Clin Ultrasound
1999;27:415420.
LWBK505-C15_p602-646.qxd 09/07/2010 07:12 PM Page 646 Aptara
646 P E D I AT R I C S O N O G R A P H Y
116. Lewis BD, James EM, Welch TJ, et al. Diagnosis of acute deep
venous thrombosis of the lower extremities: prospective evalu-
ation of color Doppler flow imaging versus venography. Radi-
ology 1994;192:651655.
117. Chin EE, Zimmerman PT, Grant EG. Sonographic evaluation of
upper extremity deep venous thrombosis. J Ultrasound Med
2005;24:829838.
118. Carroll BA. Pulsatile groin mass in the postcatherization
patient. In: Bluth EI, Arger PH, Benson CB, et al. eds. Ultra-
sound: a practical approach to clinical problems. 2nd ed. New
York: Thieme, 2008:589601.
119. Ben Romdhane HB, Neuenschwander S, Hautefort P, et al.
Pseudo-aneurysm of the popliteal artery following an arthro-
scopic meniscectomy: report of a pediatric case. Pediatr Radiol
1991;21:228.
120. Helvie MA, Rubin J. Evaluation of traumatic groin arteriove-
nous fistulas with duplex Doppler sonography. J Ultrasound
Med 1989;8:2124.
121. Sacks D, Robinson ML, Perlmutter GS. Femoral arterial injury
following catheterization. Duplex evaluation. J Ultrasound
Med 1989;8:241246.
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Spinal Ultrasonography
BRIAN D. COLEY AND MARILYN J. SIEGEL
Embryology Pseudomass
Normal Development
Spinal Dysraphism
Errors in Embryologic
Clinical Features of Spinal Dysraphism
Development
The Tethered Cord
Sonographic Technique
Overt Spinal Dysraphism (NonSkin-
Normal Anatomy Covered Lesions)
Position of the Conus Medullaris Myelocele and Myelomeningocele
Anatomic Variants Occult Spinal Dysraphism With a Mass
Ventriculus Terminalis (Transient Lipomyelocele and Lipomyelomeningocele
Dilatation of the Central Canal) Simple Meningocele
Filar Cyst Terminal Myelocystocele
ith improved resolution and advanced techniques,
W sonography plays an important role in the evalua-
tion of spinal canal lesions, especially in infants
(19). In normal infants, the spinal cord and adjacent struc-
tures can be visualized because the incompletely ossified
posterior spinal arches create an acoustic window that per-
mits transmission of the ultrasound beam, allowing
anatomic detail that is equal to that of magnetic resonance
imaging (MRI). The spinal cord also can be well visualized
in patients who have congenital or surgically created defects
in the vertebral bodies. This chapter reviews the normal
development of the spine, the techniques of spinal sonogra-
phy, and the indications for diagnostic and interventional
sonographic evaluation of the spine and spinal cord.
EMBRYOLOGY
Normal Development
The proximal spinal cord forms by the process of primary
neurulation, which occurs between the 15th and 27th days
of embryonic life (10,11). On approximately the 15th day
of embryonic life, the neural plate, composed of neuroecto-
derm, begins to form from the ectodermal plate; this process
is induced by the underlying notochord. Subsequently, the
lateral margins of the neural plate thicken to form two neu-
ral folds with a neural groove between them. By 3 weeks of
gestation, the lateral neural folds infold and close, forming
the neural tube. Tube closure begins in the lower cervical or
upper thoracic region and proceeds both cephalad and cau-
dally. The cephalic end of the tube (anterior neuropore)
closes before the caudal end (posterior neuropore).
When tube closure is complete, the neural tube sepa-
rates from the cutaneous ectoderm in a process called dis-
junction. Separation of the cutaneous ectoderm from the
CHAPTER
16
Occult Spinal Dysraphism Without
a Mass
Disorders of Primary Neurulation
Disorders of the Caudal Cell
Mass
Tumors
Syringomyelia and Hydromyelia
Spinal Cord Trauma
Other Lesions
Intraoperative Sonography
neuroectoderm allows mesodermal mesenchymal migra-
tion, leading to formation of the posterior elements of the
spine, dural coverings, and muscles of the paraspinal
region. At the same time, the neural crest tissue at the mar-
gins of the neural plate migrates laterally to form spinal
and sympathetic ganglia, Schwann cells, and the adrenal
medullae (Fig. 16.1). Errors in disjunction are responsible
for most forms of spinal dysraphism.
Caudal to the posterior neuropore, the neural tube is
formed by a process termed canalization and retrogres-
sive differentiation of the caudal cell mass, referred to as
secondary neurulation (10,11). The caudal cell mass
develops dorsal to the cloaca via neuroectodermal fusion
with the notochord. During canalization, multiple cysts
form within the caudal cell mass, which then coalesce to
form an ependyma-lined tube that fuses with the more
cephalad neural tube formed by the process of primary
neurulation. Subsequently, the cells in the caudal mass
undergo a process termed retrogressive differentiation.
During this process, cell necrosis causes a decrease in the
size of the caudal neural tube, leading to formation of the
conus medullaris, the ventriculus terminalis (a focal dilata-
tion of the central canal within the conus medullaris), and
the filum terminale (Fig. 16.2).
Errors in Embryologic Development
ABNORMALITIES SECONDARY TO ERRORS IN DISJUNCTION
Failure of normal embryologic development, especially
the process of disjunction (separation of the neural ecto-
derm from the cutaneous ectoderm), leads to the develop-
ment of spinal dysraphism (i.e., abnormalities of the spine
and spinal cord). The errors in disjunction include com-
plete absence of disjunction, partial disjunction, and pre-
mature disjunction.
647
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648 P E D I AT R I C S O N O G R A P H Y
A B
C D
E William & Wilkins, 2005:704772.)
B gestation, multiple cysts appear in
A
C roimaging. 4th ed. Philadelphia, PA:
Normal neurulation. A: Initially,
Fig. 16.1
the neural plate, which is com-
posed of neural ectoderm, is continuous with
cutaneous ectoderm on either side. The cells
at the junction of the two types of ectoderm
differentiate into neural crest cells. B: At
about 17 days of gestation, the neural plate
begins to thicken laterally, forming the neural
folds. C: Subsequently, the neural folds bend
dorsally, bringing the folds together in the
midline. D: Neurulation (closure of the neural
tube) follows with the neural folds fusing in
the midline. At the time of closure, the ecto-
derm separates from the neural tissue and
fuses in the midline, covering the neural
structures. At the same time, the neural crest
cells form a transient structure immediately
dorsal to the tube. E: Eventually, these neural
crest cells migrate to form dorsal root gan-
glia. (Modified from Barkovich AJ. Congenital
anomalies of the spine. In: Pediatric Neu-
roimaging. 4th ed. Philadelphia, PA: Lippincott
Development of the
Fig. 16.2
caudal cell mass. A: The
caudal cell mass forms as a result of
fusion of neural epithelium at the
caudal end of the embryo with the
notochord. B: At about 30 days of
the caudal cell mass. C: These cysts
coalesce to form a tubular structure
that unites with the neural tube.
D: At about 38 days, the cell mass
decreases in size through cell
necrosis in a process labeled retro-
gressive differentiation. This process
eventually forms the distalmost conus
medullaris, the filum terminale, and
the ventriculus terminalis. (Modified
from Barkovich AJ. Congenital anom-
alies of the spine. In: Pediatric neu-
Lippincott William & Wilkins, 2005:
D 704772.)
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Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 649

A B
Failure of disjunction of the neural ectoderm from the cutaneous ectoderm. A: Myelocele. The pia and arachnoid line the surface of the
Fig. 16.3
neural placode, forming a cerebrospinal fluid (CSF) sac that is continuous with the subarachnoid space. B: Myelomeningocele. This is
identical to the myelocele with the exception that there is an expansion of the CSF space, which displaces the placode posteriorly. In both condi-
tions the neural placode is exposed to the air. (Modified from Barkovich AJ. Congenital anomalies of the spine. In: Pediatric neuroimaging. 4th ed.
Philadelphia, PA: Lippincott William & Wilkins, 2005:704772.)

If disjunction fails entirely, the neuroectoderm remains

in continuity with the cutaneous ectoderm, resulting in
a nonskin-covered defect such as a myelocele and
myelomeningocele (Fig. 16.3). When disjunction is focally
incomplete, an epithelial-lined tube can connect the spinal
cord or its coverings with the skin surface, creating a dorsal
dermal sinus (Fig. 16.4). With premature disjunction, the
developing neural tube separates from the overlying cuta-
neous ectoderm prior to complete neural tube closure. This A
allows mesenchymal cells to enter the neural tube, where
they differentiate into fat. The differentiation is induced by
the underlying ependymal lining. The result is a skin-
covered, extradural fatty mass that is continuous with the
spinal cord. This group of abnormalities includes lipomye-
loceles, lipomyelomeningoceles, and terminal and intradural
lipomas (Fig. 16.5).

ABNORMALITIES SECONDARY TO ABNORMAL CAUDAL MASS DIFFERENTIATION

Abnormal development and differentiation of the caudal
cell mass produces a wide range of anomalies ranging from B
simple tethered cords and filum terminale fibrolipomas to

Focal nondisjunction. This error results in formation of a
Fig. 16.4
dorsal dermal sinus. (Modified from Barkovich AJ. Con-
genital anomalies of the spine. In: Pediatric neuroimaging. 4th ed.
Philadelphia, PA: Lippincott William & Wilkins, 2005:704772.)
C
Premature disjunction. Mesenchyme is included within
Fig. 16.5
the neural tube, where it differentiates into fat. Depending
on the timing and location, various skin-covered defects may be
produced, such as Intradural lipoma (A), lipomyelocele (B) and
lipomyelomeningocele (C). (Reprinted from Barkovich AJ. Congenital
anomalies of the spine. In: Pediatric neuroimaging. 4th ed. Philadel-
phia, PA: Lippincott William & Wilkins, 2005:704772.)
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650 P E D I AT R I C S O N O G R A P H Y

Normal spine, extended field of view. Longitudinal extended field-of-view image in a newborn infant shows the entire lower spinal cord
Fig. 16.6
and its relationship to the spine. S5 is the first ossified vertebral segment, the coccyx (arrow) is unossified, and the conus (C) ends
normally at L1-2.

more severe anomalies such as terminal myelocystoceles, Extended field-of-view imaging is useful to display the
caudal regression syndrome, and sacrococcygeal teratomas. relationship of the spinal cord with the vertebral column,
especially when trying to determine the level of the conus
DISORDERS SECONDARY TO ABNORMAL NOTOCHORD SPLITTING medullaris (Fig. 16.6) (13,14). The split-screen or dual func-
tion is similarly useful to provide a longer longitudinal view
Failure of separation of the embryonic ectoderm and endo-
of the cord and spinal canal. Three-dimensional sonography
derm can alter the development of the notochord, leading
can improve visualization of osseous structures, although
to abnormalities of the vertebral bodies or the spinal cord.
currently it does not appear to improve evaluation of the
These disorders include split cord malformations (diastem-
spinal cord (2,14,15). Newer high-resolution linear array
atomyelia), neurenteric cysts, butterfly vertebral bodies,
volumetric and 1.5-D array transducers can reduce the slice
and fistulous connections between the intestinal cavity,
thickness of the image and thus may improve visualization
spine, and skin (10,11).
of fine anatomic details.
Color Doppler is rarely useful in routine examinations.
The anterior spinal and epidural veins can be seen with
SONOGRAPHIC TECHNIQUE color Doppler imaging, especially on transverse views (16),
Because the spinal cord is a superficial structure, high- and are relatively prominent in infants compared with
frequency transducers (usually 8 to 15 MHz) provide the older children and adults (Fig. 16.7).
best images. Linear array transducers are preferred over
sector scanners because they provide a larger image in the
near field and greater spatial resolution. Linear array
transducers usually suffice for imaging the spine in
neonates and young infants. Sector scanners may be
needed in older infants when the acoustic window is small.
Scans are obtained with the patient prone and a small pil-
low placed under the chest and abdomen to create a rela-
tive kyphosis. This position splays the spinous processes,
improving acoustic access to the spinal canal, especially in
older infants and children (5). Scanning can also be per-
formed with the patient in a lateral decubitus position,
although this is more challenging than the prone position
(12).
In neonates and younger infants, the spinal canal is
usually easily scanned with the transducer positioned in
the midline over the spinous processes. In older infants
with smaller acoustic windows, the spinal contents may be
best imaged with the transducer positioned lateral and par-
allel to the spinous processes. The advantage of this
approach is that it avoids the ossified spinous processes,
which interfere with transmission of the sound beam. Epidural veins. Transverse color Doppler sonogram
Scans should be obtained in both longitudinal and trans- Fig. 16.7
through the lower spine shows normal prominent epidural
verse planes. veins surrounding the distal spinal cord (C).
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Normal longitudinal anatomy of the spinal
Fig. 16.8
cord. A: Longitudinal scan through the lower
thoracic and upper lumbar region shows the hypoechoic
cartilaginous spinous processes (p), epidural space (e),
posterior dura mater (d), hypoechoic cerebrospinal fluid
in the posterior subarachnoid space (psa), posterior sur-
face of the spinal cord (arrows), hypoechoic cord (C) with
central echogenic complex of the anterior median fissure
(*), anterior surface of the cord (arrowheads), hypo-
echoic fluid in the anterior subarachnoid space (asa),
and echogenic vertebral bodies (V). B: Longitudinal scan
through the distal cord shows the smoothly tapering
conus medullaris (C), nerve roots (arrowheads), and filum
terminale (f). B
NORMAL ANATOMY
On longitudinal scans, the posterior dura mater appears as
an echogenic line paralleling the posterior anechoic sub-
arachnoid space. The posterior subarachnoid space lies
between the dura mater and the spinal cord. The spinal
cord is a hypoechoic tubular structure with echogenic ante-
rior and posterior walls and an echogenic center, termed the
central echo complex, representing the central canal. At
histologic examination, the central canal corresponds to the
area between the myelinated ventral white commissure and
the central portion of the anterior median fissure (Fig. 16.8)
(17). The spinal cord is surrounded anteriorly by the ane-
choic anterior subarachnoid space and echogenic vertebral
bodies. The cord gradually tapers from the level of the last
thoracic to second lumbar vertebral body to form the conus
medullaris.
The conus medullaris corresponds to the caudal end of
the spinal cord. It is continuous with the fibrous filum ter-
minale that extends into the distal sacral canal. In healthy
neonates, the tip of the conus medullaris terminates above
the level of L2-3. At sonography, the filum terminale is a
cord-like echogenic structure that is surrounded by
echogenic nerve roots (the cauda equina). It is thin (nor-
Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 651
mally 2 mm) and extends caudally from the tip of the
conus medullaris (Fig. 16.9), crossing through the sub-
arachnoid space and through the dura mater, to insert on
the first coccygeal vertebral body (10).
On transverse images, the posterior dura mater appears
as an echogenic band. Superficial to the posterior dura
mater is the anechoic posterior subarachnoid space. The
spinal cord appears as an oval or round structure with the
central echogenic complex. Paired echogenic anterior and
posterior nerve roots border the conus medullaris and the
echogenic filum terminale (Fig. 16.10). Anterior to the
spinal cord are the anterior subarachnoid space and verte-
bral bodies.
The diameter of the spinal cord varies and it is broad-
est in the cervical and lumbar regions (7). In infants 1 to 3
months of age, the sagittal diameters of the cervical, tho-
racic, and lumbar portions of the cord are 5.3  0.28, 4.4
 0.42, and 5.8  0.66 mm, respectively (18,19). The cer-
vical enlargement corresponds with the origin of the nerve
roots of the cervical plexus that supplies the upper extrem-
ities. The expansion at the upper lumbar levels reflects the
large number of nerve roots of the lumbar plexus supply-
ing the lower extremities.
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652 P E D I AT R I C S O N O G R A P H Y

Normal conus and filum terminale.

Fig. 16.9
Longitudinal image through the
lower spine shows a normally tapered conus
(C) positioned at L1-2 and a normal filum, meas-
uring 2 mm in diameter (arrowheads).

Position of the Conus Medullaris
The position of the conus medullaris should be deter-
mined in all spinal sonograms. The conus medullaris in
healthy infants is located above the L2-3 disc space
(2022). The cord ends between T12 and L1-2. During
early gestation, the conus medullaris lies below the
level of L4, ascending to L2 or above by the end of ges-
tation (22). While the conus medullaris was once
thought to ascend after birth, it is now apparent that
there is minimal migration of the conus medullaris after
gestation (20,2224). The conus should not be posi-
tioned below L2-3. A conus tip below this level is
abnormal and evidence of a tethered cord (21). If the
cord is at or below the level of the L2-3 disc space, the
spinal canal should be carefully evaluated for the pres-
ence of a thick filum, mass, or other cause of tethering.

A B
Normal transverse anatomy of the spinal cord. A: Transverse scan in the thoracolumbar region shows the unossified spinous process
Fig. 16.10
(P), ossified transverse processes (t), hypoechoic cord with central echogenic complex of the anterior median fissure (arrowhead),
nerve roots (arrows), and echogenic vertebral body (V). B: Transverse scan at the level of the conus shows the tapered conus medullaris (C) and
echogenic ventral (arrows) and dorsal (arrowheads) nerve roots forming the cauda equina.
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Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 653

Estimation of the level of the conus medullaris, normal spine. Longitudinal scan through the distal spine in a term newborn shows faint
Fig. 16.11
ossification (arrow) in the last sacral segment (S5), and the two unossified cartilaginous coccygeal segments. Note the normal gut
signature of the rectum (arrowheads), characterized by an inner echogenic lining and surrounding hypoechoic wall.

It needs to be recognized that occasionally the conus is
at a normal level in patients with clinical evidence of
the tight filum terminale syndrome and cord tethering
(see below discussion).
The level of termination of the conus medullaris usu-
ally can be determined by sonography by either count-
ing down from the 12th rib or counting up from the last
ossified vertebral body. In newborns, the last ossified
vertebral body is usually S5 (Fig. 16.11) (25,26). Locat-
ing this vertebral body and counting cephalad can effec-
tively localize the level of the conus medullaris
(Fig. 16.12). Alternatively, identifying the 12th rib sono-
graphically and counting the vertebral bodies that lie
caudad can identify the position of the conus (27). Both
of these methods presume normal osseous structures.
Palpable landmarks, namely, the top of the last rib
(which usually lies at the L2 vertebral body), the top of
the iliac crest (which is about the level of the L4 verte-
bral body), and the angulation produced at the L5/S1
junction, can also be used as anatomic localizers, but
are less reliable (16).
Estimation of the level of the conus medullaris can be
complicated by segmentation and formation anomalies of
the vertebral bodies (Fig. 16.13). If there is a question
about the level of conus termination, a small radio-opaque
marker can be placed on the patients skin at the level of
the conus (based on the sonographic examination), and a
plain radiograph of the entire spine obtained to confirm
the corresponding vertebral body level.
Oscillations or movement of the cord and cauda equina
can be noted related to vascular pulsations associated
with cardiac systole (Fig. 16.14). The amplitude of these

Estimation of the level of the conus medullaris, normal spine. Longitudinal extended field-of-view image through the spine of a
Fig. 16.12
1-month-old boy. Identification of the S5 vertebral body allows the vertebral segments to be counted cranially. The conus is normally
positioned at L1. The coccyx (arrow) is usually unossified at this age.
LWBK505-C16_p647-674.qxd 09/07/2010 07:18 PM Page 654 Aptara
654 P E D I AT R I C S O N O G R A P H Y
B mission.)
oscillations is higher in healthy patients than in those with
cord tethering (28). This can help to diagnose tethering in
equivocal cases, and can be especially valuable in patients
after detethering procedures where anatomic changes may
not be apparent but changes in cord motion may indicate
retethering. In addition, anteroposterior motion of the
cord can be noted with episodes of crying. Longitudinal
movement of the spinal cord can be observed with a flex-
ion-extension motion of the neck.
ANATOMIC VARIANTS
Ventriculus Terminalis (Transient Dilatation
of the Central Canal)
Minimal dilatation of the central canal can be seen in some
healthy neonates (Fig. 16.15) (10,29,30). This variant has
Vertebral body segmentation anom-
Fig. 16.13
alies. A: Composite longitudinal scan
of the spine in a patient with VACTERL syndrome
shows irregular vertebral bodies (arrows), which
complicate counting vertebral bodies. B: Plain
radiograph in the same patient confirms multiple
vertebral body segmentation defects. Surgical
drain is from repair of duodenal atresia. (From
Coley BD, Murakami JW, Koch BL, et al. Diagnos-
tic and interventional ultrasound of the pediatric
spine. Pediatr Radiol 2001;31: 775785, with per-
no clinical significance and it regresses in size or disappears
soon after birth.
Filar Cyst
Filar cysts are of unclear etiology and are seen better at
sonography than at MRI. At sonography, they appear as
oval, hypoechoic, midline structures at the junction of the
tip of the conus medullaris and proximal filum terminale
(Fig. 16.16) (27). Their significance is unclear, but they
appear to be asymptomatic, do not progress, and do not
require further imaging or follow-up.
Pseudomass
A pseudomass refers to an aggregation of nerve roots
occurring when the patient is scanned in the decubitus
position, which leads to positional clumping of the nerve
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Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 655

Normal cord motion. Longitudinal M-mode

Fig. 16.14
image from the lumbosacral region shows nor-
mal motion of the cauda equina. The white lines mark the
borders of the anterior and posterior dura.

roots. Rescanning with the patient in a prone position
causes the mass to disappear as the nerve roots resume
a normal position.
SPINAL DYSRAPHISM
The term spinal dysraphism refers to a group of disor-
ders characterized by incomplete or absent fusion of pos-
terior midline structures. Dysraphic lesions can be classi-
fied based on their embryologic origin (i.e., failure of pri-
mary neurulation, disjunction, or canalization and retro-
gressive differentiation of the caudal cell mass) or by their
clinical presentation (10). Based on clinical classification,
they can be grouped into two categories: (a) spina bifida
aperta, which consists of nonskin-covered, open neural
tube defects (myelocele and myelomeningocele), and

Ventriculus terminalis. Longitudinal scan shows central cystic dilatation (arrowheads) of the distal cord. Arrow indicates the tip of the
Fig. 16.15
conus.
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656 P E D I AT R I C S O N O G R A P H Y
Filar cyst. Longitudinal sonogram shows an ovoid anechoic structure (*) just distal to the conus medullaris (C).
Fig. 16.16
(b) occult spinal dysraphism. The latter group can be fur-
ther subdivided into skin-covered defects associated with a
subcutaneous mass (lipomyelocele, lipomeningocele, sim-
ple meningocele, and myelocystocele) and occult skin-cov-
ered lesions without a subcutaneous mass (anomalies of
the caudal mass, such as tight filum terminale, fibrolipoma
of the filum terminale, caudal regression syndrome, and
sacrococcygeal teratoma, and anomalies of notochord for-
mation, such as split cord malformation and diastemato-
myelia). This clinical classification will be used to catego-
rize the lesions in this chapter.
There is no known male/female association with spinal
dysraphism, although a higher incidence has been noted in
individuals of British Isles descent. Folic acid deficiency has
been implicated as a potential dietary cause.
Spina bifida aperta is obvious on clinical examination
and further diagnostic imaging is not required. Sonogra-
phy of these children, however, is done to evaluate for
associated complications, such as hydrocephalus, Chiari
malformation, or syringomyelia. Spina bifida occulta is
imaged with sonography, and these conditions are dis-
cussed in more detail below.
The choice between sonography and MRI for evaluation
of the neonatal spine depends on the pretest likelihood of an
underlying abnormality, the age of the patient, and the
expertise of those performing the examination (31). The
sensitivity of sonography for evaluating the infant spine is
equivalent to MRI in experienced hands (2). Increasing
ossification of the posterior elements limits the acoustic
window in infants older than 4 to 6 months of age (6,16),
although it can suffice for the determination of the level of
the conus. In these infants, MRI becomes the imaging
study of choice.
Clinical Features of Spinal Dysraphism
Occult spinal dysraphism is of diagnostic importance
because if untreated, it can lead to progressive mechanical
traction of the cord as the growing vertebral column elon-
gates. This traction tethers the cord and impairs the micro-
circulation of the spinal cord, resulting in cord ischemia
and neural dysfunction. The ischemic injury to the caudal
spine results in a constellation of clinical findings called the
tethered cord syndrome. These findings include bowel
incontinence, back pain, and lower extremity abnormali-
ties, such as weakness, limp, atrophy, spasticity, and sen-
sory changes. Urinary problems are common and include
incontinence, retention, and frequent infections. Orthope-
dic deformities, such as scoliosis and foot deformities (pes
cavus and cavovarus), are also common.
Occult dysraphism is often associated with the forma-
tion of abnormal ectodermal tissue. At least 50% of chil-
dren affected with occult spinal dysraphism will have dor-
sal cutaneous stigmata (32,33). The stigmata are seen over
the midline of the lumbosacral spine and include masses,
skin tags, abnormal hair growth, hemangiomas, and dim-
ples (3236). These cutaneous stigmata are easily identi-
fied at birth and can serve as markers for underlying spinal
dysraphism. However, it is important to recognize that 5%
of all normal newborns will harbor lumbosacral cutaneous
stigmata. In the normal patient population, the most com-
mon lesion is a low-lying sacral dimple.
Lumbosacral cutaneous stigmata can be separated into
two groups: high-risk lesions that merit screening and
low-risk lesions that probably do not. A simple sacral
dimple is the most commonly encountered stigmata and
has a low likelihood of being associated with a tethered
cord (33,37). In contradistinction, atypical dimples are
associated with spinal dysraphism. These include dimples
that have a large size (5 mm in diameter), high location
on the back (2.5 cm from anus), or eccentric location
(off midline). Lesions elevated above the skin surface,
such as masses, skin tags, or tails and hairy patches, are
also high-risk predictors for spinal dysraphism, as are
hemangiomas. The presence of multiple stigmata also
LWBK505-C16_p647-674.qxd 09/07/2010 07:18 PM Page 657 Aptara
Tethered spinal cord. Longi-
Fig. 16.17
tudinal extended field-of-
view image shows an elongated spinal
cord (C) that is dorsally displaced within
the thecal sac. The tip of the conus (arrow)
is elongated and low lying at L4, indicating
a tethered cord. There was no appreciable
thickening of the filum and no other abnor-
mality to account for the cord tethering.
indicates high risk. Other high-risk findings include VAC-
TERL (vertebral, anal, cardiovascular, tracheoesophageal,
renal, and limb anomalies) syndrome, imperforate anus,
and cloacal exstrophy (3840).
THE TETHERED CORD
Sonographically, the diagnosis of a tethered cord is based
on the presence of caudal displacement of the conus
medullaris, below the L2-3 disc space. Other findings
include decreased or absent cord and nerve root motion
during real-time imaging, dorsal displacement of the cord
within the thecal sac, and an elongated, pointed conus
medullaris (Fig. 16.17). In addition, spinal dysraphism,
spinal masses, and sinus tracts may be seen.
It is important to recognize that the conus may be nor-
mally positioned but still be tethered, referred to as the
tight filum terminale syndrome. In this instance, assess-
ment of cord or nerve root motion may help establish the
diagnosis.
Treatment of the tethered cord consists of surgical
release of the filum. Early diagnosis and surgery are impor-
tant to prevent neurologic dysfunction (41,42). Once
symptoms develop, neurologic function can quickly deteri-
orate, and full return of neurologic function often does not
occur after surgical intervention (4345).
OVERT SPINAL DYSRAPHISM
(NONSKIN-COVERED LESIONS)
Myelocele and Myelomeningocele
Myeloceles and myelomeningoceles are the most common
congenital malformations of the spine, occurring in
approximately 2 per 1000 live births in North America
(46). The incidence is higher in the United Kingdom, in
girls, and in families with a history of neural tube abnor-
malities (47,48). The incidence of myelomeningocele is
decreasing, however, as the use of prenatal maternal folic
acid has increased (46,49,50).
Both myelocele and myelomeningocele result from fail-
ure of primary disjunction. The neural plate fails to fold,
Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 657
leaving it exposed and in continuity with ectoderm on the
skin surface. The open spinal cord, termed the neural pla-
code, along with the leptomeninges remains attached to
the skin along the lateral surface of the placode. The mes-
enchyme cannot migrate to its normal posterior position,
and therefore, the mesenchymal remnants also remain
attached to the placode, resulting in nerve roots arising
from the ventral surface of the placode (10,11). The poste-
rior elements of the bony spinal canal are widely splayed,
and vertebral body segmentation anomalies may be pres-
ent. The spinal cord is always tethered.
The placode is clinically obvious, presenting as a mass
of reddish tissue in the midline of the back. Myelomeningo-
celes have a dilated ventral subarachnoid space, displacing
the placode dorsally above the skin surface of the back (Fig.
16.3). Myeloceles lack this fluid accumulation, and thus,
they are flush with the plane of the dorsal skin surface. The
location of both lesions in descending order of frequency is
as follows: lumbosacral spine, 44%; lumbar spine, 22%;
thoracolumbar spine, 32%; and thoracic spine, 2%.
Neurologic deficits will depend on the level of the dys-
raphism, but will include some component of lower extrem-
ity motor and sensory deficit, such as paresis or paralysis.
Bladder or bowel dysfunction becomes apparent later in life.
Imaging of the myelocele or myelomeningocele is
rarely performed because of the risk of injury or infection.
The exposed placode is usually closed in the first few days
of life to minimize the risk of infection and to maximize
neurologic outcome (51). If scanning is done, caution
must be taken not to disrupt or contaminate the exposed
cord (11). Sonography should be performed utilizing ster-
ile gel, a sterile plastic wrap over the membranous sac, and
nonlatex gloves and probe covers, due to the high inci-
dence of latex allergies in these patients (52,53). Scanning
in the midline will show the splayed posterior elements of
the vertebral bodies, the spinal cord entering the sac, the
nerve roots extending from the surface of the cord, a cau-
dally displaced conus medullaris, and the neural placode
(Fig. 16.18). The cord attaches to the neural placode at the
posterior margin of the myelomeningocele sac.
If preoperative imaging is done, its major role is to iden-
tify associated anomalies, including Chiari II malformation,
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658 P E D I AT R I C S O N O G R A P H Y
Myelomeningocele. Longitudinal scan shows the distal spinal cord (arrowheads) displaced posteriorly and entering the neural pla-
Fig. 16.18
code (N) dorsal to the dilated meningocele (M). Note the last posterior spinous process (P) and the lack of posterior elements distally
at the level of the myelomeningocele.
split cord malformation, and hydromelia. Split cord malfor-
mation (diastematomyelia) occurs in at least 50% of patients
and hydromyelia in up to 70% (11). Chiari II malformation
occurs in virtually all patients with myelocele or myel-
omeningocele. In Chiari II malformation, the medulla, pons,
and vermis are displaced caudally into the spinal canal (7,54).
In addition to showing the Chiari malformation, sonography
can show other associated findings such as hydrocephalus and
congenital anomalies, including agenesis of the corpus callo-
sum and Dandy-Walker malformation. Intracranial air, which
is a rare finding, may also be noted (55).
Postoperative spinal imaging is not done routinely, but it
is indicated if there are clinical findings of recurrent tether-
ing, such as deterioration of neurologic function and devel-
opment of scoliosis (56). The untethered cord should lie in
the central or ventral portion of the spinal cord when the
patient is prone. Sonographic findings of cord retethering
include a dorsally positioned cord, attachment of the cord to
the surgical site, and decreased spinal cord and nerve root
movement. However, dorsal adhesion of the cord may also
be seen in patients without clinical evidence of cord reteth-
ering. In this instance, the evaluation of cord or nerve root
motion with respiration can be particularly helpful. Tether-
ing is unlikely if normal motion is present (26,27).
OCCULT SPINAL DYSRAPHISM WITH A MASS
Lipomyelocele and Lipomyelomeningocele
Four types of lipoma involve the spinal cord: lipomyelocele,
lipomyelomeningocele, intradural lipoma, and fibrolipoma
of the filum terminale. The latter two lesions are occult and
often associated with tight filum terminale syndrome.
Both lipomyelocele and lipomyelomeningocele result
from premature disjunction of the neural tube from the cuta-
neous ectoderm, prior to neural tube closure. This allows
mesenchymal cells to contact the ependymal lining of the
neural tube, which induces differentiation of the mes-
enchyme into fat, causing tethering of the neural tissue (Fig.
16.5). Both lesions contain a component of fat (i.e., a
lipoma) that is attached to the neural placode and subcuta-
neous fat of the back and is covered by intact skin. The
lipoma extends through the fascial soft tissues, posterior ver-
tebral elements, and dura before entering the spinal canal,
where it is contiguous with the low-lying spinal cord. With a
lipomyelomeningocele, the spinal cord and placode are dis-
placed dorsally above the skin surface by the expanded sub-
arachnoid space. With a lipomeningocele, the spinal cord is
a flat plaque in the plane of the cutaneous surface.
Lipomyeloceles and lipomyelomeningoceles account
for approximately 20% of skin-covered back masses and
50% of occult spinal dysraphism (10,57). At least 50% of
affected patients will have cutaneous stigmata, including
subcutaneous lipomas or cysts, skin tags, hemangiomas,
dermal pits, and aplasia cutis (11,3234,47). Most patients
have no neurologic deficits early in life. However, symp-
toms usually develop after infancy and include sensory and
motor deficits, orthopaedic abnormalities (hammertoes,
pes cavus), leg pain, and urinary and bowel incontinence.
Therefore, surgical repair is done early.
Sonography shows an echogenic intraspinal mass that
extends through a posterior defect in the spine, is continuous
with the echogenic subcutaneous tissue, and abuts the
hypoechoic neural placode (Fig. 16.19) (1,3,12,26). The
cord is tethered to the fatty mass. In patients with
lipomyelomeningoceles, a dilated subarachnoid space can be
seen and the individual nerve roots may be visible, extending
ventrally from the lipoma and neural placode. Segmentation
anomalies of the vertebral bodies and partial sacral agenesis
are seen in at least 40% of patients (47,58,59), diastemato-
myelia in 10% of patients (10,47),and genitourinary and
anorectal malformations in 5% to 10% of patients (59).
Simple Meningocele
Simple meningoceles are posterior herniations of cere-
brospinal fluid-filled meninges through a posterior bony
vertebral defect, producing a cyst-like mass in the subcuta-
neous tissues. They are most common in the lumbosacral
region (10,11,47). Their embryologic origin is unclear, and
they occur in approximately 0.01% of live births (11).
These arachnoid-lined sacs virtually never contain nervous
tissue, although occasionally, a nerve root may herniate
into the sac. The spinal cord is normally positioned, and
patients are usually neurologically intact (47). Imaging is
done to determine the size, shape, rare presence of nervous
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Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 659

Lipomyelocele and lipo-

Fig. 16.19
myelomeningocele. A: Lipo-
myelocele. Sagittal extended field-of-
view scan demonstrates a low-lying
spinal cord (C) with the tip at S1. There
is a large posterior lipoma (L). Note
the lack of spinous processes (p) in
the lower lumbar and sacral spine.
B: Lipomyelomeningocele. Longitudinal
scan of lumbosacral region of another
infant shows a low tethered spinal cord
(C) posteriorly positioned within the the-
cal sac. There is distal dysraphism with
a subcutaneous lipoma (L) abutting the
distal cord and posterior extension of
the meninges (arrows) containing neural
elements (arrowheads). B

tissue, and relationship of the meningocele sac to the conus
(Fig. 16.20).
Lateral meningoceles are cerebrospinal fluid (CSF)-filled
protrusions of dura and arachnoid, which extend through
the neural foramina. They are usually found in older children
Meningocele. Sagittal image shows a large cerebrospinal
Fig. 16.20
fluidfilled meningocele (M) in continuity with the spinal
subarachnoid space (arrows).
and adults with neurofibromatosis or Marfan syndrome and
almost never occur in the neonate. MRI is the study of choice
for establishing the diagnosis, rather than sonography.
Terminal Myelocystocele
Myelocystoceles are rare skin-covered lesions characterized
by a meningocele; a hydromyelic cord, which terminates in
a large cyst; and a posterior spinal defect. The dilated cord
extends through the posterior bony defect onto the back. It
is surrounded by the dilated subarachnoid space of the
meningocele, which communicates with the subarachnoid
fluid of the spinal canal but not with the dilated distal end
of the central canal (Fig. 16.21) (10,11). There may be a
lipomatous component, forming a lipomyelocystocele (60).
The spinal cord is low lying and tethered. When myelocys-
toceles occur in the lumbosacral region, they are called ter-
minal myelocystoceles. Myelocystoceles result from an
error in formation of the caudal cell mass or failure of clo-
sure of the posterior neuropore (10).
Terminal myelocystoceles occur more frequently in girls
than boys, and may be associated with the OEIS complex
(omphalocele, exstrophy of the bladder, imperforate anus,
and sacral agenesis) (61), and other abnormalities of the
spinal cord (60). Patients present with a skin-covered mass
in the lumbosacral region and varying degrees of neurologic
compromise. Myelocystoceles elsewhere in the spine are
quite rare and are probably the result of partial failure of
neurulation; these patients are often asymptomatic (62,63).
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660 P E D I AT R I C S O N O G R A P H Y
Terminal myelocystocele. The distal central canal termi-
Fig. 16.21
nates into a large cyst (C) associated with expanded
subarachnoid spaces (sas). (Reprinted from Barkovich AJ. Congenital
anomalies of the spine. In: Pediatric neuroimaging. 4th ed. Philadel-
phia, PA: Lippincott William & Wilkins, 2005:704772.)
Sonography shows the dilated spinal cord sur-
rounded by a dilated subarachnoid space (meningocele)
that is in direct continuity with the subarachnoid space
of the spinal canal, the large cyst distal to the meningo-
cele, the insertion of the cord on the posterior wall of the
meningocele, and the nerve roots exiting the spinal cord
(Fig. 16.22).
A B
Terminal myelocystocele. A: Longitudinal scan through the lower thoracic cord (C) shows marked hydromyelia (h). B: Longitudinal scan
Fig. 16.22
through the distal spine shows hydromelia (h). The large terminal myelocystocele (C) and dilatation of the adjacent subarachnoid space (S).
OCCULT SPINAL DYSRAPHISM WITHOUT A MASS
Disorders of Primary Neurulation
SPLIT CORD MALFORMATION (DIASTEMATOMYELIA)
Split cord malformation or diastematomyelia is character-
ized by a sagittal cleft in the spinal cord, dividing it into
two hemicords. Each cord contains a central canal, its own
surrounding pia, and one dorsal horn and one ventral
horn, with each horn giving rise to dorsal and ventral
nerve roots, respectively (10,64). This disorder results
from sagittal splitting of the notochord probably around
an adhesion between the endoderm and ectoderm or
another obstacle to cell migration (10,65,66). Split cord
malformations are divided into two types: type I malfor-
mations, which have a midline bony, cartilaginous, or
fibrous spur with each cord having its own arachnoid and
dural coverings, and type II malformations, which have no
septum and the hemicords share common arachnoid and
dural coverings (36,65).
Split cord malformations account for approximately
3.8% of spinal dysraphic lesions, and are most common in
the lower thoracic or lumbar region (11,36,47). Girls are
affected more often than boys, and approximately 50%
will have symptoms related to cord tethering (10,47,66).
Patients with type I malformations are generally more
symptomatic than patients with type II malformations
(10). Scoliosis is a late clinical presentation. Cutaneous
stigmata such as hypertrichosis and commonly a silky
patch of hair referred to as a fawn tail, lipomas, dimples,
hemangiomas, and dermal sinuses are present in over 50%
or cases (11,35). Other anomalies, such as myeloceles,
meningoceles, lipomas, hydromyelia, and cord tethering,
occur in over 85% of patients. Because the notochord
affects the development of the vertebral bodies, in addition
to the spinal cord, abnormalities such as hemivertebra,
butterfly vertebra, and block vertebra are common.
The most severe forms of split notochord syndrome
have dorsal enteric fistulas characterized by a communica-
tion between the gastrointestinal tract and the dorsal skin
in the midline. The fistulas cross through the prevertebral
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Split cord malformation (diastematomyelia). Transverse
Fig. 16.23
scan through the lower thoracic spine shows two dis-
tinct hemicords (C). The fibrous spur was better seen with magnetic
resonance imaging than at sonography. (From Coley BD, Murakami
JW, Koch BL, et al. Diagnostic and interventional ultrasound of the
pediatric spine. Pediatr Radiol 2001;31:775785, with permission.)
soft tissues, vertebral bodies, spinal canal, and posterior
spinal elements. The bowel lumen may communicate with
the skin. If part of the fistula involutes or becomes obliter-
ated, then fibrous cords, sinuses, or duplication cysts may
develop anywhere long the cord. Dorsal enteric sinuses
usually arise from the dorsal part of the tract; they have a
blind ending ventrally and are open to the dorsal skin sur-
face. Dorsal enteric cysts arise from trapped remnants in
the middle part of the tract; both dorsal and ventral por-
tions of the enteric fistula are closed. They are usually
found in the paraspinal region.
Sonography can demonstrate the two cords and two
central canals (Fig. 16.23) and the fibrous, cartilaginous, or
bony spur separating the cords (11,64). The two cords
Dorsal dermal sinus. Longitudinal scan through the lower lumbar spine shows a dorsal dermal sinus with a hypoechoic tract
Fig. 16.24
(arrowheads) extending through the fat to the thecal sac. The cord (C) is low lying and tethered to an associated dorsal fatty mass (F).
Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 661
often reunite below the spur. Associated abnormalities such
as low-lying conus medullaris and thickened filum indicat-
ing cord tethering, dorsal enteric cysts, hydromyelia, and
vertebral anomalies also can be observed.
It is important not to confuse a duplication artifact for
the split notochord malformation. This artifact occurs in
the transverse view and likely results from refraction of the
ultrasound beam through musclefat interfaces formed by
the rectus abdominis muscles and the fat layer deep to
them. This artifact can be minimized or obviated by slid-
ing the transducer laterally and imaging off midline in
either direction. Imaging in the longitudinal plane also can
help obviate this artifact and support the diagnosis of split
notochord syndrome (67).
DORSAL DERMAL SINUS
Dorsal dermal sinus is an epithelial-lined fistulous tract
extending from the spinal cord, cauda equina, or arach-
noid to the dorsal skin surface. It results from incomplete
separation of the cutaneous ectoderm from the neural
ectoderm during the process of disjunction (Fig. 16.4).
Dorsal sinuses occur most often in the lumbosacral and
occipital regions, but they may occur anywhere along the
spinal canal. They are associated with intraspinal lipomas,
dermoids, and epidermoid tumors (11).
Clinically, patients present with a small midline dimple
with or without discharge. Other cutaneous stigmata such
as hemangiomas, subcutaneous masses, and hairy nevi are
common (32). Because of the increased incidence of menin-
gitis, epidural and subdural abscess, or intramedullary
spinal cord abscess, early diagnosis is important (68).
Sonography can demonstrate the sinus tract, which
may be hypoechoic or hyperechoic, extending from the
skin surface into the subcutaneous soft tissues. In the
echogenic subcutaneous tissues, the tract usually appears
hypoechoic, whereas in the anechoic CSF-filled subarach-
noid space, it appears as an echogenic structure (Fig.
16.24) (68). The presence of a low conus medullaris, indi-
cating a tethered cord, is supportive evidence that the fis-
tulous tract reaches the spinal canal. Coexistent lipomas,
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662 P E D I AT R I C S O N O G R A P H Y

A B
Pilonidal sinus. A, B: Longitudinal sonograms in two different patients show a hypoechoic tract (arrow) extending from a simple sacral
Fig. 16.25
dimple (D) to the tip of the coccyx (C).

dermoids, and epidermoids can be intra- orextramedullary Sonography can show pseudothickening of the filum or
and they can be adherent to the spinal cord and nerve a nodular contour. A discrete intradural lipoma is often
roots. difficult to identify because it has the same echogenicity as
the filum terminale. MRI is the best modality to evaluate
Pilonidal Sinus/Simple Dimple patients with intradural lipomas.
Dorsal dermal sinus needs to be differentiated from a
pilonidal sinus, also known as a sacral dimple. Pilonidal Disorders of the Caudal Cell Mass
means nest of hair. Pilonidal sinuses are common
lesions, with an incidence of 2% to 9% (6,32,33). Their TIGHT FILUM TERMINALE SYNDROME
embryology is unknown, but they may result from a defect The tight filum terminale syndrome is characterized by a
in ectodermal fusion or incomplete regression of the spectrum of neurologic deficits and orthopaedic deformi-
embryonic human tail in early gestation (6,69). They typi- ties associated with a short thick filum terminale and low-
cally occur near the coccyx and can be painful. Anatomi- lying conus medullaris (at or below the level of L2-3). The
cally, the sinuses are small channels or pits that are less cause is unknown, but it may be related to incomplete invo-
than 5 mm in diameter and located less than 25 mm from lution of the spinal cord during the time of retrogressive
the anus, open to the surface of the skin, and not associ-
ated with any other cutaneous lesion. Most importantly,
simple sacral dimples do not extend to neural structures
and thus, there is no increased risk of occult spine malfor-
mation or tethered cord (4,16,32,68).
Sonography of the pilonidal sinus/simple dimple
demonstrates a short hypoechoic subcutaneous tract that
extends to the coccyx (Fig. 16.25) (32). The sinus may com-
municate with a pilonidal cyst, which is a dilated sinus. The
cyst can become infected and form an abscess. At sonogra-
phy, an infected cyst appears as an echogenic mass in the
subcutaneous tissues (Fig. 16.26).

INTRADURAL LIPOMAS
An intraspinal lipoma is a localized collection of fat within
the intradural compartment of the spinal canal, typically
in a subpial location. It is thought to result from prema-
ture separation of the neuroectoderm from the cutaneous
ectoderm. When it involves the lumbosacral area, it can
have a connection to the leptomeninges or spinal cord,
tethering the cord and leading to lower extremity weak-
ness or bowel or bladder dysfunction. With an intradural Pilonidal cyst. Longitudinal scan over the distal spine
lipoma, the plane between the lipoma and subcutaneous Fig. 16.26
(arrow  coccyx) shows a subcutaneous mass (M) with-
fat is well defined, unlike the lipomyelomeningocele, out intraspinal communication, representing an infected pilonidal
where there is no fascial plane of separation. sinus tract. The spinal cord was normal.
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Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 663

Tight filum terminale syndrome. A: Longitudinal sonogram shows a thickened filum

Fig. 16.27
terminale (arrowheads) and borderline low-lying conus at L2-3. B: Sagittal T1-
weighted magnetic resonance image of the same patient shows high-signal fat (arrow) within the
filum terminale, representing a small lipoma. B

differentiation, leading to a thickened filum terminale.
Clinical findings relate to stretching of the spinal cord and
include neurologic deficits, back pain, gait disturbance,
and bowel or bladder dysfunction. These often present
during periods of rapid growth, which presumably exacer-
bates stretching of the spinal cord (11). Symptoms are
often worse after exertion (due to stretching of nerve
roots) and in the mornings (due to cord stretching second-
ary to the accumulation of water in the intervertebral discs
during sleep) (10). Associated scoliosis is common. Histo-
logically, tight fila have increased amounts of connective
tissue and collagen fibers (44). Release of the thickened
filum can result in neurologic improvement (45).
Sonography can show an abnormally thickened filum,
which exceeds 2 mm in diameter. The conus medullaris is
nearly always low lying, although occasionally it can be at
a normal level (Fig. 16.27). Other findings include absent
or diminished spinal cord and nerve root movement. A
coexistent small lipoma or fibrolipoma may be present.
FIBROLIPOMA OF THE FILUM TERMINALE
Fibrolipomas of the filum terminale are varying sized accu-
mulations of fat within the filum terminale. In some
instances, they represent a normal variant, and small filum
fibrolipomas have been found in at least 5% of asympto-
matic adults on MRI (54). While small lesions are often
asymptomatic, larger fibrolipomas are often associated with
symptoms of cord tethering, and older patients are more
commonly symptomatic than younger patients (59,70).
On sonography, the fibrolipoma is seen as a thickened,
echogenic filum terminale (2 mm in diameter)
(Fig. 16.28). It usually cannot be clearly separated from

Filum terminale fibrolipoma. Longitudinal scan through the distal spine shows a thickened, echogenic distal filum terminale (arrow-
Fig. 16.28
heads) owing to a fibrolipoma found at surgery. The conus (C) is elongated and tapered, suggesting cord tethering.
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664 P E D I AT R I C S O N O G R A P H Y

A B
Caudal regression syndrome. A: Longitudinal scan of the distal thoracic spine shows abrupt termination of the spinal cord (C). The
Fig. 16.29
terminus of the cord has a blunted, squared shape (arrows), characteristic of caudal regression, rather than a normally tapered
configuration. B: Corresponding sagittal T1-weighted magnetic resonance image also shows the characteristic blunted shape of the cord (C). (From
Coley BD, Murakami JW, Koch BL, et al. Diagnostic and interventional ultrasound of the pediatric spine. Pediatr Radiol 2001;31:775785, with
permission.)

the filum, since both have similar echogenicity, and MRI is
the best imaging study for showing this lesion (54).
CAUDAL REGRESSION SYNDROME
Caudal regression syndrome is a spectrum of anomalies
affecting the lower spine, anorectal structures, and geni-
tourinary tract. It is the result of an insult to the caudal
mesoderm, including the caudal cell mass and the cloaca
(10,11). Approximately 15% of patients are infants of dia-
betic mothers, and approximately 1% of all infants of dia-
betic mothers will be affected (7,54). The degree of spinal
agenesis is variable, ranging from sacral hypoplasia to total
absence of the lumbar and sacral spine. The cord is fre-
quently hypoplastic and tethered. Clinical signs are variable,
ranging from mild distal muscle weakness or isolated foot
deformities with associated bladder or bowel incontinence
to total lower extremity paralysis, sirenomelia (fusion of the
lower extremities), severe genitourinary anomalies (bladder
exstrophy, renal aplasia), and anal atresia (10). Dysraphic
lesions, such as myelomeningoceles, may also occur.
Two sonographic appearances have been described in
patients with caudal regression based on the configuration
and level of the conus medullaris: (a) a blunted or wedge-
shape conus that terminates above L1 (Fig. 16.29), in con-
trast to the tapered configuration of the normal conus
medullaris (13,7,54), and (b) an elongated conus that is
tethered by a thickened filum terminale or intraspinal
lipoma and ends below L1.
SACROCOCCYGEAL TERATOMA
Sacrococcygeal teratomas represent approximately 40% of
fetal and neonatal germ cell tumors and occur in approxi-
mately 1 per 40,000 births (61,71). These tumors arise in the
coccyx from multipotential cells in the caudal cell mass of the
embryo (72). Most are sporadic, affect girls more than boys
(3.4:1 ratio) (71), and are not associated with bony defects
of the sacrum. Involvement of the sacral canal is also rare.
Sacrococcygeal teratomas are classified into four major
types according to location: type I teratomas (47%),
almost entirely external; type II tumors (34%), predomi-
nantly external with a large intrapelvic component; type III
tumors (9%), predominantly intrapelvic and intra-abdom-
inal with a small external component; and type IV tumors
(10%), entirely presacral (Fig. 16.30) (73).
Clinically, affected neonates may present with hemor-
rhage due to tumor rupture, cardiac failure or hydrops
from vascular shunting, or consumptive coagulopathy
(72,74). Early diagnosis and treatment, consisting of the
removal of the tumor in continuity with the coccyx, are
important because of the tendency for malignant degener-
ation. Approximately 10% of tumors in neonates are
malignant (71). If the diagnosis is made after the age of
2 months, the frequency of malignancy increases to 66%
in boys and 47% in girls, and is nearly 100% by the age of
3 years (71,73,7577). A rare form of sacrococcygeal ter-
atoma is familial. Familial lesions have autosomal domi-
nant inheritance, are virtually always presacral (type IV)
and benign, and are associated with sacrococcygeal defects
and anorectal stenosis (78).
Sacrococcygeal teratomas with an external component
are obvious at birth and present as large skin-covered mass
lesions. Sonography can provide information about the
internal echotexture of teratomas (79), but MRI is the pre-
ferred imaging modality to determine the total extent of
the mass. At sonography, these tumors have a heteroge-
neous appearance, with both soft tissue and cystic compo-
nents. Malignant teratomas are predominantly solid but
often contain small cystic areas (Figs. 16.31 and 16.32).
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Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 665

TYPE I TYPE II

Classification of sacrococcygeal teratomas:

Fig. 16.30
type I: predominantly external with a small pre-
sacral component; type II: external with a large intrapelvic
component; type III: predominantly internal with a smaller
external component; and type IV: entirely presacral, without
an external component. (Adapted from Altman RP, Randolph
JG, Lilly JR. Sacrococcygeal teratoma: American Academy of
Pediatrics Surgical Section Survey1973. J Pediatr Surg
1974;9:389398, with permission.) TYPE III TYPE IV

B
Malignant sacrococcygeal teratoma, type I. A: Transverse color Doppler image in a newborn with a large external mass shows a pre-
Fig. 16.31
dominantly solid heterogeneous tumor with scattered cystic areas and blood flow. B: Corresponding sagittal T2-weighted magnetic
resonance image with fat saturation shows a large solid and cystic mass arising from the coccyx. There is no intrapelvic extension.
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666 P E D I AT R I C S O N O G R A P H Y

A B
Malignant sacrococcygeal teratoma, type II. A: Transverse sonogram through the pelvis in a newborn girl shows a complex solid and
Fig. 16.32
cystic mass (arrows) posterior to the bladder (B). B: Sagittal T2-weighted magnetic resonance image shows the full intrapelvic exten-
sion of the tumor.

Benign tumors are predominantly cystic, although they

usually contain small amounts of solid tissue (Figs. 16.33
and 16.34). They usually do not enter the spinal canal.
Color Doppler can show flow in the solid components and
arteriovenous shunting may be present in malignant
tumors. Hydronephrosis may be noted if the tumor com-
presses or invades the bladder.
TUMORS
Sonography can be used in neonates to diagnose both
primary spinal canal tumors and intraspinal extension
from intrathoracic or intra-abdominal neuroblastomas,
osteosarcomas, embryonal rhabdomyosarcomas, lym-
phomas, Ewing sarcomas, rhabdoid tumors, and heman-

A B
Benign sacrococcygeal teratoma, type III. A: Longitudinal scan in a 3-month-old girl with a history of constipation and a palpable
Fig. 16.33
abdominal mass shows a predominantly cystic mass (M), with a solid mural nodule (arrows), arising from the pelvis, displacing the
bladder (B) anteriorly and superiorly. B: Longitudinal sonogram of the left kidney shows secondary hydronephrosis and hydroureter (arrows) from
bladder outlet obstruction.
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Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 667

A B
Benign sacrococcygeal teratoma, type IV. A: Longitudinal scan in a neonate with a prenatally diagnosed pelvic mass shows a com-
Fig. 16.34
plex cystic mass (M) displacing the bladder (B) anteriorly and superiorly. Arrows indicate the vertebral bodies. B: Computed tomog-
raphy scan confirms the predominantly cystic nature of the mass.

giomas (Fig. 16.35) (9,80). Most primary spinal tumors in
neonates are congenital and include teratomas, dermoids,
epidermoids, hamartomas, lipomas, and enterogenous
cysts (10).
Primary tumors of the spinal cord can be intra- or
extramedullary in location and solid, cystic, or complex.
Intramedullary tumors produce cord enlargement.
Extramedullary tumors displace the spinal cord to either
side on transverse views and either anteriorly or poste-
riorly on longitudinal views (Fig. 16.36) (81,82).
Regardless of their location, they almost always occupy
the entire spinal canal, obliterating the subarachnoid

A B
Retroperitoneal hemangioma with intrathecal extension. A: Transverse extended field-of-view image of the retroperitoneum in a
Fig. 16.35
4-month-old boy shows a large, heterogeneous hemangioma (arrows) lying lateral to the spine. The tumor extends into the epidural
space, displacing the cord (arrowhead). P  spinous process. B: Transverse power Doppler image confirms a hypervascular mass. Again, note the
paraspinal (arrows) and intraspinal (arrowheads) components of the hemangioma. The tumor displaces the cord (C) anterolaterally within the spinal
canal. The images are obtained with the patient prone.
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668 P E D I AT R I C S O N O G R A P H Y
Extradural tumor. Transverse scan through the posterior
Fig. 16.36
arches of the upper thoracic spine shows a paraspinal
mass (M) with an intraspinal component (open arrow), which dis-
places the cord (arrowheads) and dura (d). VB  vertebral body; sp 
spinous process. Intraspinal extension of neuroblastoma was shown
at operation.
space and the echogenic central canal. Motion of the
affected segment of the cord is diminished or absent.
The sonographic appearance of cord tumors is nonspe-
cific, but localization of the extent of disease allows for
minimization of surgical exposure and resection (82,83).
Following laminectomy, sonography can be used to eval-
uate patients with symptoms of recurrent tumor.
SYRINGOMYELIA AND HYDROMYELIA
Syringomyelia refers to a cavity in the spinal cord involv-
ing the parenchyma lateral to the central canal. Syringo-
hydromyelia refers to cavities involving both the
parenchyma lateral to the central canal and the central
canal. Hydromelia refers to a dilated central canal of the
spinal cord. Syringohydromyelia can occur with congeni-
tal anomalies of the spine or the cervicomedullary junc-
tion, including spinal dysraphism and Chiari malforma-
tions (2,7,10,47,48). Syringomyelia is also found in
children with spinal cord tumors.
Clinically, patients may present with sensory deficits,
muscular weakness, spastic paraparesis, or scoliosis.
Sonography shows a dilated central canal of the spinal
cord or cysts in or lateral to the central cord.
SPINAL CORD TRAUMA
Spinal cord injuries in the neonate include laceration of
the cord or the nerve roots and epidural or subdural
hematoma due to meningeal injury. Predisposing fac-
tors include difficult delivery, breech presentation, and
use of forceps leading to longitudinal traction, hyper-
flexion, or hyperextension of the spinal cord. Lumbar
puncture is another cause of epidural or subdural
hematoma.
Sonographic findings of cord disruption and laceration
include increased echogenicity of the spinal cord due to
hemorrhage or edema and displacement of the cord due to
epidural or subdural hemorrhage (Fig. 16.37) (8488). In
the acute stage, hemorrhage is echogenic, becoming com-
plex (echogenic and hypoechoic) and then predominantly
anechoic over time.
Cord disruption from in utero
Fig. 16.37
injury. Longitudinal scan of
the lower thoracic spine in a newborn
shows focal dysraphism (arrow) of the pos-
terior spinal elements. The distal part of the
cord (C) extends into the dysraphic area.
The more proximal cord is entirely cystic
(*), presumably from in utero infarction. The
patient also had hydranencephaly.
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Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 669

Traumatic epidural fluid collection after unsuccessful lumbar

Fig. 16.38
puncture. A: Longitudinal scan through the distal spine after an
unsuccessful lumbar puncture shows a heterogeneous fluid collection within
the dorsal and ventral epidural space (e). This collection, representing
epidural blood and cerebrospinal fluid, changed shape and position at real-
time imaging. The thecal sac is compressed (arrows), and no cerebrospinal
fluid is seen within it. C  conus. B: Transverse scan from another patient
shows the epidural collection (e) compressing the thecal sac (arrows). B

Lumbar puncture can result in laceration of the dura

or meninges, leading to a CSF leak or epidural or sub-
dural hematoma. The resultant fluid collections can
compress the thecal sac and obliterate the CSF space
(7,8991). Sonography can show the compressed thecal
sac due to the surrounding fluid collection (Fig. 16.38).
It can also be used to guide lumbar puncture, enabling
sampling of even small CSF collections (89) and epidural
catheter placement for anesthetic applications (92).
OTHER LESIONS
Extramedullary masses such as epidural abscesses
and arachnoid cysts can be visualized by sonography
(7,93,94).
In the setting of suspected hardware infection, sonog-
raphy can disclose abnormal fluid collections and provide
guidance for subsequent diagnostic aspiration (Fig. 16.39)
(95).
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670 P E D I AT R I C S O N O G R A P H Y

Paraspinal infection after rod placement. Longitudinal
Fig. 16.39
scan in a 14-year-old girl with pain and fever after spinal
instrumentation shows fluid (F) dorsal to the metallic hardware
(arrows). Ultrasound-guided aspiration was positive for infection.
Intraspinal cavernous hemangioma. Longitudinal intra-
Fig. 16.41
operative sonogram shows a heterogeneous echogenic
and enlarged spinal cord due to intramedullary hemorrhage (h) and
surrounding hypoechoic spinal cord tissues (arrowheads).

INTRAOPERATIVE SONOGRAPHY Intraoperative sonography has been most commonly

Intraoperative sonography is performed through a poste- used to identify the conus medullaris and localize focal
rior laminectomy with the patient in a prone position. The abnormalities, including tumors (Fig. 16.40), vascular mal-
laminectomy site is filled with sterile saline, which acts as formations (Fig. 16.41), syringomyelia (Fig. 16.42),
a coupling agent for the transducer. hydromelia, epidural hematomas and abscesses, and the

A B
Ependymoma. Intraoperative sonogram. A: Longitudinal scan directly over the dura of the lower thoracic cord (c) shows an echogenic
Fig. 16.40
intramedullary, intradural mass (m). S  saline bath. Arrowheads indicate the anterior margin of cord. B: Longitudinal scan over the
dura of the lumbar spine shows an extramedullary, intradural mass (m) displacing the spinal cord (c) anteriorly. The thoracic lesion was the primary
tumor; the lumbar lesion represented a drop metastasis. S  saline bath. Arrowhead indicates anterior cord margin.
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Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 671

A B
Intraoperative syrinx localization. A: Sagittal T1-weighted magnetic resonance image shows a syrinx (S) of the cervical cord. B: Lon-
Fig. 16.42
gitudinal intraoperative sonogram after bony decompression of the occiput and posterior arch of C1, using sterile saline in the surgi-
cal cavity as an acoustic coupling agent, clearly localizes the syrinx (S). Note also the cerebellar tonsils (T), the medulla oblongata (M), the anterior
margin of the foramen magnum (the basion, B), and the fourth ventricle (arrow).

bony or cartilaginous septum in split cord malformations
prior to surgical resection or biopsy (6,96101). Other
indications for intraoperative sonography include moni-
toring of the adequacy of posterior fossa decompression
during repair of the Chiari I malformation (Fig. 16.43)
(102), documentation of the extent of residual gibbous
deformity following straightening of spinal curvature
(103), and evaluating the degree of spinal canal decom-
pression after trauma (104).

A B
Intraoperative assessment during Chiari I decompression. A: Longitudinal intraoperative scan after posterior bony decompression
Fig. 16.43
shows cerebellar tonsillar ectopia (T) and no cerebrospinal fluid between the tonsils and the dura (arrowheads). C  spinal cord.
B: Longitudinal scan after duraplasty shows cerebrospinal fluid (arrow) between the tonsils (T) and the dura (arrowheads). C  spinal cord. (Cour-
tesy of Dr. B. L. Koch, Cincinnati, OH.)
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672 P E D I AT R I C S O N O G R A P H Y
REFERENCES
1. Deeg KH, Lode HM, Gassner I. Spinal sonography in newborns
and infantspart II: spinal dysraphism and tethered cord.
Ultraschall Med 2008;29:7788.
2. Dick EA, de Bruyn R. Ultrasound of the spinal cord in children:
its role. Eur Radiol 2003;13:552562.
3. Lowe LH, Johanek AJ, Moore CW. Sonography of the neona-
tal spine: part 2, spinal disorders. AJR Am J Roentgenol 2007;
188:739744.
4. Rufener SL, Ibrahim M, Raybaud CA, Parmar HA. Congenital
Spine and Spinal Cord MalformationsSelf-Assessment Module.
AJR 2010;194:S38S40.
5. Rubin JM, DiPietro MA, Chandler WF, et al. Spinal ultra-
sonography. Intraoperative and pediatric applications. Radiol
Clin North Am 1988;26:127.
6. Schenk JP, Herweh C, Gunther P, et al. Imaging of congenital
anomalies and variations of the caudal spine and back in
neonates and small infants. Eur J Radiol 2006;58:314.
7. Unsinn KM, Geley T, Freund MC, et al. US of the spinal cord
in newborns: spectrum of normal findings, variants, congenital
anomalies, and acquired diseases. Radiographics 2000;20:
923938.
8. Zieger M, Dorr U. Pediatric spinal sonography. Part I: anatomy
and examination technique. Pediatr Radiol 1988;18:913.
9. Zieger M, Dorr U, Schultz RD. Pediatric spinal sonography.
Part II: malformations and mass lesions. Pediatr Radiol 1988;
18:105111.
10. Barkovich AJ. Congenital anomalies of the spine. In: Pediatric
neuroimaging. 4th ed. Philadelphia, PA: Lippincott William &
Wilkins, 2005:704772.
11. Egelhoff JC, Prenger EC, Coley BD. The spine. In: Ball WS Jr,
ed. Pediatric neuroradiology. Philadelphia, PA: Lippincott-
Raven, 1997:717778.
12. Dick EA, Patel K, Owens CM, et al. Spinal ultrasound in
infants. Br J Radiol 2002;75:384392.
13. OHara SM. Extended field of view imaging: the big picture in
pediatric patients. J Ultrasound Med 2002;21:S38.
14. Riccabona M, Nelson TR, Weitzer C, et al. Potential of three-
dimensional ultrasound in neonatal and paediatric neurosonog-
raphy. Eur Radiol 2003;13:20822093.
15. Hughes JA, de Bruyn R, Patel K, et al. Three-dimensional sono-
graphic evaluation of the infant spine: preliminary findings.
J Clin Ultrasound 2003;31:920.
16. Deeg KH, Lode HM, Gassner I. Spinal sonography in newborns
and infantspart I: method, normal anatomy and indications.
Ultraschall Med 2007;28:507517.
17. Nelson MD Jr, Sedler JA, Gilles FH. Spinal cord central echo com-
plex: histoanatomic correlation. Radiology 1989;170:479481.
18. Kawahara H, Andou Y, Takashima S, et al. Normal develop-
ment of the spinal cord in neonates and infants seen on ultra-
sonography. Neuroradiology 1987;29:5052.
19. Lam WWM, Ai V, Wong V, et al. Ultrasound measurement of
lumbosacral spine in children. Pediatr Neurol 2004;30:115121.
20. DiPietro MA. The conus medullaris: normal US findings
throughout childhood. Radiology 1993;188:149153.
21. Kesler H, Dias MS, Kalapos P. Termination of the normal conus
medullaris in children: a whole-spine magnetic resonance imag-
ing study. Neurosurg Focus 2007;23:15.
22. Zalel Y, Lehavi O, Aizenstein O, et al. Development of the fetal
spinal cord: time of ascendence of the normal conus medullaris as
detected by sonography. J Ultrasound Med 2006;25:13971401.
23. Beek FJA, de Vries LS, Gerards LJ, et al. Sonographic determi-
nation of the position of the conus medullaris in premature and
term infants. Neuroradiology 1996;38:S174S177.
24. Wilson DA, Prince JR. MR imaging determination of the loca-
tion of the normal conus medullaris throughout childhood. AJR
Am J Roentgenol 1989;152:10291032.
25. Beek FJA, Bax KMA, Mali WPTM. Sonography of the coccyx
in newborns and infants. J Ultrasound Med 1994;13:
629634.
26. Korsvik HE. Ultrasound assessment of congenital spinal anom-
alies presenting in infancy. Semin Ultrasound CT MR 1994;15:
264274.
27. Lowe LH, Johanek AJ, Moore CW. Sonography of the neona-
tal spine: part I, normal anatomy, imaging pitfalls, and varia-
tions that may simulate disorders. AJR Am J Roentgenol 2007;
188:733738.
28. Schumacher R, Richter D. One-dimensional Fourier transfor-
mation of M-mode sonograms for frequency analysis of moving
structures with application to spinal cord motion. Pediatr
Radiol 2004;34:793797.
29. Kriss VM, Kriss TC, Babcock DS. The ventriculus terminalis of
the spinal cord in the neonate: a normal variant on sonography.
AJR Am J Roentgenol 1995;165:14911493.
30. Kriss VM, Kriss TC, Coleman RC. Sonographic appearance of
the ventriculus terminalis cyst in the neonatal spinal cord.
J Ultrasound Med 1999;18:207209.
31. Medina LS, Crone K, Kuntz KM. Newborns with suspected
occult spinal dysraphism: a cost-effectiveness analysis of diag-
nostic strategies. Pediatrics 2001;108:e101.
32. Kriss VM, Desai NS. Occult spinal dysraphism in neonates:
assessment of high-risk cutaneous stigmata on sonography. AJR
Am J Roentgenol 1998;171:16871692.
33. Robinson AJ, Russell S, Rimmer S. The value of ultrasonic
examination of the lumbar spine in infants with specific refer-
ence to cutaneous markers of occult spinal dysraphism. Clin
Radiol 2005;60:7277.
34. Guggisberg D, Hadj-Rabia S, Viney C, et al. Skin markers of
occult spinal dysraphism: a review of 54 cases. Arch Dermatol
2004;140:11091115.
35. Izci Y, Gonul M, Gonul E. The diagnostic value of skin lesions
in split cord malformations. J Clin Neurosci 2007;14:860863.
36. Ozturk E, Sonmez G, Mutlu H, et al. Split-cord malformation
and accompanying anomalies. J Neuroradiol 2008;35:150156.
37. Abu Sneineh AK, Gabos PG, Keller MS, et al. Ultrasonography
of the spine in neonates and young infants with a sacral skin
dimple. J Pediatr Orthop 2002;22:762762.
38. Dick EA, de Bruyn R, Patel K, et al. Spinal ultrasound in cloa-
cal exstrophy. Clin Radiol 2001;56:289294.
39. Kuo MF, Tsai Y, Hsu WM, et al. Tethered spinal cord and
VACTERL association. J Neurosurg 2007;106(suppl 3):201204.
40. Long FR, Hunter JV, Mahboubi S, et al. Tethered cord and
associated vertebral anomalies in children and infants with
imperforate anus: evaluation with MR imaging and plain radi-
ography. Radiology 1996;200:377382.
41. Koyanagi I, Iwasaki Y, Hida K, et al. Surgical treatment sup-
posed natural history of the tethered cord with occult spinal
dysraphism. Childs Nerv Syst 1997;13:268274.
42. Satar N, Bauer SB, Scott RM, et al. Late effects of early surgery
on lipoma and lipomeningocele in children less that 1 year old.
J Urol 1997;157:14341437.
43. Satar N, Bauer SB, Shefner J, et al. The effects of delayed diag-
nosis and treatment in patients with occult spinal dysraphism. J
Urol 1995;154(2 Pt 2):754758.
44. Selcuki M, Vatansever S, Inan S, et al. Is a filum terminale with a
normal appearance really normal? Childs Nerv Syst 2003;19:310.
45. Wehby MC, OHollaren PS, Abtin K, et al. Occult filum termi-
nale syndrome: results of surgical untethering. Pediatr Neuro-
surg 2004;40:5157.
46. Centers for Disease Control and Prevention. Racial/ethnic differences
in the birth prevalence of spina bifidaUnited States, 19952005.
MMWR Morb Mortal Wkly Rep 2009;57:14091413.
47. Byrd SE, Darling CF, McGlone DG, et al. MR imaging of the pedi-
atric spine. Magn Reson Imaging Clin N Am 1996;4:797833.
48. Deak KL, Siegel DG, George TM, et al. Further evidence for a
maternal genetic effect and a sex-influenced effect contributing
LWBK505-C16_p647-674.qxd 09/07/2010 07:19 PM Page 673 Aptara
to risk for human neural tube defects. Birth Defects Res A Clin
Mol Teratol 2008;82:662669.
49. Murphy M, Whiteman D, Stone D, et al. Dietary folate and the
prevalence of neural tube defects in the British Isles: the past
two decades. BJOG 2000;107:885889.
50. Thompson S, Torres M, Stevenson R, et al. Periconceptual vita-
min use, dietary folate and occurrent neural tube defected preg-
nancies in a high risk population. Ann Epidemiol 2000; 10:476.
51. Tarcan T, Onol FF, Ilker Y, et al. The timing of primary neurosur-
gical repair significantly affects neurogenic bladder prognosis in
children with myelomeningocele. J Urol 2006;176: 11611165.
52. Pittman T, Kiburz J, Gabriel K, et al. Latex allergy in children
with spina bifida. Pediatr Neurosurg 1995;22:96100.
53. Zerin JM, McLaughlin K, Kerchner S. Latex allergy in patients
with myelomeningocele presenting for imaging studies of the
urinary tract. Pediatr Radiol 1996;26:450454.
54. Rossi A, Biancheri R, Cama A, et al. Imaging in spine and
spinal cord malformations. Eur J Radiol 2004;50:177200.
55. Kao SCS, Brown BP, Goedken J. Sonography of intracranial air
in a newborn with meningomyelocele. Pediatr Radiol 1991;21:
375376.
56. Gerscovich EO, Maslen L, Cronan MS, et al. Spinal sonography
and magnetic resonance imaging in patients with repaired
myelomeningocele: comparison of modalities. J Ultrasound
Med 1999;18:655664.
57. Kim SY, McGahan JP, Boggan JE, et al. Prenatal diagnosis of
lipomyelomeningocele. J Ultrasound Med 2000;19:801805.
58. Hernanz-Schulman M. Lipomyelocele. In: Siegel BA, Siegel MJ,
eds. Pediatric diseases: test and syllabus. Reston, VA: American
College of Radiology 2001.
59. Pierre-Kahn A, Zerah M, Renier D, et al. Congenital lum-
bosacral lipomas. Childs Nerv Syst 1997;13:298335.
60. Gupta DK, Mahapatra AK. Terminal myelocystoceles: a series
of 17 cases. J Neurosurg 2005;103(suppl 4):344352.
61. Yu JA, Sohaey R, Kennedy AM, et al. Terminal myelocystocele
and sacrococcygeal teratoma: a comparison of fetal ultrasound
presentation and perinatal risk. AJNR Am J Neuroradiol 2007;
28:10581060.
62. Rossi A, Piatelli G, Gandolfo C, et al. Spectrum of nonterminal
myelocystoceles. Neurosurgery 2006;58:509515.
63. Muthukumar N. Thoracic myelocystocelestwo variants. Acta
Neurochir (Wien) 2006;148:751756.
64. Raghavendra BN, Epstein FJ, Pinto RS, et al. Sonographic diag-
nosis of diastematomyelia. J Ultrasound Med 1988;7:111113.
65. Pang D, Dias MS, Ahab-Barmada M. Split cord malformation:
part I: a unified theory of embryogenesis for double spinal cord
malformations. Neurosurgery 1992;31:451480.
66. Schijman E. Split spinal cord malformations: report of 22 cases
and review of the literature. Childs Nerv Syst 2003;19:96103.
67. Austin MJ, Gerscovich EO, Fogata M, et al. Sonographic dupli-
cation artifact of the spinal cord in children. J Ultrasound Med
2004;23:799803.
68. Lin KL, Wang HS, Chou ML, et al. Sonography for detection of
spinal dermal sinus tracts. J Ultrasound Med 2002;21:903907.
69. Bronshtein M, Solt I, Blumenfeld Z, et al. Pilonidal sinusthe
tale of the fetal tail. Eur J Obstet Gynecol Reprod Biol
2005;119:255256.
70. La Marca F, Grant JA, Tomita T, et al. Spinal lipomas in children:
outcome of 270 procedures. Pediatr Neurosurg 1997;26:816.
71. Isaacs HJ. Perinatal (fetal and neonatal) germ cell tumors.
J Pediatr Surg 2004;39:10031013.
72. Herman TE, Siegel MJ. Cystic type IV sacrococcygeal teratoma.
J Perinatol 2002;22:331332.
73. Altman RP, Randolph JG, Lilly JR. Sacrococcygeal teratoma:
American Academy of Pediatrics Surgical Section Survey
1973. J Pediatr Surg 1974;9:389398.
74. Westerburg B, Feldstein VA, Sandberg PL, et al. Sonographic
prognostic factors in fetuses with sacrococcygeal teratoma.
J Pediatr Surg 2000;35:322326.
Chapter 16 S P I N A L U LT R A S O N O G R A P H Y 673
75. Kaste SC, Bridges JO, Marina NM. Sacrococcygeal yolk sac
carcinoma: imaging findings during treatment. Pediatr Radiol
1996;26:212219.
76. Murphy JJ, Blair GK, Fraser GC. Coagulopathy associated with
large sacrococcygeal teratomas. J Pediatr Surg 1992;10:
13081310.
77. Rescorla FJ, Sawin RS, Coran AG, et al. Long-term outcome for
infants and children with sacrococcygeal teratoma: a report from
the Childrens Cancer group. J Pediatr Surg 1998;33:171176.
78. Gopal M, Turnpenny PD, Spicer R. Hereditary sacrococcygeal
teratomanot the same as its benign counterpart! Eur J Pedi-
atr Surg 2007;17:214216.
79. Hogge WA, Thiagaajah S, Barber VG, et al. Cystic sacrococ-
cygeal teratoma: ultrasound diagnosis and perinatal manage-
ment. J Ultrasound Med 1987;6:707710.
80. Garcia CJ, Keller MS. Intraspinal extension of paraspinal
masses in infants: detection by sonography. Pediatr Radiol
1990;20:437439.
81. Patel RB. Sonographic diagnosis of intraspinal neuroblastoma.
J Clin Ultrasound 1985;13:565569.
82. Regelsberger J, Fritzsche E, Langer N, et al. Intraoperative
sonography of intra- and extramedullary tumors. Ultrasound
Med Biol 2005;31:593598.
83. Maiuri F, Iaconetta G, Gallicchio B, et al. Intraoperative sonog-
raphy for spinal tumors: correlations with MR findings and sur-
gery. J Neurosurg Sci 2000;44:115122.
84. Babyn PS, Chuang SH, Daneman A, et al. Sonographic evalua-
tion of spinal cord birth trauma with pathologic correlation.
AJNR Am J Neuroradiol 1988;9:765768.
85. Caird MS, Reddy S, Ganley TJ, et al. Cervical spine fracture-dis-
location birth injury: prevention, recognition, and implications
for the orthopaedic surgeon. J Pediatr Orthop 2005;25:484486.
86. Filippigh P, Clapuyt P, Debauche C, et al. Sonographic evalua-
tion of traumatic spinal cord lesions in the newborn infant.
Pediatr Radiol 1994;24:245247.
87. Fotter R, Sorantin E, Schneider U, et al. Ultrasound diagnosis of
birth-related spinal cord trauma: neonatal diagnosis and follow
up and correlation with MRI. Pediatr Radiol 1994;24:241244.
88. Leadman M, Seigel S, Hollenberg R, et al. Ultrasound diagno-
sis of neonatal spinal epidural hemorrhage. J Clin Ultrasound
1988;16:440442.
89. Coley BD, Shiels WE II, Hogan MJ. Diagnostic and interven-
tional ultrasonography in neonatal and infant lumbar puncture.
Pediatr Radiol 2001;31:399402.
90. Kiechl-Kohlendorfer U, Unsinn KM, Schlenk B, et al. Cere-
brospinal fluid leakage after lumbar puncture in neonates: inci-
dence and sonographic appearance. AJR Am J Roentgenol
2003;181:231234.
91. Koch BL, Moosbrugger EA, Egelhoff JC. Symptomatic spinal
epidural collections after lumbar puncture in children. AJNR
Am J Neuroradiol 2007;28:18111816.
92. Kil HK, Cho JE, Kim WO, et al. Prepuncture ultrasound-mea-
sured distance: an accurate reflection of epidural depth in infants
and small children. Reg Anesth Pain Med 2007;32:102106.
93. Gudinchet F, Chapuis L, Berger D. Diagnosis of anterior cervi-
cal spinal epidural abscess by US and MRI in a newborn. Pedi-
atr Radiol 1991;21:515517.
94. Lohr M, Reithmeier T, Ernestus RI, et al. Spinal epidural abscess:
prognostic factors and comparison of different surgical treatment
strategies. Acta Neurochir (Wien) 2005;147:159166.
95. Coley BD, Murakami JW, Koch BL, et al. Diagnostic and inter-
ventional ultrasound of the pediatric spine. Pediatr Radiol
2001;31:775785.
96. Pasto ME, Rifkin MD, Rubenstein JB, et al. Real-time ultra-
sonography of the spinal cord: intraoperative and postoperative
imaging. Neuroradiology 1984;26:183187.
97. Platt J, Rubin JM, Chandler WF, et al. Intraoperative spinal
sonography in the evaluation of intramedullary tumors. J Ultra-
sound Med 1988;7:317325.
LWBK505-C16_p647-674.qxd 09/07/2010 07:19 PM Page 674 Aptara
674 P E D I AT R I C S O N O G R A P H Y
98. Post MJD, Quencer RM, Montalvo BM, et al. Spinal infection:
evaluation with MR imaging and intraoperative US. Radiology
1988;169:765771.
99. Quencer RM, Montalvo BM, Naidich TP, et al. Intraoperative
sonography in spinal dysraphism and syringohydromyelia.
AJNR Am J Neuroradiol 1987;8:329337.
100. Raghavendra BN, Epstein FJ, McCleary L. Intramedullary
spinal cord tumors in children: localization by intraoperative
sonography. AJNR Am J Neuroradiol 1984;5:395397.
101. Randel S, Gooding GAW, Dillon WP. Sonography of intraoper-
ative spinal arteriovenous malformations. J Ultrasound Med
1987;6:539544.
102. Yeh DD, Koch B, Crone KR. Intraoperative ultrasonography
used to determine the extent of surgery necessary during poste-
rior fossa decompression in children with Chiari malformation
type I. J Neurosurg 2006;105(suppl 1):2632.
103. Quencer RM, Montalvo BM, Eismont FJ, et al. Intraoperative
spinal sonography in thoracic and lumbar fractures: evaluation
of Harrington rod instrumentation. AJNR Am J Neuroradiol
1985;6:353359.
104. Lerch K, Volk M, Heers G, et al. Ultrasound-guided decom-
pression of the spinal canal in traumatic stenosis. Ultrasound
Med Biol 2002;28:2732.
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Ultrasound-Guided
Interventional Procedures
Patient Preparation General Principles
Sonographic Equipment
Sedation
Needle Guidance
Presedation Preparation
Parenteral Sedation Drugs Ultrasound-Guided Percutaneous Biopsy
Monitoring during Sedation Patient Selection
Recovery and Discharge Monitoring Needle Selection
Needle Placement
Cutaneous and Local Anesthesia
Biopsy Techniques
Imaging Methods for Interventional
Results and Complications
Procedures Selected Biopsy Sites
Ultrasonography
Ultrasound-Guided Aspiration and
Computed Tomography
Drainage
Patient Selection
nterventional radiology has dramatically changed the
I nature of patient care. In particular, ultrasound-guided
percutaneous biopsy and abscess drainage procedures
have gained widespread acceptance in a wide variety of
diagnostic and therapeutic situations (1). Many of the
techniques utilized for ultrasound-guided procedures in
adults have been adapted for use in pediatric patients for
both similar and unique disease processes. Although the
techniques are similar, children require special considera-
tion with regard to patient preparation, sedation and anal-
gesia, and equipment selection. As with any procedure,
proper training to ensure technical competence and confi-
dence is required, as is the availability of well-trained sup-
port personnel. This chapter will cover the principles of
ultrasound-guided intervention and the applications of this
procedure in children.
PATIENT PREPARATION
Before percutaneous biopsy or drainage is performed, the
radiologist should explain the procedure, its benefits and
risks, and sedation needs with the parents or caregivers.
Informed consent should be obtained. Unless there is
parental objection, assent for the procedure should be
obtained from older children and adolescents.
Prior to the procedure, the radiologist should review
the pertinent diagnostic studies, understand the diagnostic
or therapeutic intervention required, and be aware of the
patients clinical status and laboratory values (2,3). To
minimize bleeding complications, coagulation tests should
CHAPTER
17
BRIAN D. COLEY
Indications and Contraindications
Needle and Catheter Selection
Diagnostic Aspiration
Catheter Insertion Techniques
Drainage Techniques
Follow-up Management
Results and Complications
Specific Clinical Applications
Nephrostomy Tube Placement
Vascular Access
Foreign Body Removal
Lumbar Puncture
be performed and any coagulopathy corrected. Systemic
antibiotics should be administered prior to abscess
drainage, biliary intervention, and nephrostomy tube
placement to minimize the risk of septic shock (47).
SEDATION
The goal of pediatric sedation is to provide a level of seda-
tion and analgesia that allows performance of the proce-
dure with the greatest margin of safety possible. In the
United States, standards of care for sedation are dictated
by the Joint Commission (www.jointcommission.org).
These standards are based on recommendations from the
American Academy of Pediatrics and the American Society
of Anesthesiologists. Radiologists should also become
familiar with the conscious sedation protocols and guide-
lines at their particular hospital. Regardless of the drug
regimen chosen, the use of parenteral sedation requires
that appropriate monitoring equipment (electrocardiogra-
phy, blood pressure, pulse oximetry) be available during
the procedure and throughout recovery. All necessary
equipment should be immediately available should the
patient need resuscitation during or after the procedure
(810).
Sedation for imaging examinations is nearly always
conscious sedation, now often termed moderate sedation
(10). This level of sedation is defined as a minimally
depressed level of consciousness that retains the patients
abilities to maintain a patent airway, independently and con-
tinuously, and respond appropriately to physical stimulation
675
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676 P E D I AT R I C S O N O G R A P H Y
and/or verbal command. Moderate (conscious) sedation
differs from deep sedation and anesthesia, which is gener-
ally needed for interventional procedures. Deep sedation is
a controlled state of depressed consciousness or uncon-
sciousness from which the patient is not easily aroused and
which may be accompanied by a partial or complete loss
of protective reflexes. General anesthesia produces a con-
trolled state of unconsciousness accompanied by a loss of
protective reflexes (including the ability to maintain an air-
way) and the inability to respond purposefully to physical
stimulation or verbal command.
There is a trend in most pediatric centers for sedation to
be administered and overseen by anesthesiologists or other
physicians with special training who are dedicated to pedi-
atric sedation. If such resources are available, they can be a
great benefit to the interventional service as it increases the
options available to provide the most appropriate sedation
for each child and procedure. Long, complex, or particu-
larly painful procedures are best performed under general
anesthesia and not conscious sedation (810).
Depending on the patients age, level of maturity, and
understanding as well as parental desires and the nature of
the procedure, some patients may be able to tolerate cer-
tain procedures with the use of minimal or no medication
(11). Explaining the procedure in advance and what can be
expected may help to relieve anxiety. The use of distract-
ing techniques (playing music or videos) may also relax
patients and allow procedural performance without med-
ication. The use of Child Life specialists dedicated to
patient comfort during a procedure has been shown to be
useful (12). In infants and neonates, the use of oral sucrose
solutions greatly reduces the stress of minor procedures
and may be all that is required. While employing these
techniques can require a greater investment of time and
personnel, it is often worth the effort in allowing a safe
and successful procedure with greater patient and parent
satisfaction (13).
Presedation Preparation
All patients should be screened for past and current illness.
This evaluation should include (a) a health history includ-
ing allergies, current medication, current health problems,
previous hospitalizations, sedation or anesthesia, and fam-
ily history; (b) review of systems; (c) physical examination;
and (d) assessment of baseline vital signs (temperature,
heart and respiratory rate, and blood pressure), weight,
and baseline level of consciousness and motor function.
Aspiration is a major clinical concern in sedated children
and NPO (non per os or nothing by mouth) guidelines
should be followed per local hospital policy.
Parenteral Sedation Drugs
The three major classes of drugs for the conscious sedation
of children during interventional procedures are sedatives,
benzodiazepines, and narcotics (8,9,14). Depending on
local practices, propofol and ketamine may also be used.
Traditionally, patients undergoing sedation for interven-
tional procedures receive pentobarbital or midazolam,
along with a narcotic for pain control. The choice of drugs
for an individual patient depends on availability, individual
patient risk factors, and the expertise of the personnel
administering the sedation.
Pentobarbital is a barbiturate sedative. It is adminis-
tered intravenously slowly in aliquots starting at 3 mg/kg
up to 8 mg/kg (or a maximum of 200 mg), and is titrated
against patient response. Because of these dose limits, it
may be difficult to administer enough pentobarbital in
larger patients to produce the desired level of sedation. The
mean duration of drug activity from injection to the time
it is safe to release the patient is 1 hour (8), but depends on
the total amount administered. In those patients without
intravenous access who are undergoing minimally noxious
procedures, rectally administered pentobarbital at a dose
of 25 mg/kg (with a second dose of 15 mg/kg if needed)
can be used.
Midazolam is in the class of benzodiazepines. These
agents have anxiolytic, sedative, and amnestic properties,
and are also effective as muscle relaxants. Midazolam is
given intravenously in aliquots of 1 to 2 mg every 5 min-
utes until the desired effect is obtained, with most patients
requiring total doses of 4 to 6 mg. Onset of action is
almost immediate and the duration of sedation is 20 to
30 minutes. Midazolam is a successful sedative, but it may
require additional boluses for longer studies (8). Addi-
tional boluses are infrequently needed with pentobarbital,
which has a longer duration time. An advantage of mida-
zolam, when compared with the barbiturates, is the avail-
ability of an antagonist, flumazenil. The half-life of
flumazenil is less than that of midazolam and rebound
sedation can occur. Diazepam is also in the class of benzo-
diazepines, but it is not widely used in children due to its
longer duration of action.
Fentanyl citrate is in the class of narcotics. Fentanyl has
the combined benefits of sedation and analgesia. It is usu-
ally used for pain control. Fentanyl is given intravenously
over 5 minutes in doses of 1.0 g/kg. Maximum cumula-
tive dose is 3 g/kg. For those patients weighing over 25 kg,
fentanyl is given in 25-g aliquots until the desired analge-
sia is achieved. Onset is almost immediate and duration of
action is 30 to 60 minutes. Two parenteral opioid antago-
nists are available for reversing the effects of fentanyl cit-
rate: naloxone hydrochloride and nalmefene.
Oral chloral hydrate is a sedative that has been safely
used for interventional procedures in young infants. It is
given in a dose of 50 to 100 mg/kg, with a maximum
dosage of 1000 mg for infants and 2000 mg for older chil-
dren. Onset of action is usually within 20 to 30 minutes
and the duration of sedation is 30 to 90 minutes (8). While
generally safe, the ability to titrate dosing for a specific level
of sedation is limited, and there are more complications
with chloral hydrate than with the other medications dis-
cussed (15).
Propofol and ketamine are additional sedative agents
that are used in selected cases (9,16). Propofol is a short-
acting sedative with similar effects as barbiturates. It has a
rapid onset and recovery, and provides some procedural
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amnesia. Ketamine produces a dissociative state and has
sedative and analgesic properties. The use of these medica-
tions may require additional specialized personnel, as they
have potentially greater risks than pentobarbital and oral
chloral hydrate (9,16). For complex, lengthy, or potentially
very painful procedures, general anesthesia should be con-
sidered.
Monitoring during Sedation
Regardless of the choice of drug, the use of parenteral
sedation requires personnel experienced in cardiorespira-
tory support during and after the examination. This
includes an individual qualified by training to observe
and monitor the patient and administer drugs (e.g.,
physician, nurse, and/or physicians assistant) and other
individuals as needed to assist those performing the pro-
cedure (9,10).
Intravenous access should be continuously maintained
and a person skilled in establishing an intravenous line in
pediatric patients needs to be present to re-establish vas-
cular access if the existing line fails. Continuous monitor-
ing of vital signs (at a minimum, heart rate, oxygenation,
and respiratory rate) must be performed and recorded at
least every 5 minutes. Suction apparatus and supplemen-
tal oxygen, with age- and size-appropriate equipment,
also must be immediately available during each sedation
procedure.
Recovery and Discharge Monitoring
All patients should be recovered from sedation in a desig-
nated area where continuous monitoring and resuscitative
equipment are available. Level of consciousness and vital
signs should be monitored and recorded regularly per local
guidelines and protocol. Patients should not leave the
recovery area until they are awake, alert, oriented (or
return to baseline level of consciousness), hemodynami-
cally stable, and able to maintain a patent airway without
assistance.
Patients can be discharged when they are completely
recovered from sedation and their vital signs, level of con-
sciousness, and motor function (appropriate for age) have
returned to presedation ranges. It is desirable that patients
also be able to tolerate oral fluids. Written discharge
instructions should be given to the family or caretaker. The
discharge orders should include information on diet and
activity, use of prescribed drugs, conditions requiring con-
tact of a physician, and physician contact information for
postprocedural problems.
CUTANEOUS AND LOCAL ANESTHESIA
Cutaneous and local anesthesia are recommended prior
to needle insertion, and may be the only pain relief
required in older patients. Topical anesthetic creams have
been shown to be useful to decrease pain at the skin entry
site of the needle. To provide effective anesthesia, these
agents should be applied 30 to 60 minutes prior to the
procedure.
677
Deeper local anesthesia is particularly important because
the periosteum, pleura, and capsules of solid organs
are richly innervated and their transgression produces
intense pain. Anesthetics, such as lidocaine, when injected
along the expected course of the needle or biopsy device,
provide effective local pain control and may decrease the
depth of conscious sedation required. Lidocaine produces
a burning sensation when first administered, which can be
minimized by a slow injection and the addition of sodium
bicarbonate to the lidocaine solution (17). The time from
the injection of the lidocaine to the onset of activity is
about 1 minute.
IMAGING METHODS FOR INTERVENTIONAL PROCEDURES
The mainstays of image guidance include ultrasonography,
fluoroscopy, and computed tomography (CT). While mag-
netic resonance imaging is being used in some centers, its
role remains limited. The choice of image guidance should
be based on lesion size and location, conspicuity of the
lesion on the various imaging studies, nature of the proce-
dure, and experience of the physician performing the pro-
cedure.
Ultrasonography
Sonography is well suited for pediatric interventional pro-
cedures, since children generally have a thin body habitus
favorable for sonographic imaging. Sonography has the
advantage of being readily available, portable, and rela-
tively inexpensive, and it does not utilize ionizing radiation.
Unlike CT, where visualization of the needle is confined to
the axial plane, sonography allows multidirectional visual-
ization, permitting selection of the safest percutaneous
route. Biopsy or drainage also can be performed with
patients in a variety of positions. However, the greatest
advantage of sonography may be that it allows precise depic-
tion of the needle tip as it passes through the skin into the tis-
sues and then to the target area (18). This increases the suc-
cess rate of aspiration or drainage procedures and decreases
the risk of complications. Ultrasonography is often coupled
with fluoroscopy after initial needle placement to improve
visualization of guidewires, catheters, and the instillation of
contrast (19,20).
Computed Tomography
There are limitations in the use of sonography for drainage
or biopsy, especially in the lungs, mediastinum, and mida-
bdomen, where bone or bowel gas can obscure detail.
Open wounds, dressings, and surgical drains can also be
obstacles to ultrasound scanning. In these scenarios, CT
guidance is usually performed.
GENERAL PRINCIPLES
Sonographic Equipment
Multiple transducers should be available to facilitate
detection of the structure of interest. Superficial lesions are
best visualized with high-frequency linear or curved linear
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678 P E D I AT R I C S O N O G R A P H Y
Multiplanar needle display. Simultaneous image displays during ultrasound-guided biopsy of a focal liver mass show the biopsy needle
Fig. 17.1
tip (arrowheads) in the longitudinal (right) and transverse (left) planes ensuring needle placement precisely in the center of the lesion.
array transducers. Deeper lesions usually are best seen
with lower-frequency curved or sector transducers. When
there is a limited acoustic window, such as that associated
with an intercostal approach, small-footprint sector trans-
ducers are invaluable.
Transducer and needle guide. The guide (arrow) is
Fig. 17.2
attached to the transducer, and the needle (arrowheads)
is placed within the guide.
Color flow and pulsed Doppler sonography have been
shown to be useful in guiding aspiration biopsy and
drainage procedures and can facilitate recognition of vas-
cular structures, thereby minimizing the risk of hemor-
rhage associated with needle or catheter placement (21).
Pulsed Doppler imaging also can be useful in ensuring that
the appropriate vessel (vein or artery) is accessed for vas-
cular procedures (22).
Multiplanar displays, volume-rendered images, and simul-
taneous display of images in different scan planes may help
with needle guidance. These methods allow visualization of
the needle tip in multiple planes of view, and may assist in
more precise needle placement (Fig. 17.1) (23,24). The fusion
of CT data sets with real-time ultrasound images can also
facilitate localizing lesions that are poorly visualized by ultra-
sound, bringing the strengths of each modality to the inter-
ventional procedure (25).
Needle Guidance
Ultrasound-guided biopsy can be accomplished with either a
needle guidance system or freehand method. Needle guid-
ance systems use an attachable biopsy guide that is clipped
or screwed onto the end of the transducer (Fig. 17.2). With
this system, software modifications permit continuous mon-
itoring of the angle, direction, and depth of the needle. The
angle of the guide relative to the transducer is preselected.
The proposed course of the needle is displayed as parallel
dotted lines, which helps to guide the insertion of the needle
into the lesion (Fig. 17.3). This approach may be useful in
accessing very deep lesions, and may be especially useful for
less experienced interventionalists (26). Disadvantages
include a more limited selection of transducers, the need for
a specific guide for each transducer, and the loss of the abil-
ity to alter the angle of approach during the procedure.
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A B
Aspiration with needle guide. A: The fluid collection (F) is initially localized and positioned within the dotted parallel guide lines on the
Fig. 17.3 ultrasound screen. B: The needle (arrow) is then placed into the attachable biopsy guide and directed into the collection under con-
tinuous ultrasound monitoring.

Another method of biopsy is the free-hand puncture.
With this approach, the needle is guided through the soft
tissues in the field of view of the transducer without the use
of a needle guidance system. The major advantage of this
approach is the ability to alter the angle of the needle rel-
ative to the transducer. In expert hands, this method is
quick and capable of considerable accuracy.
Contact scanning. The transducer is held in the first
Fig. 17.4
three fingers while the hypothenar surface of the hand
and the fourth and fifth digits (arrowheads) rest against the patient.
This approach provides constant patient contact and visualization of
the needle during the procedure.
While either hand may be used to guide the needle or
transducer, most interventional radiologists hold the needle
in their dominant hand and scan with their nondominant
hand. Holding the transducer with the first three fingers
while resting the fourth and fifth fingers and the hypothenar
surface of the hand against the patient (Fig. 17.4) will ensure
steady patient contact and continuous target and needle
visualization (27).
The needle is inserted longitudinal to the ultrasound
beam, either perpendicular to the transducer or at an
oblique angle relative to the transducer (the most fre-
quently used approach) (Fig. 17.5) (27). The focal
zone(s) of the transducer should be placed along the
course of the needle and at the site where the needle is
expected to intersect the target. The time gain compen-
sation curve should be adjusted to reduce near-field
echoes from skin reverberation, which allows improved
needle visualization.
The key to a successful interventional procedure is con-
tinuous real-time visualization of the needle tip as it is
advanced into the soft tissues. Specially treated (echo-
coated) needles can be easier to visualize (2,28,29). The tip
appears as a bright dot on the screen often with an associ-
ated comet-tail or reverberation artifact (Fig. 17.6) (30,31).
However, even in the best of hands, continuous visual-
ization of the needle tip may be technically difficult. The
most common reason for nonvisualization of the tip is mis-
alignment of the needle tip and the transducer (31). The
needle and ultrasound beam need to be in the same plane.
Sweeping the transducer slowly back and forth will usually
help relocate the needle. Gentile motion or jiggling of the
needle or short in-and-out movements of the needle or the
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680 P E D I AT R I C S O N O G R A P H Y

A B
Free hand biopsy method. A: Oblique and B: parallel insertion angles of the needle relative to the transducer. Note that the needle
Fig. 17.5
echogenicity and reverberation artifact (arrowheads) are more intense with the parallel approach. Also note the artifact created by the
needle tip (arrow).

stylet can also improve visualization of the needle tip. tional radiology can be acquired with experience and
Large-caliber needles are usually more easily seen than with the use of biopsy phantoms (27,32,33).
small-caliber needles. Once the needle is relocated, the nee-
dle trajectory should be reassessed. If misalignment is min-
imal, then the course usually can be altered without with-
ULTRASOUND-GUIDED PERCUTANEOUS BIOPSY
drawing the needle. If there is substantial misalignment, Patient Selection
the needle should be withdrawn to a subcutaneous loca- Percutaneous biopsy is one of the most frequently per-
tion and redirected along a more appropriate path (18). In formed sonographically guided procedures. Virtually any
some instances, it may be necessary to choose a new skin lesion that can be seen sonographically can be biopsied.
entry site and to reinsert the needle. Ultrasound-guided biopsy is commonly used to aid in the
Errors in needle placement can be the result of (a) near- documentation of neoplastic or inflammatory disease, and
field echoes, which obscure the needle trajectory (Fig. 17.7);
(b) volume-averaging artifact due to the finite width of the
ultrasound beam (Fig. 17.8); and (c) oblique positioning
of the transducer beam relative to the needle, which fore-
shortens the length of the needle and creates the appear-
ance of a beveled tip (Fig. 17.9). Visualization of the
entire shaft of the needle and identification of the needle
tip or comet-tail artifact will prevent these pitfalls.
Increased confidence in the technical aspects of interven-

Needle tip echogenicity. The beveled tip of the needle is
Fig. 17.6
clearly visible (arrow) and creates a bright echo, and often
creates a reverberation or comet-tail artifact (arrowhead).
B
Obscuration of needle path by near-field echogenicity. A: A
Fig. 17.7
22-gauge Chiba needle (arrowheads) is difficult to visualize
with high near-field gain and increased echoes. B: The needle (arrow-
heads) becomes much more conspicuous once the gain is reduced.
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Chapter 17 U LT R A S O U N D - G U I D E D I N T E R V E N T I O N A L P R O C E D U R E S 681

C C

A B
Partial volume artifact. A: The needle (arrow) appears to be directed into the cyst (C) on the longitudinal image. B: Transverse image
Fig. 17.8
shows that the needle (arrow) is actually adjacent to the cyst (C). Note the reverberation artifact distal to the beveled tip (arrowhead).

in the diagnosis of complications of renal or hepatic trans-
plantation. The advantage of ultrasound-guided biopsy is
that it may obviate surgery, thus decreasing patient costs
and the duration of hospitalization.
Contraindications to needle biopsy are an uncor-
rectable coagulopathy and the absence of a safe biopsy
pathway. A biopsy route that does not transgress bowel is
desirable, although puncture of the small bowel is not an
absolute contraindication to biopsy if small-gauge needles
are used. Ascites was at one time considered to be a con-
traindication, but biopsy through ascites can be performed
if other alternatives are not available (31). Hypervascular
lesions can also be biopsied safely, but the use of smaller-
gauge needles and the use of coaxial technique to allow
tract embolization should be considered.

A for performing fine-needle aspirations for cytologic analy-
B needle into the tissue. The distance the needle extends into
Oblique positioning artifact. A: Oblique imaging of needle
Fig. 17.9
foreshortens the shaft and may create the appearance of a
beveled tip (arrow), resulting in misplacement. B: With the needle and
transducer parallel to each other, the entire shaft of the needle is visible
as an echogenic line and the actual needle bevel (arrow) is clearly seen.
Needle Selection
The character of the mass, its location, and the amount of
tissue required for diagnosis are important factors in
determining the choice of needle for biopsy. Small-gauge
needles (22 to 25 gauge) with a simple beveled tip are used
sis. These small needles are useful when lesions are deep
and bowel or other structures must be crossed to reach the
lesion. Core biopsy needles are typically constructed with
an inner slotted stylet (which contains the specimen) and
an outer cutting cannula to yield a core of tissue (Fig.
17.10). These needles may be operated manually or
fired by automated spring-loaded devices. Smaller-
gauge core biopsy needles (20 and 21 gauge) can be used
in superficial structures and the lung. Larger-gauge core
biopsy needles (14 to 18 gauge) are more commonly used
when a direct path to the biopsy target is available. They
allow larger specimen samples for histologic analysis.
Spring-loaded biopsy needles rapidly fire a cutting
the tissue (the throw) differs among manufacturers
(with some models allowing a selection of distances) to
obtain a specimen core (Fig. 17.11). In general, the greater
the length of throw of the biopsy device, the better the tis-
sue sample (34). Advantages over nonautomated biopsy
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682 P E D I AT R I C S O N O G R A P H Y

Core biopsy needle: the inner slotted needle (arrow-

Fig. 17.10
heads) used to collect the tissue sample (A) and the
outer cutting cannula (B) (arrow).

needles include more uniform sampling of tissue, mini-

mization of crush artifact, reduced patient discomfort, and
decreased procedure time. The spring-loaded devices pro-
vide consistently high-quality samples with fewer major
complications.
Needle Placement
After diagnostic imaging studies have been reviewed, opti-
mal patient position (prone, oblique, or decubitus) for
biopsy is chosen and the area of interest is localized. The
phase of respiration that allows the best access to the
lesion is determined. Once the appropriate area is found,
the site for needle entry is marked; the overlying skin is
cleansed and draped; and local anesthesia is administered
from the skin to the target. It is important to make sure
there is no air in the anesthetic syringe, as injection of air
will obscure the desired target (Fig. 17.12). A sterile sleeve
Air obscuring biopsy target. Inadvertent injection of air
Fig. 17.12
(arrowheads) during placement of local anesthesia is seen
around the renal capsule obscuring the lower pole of the kidney (K).
filled with a sterile coupling gel is placed over the trans-
ducer. Additional sterile gel is applied to the patients skin
directly over the needle entry site. If an attachable guide is
used, it is snapped onto the transducer over the sterile
sleeve and the appropriate needle inserted through the
guide. The needle is then advanced to the correct depth. If
relevant to the procedure, the patient is instructed to sus-
pend respiration during passage of the needle.
Biopsy Techniques
Prior to any biopsy procedure, it is essential to know the
type, size, and quantity of tissue needed. Optimally, a

A B
Spring-loaded biopsy. A: Image during biopsy of an axillary mass in a 15-year-old boy shows the needle tip (arrow) just within the mass
Fig. 17.11
(M). B: Image obtained after deploying the device shows the needle (arrowheads) being fired into the mass. Final pathology was
hemangiopericytoma.
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Chapter 17 U LT R A S O U N D - G U I D E D I N T E R V E N T I O N A L P R O C E D U R E S
pathologist or skilled cytotechnologist should be present in
the radiology suite at the time of the procedure to determine
the adequacy of the specimen and to provide a preliminary
reading. This approach limits the number of passes required
for accurate diagnoses. For fine-needle aspiration, close
cooperation with the cytopathologist is essential.
For fine-needle aspiration, a syringe is attached to a
small-gauge needle (usually 22 to 25 gauge), which is
inserted in the proper location. Negative pressure is placed
on the attached syringe while moving the needle back and
forth within the target of interest. The negative suction is
released before the needle is removed from the body, so that
the specimen remains in the needle, rather than being drawn
into the syringe. The specimen is then placed into preserva-
tive fluid for subsequent analysis. For superficial lesions, just
moving the needle back and forth within the lesion (i.e., cap-
illary action) may allow acquisition of sufficient cells for
diagnosis. This technique may be simpler than suction aspi-
ration, and is successful with very small needles (31,35).
Core biopsy tissue samples are obtained by either a sin-
gle-needle pass or a coaxial double-needle approach. Sin-
gle-needle passes require a separate puncture into the
object of interest for each sample obtained. The double-
needle or coaxial technique uses a larger-gauge needle (14
to 19 gauge) as a stabilizing sleeve through which a
smaller-gauge biopsy needle (15 to 20 gauge) is placed.
This allows multiple tissue samples to be obtained with
only one puncture into the target. Before removing the
outer guiding needle, thrombotic agents (such as Gelfoam)
can be placed to minimize postbiopsy bleeding (3638).
The disadvantage of this method is the use of a larger
gauge needle, which is inflexible and may cause damage to
internal organs with respiratory motion.
Results and Complications
Depending on the location and disease, sonographically
guided biopsies have an accuracy of 83% to nearly 100%
(2,36,3848). False-positive diagnoses are exceedingly
rare. Nondiagnostic biopsies do occur and are more com-
A B
Renal biopsy. A: Longitudinal scan of a kidney prior to percutaneous biopsy shows the left lower pole parenchyma positioned between the
Fig. 17.13
needle guide lines. B: During biopsy, the needle (arrow) is appropriately positioned between the guide lines within the lower pole renal cortex.
683
mon with benign than malignant conditions (37). Although
larger lesion sizes, and thus potentially larger sample sizes,
increase biopsy sensitivity (37), even small lesions can be
successfully characterized (40).
Biopsy complications depend on the organ or mass
being biopsied, the number of samples, and the presence of
coagulopathy. Major complications are uncommon, occur-
ring in less than 1%, although rates as high as 9% have
rarely been reported (36,38,4853). Most major complica-
tions are related to bleeding, but peritonitis, sepsis, pancre-
atitis, and pneumothorax are also reported. Minor complica-
tions include inadvertent puncture of vessels, bowel, or other
structures and are almost always without sequelae. After the
procedure is completed, the radiologist should have an active
role in the follow-up evaluation of the patient to detect com-
plications as early as possible (54).
Selected Biopsy Sites
KIDNEY
The kidney is the most common site of ultrasound-guided
biopsy. The common indication for renal biopsy is evaluation
of diffuse parenchymal disease. The overall accuracy rates for
percutaneous biopsy exceed 90%. The optimal site for biopsy
of native kidneys is the lower pole, lateral to the collecting
systems and below the ribs (Fig. 17.13). The needle should
enter the inferior renal cortex. To minimize bleeding, care
must be taken to avoid the renal medulla, corticomedullary
junction, and hilar vessels. Ideally, respiratory motion should
be suspended at the time of biopsy. However, this procedure
can be performed in sedated children who cannot hold their
breath if respiratory excursion is reproducible and shallow.
Large sample volumes, typically obtained with 14- or 15-
gauge needles, are usually required for evaluation of renal
architecture, although there are reports of adequate speci-
mens obtained with 18-gauge automated devices (55,56).
The incidence of substantial postbiopsy hematuria or hemor-
rhage is low, although bleeding from the biopsy site itself or
from a postbiopsy arteriovenous fistula can occur in up to
17% of patients (57). Most bleeding resolves spontaneously
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684 P E D I AT R I C S O N O G R A P H Y

without sequelae, but patients with persistent symptoms may
need interventional occlusion (55,57).
Biopsies of renal transplants with sonographic guidance
are also frequently performed to diagnose the presence or
absence of rejection. The ability of ultrasonography to
visualize directly the renal parenchyma and to avoid large
vessels and the renal pelvis are advantages over blind
biopsy. Respiratory motion is not as important in iliac
fossa transplants as it is in biopsies of native kidneys.
Ultrasonography also is useful in the treatment of post-
transplant fluid collections and hydronephrosis.
Renal tumor biopsy is more common in adults. Despite
concerns about tumor tract seeding, percutaneous renal
mass biopsy is an effective technique that can alter patient
management, with over 80% of biopsies providing conclu-
sive diagnoses (51,58). Although not often necessary, the
diagnosis of Wilms tumor by renal biopsy has an accuracy
of 88% (41).
LIVER
Percutaneous biopsy is the procedure of choice to diagnose
and characterize diffuse hepatic disease (2,36,59). While
biopsies without guidance have a high success rate, ultra-
sound-guided biopsy has a higher success rate and lower
complication rate (59). The right lobe is usually biopsied
as it contains the greatest volume of parenchyma. A 16- to
18-gauge needle usually suffices for routine histologic
studies.
Ultrasonography is also used to guide biopsy of focal
hepatic lesions (39,40). It is particularly useful in children
with unresectable lesions and those unable to undergo an
operative procedure. While small-gauge needle biopsy or fine-
needle aspiration may allow evaluation of potential metasta-
tic disease, the rate of positive and accurate diagnoses is
greater with core biopsy samples. If possible, liver lesions
should be biopsied via a subcostal approach, rather than an
intercostal approach, to avoid entering the pleural space.
Complications of biopsy for diffuse or focal lesions range
from zero to 5%, and include hemorrhage or passage of the
needle through the gallbladder, interposed lung, or colon
(36,52,59). Most complications can be avoided by meticu-
lous attention to localization of the biopsy site. Bleeding can
be minimized by correction of coagulation abnormalities
prior to biopsy. For patients at high risk of bleeding, biopsies
may be better performed using a coaxial technique with sub-
sequent tract embolization, or a via transvenous route
(Fig. 17.14) (36,37,39). Transjugular liver biopsy tradition-
ally has been fluoroscopically guided and has not involved
ultrasound. However, more recent experience that includes
ultrasound guidance during needle placement has shown a

A B

Coaxial liver biopsy with tract embolization. A: Image

Fig. 17.14
of the liver in a 3-year-old with severe combined
immunodeficiency syndrome with new liver masses after bone
marrow transplantation shows a cannula (arrowhead) at the
periphery of one of the masses (M). B: The biopsy needle has been
deployed, with the needle tip (arrow) seen at the edge of the mass.
C: As the outer cannula was removed, three small Gelfoam pledgets
(arrowheads) were placed into the biopsy tract extending to the
liver capsule. Air trapped within the Gelfoam causes it to be very
echogenic. Final diagnosis was posttransplant lymphoproliferative
C disorder.
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Thyroid fine-needle aspirate. Image during fine-needle
Fig. 17.15
aspiration of a thyroid mass in a 7-year-old girl with thy-
roid dysfunction shows an irregular mass with punctate calcifications
(M). The shaft of the 23-gauge needle (arrowheads) is clearly seen
from skin entry to needle tip (arrow). Cytologic examination showed
papillary thyroid carcinoma.
better success rate, fewer complications, and the ability to
successfully biopsy smaller livers (49).
THYROID
Thyroid nodules are much less common in children than
in adults, and the vast majority of thyroid nodules in chil-
dren are benign. However, malignancies do occur (60).
Fine-needle aspiration biopsy allows nonoperative diag-
nosis of these nodules (Fig. 17.15). This results in a sub-
stantial reduction in unnecessary surgical resections. The
suspicious lesion is identified by sonography and the best
site of skin entry chosen to avoid underlying vessels and
Pleural mass biopsy. Sonogram of the right chest of a 10-
Fig. 17.16
year-old with a left renal mass and lung nodules shows a
biopsy needle (arrow) within a subpleural mass (M). Histologic exami-
nation showed metastatic Wilms tumor.
the trachea. A fine needle (23 or 25 gauge) is used for aspi-
ration with either suction or capillary action (31). Overall
accuracy for thyroid biopsy is greater than 90% (61).
False-positive diagnoses suggesting cancer can occur, usu-
ally in the presence of thyroiditis or colloid goiter.
OTHER SITES
Chest and mediastinal masses can be sampled provided that
the lesions abut the chest wall and there is a good acoustic
window to facilitate access to the lesion (Fig. 17.16)
(18,21,45,62). Focal lesions within the spleen, retroperi-
toneum, and mesentery have all been successfully biopsied
in children (Fig. 17.17) (44,50,53,63). Ultrasound-guided

A B
Mesenteric mass biopsy. A: Contrast-enhanced computed tomography scan of a 5-year-old boy with abdominal pain and fatigue
Fig. 17.17
shows a large mesenteric mass (M) encasing contrast-filled bowel. B: Sonogram during biopsy through a 15-gauge guiding cannula
shows a 16-gauge needle (arrowheads) within the solid mesenteric mass (M). Histologic examination showed B-cell lymphoma.
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686 P E D I AT R I C S O N O G R A P H Y
A B
Wrist mass biopsy. A: Longitudinal sonogram of the right wrist in a 10-year-old shows a solid mass (M). A manual cutting biopsy nee-
Fig. 17.18
dle has been placed into the mass with visualization of the open slotted part of the needle (arrowheads) and the outer cutting portion
of the needle (arrow). B: The biopsy needle appears uniform on an image acquired after advancement of the outer cutting needle. Histologic exam-
ination revealed benign inflammatory tissue.
biopsy is also useful for extremity soft tissue masses
(Fig. 17.18), and has been used to confirm a site of abnor-
mality and guide biopsy in myopathies (46,47,50,64).
When biopsying suspected malignant disease, proper
planning of the skin entry site and approach is essential
to optimize subsequent limb salvage surgery (65).
ULTRASOUND-GUIDED ASPIRATION AND DRAINAGE
Patient Selection
Any anatomic area that allows safe needle and catheter
passage is amenable to percutaneous aspiration and
drainage. Common drainage sites include the peritoneal
cavity, cul-de-sac, and pleural spaces. Additionally, sono-
graphic guidance can be useful to drain fluid collections in
solid organs, such as the liver, kidney, and spleen. The abil-
ity of ultrasonography to continuously monitor advance-
ment of the needle tip into fluid collections has played an
important role in the success of these aspiration and
drainage procedures.
Indications and Contraindications
The most common indication for percutaneous aspira-
tion and drainage is an enteric-related abscess, usually
secondary to appendicitis or Crohn disease. Other indi-
cations include postoperative or posttraumatic fluid col-
lections or abscesses, solid organ abscesses, and tubo-
ovarian abscesses. Percutaneous drainage is most
successful if the lesion is well defined and unilocular.
However, it can be performed in multilocular lesions,
although frequent catheter manipulation or multiple
catheters may be necessary.
Ultrasonography is often used in combination with
fluoroscopy to guide catheter placement. Ultrasonog-
raphy is used to select the skin entry site and for nee-
dle guidance, and fluoroscopy is used to monitor
guidewire and catheter placement. Fluoroscopy may
then be used to monitor contrast opacification of the
area of interest to confirm adequate catheter place-
ment and adequate drainage.
Contraindications to image-guided drainage are similar
to those discussed earlier for percutaneous biopsy. How-
ever, a lack of a safe access pathway may preclude drainage
catheter placement. Abscess drainage through bowel needs
to be avoided, in contrast to a fine-needle biopsy or aspi-
ration, where bowel may be transgressed without adverse
effects (44,63).
Needle and Catheter Selection
For simple aspiration of thin fluid collections, small nee-
dles with or without an internal stylet are adequate.
Coaxial systems with removable stylets (with or without
external sheaths) are most commonly used for drainage
access. Similar to biopsy, the choice of a catheter in large
part depends on personal expertise and the requirements
of the case.
Small-caliber catheters (6 to 10 French) are usually ade-
quate for aspiration and drainage of most collections
(6668). However, the small side holes of these single-
lumen catheters may limit their use in draining thicker
purulent collections (69). Larger single-lumen catheters (12
to 16 French) are available for highly viscous fluid collec-
tions. Although rarely needed, a sump (double-lumen)
catheter may also help in the drainage of very thick collec-
tions. Self-retaining catheters that have an inner monofila-
ment suture to secure the pigtail configuration are most
commonly used to minimize accidental catheter dislodge-
ment.
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Paracentesis. Longitudinal sonogram confirms the posi-
Fig. 17.19
tion of the needle (arrow) in the ascitic fluid. Ultrasound
guidance ensures appropriate placement of the needle for aspiration
and decreases the risk of transgressing bowel loops (B). Note the fluid
in the abdominal wall (arrowheads) from placement of local anesthe-
sia along the path of the needle.
Diagnostic Aspiration
Aspiration may be purely diagnostic, or it may be the prelim-
inary procedure prior to placing drainage catheters (69,70).
Sonography can disclose characteristics of the fluid collection
(debris, presence of septations) that may influence the deci-
sion to perform drainage and the type of catheter used.
The shortest and safest access route that will allow
for optimal fluid drainage should be used for aspiration
and drainage. When the needle is within the lesion, a
diagnostic aspiration should be performed to determine
the nature of the fluid (Fig. 17.19). Although ultra-
sonography is sensitive for localizing a fluid collection, it
cannot reliably separate pus from blood, bile, lymph, or
urine. Only a small amount of fluid should be aspirated,
because a decrease in cavity size may make subsequent
catheter placement and drainage more difficult. Aspira-
tion can usually be performed with a small needle (20 or
22 gauge); however, aspiration of viscid material may be
difficult. If aspiration is unsuccessful and the needle tip
is correctly positioned, placing a larger-gauge needle
may be necessary for successful aspiration.
If purulent fluid is recovered, a drainage catheter can be
placed immediately. If the fluid is not obviously infected,
catheter drainage may be delayed until the results of Gram
stain, cultures, and chemical analysis are known. Alterna-
tively, a catheter can be placed at the time of diagnostic
aspiration to allow complete drainage, and can be
removed once infection or fistula has been excluded.
Catheter Insertion Techniques
Drainage catheters can be placed either by the Seldinger
technique or the trocar technique. With the Seldinger
687
technique, a needle is placed into the fluid collection.
After diagnostic aspiration, a guidewire with a floppy tip
is passed through the needle or sheath into the fluid col-
lection. Once the guidewire is in place, the remainder of
the procedure is usually performed with fluoroscopic
guidance, although ultrasound guidance can also be used
and is usually required when performing drainages out-
side of the interventional radiology suite (such as in the
intensive care unit). After the wire is in place, the needle
is removed and the access tract dilated to the size of the
catheter. The catheter is then advanced into the cavity
and coiled in place (Fig. 17.20). Proper catheter position
is confirmed by fluid aspiration and by sonographic
demonstration of a decrease in size of the original fluid
collection. If fluoroscopy is available, catheter position
can also be confirmed by the injection of iodinated con-
trast material.
The trocar technique may be used when the fluid
collection is large, superficial, and easily accessible.
With the trocar technique, the metal stylet and catheter
function as a single unit. The entire unit is advanced
through the front wall of the lesion into the fluid cav-
ity. The catheter is advanced over the stylet into the
lesion and the stylet removed (Fig. 17.21). Potential
advantages of the trocar technique over the Seldinger
technique are its speed and the decreased frequency of
bacteremia that can occur during dilation and catheter
exchanges associated with the Seldinger technique (4).
Because considerable force may be necessary to
advance the catheter through the overlying soft tissues,
there is a risk of perforating the far wall of the fluid
collection. This technique is used more often in adults
than in children.
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688 P E D I AT R I C S O N O G R A P H Y

A B

C D
Transabdominal abscess drainage. A: Computed tomography scan shows a large pelvic abscess (A) secondary to perforated appen-
Fig. 17.20
dicitis. B: Longitudinal sonogram prior to drainage shows the abscess (A) immediately superior and posterior to the bladder (B).
C: Transverse scan used to guide diagnostic aspiration documents needle position (arrow) within the abscess; aspiration confirmed infection.
D: A guidewire (arrowheads) was then passed through the needle into the abscess. The needle was subsequently removed, leaving the guidewire
in place. (continued)
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Chapter 17 U LT R A S O U N D - G U I D E D I N T E R V E N T I O N A L P R O C E D U R E S 689

E F

(Continued) E: Fluoroscopy was then used to guide tract

Fig. 17.20
dilation (arrow indicates dilator). F: The catheter (arrow)
was then placed and coiled in the abscess cavity. G: Longitudinal sono-
gram after removal of 150 mL of purulent fluid shows the catheter
G (arrows) superior to the bladder (B) and collapse of the abscess cavity.

Drainage Techniques
After catheter placement, the cavity is completely emptied
by syringe aspiration and it may be gently irrigated with
saline until drainage is clear. Vigorous irrigation should be
avoided, since it can force infected material into the circu-
lation, leading to sepsis (4). Bleeding is not uncommon as
the abscess cavity collapses and should cease when the
aspiration is terminated.
The catheter is then secured and left to dependent
drainage or low suction. Proper catheter fixation is as
important as proper catheter size selection and placement.
The first line of fixation is the internal locking loop of the
catheter itself. Secondly, the external portion of the
catheter needs to be secured to the skin. Sutures must be
placed full thickness to help prevent tearing of the skin.
Wrapping a piece of plastic adhesive tape around the tube
to form a mesentery and then suturing to the tape can also
help to hold the tube in place. There are also a number of
retention devices available that adhere to the skin, thus
avoiding suturing. A bio-occlusive dressing is placed over
the skin entry site and catheter, which further helps to
secure the catheter to the patient.
Follow-up Management
Performing daily rounds on patients and communicating
directly with the primary clinical service can improve
patient care and increase the success rate of the interven-
tional procedure (4,54,71). If catheter drainage decreases
or stops and the patient is still symptomatic, the catheter
may need to be irrigated or repositioned (54). If drainage
persists or increases or if the white blood cell count
increases or fever recurs, a repeat sonogram, CT, or con-
trast medium injection should be done to evaluate the cav-
ity size, completeness of drainage, catheter position, and
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690 P E D I AT R I C S O N O G R A P H Y

A B
Trocar drainage. A: Contrast-enhanced computed tomography scan in a patient with fevers after liver transplantation shows a fluid
Fig. 17.21
collection (F) between the liver and kidney. Small needle (arrow) has been placed to determine the best direction for catheter place-
ment. B: Image after direct advancement of a drainage catheter (arrowheads) into the collection shows drainage of the collection.

presence or absence of a fistulous communication (4). If Pelvic abscesses in children are most often the result of
necessary, additional catheters can be placed into intestinal perforation secondary to appendicitis or Crohn
undrained locules or the existing catheter can be manipu- disease (6668). The traditional approaches for drainage
lated. If drainage stops and the patient shows clinical have been the anterior transperitoneal route and the pos-
improvement, follow-up imaging does not necessarily have terior transgluteal route. Drainage of pelvic abscesses is
to be performed prior to catheter removal (4). best performed with the catheter positioned in the most
dependent part of the peritoneal cavity (Fig. 17.22).
Results and Complications Multiple catheters may be required for successful drainage
Percutaneous drainage decreases hospital costs and avoids
the risk of surgery and anesthesia. Success rates of approx-
imately 80% to 95% have been reported and compare
favorably with surgical management (4,19,6668,70).
Failure of complete resolution of a fluid collection is usu-
ally due to loculations or septations, premature catheter
removal, or a fistulous communication with the bowel.
Complications occur in 10% to 15% of patients. Major
complications include significant hemorrhage and sepsis;
minor complications include mild bleeding, transient bac-
teremia, bowel puncture, and superficial skin infection.
Abscess recurrence rates are approximately 5% (67).

Specific Clinical Applications

ABDOMINAL AND PELVIC ABSCESSES
Percutaneous drainage has become the technique of choice
for drainage of intra-abdominal abscesses. The subphrenic,
subhepatic, intrahepatic, and peripancreatic spaces are
drained easily by percutaneous techniques (4). When a
subcostal approach to upper abdominal collections is not
possible because of interposed bowel, an intercostal access Abscess drainage. Longitudinal sonogram in a patient
can be used. Catheters placed between the ribs may cause Fig. 17.22
with a large abscess (A) below the liver (L) in Morrison
more postprocedural discomfort, and care must be taken pouch shows placement of a guidewire (arrowhead) into the deepest
to avoid crossing the pleural space and spreading infection portion of the fluid collection. Subsequent catheter placement allowed
to the thorax. complete drainage of the abscess.
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Chapter 17 U LT R A S O U N D - G U I D E D I N T E R V E N T I O N A L P R O C E D U R E S 691

(67). A limitation of the traditional approaches is that deep
pelvic abscesses may be difficult to access due to overlying
bowel, blood vessels, urinary bladder, or osseous structures.
Transgluteal drainage is usually performed with CT guid-
ance, although ultrasound guidance can be successfully used
(66,72). An additional limitation of the transgluteal route is
that it is relatively painful and there is the risk of injury to
the sciatic nerve and deep pelvic vasculature (66,72,73).
Ultrasound-guided transrectal drainage is an alterna-
tive route for drainage of deep pelvic abscesses or fluid col-
lections, particularly when access is limited secondary to
overlying bowel or vessels (4,19,67,74). An endocavitary
transducer or imaging from the anterior abdominal wall
through a full urinary bladder is used for visualization and
guidance of the needle into the abscess or fluid collection
(Fig. 17.23). The drainage procedure is often performed in
conjunction with fluoroscopy. Results are comparable to
percutaneous drainage via an anterior approach with
regard to success and safety of this technique (69). Advan-
tages of the transrectal techniques include avoidance of
traversing the gluteal muscles (which can be painful),
avoidance of sciatic nerve or vascular injuries, and improved
visualization and access in some patients. While the peri-
toneum has pain fibers, the rectum itself does not have

A B

C D
Endocavitary and transabdominal imaging for transrectal drainage. A: Transrectal sonogram of a boy with ruptured appendicitis shows
Fig. 17.23
an abscess (A) within the cul-de-sac. Needle (arrow) is seen along the biopsy guide lines. Subsequent placement of a catheter over
a guidewire allowed complete abscess drainage. B: Transabdominal sonogram through a full urinary bladder (B) of another child with an appen-
diceal abscess (A) shows a catheter and stylet (arrowhead) that have been advanced into the collection with the trocar technique. C: The echogenic
metal trocar and stiffener have been removed, and the drainage catheter (arrow) is being advanced and coiled within the abscess (A). D: After aspi-
ration, the drainage catheter (arrow) is seen in the now collapsed abscess cavity.
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692 P E D I AT R I C S O N O G R A P H Y
somatic sensation above the level of the dentate line, mini-
mizing catheter discomfort once the drain has been placed.
These catheters may be placed by either the trocar or
Seldinger technique (69,75,76).
PANCREATIC FLUID
Peripancreatic fluid collections are usually the result of
acute pancreatitis or trauma. These fluid collections can
resolve spontaneously, but some will develop a fibrotic
wall, forming a pseudocyst. Sonographically guided percu-
taneous puncture may be used to determine the presence or
absence of infection and to guide drainage. The overall
cure rates (i.e., resolution of the pseudocysts) by catheter
drainage are over 90% (77,78). Prolonged drainage may
be needed when there is communication of the collection
with the pancreatic duct. Both transperitoneal and trans-
gastric approaches have been used for drainage.
BILIARY TRACT
Ultrasonography in combination with fluoroscopy has been
used to guide transhepatic cholangiography and drainage in
patients with obstructive lesions of the biliary tract (79). The
use of sonography to guide initial needle puncture of the
dilated ducts has been shown to be safer and more rapid than
without guidance (80). Once a duct or the gallbladder is
accessed (Fig. 17.24), fluoroscopy is used to monitor contrast
injection as well as guidewire and catheter manipulation.
THORAX
Pleural Effusion
The most frequent indication for percutaneous interven-
tion in the chest is the aspiration of pleural fluid. Sono-
graphic guidance can be used to provide a diagnosis, and
Biliary access. Sonogram of a young child with jaundice
Fig. 17.24
shows a needle tip (arrow) within the gallbladder (G).
The needle has traversed a small portion of the liver (arrowhead) to
minimize the chance of bile leak.
Intercostal neurovascular bundle. Longitudinal sono-
Fig. 17.25
gram of the thorax shows echogenic ribs (R) with poste-
rior acoustic shadowing. Immediately below the upper rib, the inter-
costal artery (A) and vein (V) are clearly seen.
percutaneous drainage can follow if indicated. Access to the
pleural space may be obtained by scanning through sub-
costal or intercostal spaces.
The site of thoracentesis can be marked and the patient
returned to the floor for thoracentesis, or the procedure may
be performed in the interventional radiology suite. Small-
gauge needles are adequate for diagnostic thoracentesis. The
needle should be placed over the top of the rib to avoid the
neurovascular bundle, which courses below (Fig. 17.25). In
adolescents, fluid localization and thoracentesis can be per-
formed with local anesthesia and the patient placed in an
upright position. In younger children, localization and tho-
racentesis are generally performed with the patient sedated
and placed in an oblique decubitus position.
Thoracentesis is successful in the majority of patients.
The most useful sonographic criteria for determining
whether thoracentesis will be successful are (a) presence of a
change in shape of the fluid with inspiration and expiration
and (b) the absence of septations. Free-flowing fluid that
changes shape with respiratory motion and nonseptated
collections are more likely to be completely aspirated than
loculated, septated collections.
At times, thoracentesis is unsuccessful even when the
fluid is hypoechoic and the needle is in good position. Pre-
sumably, the fluid in these cases is quite viscous or contains
pus or clotted blood. In these instances, a larger-gauge nee-
dle should be used for aspiration. The rate of pneumotho-
rax is much lower with ultrasound-guided thoracentesis
than without image guidance (81).
Empyema
Controversy continues regarding the most appropriate man-
agement of children with infected pleural collections (8286).
Empyema can be drained surgically or percutaneously with
sonographic guidance. For maximal drainage, the needle
should be placed into the chest through a posterolateral
approach. Small catheters (8 or 10 French) may suffice for
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Chapter 17 U LT R A S O U N D - G U I D E D I N T E R V E N T I O N A L P R O C E D U R E S 693

thin fluid collections, but larger catheters (12 or 14 French)
are necessary in order to drain thicker bloody or purulent
material.
Local anesthesia is placed along the path of the
catheter, in the periosteum of the superior rib surface, and
at the pleura. The catheter should be placed in the most
dependent position possible to facilitate drainage. How-
ever, care should be taken not to place the catheter imme-
diately on top of the diaphragm, if possible, as diaphrag-
matic irritation and shoulder pain may develop.
Interventional pleural catheters can be as effective as
larger surgical chest tubes provided that fibrinolytic therapy
is also used (20,83,87). Ultrasonography is valuable in
assessing the need for fibrinolytic therapy by showing
whether or not the empyema is septated or loculated
(85,86,88,89). If there are no septations, or just a few that
are thin and mobile, simple drainage is usually effective. If
the collection has multiple compartments or thick septa-
tions, adjunctive lytic therapy will be required. Intrapleural
lytic therapy has few complications except in the presence of
necrotizing pneumonia. In this setting, a bronchopleural fis-
tula may result (20,82,83). If the collection is highly organ-
ized or appears solid, then surgical intervention and pleural
decortication will likely be necessary (Fig. 17.26) (89,90).
OTHER SITES
Fluid collections virtually anywhere in the body have been
successfully accessed and drained with ultrasound guidance.
Liver and splenic abscesses can be successfully aspirated for
diagnosis; this may suffice for treatment of smaller lesions,
but larger collections respond better to catheter drainage
(Fig. 17.27) (9193). Lung abscess can be successfully
accessed and drained if it abuts the pleural surface, thus
allowing an acoustic window (82,83). Other procedures
include aspiration of neonatal ovarian cysts to help mini-
mize torsion (94), and drainage of abdominal cerebrospinal
fluid pseudocysts in patients with shunt dysfunction (95).
Nephrostomy Tube Placement
The development of sonographically guided catheter place-
ment techniques has made percutaneous nephrostomy and
antegrade pyelography common procedures in children

A B

Pleural fluid collections. Longitudinal sonograms in three

Fig. 17.26
patients showing varying appearances of empyema.
A: Longitudinal sonogram through the left hemithorax in a 5-year-old
girl with pneumonia shows a nonseptated hypoechoic pleural effusion
(E) containing low-level echoes. Also note underlying consolidated
lung (L) with air bronchograms (arrowheads). Simple catheter
drainage was effective. B: Young child with a septated pleural effusion
(E) with echogenic mobile debris adjacent to consolidated lung (L).
This collection responded to catheter drainage and thrombolytics. C: A
highly organized nearly solid empyema (E) that required surgical inter-
C vention.
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694 P E D I AT R I C S O N O G R A P H Y
A B
Liver abscess drainage. A: Sonogram of a 15-year-old boy with a liver abscess (arrowheads) in the left lobe of the liver complicating
Fig. 17.27
Crohn disease. A needle (arrows) has been placed into the far side of the abscess cavity. B: After placement of a drainage catheter
and aspiration, there is near-total collapse of the abscess cavity (arrow).
(5,96). Indications for percutaneous nephrostomy include
decompression of obstruction, treatment of infected col-
lecting systems, and guidance of endourologic procedures
such as stone extraction (5,55,70,96). The technique
requires a posterolateral approach below the 10th rib to
avoid traversing the pleural space. A subcostal approach is
preferred over an intercostal approach to minimize pain. A
transparenchymal approach is preferred over a transpelvic
approach because there is less risk of renal vascular injury
and urine leak. Broad-spectrum antibiotics should be
administered in the setting of obstructive uropathy to
decrease the possibility of sepsis.
The site of renal access depends on the clinical situation
and possible future interventional procedures. A lower
pole calyx suffices for simple drainage. If other interven-
tion, such as stent placement or stone extraction, is being
considered, a middle or upper pole calyx may be more suit-
able for catheter placement if technically possible. With the
patient in a prone position, an appropriate posterior calyx
can be identified for puncture (Fig. 17.28). If access to a
nondilated collecting system is required, a 22-gauge needle
can be placed into the renal pelvis with sonographic guid-
ance. Distension of the collecting system can then be
achieved by infusing saline, allowing identification of an
appropriate calyx for puncture and subsequent catheter
placement. A needle that can accept a 0.035- or 0.038-inch
guidewire is then placed under direct sonographic visuali-
zation into the collecting system, and the wire advanced
with fluoroscopic monitoring. The needle then is removed
and fascial dilators are inserted to enlarge the tract. Finally,
a self-retaining pigtail catheter is placed over the wire and
into the collecting system. The tube is securely fastened to
the skin and placed to dependent drainage. An 8-French
catheter usually is suitable for drainage procedures in chil-
dren and adolescents, whereas a 5- or 6-French catheter is
used in infants.
In the infant with hydronephrosis, who often has con-
comitant renal dysplasia, it is tempting to access the kidney
initially with a small needle and guidewire to prevent renal
injury. However, it is often very difficult to perform the sub-
sequent dilation required to place the larger working wire
required for nephrostomy tube placement, as the renal
parenchyma can be tough and unyielding, the neonatal kid-
ney is poorly fixed in the retroperitoneum, and the smaller
guidewire provides inadequate support. When a small
guidewire is used, it is often dislodged and access to the kid-
ney lost. The hydronephrotic kidney may then decompress
into the retroperitoneum, making subsequent access diffi-
cult. With proper technique and direct sonographic visuali-
zation, a larger sheathed needle can be placed initially with
a single pass, a larger adequate working wire placed directly,
and the procedure completed less traumatically (5,79,97).
Percutaneous nephrostomy also may be used to treat
obstructive uropathy in patients with renal allografts.
Sonographic guidance is helpful to avoid transgressing per-
inephric fluid collections and adjacent bowel loops. In
addition, sonography can help to identify an anterior
calyx, which is the preferred location for nephrostomy
placement in renal transplantation. This position mini-
mizes damage to renal parenchyma, and if percutaneous
intervention is anticipated, it facilitates guidewire and
catheter manipulation within the ureter.
VASCULAR ACCESS
Central venous catheters play a crucial role in patient care,
allowing the administration of parenteral nutrition,
chemotherapy, and antibiotics. The use of sonographic
guidance can facilitate catheter placement. While fluoro-
scopic guidance with venography is an alternative method
for guiding catheter placement, this requires access to a
distal vein for contrast medium injection. Additionally, this
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Chapter 17 U LT R A S O U N D - G U I D E D I N T E R V E N T I O N A L P R O C E D U R E S
C grade ureteropelvic junction obstruction.
is a two-dimensional approach, and does not allow real-
time visualization of needle depth or visualization of the
adjacent artery (98,99).
The type of catheter to be placed depends on the needs
of the patient. Long-term access needs are best met with
tunneled catheters or implanted ports. Regardless of whether
these are placed by interventional radiologists or surgeons
(depending on the institution), ultrasound guidance facili-
tates safe and accurate access (99,100). Peripherally
inserted central catheters (PICCs) are useful for short- to
intermediate-length central access. Generally, single-lumen
catheters of 3- or 4-French size are sufficient, but patients
receiving multiple medications often require placement of
a double-lumen catheter, available in 4- to 6-French sizes.
If possible, a catheter with an internal valve mechanism
should be placed, as these have been shown to minimize
clotting complications (101).
Peripherally inserted central catheters are generally
placed in either the basilic or brachial vein. Lower extremity
access can be used in very small infants or in those with
upper extremity venous occlusion. Sonography is first used
to establish the presence of a suitably sized vessel and to
695
Percutaneous nephrostomy. One-day-old infant with
Fig. 17.28
elevated serum creatinine. A: Longitudinal sonogram
shows a hydronephrotic left kidney. B: Ultrasound guidance was
used to puncture a posterior calyx (arrowhead) with a 19-gauge
sheathed needle (arrow). C: Follow-up sonogram after placement
of a 6-French catheter (arrow) documents decompression of the
collecting system. The cause of the hydronephrosis was a high-
ensure that it is patent. An appropriate site for puncture is
chosen, and local anesthesia placed. In small children and
infants, the amount of lidocaine injected immediately adja-
cent to the vein should be as minimal as possible, as com-
pression of the vein or venospasm may result and preclude
immediate use of that vessel. The vessel is then entered under
direct sonographic guidance with a needle, and a 0.018-inch
mandril-type guidewire is passed. The tract is then dilated to
the appropriate size with a peel-away sheath-dilator system,
and the catheter placed. Fluoroscopy is used to document
appropriate catheter tip position in the central circulation.
The sheath is removed and pressure applied to produce
hemostasis. The catheter is secured by suturing it directly to
the patients skin or by the use of adhesive retention devices,
and a sterile dressing is applied.
Unlike other ultrasound-guided procedures that use a
longitudinal alignment of needle and transducer, the use of
transverse imaging has been advocated when performing
vascular access (99). The transverse approach usually
ensures that the needle is centered within the vessel. With the
longitudinal approach, partial volume averaging can occur,
and the needle may appear to be in the vessel when in fact it
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696 P E D I AT R I C S O N O G R A P H Y

A B
Vascular access. A: Longitudinal sonogram of the basilic vein shows an anechoic lumen and echogenic posterior wall (arrowheads).
Fig. 17.29
A 21-gauge thin-wall needle has been placed into the vein (arrow). B: A guidewire (arrowheads) was then passed through the needle
into the vein. The tract was dilated and a 4-French catheter placed.

is beside the vessel. The longitudinal approach can be used if
meticulous attention is paid to the scanning technique. The
posterior wall of the vessel produces a bright echo when the
transducer beam is precisely aligned (Fig. 17.29).
FOREIGN BODY REMOVAL
Sonography is also useful in identifying foreign objects
and in guiding their surgical or percutaneous removal
(102,103). The appearance of an object depends on its
composition (Fig. 17.30) and the length of time that it has
resided within the soft tissues (104,105). If surgical
removal is planned, the location of the object should be
marked on the patients skin and the depth from the skin
surface measured and reported. Alternatively, a localization
guidewire can be placed adjacent to the foreign body to
facilitate surgical removal. Ultrasound-guided removal is an
alternative to surgical or blind dissection. A small skin inci-
sion is made and a small hemostat with its teeth closed is
advanced under ultrasound guidance until the foreign body

A B

Sonographic appearance of foreign bodies. A: Metal

Fig. 17.30
(sewing needle). Note reverberation artifact from body of
needle (arrowhead) as well as the angled reverberation artifact from
the beveled tip (arrow). B: Wood (toothpick). Note posterior acoustic
shadowing. The echogenicity of wood depends on the amount of
entrapped air. C: Glass (bottle). Note moderate echogenicity. Glass has
a variable appearance depending on its thickness and surface irregu-
C larity.
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Chapter 17 U LT R A S O U N D - G U I D E D I N T E R V E N T I O N A L P R O C E D U R E S 697

A B

C D
Foreign body removal. A: Transverse scan shows a faintly echogenic foreign body (cursors) within the soft tissues of the thigh. B: A
Fig. 17.31
needle (arrow) is placed into the soft tissues. Note the fluid (arrowheads) in the soft tissues around the foreign body from use of local
anesthesia to provide pain relief and tissue dissection. C: The hemostat (arrow) is then advanced and the foreign body (arrowhead) gently grasped
and removed. D: Follow-up sonogram demonstrates no evidence of residual foreign body. The tract caused by the foreign body (*) is filled by blood
or edema. The foreign body was a wooden splinter.

is reached. When the foreign object is reached, the hemostat

teeth are gently opened and the object is grasped and slowly
removed, while still being monitored with sonography. The
area should then be rescanned to ensure that no residual
fragments remain (Fig. 17.31). Ultrasound-guided removal
requires smaller incisions than surgical removal, and is gen-
erally faster and more comfortable for the patient.

Lumbar puncture. Posterior longitudinal sonogram of a
Fig. 17.32
neonate shows a needle passing between hypoechoic
cartilaginous spinous processes (P) with the needle tip (arrow) within
the thecal sac (T). Clear cerebrospinal fluid was successfully obtained.
LUMBAR PUNCTURE
Lumbar puncture is routine in the evaluation of febrile
neonates, as well as in older children suspected of having
central nervous system infection or neoplasia. Most of the
time lumbar puncture is readily performed by the clinical
service without imaging guidance. However, in neonates
and infants in whom there have been failed attempts, ultra-
sound can disclose complications of earlier attempts as
well as guide successful puncture (Fig. 17.32) (106).
Although not a common indication, ultrasound can assist
in localizing the midline and identifying the spinous
processes in larger patients, and has been shown to facili-
tate successful access into the thecal sac (107).
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698 P E D I AT R I C S O N O G R A P H Y
REFERENCES
1. McGahan JP. The history of interventional ultrasound. J Ultra-
sound Med 2004;23:727741.
2. Nazarian LN, Feld RI, Herrine SK, et al. Safety and efficacy of
sonographically guided random core biopsy for diffuse liver dis-
ease. J Ultrasound Med 2000;19:537541.
3. Murphy TP, Dorfman GS, Becker J. Use of preprocedural tests
by interventional radiologists. Radiology 1993;186:213220.
4. Gervais DA, Mueller PR. Percutaneous abdominal and pelvic
abscess drainage in children a practical approach. Semin
Interv Radiol 2002;19:1322.
5. Schmidt MB, James CA. Genitourinary intervention in children.
Semin Interv Radiol 2002;19:5157.
6. Spies JB, Rosen RJ, Lebowitz AS. Antibiotic prophylaxis in vas-
cular and interventional radiology: a rational approach. Radi-
ology 1988;166:381387.
7. Thomas J, Turner SR, Nelson RC, et al. Postprocedure sepsis in
image-guided percutaneous hepatic abscess drainage: how often
does it occur? AJR Am J Roentgenol 2006;186:14191422.
8. Frush DP, Bissett GS III, Hall SC. Pediatric sedation in radiol-
ogy: the practice of safe sleep. AJR Am J Roentgenol 1996;167:
13811387.
9. Mason KP. The pediatric sedation service: who is appropriate to
sedate, which medications should I use, who should prescribe
the drugs, how do I bill? Pediatr Radiol 2008;38(suppl 2):
S218S224.
10. Shankar VR. Sedating children of radiological procedures: an
intensivists perspective. Pediatr Radiol 2008;38(suppl 2):
S213S217.
11. Koch BL. Avoiding sedation in pediatric radiology. Pediatr
Radiol 2008;38(suppl 2):S225S226.
12. Mcgee K. The role of a child life specialist in a pediatric radiol-
ogy department. Pediatr Radiol 2003;33:467474.
13. Khan JJ, Donnelly LF, Koch BL, et al. A program to decrease
the need for pediatric sedation for CT and MRI. Appl Radiol
2007;4:3033.
14. Kaye RD, Sane SS, Towbin RB. Pediatric intervention: an
update part I. J Vasc Interv Radiol 2000;11:683697.
15. American Society of Anesthesiologists Task Force. Practice
guidelines for sedation and analgesia by non-anesthesiologist: a
report by the American Society of Anesthesiologists Task Force
on sedation and analgesia by non-anesthesiologists. Anesthesi-
ology 1996;84:459471.
16. Cotsen MR, Donaldson JS, Uejima T, et al. Efficacy of ketamine
hydrochloride sedation in children for interventional radiologic
procedures. AJR Am J Roentgenol 1997;169:10191022.
17. McNaughton C, Zhou C, Robert L, et al. A randomized,
crossover comparison of injected buffered lidocaine, lidocaine
cream, and no analgesia for peripheral intravenous cannula
insertion. Ann Emerg Med 2009;54:214220.
18. Burke BJ. Sonographic guidance for nonvascular interventions in
the chest, abdomen, and pelvis. Ultrasound Q 2000;16:185202.
19. Chung T, Hoffer FA, Lund DP. Transrectal drainage of deep pelvic
abscesses in children using a combined transrectal sonographic
and fluoroscopic guidance. Pediatr Radiol 1996;26:874878.
20. Norman JTI, Donaldson JS. Interventional procedures in the
pediatric chest: biopsy and drainage. Semin Interv Radiol 2002;
19:3950.
21. Gorguner M, Misirlioglu F, Polat P, et al. Color Doppler sono-
graphically guided transthoracic needle aspiration of lung and
mediastinal masses. J Ultrasound Med 2003;22:703708.
22. Longo JM, Bilbao JI, Barettino MD, et al. Percutaneous vascu-
lar and nonvascular puncture under US guidance: role of color
Doppler imaging. Radiographics 1994;14:959972.
23. Albrecht H, Stroszczynski C, Felix R, et al. Real time 3D (4D)
ultrasound-guided percutaneous biopsy of solid tumours.
Ultraschall Med 2006;27:324328.
24. Rose SC, Nelson TR, Deutsch R. Display of 3-dimensional
ultrasonographic images for interventional procedures: volume-
rendered versus multiplanar display. J Ultrasound Med 2004;
23:14651473.
25. Nakai M, Sato M, Sahara S, et al. Radiofrequency ablation
assisted by real-time virtual sonography and CT for hepatocel-
lular carcinoma undetectable by conventional sonography. Car-
diovasc Intervent Radiol 2009;32:6269.
26. Phal PM, Brooks DM, Wolfe R. Sonographically guided biopsy
of focal lesions: a comparison of freehand and probe-guided
techniques using a phantom. AJR Am J Roentgenol 2005;184:
16521656.
27. Georgian-Smith D, Shiels WE II. Freehand interventional
sonography in the breast: basic principles and clinical applica-
tions. Radiographics 1996;16:149161.
28. Culp WC, McCowan TC, Goertzen TC, et al. Relative ultra-
sonographic echogenicity of standard, dimpled, and polymeric-
coated needles. J Vasc Interv Radiol 2000;11:351358.
29. Jandzinski DI, Carson N, Davis D, et al. Treated needles: do
they facilitate sonographically guided biopsies. J Ultrasound
Med 2003;22:12331237.
30. Bondestam S. The needle tip echo. J Ultrasound Med 1992;11:
253256.
31. Feld RI. Ultrasound-guided biopsies: tricks, needle tips, and
other fine points. Ultrasound Q 2004;20:9199.
32. Harvey JA, Moran RE, Hamer MM, et al. Evaluation of a
turkey-breast phantom for teaching freehand US-guided core-
needle breast biopsy. Acad Radiol 1997;4:565569.
33. Georgian-Smith D, Lyon RD, Schwartzberg BS, et al. A smorgas-
bord of interventional phantoms. Semin Interv Radiol 1997;14:4.
34. Hopper KD, Abendroth CS, Sturtz KW, et al. Automated biopsy
devices: a blinded evaluation. Radiology 1993;187:653660.
35. Degirmenci B, Haktanir A, Albayrak R, et al. Sonographically
guided fine-needle biopsy of thyroid nodules: the effects of nod-
ule characteristics, sampling technique, and needle size on the
adequacy of cytological material. Clin Radiol 2007;62:798803.
36. Amaral JG, Schwartz J, Chait P, et al. Sonographically guided
percutaneous liver biopsy in infants: a retrospective review. AJR
Am J Roentgenol 2006;187:W644W649.
37. Bittles MA, Hoffer FA. Interventional radiology and the care of
the pediatric oncology patient. Surg Oncol 2007;16:229233.
38. Sebire NJ, Roebuck DJ. Pathological diagnosis of paediatric
tumours from image-guided needle core biopsies: a systematic
review. Pediatr Radiol 2006;36:426431.
39. Hoffer FA. Liver biopsy methods for pediatric oncology
patients. Pediatr Radiol 2000;30:481488.
40. Yu SCH, Liew CT, Lau WY, et al. US-guided percutaneous biopsy
of small (1 cm) hepatic lesions. Radiology 2001;218:195199.
41. Garrett K, Fuller C, Santana V, et al. Percutaneous biopsy of
pediatric solid tumors. Cancer 2005;104:644652.
42. Konermann W, Wuisman P, Ellermann A, et al. Ultrasono-
graphically guided needle biopsy of benign and malignant
soft tissue and bone tumors. J Ultrasound Med 2000;19:
465471.
43. Liu JC, Chiou HJ, Chen WM, et al. Sonographically guided
core needle biopsy of soft tissue neoplasms. J Clin Ultrasound
2004;32:294298.
44. Marco-Domenech SF, Gil-Sanchez S, Fernandez-Garcia P, et al.
Sonographically guided percutaneous biopsy of gastrointestinal
tract lesions. AJR Am J Roentgenol 2001;176:147151.
45. Morvay Z, Szabo E, Tiszlavicz L, et al. Thoracic core needle
biopsy using ultrasound guidance. Ultrasound Q 2001;17:
113121.
46. Shin HJ, Amaral JG, Armstrong D, et al. Image-guided percu-
taneous biopsy of musculoskeletal lesions in children. Pediatr
Radiol 2007;37:362369.
47. Soudack M, Nachtigal A, Vladovski E, et al. Sonographically guided
percutaneous needle biopsy of soft tissue masses with histopatho-
logic correlation. J Ultrasound Med 2006;25:12711277.
LWBK505-C17_p675-700.qxd 09/07/2010 07:15 PM Page 699 Aptara
Chapter 17 U LT R A S O U N D - G U I D E D I N T E R V E N T I O N A L P R O C E D U R E S
48. Skoldenberg EG, Jakobson AA, Elvin A, et al. Diagnosing child-
hood tumors: a review of 147 cutting needle biopsies in 110
children. J Pediatr Surg 2002;37:5056.
49. Habdank K, Restrepo R, Ng V, et al. Combined sonographic
and fluoroscopic guidance during transjugular hepatic biopsies
performed in children: a retrospective study of 74 biopsies. AJR
Am J Roentgenol 2003;180:13931398.
50. Hussain HK, Kingston JE, Domizio P, et al. Imaging-guided
core biopsy for the diagnosis of malignant tumors in pediatric
patients. AJR Am J Roentgenol 2001;176:4347.
51. Johnson PT, Nazarian LN, Feld RI, et al. Sonographically
guided renal mass biopsy: indications and efficacy. J Ultrasound
Med 2001;20:749753.
52. Lachaux A, Le Gall C, Chambon M, et al. Complications of
percutaneous liver biopsy in infants and children. Eur J Pediatr
1995;154:621623.
53. Muraca S, Chait PG, Connolly BL, et al. US-guided core biopsy
of the spleen in children. Radiology 2001;218:200206.
54. Goldberg MA, Mueller PR, Saini S, et al. Importance of daily
rounds by the radiologist after interventional procedures of the
abdomen and chest. Radiology 1991;180:767770.
55. Riccabona M, Sorantin E, Hausegger K. Imaging guided inter-
ventional procedures in paediatric uroradiology a case based
overview. Eur J Radiol 2002;43:167179.
56. Sahney S, Mohan GC. Renal biopsy in infants and children. Am
J Kidney Dis 1994;23:3132.
57. Brandenberg VM, Frank RD, Riehl J. Color-coded duplex
sonography study of arteriovenous fistulae and pseudo-
aneurysms complicating percutaneous renal allograft biopsy.
Clin Nephrol 2002;58:398404.
58. Maturen KE, Ngheim HV, Caoili EM, et al. Renal mass core
biopsy: accuracy and impact on clinical management. AJR Am
J Roentgenol 20007;188:563570.
59. Nobili V, Comparcola D, Sartorelli M, et al. Blind and
ultrasound-guided percutaneous liver biopsy in children. Pedi-
atr Radiol 2003;33:772775.
60. Josefson J, Zimmerman D. Thyroid nodules and cancers in chil-
dren. Pediatr Endocrinol Rev 2008;6:1423.
61. Izquierdo R, Shankar R, Kort K, et al. Ultrasound-guided fine-
needle aspiration in the management of thyroid nodules in chil-
dren and adolescents. Thyroid 2009;19:703705.
62. Middleton WD, Teefey SA, Dahiya N. Ultrasound-guided chest
biopsies. Ultrasound Q 2006;22:241252.
63. Ho LM, Thomas J, Fine SA, et al. Usefulness of sonographic
guidance during percutaneous biopsy of mesenteric masses.
AJR Am J Roentgenol 2003;180:15631566.
64. OSullivan PJ, Gorman GM, Hardiman OM, et al. Sonograph-
ically guided percutaneous muscle biopsy in diagnosis of neu-
romuscular disease: a useful alternative to open surgical biopsy.
J Ultrasound Med 2006;25:16.
65. Liu PT, Valadez SD, Chivers S, et al. Anatomically based guide-
lines for core needle biopsy of bone tumors: implications for
limb-sparing surgery. Radiographics 2007;27:189206.
66. Cahill AM, Baskin KM, Kaye RD, et al. Transgluteal approach
for draining pelvic fluid collections in pediatric patients. Radi-
ology 2005;234:893898.
67. McCann JW, Maroo S, Wales P, et al. Image-guided drainage of
multiple intraabdominal abscesses in children with perforated
appendicitis: an alternative to laparotomy. Pediatr Radiol 2008;
38:661668.
68. Rypens F, Dubois J, Garel L, et al. Percutaneous drainage of
abdominal abscesses in pediatric Crohns disease. AJR Am J
Roentgenol 2007;188:579585.
69. Sudakoff GS, Lundeen SJ, Otterson MF. Transrectal and trans-
vaginal sonographic intervention of infected pelvic fluid col-
lections: a complete approach. Ultrasound Q 2005;21:
175185.
70. Hoffer FA. Interventional radiology in the acute pediatric
abdomen. Radiol Clin North Am 1997;35:977987.
699
71. Connolly B, Mahant S. The pediatric hospitalist and interven-
tional radiologist: a model for clinical care in pediatric inter-
ventional radiology. J Vasc Interv Radiol 2006;17:17331738.
72. Walser E, Raza S, Hernandez A, et al. Sonographically guided
transgluteal drainage of pelvic abscess. AJR Am J Roentgenol
2003;181:498500.
73. Harisinghani MG, Gervais DA, Hahn PF, et al. CT-guided
transgluteal drainage of deep pelvic abscesses: indications, tech-
nique, procedure-related complications, and clinical outcome.
Radiographics 2002;22:13531367.
74. Pereira JK, Chait PG, Miller SF. Deep pelvic abscesses in chil-
dren: transrectal drainage under radiologic guidance. Radiol-
ogy 1996;198:393396.
75. Nielsen MB, Torp-Pedersen S. Sonographically guided transrec-
tal or transvaginal one-step catheter placement in deep pelvic
and perirectal abscesses. AJR Am J Roentgenol 2004;183:
10351036.
76. Rao S, Hogan MJ. Trocar transrectal abscess drainage in chil-
dren: a modified technique. Pediatr Radiol 2009;39:982984.
77. de Blaauw I, Winkelhorst JT, Rieu PN, et al. Pancreatic injury
in children: good outcome of nonoperative management.
J Pediatr Surg 2008;43:16401643.
78. Wales PW, Shuckett B, Kim PC. Long-term outcome after non-
operative management of complete traumatic pancreatic tran-
section in children. J Pediatr Surg 2001;36:823827.
79. Coley BD, Hogan MJ. Image-guided interventions in neonates.
Eur J Radiol 2006;60:208220.
80. Lorenz JM, Leef JA, Chou CH, et al. Sonographic needle guidance
in cholangiography in children. J Vasc Interv Radiol 2001;12:
342346.
81. Barnes TW, Morgenthaler TI, Olson EJ, et al. Sonographically
guided thoracentesis and rate of pneumothorax. J Clin Ultra-
sound 2005;33:442446.
82. Hoffer FA, Bloom DA, Colin AA, et al. Lung abscess versus
necrotizing pneumonia: implications for interventional therapy.
Pediatr Radiol 1999;29:8791.
83. Hogan MJ, Coley BD. Interventional radiology treatment of
empyema and lung abscess. Paediatr Respir Rev 2008;9:7784.
84. Pierrepoint MJ, Evans A, Morris SJ, et al. Pigtail catheter drain
in the treatment of empyema thoracis. Arch Dis Child 2002;87:
331332.
85. Ramnath RR, Heller RM, Ben-Ami T, et al. Implications of
early sonographic evaluation of parapneumonic effusions in
children with pneumonia. Pediatrics 1998;101:6871.
86. Shankar S, Gulati M, Kang M, et al. Image-guided percuta-
neous drainage of thoracic empyema: can sonography predict
the outcome? Eur Radiol 2000;10:495499.
87. Gervais DA, Levis DA, Hahn PF, et al. Adjunctive intrapleural
tissue plasminogen activator administered via chest tubes
placed with imaging guidance: effectiveness and risk for hem-
orrhage. Radiology 2008;246:956963.
88. Calder A, Owens CM. Imaging of parapneumonic pleural effu-
sions and empyema in children. Pediatr Radiol 2009;39:527537.
89. Chiu CY, Wong KS, Huang YC, et al. Echo-guided management
of complicated parapneumonic effusion in children. Pediatr
Pulmonol 2006;41:12261232.
90. Chen KY, Liaw YS, Wang HC, et al. Sonographic septation: a
useful prognostic indicator of acute thoracic empyema. J Ultra-
sound Med 2000;19:837843.
91. Kang M, Saxena AK, Gulati M, et al. Ultrasound-guided per-
cutaneous catheter drainage of splenic abscess. Pediatr Radiol
2004;34:271273.
92. Lee SH, Tomlinson C, Temple M, et al. Imaging-guided percu-
taneous needle aspiration or catheter drainage of neonatal liver
abscesses: 14-year experience. AJR Am J Roentgenol 2008;190:
616622.
93. Zerem E, Hadzic A. Sonographically guided percutaneous catheter
drainage versus needle aspiration in the management of pyogenic
liver abscess. AJR Am J Roentgenol 2007;189:W138W142.
LWBK505-C17_p675-700.qxd 09/07/2010 07:15 PM Page 700 Aptara
700 P E D I AT R I C S O N O G R A P H Y
94. Kessler A, Nagar H, Graif M, et al. Percutaneous drainage as
the treatment of choice for neonatal ovarian cysts. Pediatr
Radiol 2006;36:954958.
95. Coley BD, Shiels WE II, Elton S, et al. Sonographically guided
aspiration of cerebrospinal fluid pseudocysts in children and
adolescents. AJR Am J Roentgenol 2004;183:15071510.
96. Hogan MJ, Coley BD, Shiels WE, II. Percutaneous nephros-
tomy in children and adolescents: outpatient management.
Radiology 2001;218:207210.
97. Koral K, Saker M, Morello F, et al. Conventional versus modi-
fied technique for percutaneous nephrostomy in newborns and
young infants. J Vasc Interv Radiol 2003;14:113116.
98. Chrisman HB, Omary RA, Nemcek AA, et al. Peripherally
inserted central catheters: guidance with use of US versus venog-
raphy in 2650 patients. J Vasc Interv Radiol 1999;10:473475.
99. Donaldson JS. Pediatric vascular access. Pediatr Radiol
2006;36:386397.
100. Chait P, Temple M, Connolly B, et al. Pediatric interventional
venous access. Tech Vasc Interv Radiol 2002;5:95102.
101. Hoffer EK, Borsa J, Santulli P, et al. Prospective randomized
comparison of valved versus nonvalved peripherally inserted
central vein catheters. AJR Am J Roentgenol 1999;173:
13931398.
102. Shiels WE II. Soft tissue foreign bodies: diagnostic and thera-
peutic radiological management. In: Postgraduate course:
emergency radiology in childhood, European society of pedi-
atric radiology. Berlin, Germany: Springer-Verlag, 1998:
4655.
103. Shiels WE II, Babcock DS, Wilson JL, et al. Localization and
guided removal of soft-tissue foreign bodies with sonography.
AJR Am J Roentgenol 1990;155:12771280.
104. Gilbert FJ, Campbell RSD, Bayliss AP. The role of ultrasound in
the detection of non-radiopaque foreign bodies. Clin Radiol
1990;41:109112.
105. Schlager D. Ultrasound detection of foreign bodies and proce-
dure guidance. Emerg Med Clin North Am 1997;15:895912.
106. Coley B, Shiels W II, Hogan M. Diagnostic and interventional
sonography in neonatal and infant lumbar puncture. Pediatr
Radiol 2001;31:399402.
107. Nomura JT, Leech SJ, Shenbagamurthi S, et al. A randomized
controlled trial of ultrasound-assisted lumbar puncture. J Ultra-
sound Med 2007;26:13411348.
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HEAD ULTRASOUND
Transducer
1. 7.5-MHz phased array or vector transducer for evalua-
tion of the premature infant
2. 5-MHz may be needed in term or older, larger infants
with closing fontanelles.
3. 7.5- to 12-MHz linear array to image extracerebral
spaces, brain cortex, and superior sagittal sinus
Coronal Images through the Following Levels
1. Frontal horns
2. Foramen of Monro (level of third ventricle)
3. Posterior to third ventricle: three-dot sign (representing
choroid plexus in floor of lateral ventricles and in roof
of third ventricle)
4. Quadrigeminal cistern
5. Choroid plexus in atria of the lateral ventricles
6. Cephalad to lateral ventricles (periventricular area of
occipital lobes)
Sagittal Images through the Following Levels
1. Midline to include corpus callosum, cavum septi pellu-
cidi, area of third ventricle, brain stem, cerebellum, and
fourth ventricle.
2. Caudothalamic groove
3. Elongated view of the lateral ventricle
4. Periventricular area and peripheral brain parenchyma
5. Repeat the caudothalamic groove image on the opposite
side.
6. Repeat the elongated view of the lateral ventricle on the
opposite side.
7. Repeat periventricular area and peripheral brain
parenchyma image on the opposite side.
Doppler Imaging
1. Spectral and color Doppler imaging is performed to
identify flow direction, flow velocity, and vascular
resistance in the major cerebral vessels.
2. Power mode Doppler (amplitude mode color or color
flow Doppler energy) improves detection of low veloc-
ity and low amplitude flow.
3. In neonates with a history of ischemia and vascular
malformations, Doppler imaging is performed obtained
through the anterior fontanelle.
4. In patients with sickle cell anemia, Doppler images
should be obtained through a transtemporal approach.
Appendix
Additional Views
1. Transmastoid view through (posterolateral) fontanelle
can enhance visualization of the posterior fossa.
2. Image through posterior fontanelle to enhance visuali-
zation of periventricular white matter and occipital
horns.
3. Transtemporal view to show vessels in the circle of
Willis
4. Coronal and squamosal sutures for visualizing convex-
ities of the brain and extracerebral fluid collections.
5. Foramen magnum to visualize the upper cervical
spinal canal, particularly in patients with Chiari mal-
formation.
SALIVARY GLANDS
Transducer
1. 7.5- to 15-MHz linear or curvilinear array transducer,
with or without a stand-off pad
Patient Position
1. Supine
Views
1. Parotid gland views are obtained by placing the trans-
ducer perpendicular and inferior to the earlobe.
2. Submandibular gland is evaluated by placing the trans-
ducer in a submental position.
3. Sublingual glands are imaged with the transducer per-
pendicular and parallel to the submental mandible.
NECK
Transducer
1. 7.5- to 15-MHz linear array transducer
Patient Position
1. Supine with the neck hyperextended. Neck is rotated to
the right to examine the left side and to the left to exam-
ine the right side.
Longitudinal Views
1. Images showing course of jugular vein and carotid
artery
2. Images extending from anterior to posterior through
the entire neck
701
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702 APPENDIX

Transverse Views 8. Posterior paraspinal: transducer parallels the spine.

1. Images showing jugular vein and carotid artery Improves visualization of posterior mediastinal masses.
2. Images extending from inferior to superior through the Special Techniques
entire neck
3. Images showing the thyroid isthmus DIAPHRAGM MOTION
4. Midline image to compare echogenicity between the 1. Patient position: supine
two lobes of the thyroid 2. Transverse plane through xiphoid tip shows both
hemidiaphragms
Doppler Imaging 3. Images in inspiration and expiration
1. Spectral and color Doppler images to show patency of
the jugular vein and carotid artery THORACENTESIS
2. Doppler imaging to characterize vascularity of soft tis- 1. Patient position: upright in oblique decubitus position
sue, thyroid and parathyroid masses, and inflammatory 2. Longitudinal and transverse images using a posterior
lesions and parasagittal scan plane through pleural cavity
3. Document level of fluid relative to rib space and mark
skin.
CHEST
Transducer
1. 7.5- or 10-MHz transducer used for evaluation of near
THORACIC GREAT VESSELS
field structures in infants and children Transducer
2. 5-MHz transducer for evaluation of larger patients and 1. 5- to 10-MHz linear array transducer for parasternal
deep pleural space, lung, or mediastinum. approach
3. Curved or linear-array transducers used for evaluation 2. Sector or small footprint transducer with narrow field of
of lung, pleura, mediastinum, and chest wall view helpful if insonation performed through supraster-
4. Sector or small foot print transducers with narrow field nal or intercostal windows.
of view helpful for insonation of suprasternal, inter-
costal, and subxiphoid spaces. Patient Position
1. Supine
Patient Position
1. Supine Views of Arterial Anatomy
2. Decubitus position can help visualize posterior thoracic 1. Transverse and longitudinal planes to include the
structures. following:
3. Upright scanning used to evaluate free flowing fluid. a. Junction of left carotid artery and left subclavian
artery with aortic arch
Longitudinal and Transverse Views through Area of Interest b. Junction of right and left innominate artery with aor-
1. Supraclavicular: transducer positioned above the clavi- tic arch
cle. Used to evaluate the lung apices, upper medi- c. Left and right subclavian artery becoming axillary
astinum, and great vessels. artery
2. Suprasternal: transducer placed above the manubrium
in the suprasternal notch and angled caudally. Used to Views of Venous Anatomy
evaluate the lung apices, upper mediastinum, and great 1. Transverse and longitudinal planes to include the fol-
vessels lowing:
3. Parasternal: transducer paralleling the sternum with a. Junction of superior vena cava and right atrium
patient in lateral decubitus position, which shifts medi- b. Junction of right and left innominate veins with
astinum downward enlarging the acoustic window. superior vena cava
Used to evaluate mediastinum and great vessels. c. Left and right jugular veins
4. Transsternal: transducer placed over the sternum. In
neonates, this view is useful to image the thymus.
5. Intercostal: transducer positioned between ribs. Used to BREAST
image pleural space and peripheral lung parenchyma. Transducer
6. Subxiphoid: transducer placed beneath the xiphoid mar- 1. 7- to 15-MHz linear array transducer
gin and angled cephalad. Used to evaluate deep sulcal
spaces (lower lung and pleural space) and diaphragm. Patient Position
7. Subdiaphragmatic transducer placed beneath the costal 1. Supine
margins, using the liver or spleen as acoustic window,
and angled cranially. Used to evaluate deep sulcal Longitudinal Views
spaces and diaphragm. 1. Images showing entire breast from medial to lateral.
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APPENDIX 703

Transverse Views Comment

1. Images showing entire breast from skin surface to chest 1. The diameter of the portal vein should be measured just
wall. beyond the junction of the splenic and superior mesen-
teric veins.
Comment
1. Images need to include skin with nipple, subcutaneous GALLBLADDER
fat, subadjacent fibrofatty and glandular tissue, pec-
toralis muscle, and ribs. Transducer
1. 5- to 7.5-MHz curved linear array transducer
2. 3- to 5-MHz transducer may be needed in large or
LIVER obese patients.

Transducer Patient Position

1. 5- to 7.5-MHz linear or curved linear array transducer 1. Multiple positions, including supine, left posterior
in infants and smaller children oblique, and left lateral decubitus
2. 3- to 5-MHz transducer may be needed to penetrate
larger right lobe in larger children Longitudinal and Transverse Views through
3. 7.5- to 12-MHz transducer may help define very super- the Following Levels
ficial lesions and liver surface 1. Gallbladder neck
4. Anterior approach used most often, but an intercostal 2. Gallbladder body
approach with a small footprint transducer may be 3. Gallbladder fundus
necessary for evaluation of the subcostal parts of the
liver. Doppler Imaging
1. Color Doppler images useful to confirm inflammation.
Patient Position 2. Color and pulsed Doppler images can confirm varices
1. Supine or posterior oblique by showing venous flow with portal venous wave-
forms.
Longitudinal Images through the Following Levels Comments
1. Extreme left lobe
1. Patients should have nothing per os for 4 to 6 hours
2. Left lobe with aorta posterior to liver
before the study.
3. Right lobe with inferior vena cava posterior to liver
2. When stones or sludge are identified, additional views
4. Interface of right lobe with diaphragm
of the gallbladder should be obtained in the left lateral
5. Interface of right lobe with right kidney (to compare
decubitus, prone, and erect positions.
echogenicity)
3. Feeding of a fatty meal can be useful to assess patency
6. Interface of left lobe with left kidney (to compare
of the cystic duct.
echogenicity)
7. Main portal vein, including common bile duct
BILE DUCTS
Transverse Images through the Following Levels Transducer
1. Left lobe and left hepatic vein 1. 5- to 7.5-MHz curved linear array transducer.
2. Right lobe and right hepatic vein 2. 3.5- to 5-MHz transducer may be needed in large or
3. Three hepatic veins draining into inferior vena cava obese patients.
4. Main portal vein and right and left branches
5. Interface of liver with right kidney Patient Position
1. Multiple positions, including supine, left posterior
Doppler Imaging oblique, and left lateral decubitus
1. Pulsed waveforms should be obtained from the main, 2. The erect position may improve visualization of the
left, and right portal veins, the three hepatic veins, and distal common bile duct.
the hepatic artery.
2. The portal veins show low-velocity continuous, Longitudinal and Transverse Views through
monophasic flow toward the liver. the Following Areas
3. The hepatic veins show a triphasic waveform, which 1. Intrahepatic ducts
reflects cardiac activity. 2. Common hepatic duct
4. The hepatic artery shows a low resistance waveform 3. Common bile duct
with antegrade flow throughout diastole. 4. Junction of common bile duct with pancreatic duct
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704 APPENDIX

Comments Image Plane

1. Patient should be fasting for 4 to 6 hours.
2. Measurements of common bile duct size performed
during suspended respiration.
3. Feeding of a fatty meal is useful to assess cystic duct
patency. Nonobstructed ducts either remain unchanged
or decrease in caliber Obstructed ducts often increase in
size.
SPLEEN
Transducer
1. 5- to 7.5-MHz curved linear array transducer
2. 3- to 5-MHz transducer may be needed in large or
obese patients.
Patient Position
1. Supine
2. Right lateral decubitus view is helpful if the gas-filled
colon or stomach obscure visualization of the spleen.
Longitudinal and Transverse Views through
the Following Areas
1. Splenic hilum and vessels
2. Spleen and left kidney interface
3. Splenic parenchyma
1. Transducer positioned in the transverse plane of the
patients body will demonstrate the pylorus in its long
axis.
2. Transducer positioned in the longitudinal plane of the
patients body will demonstrate the pylorus in its short
axis.
3. Measure pyloric wall thickness (normal thickness
should not exceed 3 mm).
Comments
1. Patient should be given clear liquid to drink if stomach
is empty. Be careful not to overfeed because the pylorus
will be pushed posteriorly, making evaluation difficult.
If this occurs, consider scanning from a posterior
approach with the patient in a prone or right lateral
decubitus position, or remove some fluid from the
stomach through a nasogastric tube.
2. Longitudinal and transverse images through the gas-
troesophageal junction can be useful to show associated
reflux.
3. Transverse image should be obtained to show the supe-
rior mesenteric artery and vein relationship. Normal
superior mesenteric vein lies to the right of the artery.
This view may help in diagnosis of malrotation, which
is included in the diagnosis of vomiting.

Doppler Imaging
1. Color and spectral Doppler images to show patency of BOWEL ULTRASOUND
artery and vein and diagnose thrombus and infarct. Transducer
2. Doppler images to characterize vascularity of neoplasms
1. 5- to 7.5-MHz curved linear or linear array transducer
and inflammatory lesions.
for survey examination of the entire abdomen
Comments 2. 7.5- to 12-MHz transducer for more detailed examina-
tion if wall thickening is detected
1. Splenic length is measured is measured in the coronal
plane at the level of the splenic hilum.
Patient Position
1. Supine
PERITONEAL CAVITY-MESENTERY AND LIGAMENTS
Transducer Image Planes
1. 5- to 7.5-MHz curved linear array transducer 1. Longitudinal and transverse views through area of
interest
Patient Position
1. Supine Doppler Imaging
1. Color Doppler images to confirm and characterize
Longitudinal and Transverse Views bowel wall thickening.
1. Views should include the entire depth of the peritoneal
cavity. Comments
1. Graded compression technique is used to displace inter-
posed gas-filled bowel loops and increase conspicuity of
PYLORUS ULTRASOUND abnormal bowel loops.
Transducer 2. In patients with acute abdominal pain, no preparation
1. 7.5-MHz curved linear or linear array transducer is required. In patients without acute symptoms, 4 to
5 hours or fasting can be helpful to minimize bowel
Patient Position gas.
1. Right lateral oblique or decubitus, with the liver used as 3. High-resolution transducers can increase resolution of
an acoustic window the five separate layers of the small bowel.
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APPENDIX ULTRASOUND
Transducer
1. 7.5-MHz curved linear or linear array transducer
Patient Position
1. Supine
Transverse and Longitudinal Images
1. Image the entire right lower quadrant.
2. Start at the level of the iliac vessels and continue to the
inferior aspect of the bladder.
3. Image the right flank (retrocecal area) if appendix is not
visualized in the normal position.
4. Measurements of the appendix should be obtained.
Doppler Imaging
1. Color Doppler images can show hyperemia in acute
appendicitis, increasing confidence in diagnosis.
Comments
1. Graded compression technique is used to displace inter-
posed gas-filled bowel loops.
KIDNEY
Transducer
1. 5- to 7.5-MHz curved linear or linear transducer for
infants and small children
2. 3- to 5-MHz transducer may be required for adequate
penetration in larger patients.
Patient Position
1. Images obtained with patient supine or in lateral decu-
bitus position
2. Right kidney scanned with the patient in the supine or left
lateral decubitus position, using liver as acoustic window
3. Left kidney imaged with the patient in the supine or the
right lateral decubitus position, using the spleen as an
acoustic window
4. Scan using ventral scan approach
5. Scanning with patient prone using a dorsal approach
may improve visualization of the left kidney if air-filled
stomach or loops of bowel impede sound transmission
Longitudinal Images at the Following Levels
1. Liverright kidney interface, spleenleft kidney interface
2. Longest axis through collecting system with measure-
ment of renal length
3. Two views angled medially to show vessels and cortex
4. Two views angled laterally to show cortex and pyra-
mids
Transverse Images at the Following Levels
1. Two views of upper pole to show cortex and pyramids
2. Two views of mid pole to show renal artery, vein, and
renal pelvis
3. Two views of lower pole to show cortex and pyramids
APPENDIX 705
Doppler Imaging
1. Pulsed and Doppler imaging used to evaluate integrity
of renal vessels.
2. Resistive index (RI) obtained in the main renal artery
and the arcuate and interlobar arteries. At least three
different areas in each kidney are sampled to obtain a
mean RI.
3. Color Doppler images obtained to characterize tumor,
infection, and infarction and increase confidence in
diagnosis.
BLADDER AND URETHRA
Transducer
1. 5- to 7.5-MHz curved linear or linear transducer
Patient Position
1. Images obtained with patient supine or in lateral decu-
bitus position.
Longitudinal Views at the Following Levels
1. Midline images and images of both sides of bladder
2. Images of distal ureters if dilated
Transverse Views at the Following Levels
1. Images from dome to neck
2. Images of dilated ureters if present
Comment
1. Overdistention of the bladder should be avoided
because it increases patient discomfort.
ADRENAL GLANDS
Transducer
1. 7.5- to 10-MHz curved linear array transducer for
neonates and infants
2. 3- to 5-MHz linear or curved linear array transducer
for larger patients
Patient Position
1. Supine
2. In neonates and young infants, the right adrenal gland
can be visualized by an anterolateral or right flank
approach, using the right hepatic lobe as an acoustic
window. The left adrenal gland is usually best seen from
a left flank approach.
3. In older children and adolescents, the right adrenal
gland is best evaluated with an intercostal approach in
the anterior axillary or midaxillary line, using the liver
as an acoustic window. The left adrenal gland is best
evaluated with an intercostal approach in the posterior
axillary or midaxillary line, using the spleen or left kid-
ney as an acoustic window.
Transverse and Longitudinal Images
1. Images should show entire extent of glands.
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706 APPENDIX
Doppler Imaging
1. Doppler images to characterize vascularity of neo-
plasms and inflammatory lesions
Comment
1. Patients should have nothing per os for 4 to 6 hours
before the study to minimize the amount of intervening
bowel gas.
PANCREAS
Transducer
1. 7.5-MHz curved linear array transducer for infants and
small children
2. 3- to 5-MHz linear or linear array transducer for larger
patients
Patient Position
1. Supine
2. Neck and body are often best imaged with the trans-
ducer positioned in the midline below the xiphoid using
the left lobe of the liver as an acoustic window.
3. Head and uncinate process best seen through a right
subcostal approach
4. Tail visualized best using the spleen or left kidney as a
window
Transverse Images
1. Head of pancreas to include distal common bile duct
and uncinate process
2. Neck, body, and tail of pancreas anterior to splenic vein
Doppler Imaging
1. Doppler images to characterize vascularity of neo-
plasms and inflammatory lesions
Comments
1. Portion of the liver should be included so that pancre-
atic and liver echotexture can be compared.
2. Scans should extend cephalad at least to the celiac axis
and caudad to the level of the portal vein to ensure cov-
erage of the entire gland.
3. If unable to visualize the pancreatic tail from an ante-
rior approach, turn patient into right lateral decubitus
position and scan coronally through the spleen.
4. A fluid-filled stomach may help to visualize tail of pan-
creas with the patient in a right posterior oblique position.
5. Patients should have nothing per os for 4 to 6 hours
before the study to minimize the amount of intervening
bowel gas.
AORTA AND INFERIOR VENA CAVA
Transducer
1. 7- to 10-MHz linear array transducer for newborns and
infants
2. 5- to 7-MHz transducer for larger patients
Patient Position
1. Supine or decubitus
2. Scanning through the anterior abdominal wall to visu-
alize superior portions of the inferior vena cava and
abdominal aorta.
3. Coronal scans through both flanks can improve demon-
stration of the more inferior segments of the vessels and
sometimes the superior segments of the vessels.
Aorta, Views to Include the Following
1. Entire length of aorta from diaphragmatic hiatus to
bifurcation
2. Celiac axis
3. Superior mesenteric artery
4. Both renal arteries
5. Bifurcation of aorta into common iliac arteries
Inferior Vena Cava, View to Include the Following
1. Entire length of cava from right atrium to common iliac
veins
2. Junction of hepatic veins with vena cava
3. Left and right renal veins
4. Bifurcation into iliac veins
Doppler Imaging
1. Color and spectral Doppler are required to show vessel
patency and assess thrombotic, aneurysmal, or occlu-
sive disease.
Comments
1. Patients should have nothing per os for 4 to 6 hours
before the study to minimize the amount of intervening
bowel gas.
FEMALE PELVIS
Transducer
1. 5- to 7-MHz or higher linear array transducer for trans-
abdominal insonation in infants and smaller children
2. 3.5- to 5-MHz transducer for larger patients
3. Endovaginal transducer may be used in sexually active
adolescent girls or girls who use tampons.
Longitudinal Images at the Following Levels
1. Midline view to show vagina, cervix, and uterus in
longest axis. Measure uterine length and width.
2. Right ovary. Measure length and width.
3. Left ovary. Measure length and width.
Transverse Images at the Following Levels
1. Body and fundus of uterus
2. Endometrial canal. Measure endometrial thickness.
3. Right ovary. Measure height and width.
4. Left ovary. Measure height and width.
5. Caudal image to show vaginal canal
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Doppler Imaging
1. Color and spectral Doppler imaging should be per-
formed if inflammation, tumor, or torsion is suspected.
Comments
1. A distended bladder is needed for transabdominal
sonography. Bladder filling can be achieved with oral
intake of fluid or bladder catheterization with instilla-
tion of sterile fluid.
2. To visualize ovaries with a transabdominal technique,
keep transducer in the midline and angle laterally using
the bladder as a window.
3. Placing the patient in a decubitus position and scanning
directly over the adnexa can improve visualization of
the ovaries
4. In a patient with a history of precocious puberty, both
adrenal glands should be imaged.
SCROTUM
Transducer
1. 7.5- to 12-MHz transducer
Patient Position
1. Supine. Scrotum should be elevated by towels.
Longitudinal Views to Include the Following
1. Full extent of testis from medial to lateral
2. Epididymal head and its relationship to testis
3. Body and tail of epididymis
4. Measure testicular width and length in longest axis.
Transverse Views to Include the Following
1. Full extent of testis from superior to inferior
2. Epididymis
3. Midline transverse image to show echogenicity of both
testes
4. Measure testicular width at widest point.
Doppler Imaging
1. Color Doppler images should evaluate flow in testis,
epididymis, paratesticular tissues, and scrotal skin.
2. Transverse image of both testes should be obtained to
allow comparison of flow.
3. Spectral waveform should be obtained to confirm
intratesticular arterial flow.
Comment
1. Image the inguinal canal when looking for a hernia as
well as an undescended testis.
MUSCULOSKELETAL IMAGING: GENREAL IMAGING
Transducer
1. 7.5- to 15-MHz linear or curvilinear array transducer
APPENDIX 707
Patient Position
1. Supine
2. Patients should be positioned so that the area of inter-
est is in an advantageous position for interrogation
while the patients comfort is maintained.
Longitudinal and Transverse Views
1. To show full extent of soft tissue lesion
Doppler Imaging
1. Color, power, and pulsed Doppler techniques to char-
acterize the vascularity of soft tissue masses and inflam-
matory lesions.
Comment
1. Extended field of view software is used to show large
continuous areas of anatomy and full extent of lesions
2. Split screen function used for side-by-side comparisons
of the affected and normal contralateral extremity.
HIP: DEVELOPMENTAL DYSPLASIA-DYNAMIC
TECHNIQUE
Transducer
1. 5- to 10-MHz linear array transducer. Use highest-
frequency transducer that allows penetration of poste-
rior joint.
Patient Position
1. Supine, with transducer over the lateral or posterolat-
eral aspect of the hip
Coronal Images
1. Leg flexed to show femoral head and acetabulum
2. Leg extended to show femoral head and acetabulum
Transverse Views
1. Leg extended to show femoral head and acetabulum
2. Leg flexed and knee in a neutral position to show
femoral head and acetabulum
3. Leg flexed and Barlow maneuver performed to assess
laxity or displacement
4. Leg flexed and Ortolani maneuver performed to assess
laxity or displacement
Comments
1. Examination limited to infant with unossified epiphyses
(i.e., usually patients younger than 6 months of age)
2. If patient is in a harness, only flexed views are obtained.
Stress views are not performed.
HIP: DEVELOPMENTAL DYSPLASIA-GRAF
TECHNIQUE
Transducer
1. 5- to 10-MHz transducer
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708 APPENDIX

Patient Position LOWER EXTREMITY ARTERIAL DOPPLER

1. Left lateral decubitus with femur extended. Coronal Transducer
sonogram obtained through hip.
1. 5- to 10-MHz linear array transducer
Coronal Image Patient Position
1. Three lines and two angles (alpha and beta) are drawn
1. Supine, with leg slightly abducted and externally
around the acetabulum.
rotated and the knee slightly flexed
2. Alpha angle is the angle between one line drawn along
the straight edge of the iliac bone and a second line Transverse and Longitudinal Images
along the bony acetabular roof. to Include the Following
3. Beta angle is the angle between a line through the
1. Iliac artery
straight edge of the iliac bone and a line through the
2. Common femoral artery
echogenic fibrocartilaginous labrum.
3. Deep and superficial femoral arteries
4. Popliteal artery
HIP EFFUSION 5. Posterior tibial, anterior tibial, peroneal arteries
Transducer Doppler Imaging
1. 5- or 7.5-MHz linear array transducer 1. Color and spectral Doppler scans to show patency of
Patient Position arteries
1. Supine with the feet externally rotated to open the joint
space UPPER EXTREMITY VENOUS DOPPLER
Sagittal Plane Only Transducer
1. Anterior image through the femoral head to show the 1. 5- to 10-MHz linear array transducer
joint capsule
2. Dual image obtained to allow comparison of widths of Patient Position
symptomatic and asymptomatic sides. 1. Supine, with arm slightly abducted and externally
3. Measure width of both joint capsules. rotated
2. Patients head turned away from the transducer to help
Doppler Imaging visualize more proximal parts of the subclavian and
1. Color Doppler may show color signal in the capsule and brachiocephalic veins
soft tissues in septic arthritis
Transverse and Longitudinal Images to Include the Following
1. Brachial vein
LOWER EXTREMITY VENOUS DOPPLER 2. Basilic vein
Transducer 3. Axillary vein
1. 5- to 10-MHz linear array transducer 4. Subclavian vein
5. Caudal segment of internal jugular vein
Patient Position
1. Supine, with leg slightly abducted and externally
Doppler Imaging
rotated and the knee slightly flexed 1. Color Doppler scans to show patency of vein
2. Pulse Doppler waveforms to show response to augmen-
Transverse and Longitudinal Images tation and Valsalva maneuvers
to Include the Following Comment
1. Iliac vein
1. Infraclavicular approach is used to image lateral por-
2. Common femoral vein
tion of the subclavian vein, while a supraclavicular
3. Deep and superficial femoral veins
approach is used to study medial segment of the sub-
4. Popliteal vein
clavian vein and caudal segment of the internal jugular
5. Posterior tibial, anterior tibial, peroneal veins
vein.
6. Compressibility assessed on transverse views

Doppler Imaging UPPER EXTREMITY ARTERIAL DOPPLER

1. Color Doppler scans to show patency of vein
2. Pulse Doppler waveforms to show response to augmen- Transducer
tation and Valsalva maneuvers 1. 5- to 10-MHz linear array transducer
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APPENDIX 709

Patient Position 2. Imaging should begin at the midthoracic level and con-
1. Supine, with arm slightly abducted and externally rotated tinue to the sacrum
2. Patients head turned away from the transducer to help
visualize more proximal parts of the subclavian and Longitudinal and Transverse Images to Show the Following
brachiocephalic arteries. 1. Conus
2. Filum terminale
Transverse and Longitudinal Images to Include the Following 3. Cauda equina
1. Subclavian artery 4. Sacral dimple, if this is clinical indication for examina-
2. Axillary artery tion
3. Brachial artery
4. Ulnar artery Doppler Imaging
5. Radial artery
1. Color Doppler is rarely useful in routine examinations.
Doppler Imaging
1. Color and spectral Doppler scans to show patency of Comments
arteries 1. Extended field of view or split screen function in the
longitudinal plane is useful to show both the level of
the cord and the inferior contents of the canal on one
SPINE view.
Transducer 2. The level of spinal cord termination must be shown.
1. 7- to 15-MHz linear array transducer This can be done by either:
a. Counting cephalad from the sacrum. Transverse
Patient Position processes are counted to determine the level of cord
1. Prone. The back needs to be rounded to separate the termination.
vertebral bodies. To achieve this, place a pillow beneath b. Counting caudad from the last rib, presumed to be
the back. T12 (cord should terminate at the level of L1 or L2)
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Index

Page numbers followed by f indicate figures; page numbers followed by t indicate tables.

A Acute renal cortical necrosis, 432 Adrenarche, premature, 547

Abdomen. see also Specific organs; Specific tissues Acute renal failure, 430 Adrenocortical adenoma, 472473
abscesses, 690692 Acute scrotum, causes of, 571 Adrenocortical carcinoma, 472
normal anatomy, 367f Acute splenic sequestration, 311 Adrenocortical macrocyst, 475f
Abscesses Acute terminal ileitis, 361362 Adrenocorticotropic hormone (ACTH),
abdominal, 690692 Acute tubular necrosis, 431f 462, 476
acute suppurative thyroiditis and, 155f Addison disease, 156 Adrenogenital syndrome. see Congenital adrenal
adrenal, 476f Adenocarcinoma hyperplasia (CAH)
amebic, 242243 brain, 123 Agyria-pachygyria complex, 9798
appendiceal, 370f breast, 211212 Aicardi syndrome, 91
aspiration of, 686 colon, 378, 378f Alagille syndrome, 292, 294
brain, 106 pancreatic, 483484, 484f Aldosterone overproduction, 473
breast, 206207, 206f small bowel, 365 Aldosteronism, primary, 473
cervical, 142f uterine, 546 Aliasing, 1718, 3536, 36f
chest wall, 194195, 194f vaginal, 546 -Fetoprotein, 226227, 562
Crohn disease and, 361, 361f Adenomas. see also Cystadenomas; Amastia, 203
drainage techniques, 689, 690692, 690f, Fibroadenomas Ambiguous genitalia, 476
694f adrenal, 472f, 547 Amebiasis, 242243
enteric, 686 adrenocortical, 472473 Amebic abscesses, 242243, 243f
fungal, 241242, 318319 embryonal, 424 Amebic colitis, 376377
hepatic, 694f hepatic, 238, 238f, 239 Amenorrhea, 547548, 549
identification of, 670 lactating, 208209, 209f Ampulla of Vater, 480
intraperitoneal, 333, 334f liver, 238 Anabolic steroids, 260
liver, 241243 metanephric, 424 Anaplastic carcinoma of the thyroid, 152
lung, 176177, 177f parathyroid, 159, 159f Anechoic cyst, kidney, 410f
pancreatic, 490 parathyroid glands, 159, 159f Anencephaly, 85
parotid gland, 126f pleomorphic, 122, 123f Anesthesia, 677
pelvic, 690692 thyroid, 150151, 151f Aneurysms
percutaneous aspiration, 628f Adenomatoid tumors, 569 carotid arteries, 146
periappendiceal, 369f Adenomyomatosis, 279, 288f chest, 188
post renal transplant, 445446, 446f Adenomyosis, 542, 543f jugular vein, 146f
psoas muscle, 499, 500f Adenopathy. see also Lymphadenopathy vein of Galen, 83f
pyogenic, 241, 318 HIV and, 142 Angiomyolipomas, 239, 423424, 424f
renal, 426427, 427f infectious, 141 Angiosarcomas, 226, 230, 317, 422
scrotal, 582583 mediastinal, 185 Anisotropy, 33, 33f
soft tissue, 628, 628f tuberculous, 142f Annular pancreas, 350
sonographic findings, 630 Adnexal torsion, 514, 530533, 531f, 532f Antegrade pyelography, 694
splenic, 318 Adrenal glands Anterior cerebral arteries, 55
subperiosteal, 630 abscesses, 476f Anterior fontanelle, 4344
testicular, 582583, 582f accessory glands, 464 Anterior tibial artery, 640
transabdominal drainage, 688f689f adenoma of, 472f, 547 Anterior tibial vein, 637
tubo-ovarian complex, 529f, 530f adrenocortical tumors, 471473 Anticoagulant therapy, 475
Absorption, of sound, 2 congenital anomalies, 463465 Antral dyskinesia, 344
Acceleration time (AT), systolic, 387 cysts, 475f Antral membranes, 345
Accessory duct of Santorini, 480 embryology, 461462 Antrum, normal anatomy, 341f
Accessory hepatic vein, 220f hyperplasia, 476477 Anus, imperforate, 373, 373f
Accessory spleen, 308, 308f infections, 476477 Aorta
Achilles tendon, 604f, 606, 636f medullary neoplasms, 465470 aneurysm, 493
Acinar cell carcinomas, 122, 123f metastatic disease, 471 dissection, 494495, 495f
Acoustics, 2 neonatal, 463f idiopathic arterial calcification, 495
Acquired immunodeficiency syndrome (AIDS), neonatal hemorrhage, 473475, 474f mycotic pseudoaneurysm, 494f
142 normal anatomy, 462, 463f normal anatomy
cholangitis related to, 299, 299f posttraumatic hemorrhage, 475 neonatal, 492f
fungal infections and, 427428 scanning techniques, 461 sonographic findings, 169
infections and, 319, 428 size of, 463f occlusive disease, 493494
liver in, 244, 244f sonographic findings pulsed Doppler examination, 492f
Acute bacterial pyelonephritis, 425, 425f, echo texture, 462463 stenosis, 493494, 494f
426427, 426f, 427f shape, 462, 462f thrombi, 492493, 493f
Acute glomerulonephritis, 430f traumatic hematoma, 475f umbilical arterial catheter, 492
Acute interstitial nephritis, 432 Wolman disease, 477478 Aortoiliac aneurysms, 493
Acute pancreatitis, 488491 Adrenal hemangioendothelioma, 473 Appendiceal abscess, 370f
Acute perirenal hematoma, 439f Adrenal rest tissue, 464, 566, 567f Appendicolith, 368

711
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712 INDEX

Appendix Asplenia, 309310, 310f, 496 Bone, 604, 604f

appendicitis, 333, 366 Astrocytomas, 110, 111f Bone marrow transplantation, 258f
acute, 368f, 369f Atelectasis, consolidation and, 175176 Bourneville disease. see Tuberous sclerosis
complications, 369370 Attenuation, of sound, 2 Bowel
diagnosis, 370373 Autoimmune diseases, 126127, 155157 air in, 301
focal, 371f Autosomal dominant polycystic disease, 482, ischemic disease, 374
retrocecal, 371f 483f obstruction by gas, 384385
scrotal abscesses and, 583 Autosomal dominant polycystic renal disease, Bowman spaces, 408
normal anatomy, 366368, 367f 407408 Brachial artery, 640
Appendix epididymis, 556, 556f, 577580 Autosomal recessive polycystic disease, 239f, 246, Brachicephalic vein, 638
Appendix testis, torsion of, 577580 405407, 406f, 407f Brain
Aqueductal stenosis, congenital, 107f Axillary artery, 640 abscesses, 106
Arachnoid cysts, 90f, 109 Azathioprine, 261 congenital infections, 102103, 102f
Arcuate uterus, 540 Azygos-hemiazygos systems, 495496 cross-sectional anatomy, 4555
Arms, vascular imaging, 639 imaging techniques, 4344
Arnold-Chiari malformation, 54 normal variants
Array transducers B calcar avis, 55
conventional versus two-dimensional, 9f Backscatter, causes of, 2 cavi septi pellucidi, 52
multiple-element Bacteremia, aortic aneurysms in, 493 cavum vergae, 52
conventional, 9f Bacteroides sp. infections, 204 choroid plexus, 5254
focusing, 4f Baker cysts, 622 cisterna magna, 54
linear array, 47 Bandwidth, transducer, 3 extra-axial fluid spaces, 5455
phased array sector, 4f, 5f Barlow maneuver, 607 germinal matrix, 52
sequenced array, 47 Bartonella henselae, 318 lateral ventricles, 5152
standard array, 8f Bartter syndrome, 437 parenchyma, 4951
three-dimensional volume probes, 810 Basilar artery, 57f peritrigonal echogenicity, 54
two-dimensional arrays, 78, 9f Bat-wing appearance, 86, 87f posterior fossa vallecula, 55
Arrays, types of, 3 Beckwith-Wiedmann syndrome, 226 thalamic pseudolesion, 55
Arterial occlusive disease, neonatal, 7778, 77f adrenal carcinoma and, 472 premature infants, 50f
Arterial resistance, calculation of, 385 adrenal cysts and, 475 sagittal sections, 4648
Arterial stenosis, 145146, 188 nephroblastomatosis in, 417 scanning artifacts, 4849
Arterial thrombosis, 145146 pancreaticoblastoma and, 483 term infants, 50f
Arteriovenous fistulae (AVFs) renal cell carcinoma in, 418 ultrasound equipment, 4344
after renal transplants, 442, 444 splenic hemangiomas and, 313 Brainstem, 45, 50f, 110, 111f
hepatic, 257259 Wilms tumor and, 413, 416, 417 Branchial apparatus, 121
hepatic artery, 266, 267f Bell clapper deformity, 572f Branchial cleft cysts, 121122, 132134, 133f,
neck, 131 Bell clapper sign, 636 134f
renal, 434435, 434f Benign cystic nephroma. see Multilocular cystic Branchial cleft sinus, 134f
sonographic findings, 643, 643f renal tumors BRCA genes, 211212
Arteriovenous malformations (AVMs), 8183, Benign hydatidform mole, 544 Breast, 200213
619f Benzodiazepines, 676677 benign masses, 207208
hepatic, 257259 Bezoars, 348349, 349f cystic lesions, 203207
high flow, 619f Biceps groove, 606 developmental abnormalities, 203
neck, 131, 132 Biceps tendon, 606 malignant tumors, 211212
pulmonary, 182, 182f Bicornate uterus, 539540 nipple, 203
Arteritis, 146 Bile ascites, 296 normal anatomy, 200201, 202f
Arthritis, septic, 624625 Bile ducts premature development, 547
Articular cartilage, 604 choledochlithiasis, 300301 sonography, 200203
Artifacts, 2142 cystic duct stones, 301 Breast cancer, 211212
aliasing, 1718, 3536, 36f, 37f extrahepatic, 296297 Bronchogenic cysts, 136f, 177, 178, 178f
gallbladder sludge, 284285 inflammatory diseases, 299 Bronchopulmonary sequestration, 179180
gray-scale, 2134 neoplasms, 301302 Budd-Chiari syndrome, 256257, 256f, 413
harmonic imaging and, 1112, 384385 normal anatomy, 291 Bursae, sonographic anatomy, 604
hepatic Doppler sonography, 224225 pseudocalculi, 301 Bursitis, septic, 631
oblique-positioning, 681f scanning techniques, 290291 Butterfly vertebral bodies, 650
partial volume type, 681f sonographic measurements, 291 Byler syndrome, 239, 294, 294f
three-dimensional ultrasound artifacts, 40 spontaneous perforation, 296297, 298f
Ascaris infections, 243 strictures, 302
Ascaris lumbricoides, 243 structure of, 268f C
Ascites Bile plug syndrome, 297298 Calcar avis, 55, 56f
bloating bowel and, 326f Biliary atresia, 292294, 293f Calcitonin levels, 152
causes of, 325 Biliary tract Caliectasis, megaureter and, 396
loculated, 327f drainage procedures, 692 Callosal agenesis, 85
urinary, 401402 needle access, 692f Callosal marginal artery, 57f
urine, 327 obstructions, 299301, 301f Calvarial masses, 112
Aspergillus spp., abscesses and, 241 Bilomas, 263, 327 Campylobacter jejuni, 361
Asphyxia Biopsies Cancer. see Specific cancers
neonatal, 72 complications of, 684 Candida albicans
perinatal, 59f false-positive, 683 CNS infections, 104
Aspiration free hand biopsy method, 679, 680f fungal abscesses and, 241, 242f, 318319
catheter insertion, 687689 needles, 681682, 682f post renal transplantation, 447
diagnostic, 687 percutaneous, 680686 urinary tract infections, 428f
of hip joint effusion, 626, 627f sites, 683684, 683f Capillary malformations, 131132, 619
needle guidance, 679f techniques, 682683 Caput medusae, 250
percutaneous, 628f Blooming artifact, 40 Carcinoid tumors, 230, 347
of pleural effusion, 174f Blue rubber bleb nevus syndrome, 619 Carcinomas
ultrasound-guided, 686695 Bochdalek hernia, 188, 189f, 391 acinar cell, 122, 123f
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INDEX 713
anaplastic, 152 Chiari malformations, 8587 subdural fluid, 71f
breast, 211212 Chiari I type, 671f techniques, 5558
colon, 378 Chiari II type, 87f, 657658 term infants, 7172, 72f
fibrolamellar, 227228, 229f sonographic findings, 8587 Color noise artifacts, 37
follicular, 152 types of, 86 Colpocephaly, 86
hepatocellular, 226227, 228f, 229f vena cava thrombi and, 497498 Column of Bertin, hypertrophied, 389f
invasive ductal, 212f Chlamydia trachomatis, 528, 580 Comet-tail artifacts, 28, 29f
islet cell, 230 Chloral hydrate, 676 Common bile duct, 479
medullary, 152 Cholangitis, 243, 299, 299f Common femoral vein, 637
mucoepidermoid, 122 Cholecystitis Common pancreaticobiliary channel, 481
papillary thyroid, 152, 153f acute, 285287, 286f Common tibioproneal trunk, 640
renal cell, 418419, 419f alcalculous, 287288, 287f Computed tomography, interventional
renal medullary, 421422 ascaris and, 243 procedures, 677
squamous cell, regional spread, 123 chronic, 287 Congenital adrenal hyperplasia (CAH), 476, 477f
thyroid, 152, 157 complications, 286287 Congenital aqueductal stenosis, 107f
transitional cell, 452 emphysematous, 286f Congenital hemihypertrophy, 416
Carcinomatosis, peritoneal, 333f gallbladder wall thickening and, 279 Congenital hip dislocation. see Developmental
Cardiophrenic angle masses, 187 gangrenous, 286, 287f dysplasia of the hip (DDH)
Cardiosplenic syndromes, 308 perforated, 287f Congenital hydronephros, 393405, 394f
Carney complex, 473 Cholecystoses, hyperplastic, 288289 imaging, 393394
Caroli disease, 295296, 297f Choledochal cysts, 294295, 295f, 296f posterior urethral valves and, 400403
Caroli syndrome, 246 Choledocholithiasis, 300301, 300f, 301f primary megaureter and, 395397, 396f, 397f
Carotid arteries, 38f, 143, 146, 146f Cholelithiasis, 279283 prune belly syndrome and, 403405
Carotid ghosts, 37 Cholestatic diseases, 291292 retrocaval ureter, 405
Cartilage, 604, 604f Cholesterol, accumulation of, 477 simple ureterocele and, 400
Cartilaginous epiphyses, 604, 605 Cholesterol crystals, 134 ureteral duplication and, 399400
Castleman disease, 329, 330f Cholesterolosis, 288, 289f uteropelvic junction obstruction and, 394395,
Cat-scratch disease, 143, 244, 244f, 310, 318f Chorioamnionitis, 72 395f
Catecholamines, 462, 465 Choriocarcinomas, 562 vesicoureteral reflux and, 397398
Catheterization hepatic, 230 Congenital hyperinsulinism, 482483
catheter insertion, 687689 ovarian, 522 Congenital intrathoracic kidney, 391
central venous catheters, 695696 sonographic findings, 563 Congenital lobar emphysema, 177, 178, 178f
peripherally inserted central catheters (PICCs), uterine, 544 Congenital malformations, 81102
695 Choroid plexus, 5254 arch anomalies, 188
umbilical artery, 492, 492f cysts, 54f, 110, 110f cerebral development disorders, 97100
umbilical vein, 263 hemorrhage, 72 destructive brain lesions, 100102
urinary bladder infections and, 454 papillomas, 110 diverticularion disorders, 9297
Caudal cell mass, 648f, 662666 Chromosome 4, 407 histogenesis disorders, 8185
Caudal regression syndrome, 664, 664f Chromosome 7, 481 lung, 177182
Caval thrombosis, 497498 Chromosome 9, 410 neck, 129
Cavernous hemangiomas, 233234, 235f, 670f Chromosome 11, 422423 neural tube closure disorders, 8592, 91f
Cavernous malformations, 8384 Chromosome 16, 407 stomach, 341
Cavi septi pellucidi, 44f, 47f, 52 Chromosome 22, 422 thyroid gland, 148149
Cavi veli interpositi, 53f Chronic granulomatous disease, 243, 345346, Congenital vertical talus, 617
Cavum vergae, 52 346f Congestive heart failure, 222, 325
Cecal duplication, 358f Chylothorax, 171 Conn syndrome, 473
Celiac artery, 221f Chylous effusions, pleural, 171 Conscious sedation protocols, 675
Cellulitis Circle of Willis, 44, 58f Continuous-wave Doppler, 15f, 16
chest wall, 194, 194f, 195f Circumaortic renal vein, 497 Contrast agents, 1819, 4041
description, 626627, 627f Cirrhosis, 247248, 247f, 325 Conus medullaris, 651
Central hypothyroidism, 149 Cisterna magna, 49, 54 identification, 670
Central sinus echogenicity (CSE), 385f Citrobacter diversus, 106, 106f normal, 652f
Central venous catheters, 695696 Clear cell sarcoma, renal, 421, 422f position of, 652654, 653f
Cerebellar hemorrhage, 72 Cleft sign, 53f termination of, 653
Cerebellar ischemia of prematurity, 75 Clostridium difficile, 375 Core biopsy needles, 681, 682f, 683
Cerebellum, scanning planes, 44f Clostridium perfringens, 629 Coronal sutures, 44, 112f
Cerebral arteries, 55, 57f, 78 Clubfoot, 616617, 617f Corpus callosum
Cerebral blood flow (CBF), 58 Cocaine, maternal use of, 77 abnormalities, 9092
Cerebral cortex, development, 97 Colloid cysts, 151152, 152f agenesis, 91f, 93f, 658
Cerebral edema, 105, 105f Colon lipoma of, 92, 93f
Cerebral hemispheres, cortical pseudolesion, anorectal malformations, 373374 periventricular leukomalacia, 75f
51f benign masses, 377 scanning planes, 44f
Cerebral peduncles, 49 malignant masses, 378 Corpus hemorrhagicum, 512
Cerebritis. see Cerebral edema normal anatomy, 373 Cortical hemartomas, 85
Cerebrohepatorenal syndrome, 410. see also scanning technique, 373 Cortical pseudolesions, 51f
Zellweger syndrome wall diseases, 374376 Corticosteroids, 261
Cerebrospinal fluid (CSF), 106107, 327, 328f Color bleed. see Blooming artifact Corticotropin-releasing hormone, 462
Cervical lymph nodes, 129f Color Doppler imaging, 1617, 37f, 5560 Costal cartilage, prominent, 197f
Cervical sinus of His, 133 aliasing, 37f Costoclavicular trunk, 640
Cervical thymic cysts, 134136 arteriovenous fistula, 643f Craniosynostosis, 111
Chest epidural hemorrhage, 71 Cremasteric artery, 556
masses, 685686 insonation angle and, 37f Cremasteric fascia, 554
sonography, 171 normal blood flow patterns, 5860 Crohn disease, 333, 359361, 359f, 360f.
sonography techniques, 164165 pulsation artifact, 39f see also Granulomatous colitis
ultrasonography, 164199 scrotal sonography, 554 Cronkhite-Canada syndrome, 365
Chest wall, osseus lesions, 195197 subarachnoid fluid on, 71f, 104105 Crura, diaphragmatic, 498, 499f
Chest wall lesions, 191197 subarachnoid versus subdural, 71 Cryptorchidism, 562f, 569
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714 INDEX

Curved array transducer, 7f, 8f thymic, 136, 136f tissue vibration artifacts, 3739
Cushing syndrome, 472473, 472f thyroglossal duct, 132, 133f twinkle artifacts, 39, 40f
Cutaneous stigmata, 656, 660 thyroid, 151152 Doppler frequency shifts, 15
Cutis laxa, 449 tunical, 571f Doppler sonography, 1518. see also Color
Cyclosporine, 442 urachal, 451f Doppler imaging; Specific organs;
Cystadenomas, 122. see also Adenomas vaginal, 546547 Specific tissues
mucinous, 523f Cytomegalovirus acceleration time (AT), 387
ovarian, 522, 523f in AIDS, 244, 319 color Doppler, 1617
pancreatic, 487488 congenital infections, 103 continuous-wave Doppler, 15f, 16
serous, 522 lentriculostriate vasculopathy and, 103, 103f duplex, 16f
Cystic adenomatoid malformations, 177179, opportunistic infections, 428 power mode Doppler, 1718
179f, 181f post renal transplantation, 447 pulsed Doppler, 16, 36f
Cystic duct, stones, 301 salivary gland inflammation, 124126 Dorsal cutaneous stigmata, 656
Cystic dysplasia, testicular, 561, 561f, 566 viral hepatitis and, 240 Dorsal dermal sinus, 649f, 661662, 661f
Cystic encephalomalacia, 102 Dorsalis pedia artery, 640
Cystic fibrosis Double-arc shadow sign, 282
bowel wall and, 377f D Down syndrome, 156
chronic pancreatitis and, 490 D-dimer tests, 639 Drash syndrome, 413, 416
epididymal cysts, 569 Dandy-Walker complex, 8790 Dromedary hump, 390
fatty infiltration of liver, 245f Dandy-Walker malformation, 658 Drug toxicity, tubular necrosis and, 442
liver and, 248 Dandy-Walker syndrome, 54, 85, 88f, 90f Duct of Wirsung, 480
microgallbladder, 279f Dandy-Walker variant, 90f Ductal ectasia, 203204, 204f
pancreas and, 481482 Dartos muscle, 554 Ductus venosus, 218219, 218f
pancreatic cysts, 482f De Morsier syndrome, 9697 Duodenal atresia, 350351, 350f
small bowel, 363 De Quervain thyroiditis, 154155, 155f Duodenal bulb, 349
sonogram, 481f Deep femoral artery, 640 Duodenal hematoma, 363f
thickened gut wall, 364f Deep femoral vein, 637 Duodenal membrane, 350, 351f
Cystic hamartoma. see Multilocular cystic Deep vein thrombosis (DVT), 639, 640f Duplication cysts, 136
renal tumors Deferential artery, 556 duodenal, 364f
Cystic hygromas, 121, 129130, 146f, 185f, Dermoid cysts, 112f, 134, 135f enteric, 364365, 377
620f. see also Lymphatic malformations Desmoid tumors, 330 esophagus, 186f
Cystic mesenchymal hamartoma, 236f Desmoplastic round cell tumor, 332 gastrointestinal tract, 346, 346f
Cystic peritoneal mesothelioma, 330, 330f Developed collaterals, 249250, 250f Dura mater, 651
Cystic teratomas, 486, 519521 Developmental dysplasia of the hip (DDH), Dural arteriovenous fistula, 84f
Cystitis, 454 607613 Dysgerminoma, ovarian, 523, 524f
Cystitis cystica, 454 associated abnormalities, 611 Dyshormonogenesis, 149
Cystography, sonographically-guided, 397 clinical diagnosis, 607
Cysts description, 607
acoustic enhancement, 203 dynamic imaging, 607611, 608f E
arachnoid, 109 pathology, 610611 Eagle-Barrett syndrome. see Prune belly syndrome
branchial cleft, 132134, 133f, 134f posttreatment imaging, 611613 Early systolic peak (ESP), 387
breast, 203207 screening, 613 Echinococcsis, 242
bronchogenic, 177, 178f sequelae, 611613 Echinococcus alveolaris, 242
cervical thymic, 134136 three-dimensional sonography, 613 Echinococcus granulosus, 242
choledochal, 294295, 295f, 296f Dexamethasone, 472 Echoes, artifactual, 26
choroid plexus, 110, 110f Diaphragm, 350351 Ectodermal sinus tumor, ovarian, 523, 525f, 526
colloid, 151152, 152f duplication artifacts, 21, 22f, 25f Ectomesenchymoma, mesenchymal, 332
dermoid, 112f eventration, 190, 191f Ectopic thymus, 136137, 137f
duplication, 136, 186f juxtadiaphragmatic masses, 191 Edema
ectopic bronchogenic, 136f motion of, 170171 cerebral, 105, 105f
foregut, 185 normal anatomy, 169171, 171f male genital tract, 584
ganglion, 622, 622f paralysis, 190191, 191f ovarian, 533
harmonic imaging, 11f traumatic rupture, 391 scrotal, 571, 584, 584f
hemorrhagic, 152, 515f, 516517, 516f, 518f Diaphragmatic crura, 498, 499f Eggshell calcifications, 151
hepatic, 239240, 239f Diaphragmatic hernias, 188190 Ehlers-Danlos syndrome, 449, 493
mediastinal, 184185 Diaphragmatic lesions, 188191 Elastography, 18, 247
meniscal, 623 Diaphragmatic slips, 224225 Elbow, normal anatomy, 606f
mesenteric, 327328, 328f, 329f Diastematomyelia, 650, 660661 Embryology
mesothelial, 240f Diazepam, 676 adrenal gland, 461462
mucus retention, 123124 Diethylstilbesterol, prenatal, 540 filum terminale fibrolipomas, 649650
ovarian, 514517, 515f, 516f, 517f, 518f Digital Imaging and Communications in Medicine inferior vena cava, 496f
pancreatic, 482f, 487488 (DICOM), 3 pancreas, 480
parathyroid, 159160, 160f Dimercaptosuccinic acid (DMSA), 425 spine, 647650, 648f, 649f
paraurethral, 547f Distance gain compensation, 2 tethered cords, 649650
paravaginal, 546547 Diuretic scintigraphy, 394 uterus, 536
parovarian, 518519, 518f Diverticularion disorders, 9297 Embryonal adenofibroma, 424
peritoneal inclusion, 519 Doppler artifacts, 3439 Embryonal adenoma, 424
popliteal, 622, 623f anatomically-related Embryonal carcinomas, 562, 563
renal cystic disease, 405413 aliasing, 37f Embryonal rhabdomyosarcoma, 568
seminal vesicle, 595f color noise artifacts, 37 Emphysematous cholecystitis, 286f
simple, 152 mirror-image artifacts, 22f, 37 Empyemas, 173174, 692693
sonographic findings, 622623 pulsality artifacts, 37 Encephalocele, 85, 86f, 112
splenic, 311313, 312f technically-related Encephalomalacia, 66f
subhyoid, 133f absent Doppler signal, 34 Encephalotrigeminal angiomatosis, 84.
supracerebellar, 90f aliasing, 3536 see also Sturge-Weber syndrome
suprahyoid, 133f Doppler noise, 3435 End-diastolic velocity (EDV), 58
testicular, 26f, 571f flow directional abnormalities, 36 Endometritis, 528f
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INDEX 715
Endophlebitis, suppurative, 370 Fentanyl citrate, 676 sonographic findings, 634635
Endoscopic probes, 11 Fetal alcohol syndrome, 129, 226 testicular, 585, 586f
Endotracheal tubes, positioning, 188 Fetal renal hamartoma, 422423 Frantz tumor, 484
Entamoeba histolytica, 242243, 376377 Fibrin, pleural deposition, 173, 175 Free hand biopsy method, 679, 680f
Enteric duplication cysts, 377 Fibroadenomas, 207208, 207f, 208f. Frequency
Enteritis, infectious, 361362 see also Adenomas range of, 3
Enterobacter sp., 106 Fibrocystic disease, breast, 205 ultrasound, 2
Enteroenteric fistulae, 361f Fibroepithelial polyps, urethral, 594 Fungal abscesses, hepatic, 241242
Eosinophilic gastroenteritis, 346 Fibroids, uterine, 542544, 544f Fungal infections, 104, 427428, 428f
Ependymomas, 110, 670f Fibrolamellar carcinoma, 227228, 229f Fusobacterium necrophorum, 144
Epidermoid cysts, 566, 566f Fibromatosis, aggressive, 138
Epididymal cystenadenomas, 569 Fibromatosis colli, 137138, 138f
Epididymal cysts, 569570, 570f Fibromuscular dysplasia, 432 G
Epididymis, 555, 558f, 585f Fibrosarcomas, 195, 422, 487 Galactoceles, 205, 205f
Epididymitis paratesticular, 568 Galactosemia, 248
acute, 580583, 580f, 581f Fibrosis, hepatic, 246 Galenic malformations, 81, 82f, 83f
acute scrotum and, 571 Fibrothorax, 173175, 174f Gallbladder
chronic, 583, 583f Fibrous histiocytoma, 501 agenesis, 277
testicular abscess and, 582f Fibrous histiocytomas, 487 air in, 283f
Epidural hematomas, identification, 670 Fibroxanthoma, 346 bilobed, 279f
Epimysium, 603 Filar cysts, 654, 656f with calculi (see also Gallstones)
Epstein-Barr virus, 240, 310 Filum terminale, normal, 652f acoustic shadowing, 31f
Escherichia coli Filum terminale fibrolipomas, 649650, 663664, multiplanar image displays, 14f
acute epididymitis/orchitis and, 580 663f reverberation artifacts, 26f
acute pyelonephritis, 425 Filum terminale syndrome, 662663, 663f threshold artifacts, 41f
cellulitis and, 626627 Fine-needle aspirate, thyroid, 685f congenital anomalies, 277278
chronic granulomatous disease and, 243 Fistulae disease symptoms, 280
hemolytic uremic syndrome and, 430431 in Crohn disease, 360361 duplicated, 278f
hepatic pyogenic abscess, 241 diagnosis, 374 ectopic, 278
meningitis and, 103 enteroenteric, 361f folds, 277f
osteomyelitis and, 630 Fitz-Hugh-Curtis syndrome, 530 hepatization, 284f
post renal transplantation infection, 447 Flexor pollicis longus tendon, 33f hydropic, 284f, 288, 288f
pyelonephrosis, 427 Flow directional abnormalities, 36 inflammatory polyps, 289f
Esophageal varices, 250, 251f Fluid collections normal anatomy, 275, 276f
Esophagus aspiration of, 686 variants, 277278
atresia, 188 extended-field-of-view scans, 12f normal sonographic anatomy, 275277, 276f
duplication cyst, 186f extra-axial, 70f perforation, 286, 290f
normal anatomy, 168, 339 pleural, 693f pseudosludge, 29, 32
scanning technique, 339 Fluid color sign, 173f scanning technique, 275
Estrogens, precocious puberty and, 547 Flumazenil, 676 septate, 278, 279f
Ewing family tumors, 195 Focal fatty sparing, 245, 245f, 246f side-lobe artifacts, 30f
Ewing sarcomas, 332, 501, 624f Focal foveolar hypoplasia, 347, 347f sonographic findings, 279, 280f
Extended-field-of-view (EFOV) imaging, 12, 12f Focal nodular hyperplasia, hepatic, 226, thick-wall, hepatitis and, 240241, 240f
External carotid artery, 119, 143f 237, 237f torsion, 288
External spermatic fascia, 554 Focused abdominal sonography for trauma trauma, 290
Extracorporeal membrane oxygenation (ECMO) (FAST), 262 varices, 289290
arterial thrombosis and stenosis, 145146 Folic acid deficiency, 656 Gallstones
cerebral abnormalities, 79 Follicular carcinoma, 152 in children, 280281
oxygenation patterns, 78, 78f Follicular thyroid cancer, 153f composition of, 280281
parenchymal hemorrhage and, 7172, 72f Fontanelle, closing of, 43 false-negative diagnoses, 281283
spenomegaly and, 311 Foramen magnum, as acoustic window, 44 false-positive diagnoses, 283
vendarterial cannulation, 7879 Foramen of Monroe, 45, 45f fetal, 283
Extradural tumors, 668f Foramen of Winslow, 325 nonshadowing, 282f
Extralobar sequestration, 181f Forearm, veins of, 638 obesity and, 281
Extrarenal pelvis, 396f Foregut cysts, 185 sludge, 283285, 283f, 284f
Foreign bodies sonographic findings, 281
ingested, 378f Gangliogliomas, in infants, 110
F localization, 378379 Gangliomas, location of, 110
Facial artery, 120, 120f removal, 696697, 697f Ganglion cysts, 622, 622f
Facial vein, 120 soft tissue, 535f, 636 Ganglioneuroblastomas, 185, 470, 470f
Factor V Leiden, 435 sonographic appearance, 535f, 696f Ganglioneuromas, 139140, 185, 470
Falciform ligament, 215, 217f urethral, 596f Gardner syndrome, 226, 330, 365
Fallopian tubes urinary bladder, 452 Gartner cysts, 546547
adnexal torsion, 530533 Fournier gangrene, 583 Gas gangrene, 629
parovarian cysts, 518519, 518f Fourth ventricle Gastric duplication, 346f
torsion, 533, 533f dilated, 87, 107f Gastric polyps, 347f
Familial intrahepatic cholestasis, 239 mastoid fontanelle scan, 49 Gastric vein, enlarged, 250, 251f
Familial polyposis coli, 226 sagittal scan, 47 Gastric wall thickening, 345346
Fasciitis, 628f scanning planes, 44f Gastrinomas, 485
Fat necrosis, 633 trapped, 67f Gastritis, ulcer disease and, 345
Fatty tumors, 331, 622 Foveolar hyperplasia, 344 Gastrocnemius muscle, 606
Female pelvis, 509553 Foveolar hypoplasia, focal, 347f Gastroesophageal junction, 340f
Femoral vein, 639f Fractures Gastroesophageal reflux, 339341, 340f
Femur hepatic, 262 Gastrointestinal stromal tumors (GISTs), 332,
neonatal fracture, 634f neonatal femur, 634f 348, 348f
normal anatomy, 625626 renal, 439f Gastrointestinal tract, 339383. see also Specific
slipped capital epiphysis, 636f rib, 197 organs; Specific tissues
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716 INDEX
Gastrosplenic ligament, 306f, 307
Gaucher disease, 248, 311, 321322, 322f
Genital tract, male, 554601
Genu recurvatum, 616, 616f
Germ cell neoplasms
extragonadal, 332
malignant, 565
mixed, 564f
ovarian, 522526, 525f
primary testicular, 562563
retroperitoneal, 501
testicular, 563
Germinal matrix, 52, 60, 62f
Germinomas, 110
Gestational trophoblastic disease, 544
Gian cell arteritis, 146
Glands of Montgomery, 204205
Gliomas, location of, 110
Globus major, 555
Glomerulocystic disease, 408409, 408f, 409f
Glomerulonephritis, 430f
Glomerulonephritis, acute, 430f
Glomerulonephrosis, 430
Glucagonoma, 485
Glucocerebrosidase deficiency, 321
Glucocorticoids, synthesis of, 462
Glucose transporter-1 (GLUT-1), 232233
Glycogen storage disease, 248
Goiter, 148, 150f, 154, 157158, 158f
Goldston syndrome, 88, 90f
Gonadal dysgenesis, 549
Gonadoblastomas, 565
Graafian follicles, 512, 512f
Graf technique, 611, 612f
Graft-versus-host disease (GVHD), 363364
Granular cell tumors, 209210, 210f, 302
Granulomatous colitis, 374375, 375f
Granulomatous disease, 126127
Granulosa cell tumors, 526
Graves disease, 154, 157
Gray matter, heterotopic, 99100, 101f
Gray-scale artifacts, 2134
anisotropy, 33, 33f
increased through-transmission, 31, 33f
mirror-image artifacts, 21
refraction artifacts, 2125
reverberation artifacts, 2527
ring-down artifacts, 2728
shadowing, 24f, 3031
side-lobe artifacts, 2830, 29f
slice-thickness artifacts, 3133
Gray-scale sonography, 16, 4344. see also
Specific organs; Specific tissues
Great vessels, 143144, 168169, 169f
Greater saphenous veins, 637
Gut, pseudothickened, 21
Gynecomastia, 203, 204f, 310, 563
H stenosis, 267f
Hamartomas, 315, 315f, 316f, 566
Hand, normal anatomy, 606, 607f
Harmonic imaging, 1112, 11f, 384385
Hashimoto thyroiditis, 154, 155157, 156f
Helicobacter pylori, 345
Hemangioendothelioma, 226, 232233, 487
Hemangiomas
breast, 208, 209f
calvarial, 112
chest wall, 192f
description, 121, 618, 618f
gastric, 347
hepatic, 22f, 226
neck, 130132, 131f
parotid gland, 122f
peritoneal, 328329, 329f
pleural, 175f
retroperitoneal, 501, 502, 667f Morgagni, 188189, 190f
splenic, 313, 313f muscle, 623
Hemangiopericytoma, renal, 422 strangulated, 571, 592f
Hemartomas, 85 Herpes simplex encephalitis, 103
Hematoceles, 585, 586f, 590 Herpes simplex virus (HSV), 102103, 240,
Hematocolpos, 540, 541, 542f 447, 476
Hematomas Heterotaxy, 308
acute perirenal, 439f Heterotopic gray matter, 99100, 101f
acute subcapsular, 446f High-dose dexamethasone suppression test, 472
breast, 206, 206f High-intensity transient signals, 41
chest wall, 194 Hindfoot, congenital anomalies, 616617
chronic, 633f Hip
epididymal, 585f capsule, normal, 625f
gastric, 347 congenital anomalies, 607613
GI tract, 363f developmental dysplasia, 607613
hepatic, 262f dislocated, 610f
penile, 596f Graf technique classification, 611, 612f
post renal transplant, 445 joint effusion, 624626, 627f
soft tissue trauma and, 632633, 633f normal anatomy of, 605, 608f, 609f
splenic, 322f, 323f subluxed, 610f
testicular, 584585, 585f types of, 612f
Hematometrocolpos, 540 Histogenesis disorders, 8185
Hematopoiesis, 305 Histoplasmosis, 476
Hemidiaphragm, 170 HIV (human immunodeficiency virus), 102103,
Hemimegalencephaly, 97, 98f 124, 125f, 142, 313314
Hemobilia, 285 Hodgkin lymphoma, 138, 184f, 317, 331
Hemochromatosis, 246247, 246f Hole sign, 286
Hemoglobinopathies, 310, 320f Holoprosencephaly, 85, 9197, 95f, 96f
Hemolytic uremic syndrome (HUS), 376, 376f, Homovanillic acid (HVA), 465
430431, 431f Horner syndrome, 139140
Hemoperitoneum, 335336 Horseshoe kidney, 392393, 393f
Hemorrhages -human chorionic gonadotropin, 562
adrenal glands, 473475 Human immunodeficiency virus. see HIV
neonatal, 473475, 474f Humerus, epiphyseal separation, 634f
retroperitoneal, 503 Hydatid disease, liver, 242
Hemorrhagic effusion, pleural, 171 Hydatidform mole, 544, 545f
Hemothorax, 171, 183f Hydrancephaly, 100102, 101f
Henoch-Schnlein purpura, 362, 362f Hydroceles, 587590, 587f, 588f
epididymis enlarged in, 584f Hydrocephalus, 106109
renal disease and, 431 benign external, 109f
scrotal skin thickening in, 584, 584f benign extra-axial, 109f
Hepatic adenoma, 238, 238f communicating, 107
Hepatic arteries CSF disturbances, 107
anatomy, 220 in Dandy-Walker malformations, 87
blood flow, 224f Doppler interrogation, 108
normal Doppler anatomy, 221f, 224 meningitis and, 106
replaced, 221f noncommunicating, 107
thrombosis, 265 normal CSF production, 106107
Hepatic cysts, 239f occult spinal dysraphism and, 658
Hepatic fibrosis, 246, 246f, 405 sonographic findings, 107108
Hepatic hemangioma, 22f subdural hematoma and, 69, 71
Hepatic infarction, 260 ventricular herniation, 108f
Hepatic lesions, duplication of, 21 ventricular shunt, 108f
Hepatic peliosis, 261, 261f Hydrocolops, 540, 541, 541f
Hepatic veins Hydrometrocolopos, 540
blood flow, 223f Hydromyelia, 658, 668, 670
complications of transplantation, 266f Hydronephros, 394, 400405
normal Doppler anatomy, 222223 Hydronephrosis, 694
occlusion, 256257, 257f Hydrosalpinx, 530f
Hydroureter, 447f
variations, 219, 220f 17-Hydroxycorticoids, 472
Hepatitis 11-Hydroxylase, 476
acute, 240f 21-Hydroxylase deficiency, 476, 477f
neonatal, 292294, 293f 3-Hydroxysteroid dehydrogenase, 476
viral, 240241 Hyperbilirubinemia, 292
Hepatitis viruses, 240241 Hypercalciuria, calculi and, 452
Hepatobiliary scintigraphy, 292 Hyperinsulinism, congenital, 482483
Hepatoblastoma, 226, 227f, 228f, 229f Hyperparathyroidism, 159, 490
Hepatocellular carcinoma, 226228, 228f, 229f Hyperthyroidism, 148
Hepatosplenomegaly, 232 Hypertrichosis, 660
Hereditary autosomal dominant hyperthyroidism, Hypertrophic pyloric stenosis (HPS), 342344
157 Hypoalbuminemia, 325
Hermaphrodites, 549550, 550f Hypodermis, 603
Hernias Hypogenetic lung syndrome, 180
acquired, 189 Hypoglycemia, 482
Bochdalec, 188 Hypokalemia, 473
inguinal, 590591, 591f, 592f Hypoparathyroidism, 156
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Hypopituitarism, 96
Hypotension, 430
Hypothyroidism, 148
Hypoxic-ischemic encephalopathy (HIE), 72
Hypoxic-ischemic injury, 7277, 77f
I Internationial Neuroblastoma Staging System
Idiopathic arterial calcification, 495
Idiopathic fibrosing pancreatitis, 490
Idiopathic infantile hypercalcemia, 432
Idiopathic scrotal edema, 571, 584
Ileal atresia, 351
Ileal stenosis, 351
Iliac arteries, uterine, 536
Iliopsoas muscle, 499
Image displays, 3, 14f
Image storage, 3
Impedence, 2
Inclusion cysts, vaginal, 546547
Increased through-transmission, 31, 33f
Infantile hemangioendothelioma, 232233, 233f,
234f, 235f
Infantile polycystic kidney disease, 405
Infants, term. see also Premature infants
brain, 50f
hypoxic-ischemic injury, 7577
intracranial hemorrhage, 6872
normal spine, 650f
normal venous waveforms, 60f, 60t
renal imaging, 386
spinal sonography, 650651
subarachnoid hemorrhage, 68
testis, 556559
urinary tract, 385386
Infections. see Specific conditions; Specific
organisms; Specific tissues
Infectious colitis, 377f, 378
Infectious enteritis, 361362
Infectious tenosynovitis, 630631
Inferior vena cava (IVC)
anatomy, 495
caval thrombosis, 497498, 497f, 498f
complications of transplantation, 266f
congenital anomalies, 495497
dilated, 495f
embryologic segments, 496f
fistula, 260f
infrahepatic interruption, 496f
interrupted, 495496, 496f
normal, 495f
occlusion, 257
stenosis, 267f
tumor thrombus, 498f
Wilms tumor invasion, 415f
Inflammatory myofibroblastic tumors,
501f
Inflammatory pseudotumor, 329330
gastrointestinal tract, 346347
pancreatic, 487
spleen, 315, 316f
Inflammatory pseudotumors, renal, 425
Infradiaphragmatic extralobar pulmonary
sequestration, 474475, 475f
Infrapatellar bursa, 606
Infraspinatus muscle, 606
Infratentorial subdural hematoma, 6971, 69f,
70f
Inguinal hernias, 590591, 592f
Inspissated bile syndrome, 297298, 298f
Instrumentation, 23
image display, 3
image storage, 3
receivers, 3
transducers, 23
transmitters, 2
Insulinomas, 485f
Intercostal views, chest, 165
Internal carotid artery, 55, 143f
Internal jugular vein, 143145, 144f
Internal mammary artery, 38f, 169, 170f, 640
Internal mammary compartment, 168169,
188
Internal mammary vein, 169
(INSS), 465, 465t
Intersex disorders, 549550
Interventional procedures, ultrasound-guided,
675700
Intra-arterial probes, 11
Intracavitary probes, 1011
Intracerebellar hemorrhage, 6768, 68f
Intracranial hemorrhage, 6072
cerebellar, 72
choroid plexus, 72
epidural, 71
parenchymal, 7172
premature infants, 6068, 62f, 65f
prenatal, term infants, 72
subdural, term infants, 6971
subependymal, 62f, 63f, 72
Intraductal papillary mucinous neoplasms, 487
Intraductal papilloma, 210211, 211f
Intradural lipomas, 662
Intralobar sequestration, 180f
Intraluminal probes, 1011
Intramammary lymph nodes, 211
Intraparenchymal hemorrhage (IPH), 6567, 66f
Intraspinal cavernous hemangioma, 670f
Intrauterine diagnoses, 393
Invasive ductal carcinoma, 212f
Iodine, 147
Islet cell tumors, 230, 485486, 486f
Isosexual precocity, 547, 548f
Ivemark syndrome, 246
J nephromegaly, 416417
Jaundice, 291292, 300f
Jejunal atresia, 351
Jejunal stenosis, 351
Jejune syndrome, 246
Jeune asphyxiating thoracic dystrophy, 410
Johanson-Blizzard syndrome, 482
Joint Commission on sedation, 675
Joints, normal anatomy of, 605607
Jorgenson syndrome, 156
Joubert syndrome, 88, 246
Jugular vein, 146f
Jugular vein thrombosis, 145f
Jugulodigastric node, 128
Juvenile granulosa cell tumors, 563, 566f
Juvenile nephronophthisis, 409
Juvenile papillomatosis, 310, 310f
Juvenile polyps, 377
Juvenile rheumatoid arthritis, 304
Juvenile (virginal) hypertrophy, 203
Juxtadiaphragmatic masses, 191
Juxtarenal processes, 438
K congenital anomalies, 616
Kallmann syndrome, 549
Kasabach-Merritt syndrome, 233, 313
Kasai hepatoportoenterostomy, 292
Kawasaki disease
aneurysms, 188
aortoiliac aneurysm and, 493
arterial stenosis, 188
carotid artery aneurysms and, 146
cervical node enlargement, 143
small bowel, 363
Ketamine, 676677
Kidney. see also Renal entries
INDEX 717
acute glomerulonephritis, 430f
acute perirenal hematoma, 439f
agenesis, 464f
anatomic variations, 389390, 389f,
390f
anechoic cyst, 410f
benign tumors, 422425, 423f, 424f
central renal sinus, 386f
central sinus echogenicity, 385f
congenital anomalies, 390405, 390f, 392f,
393f, 394f
cortical echogenicity, 385f, 386f
with curved array, 8f
dilated calyces, 401f
dilated renal pelvis, 398f
drug toxicity, 442
duplication artifacts, 24, 25f
ectopic, 391392
extrarenal pelvis, 396f
flow detection, 35f
injuries, categories of, 438440
juxtarenal processes, 438
left, scanning technique, 384
malignant neoplasms, 413422, 419f, 420f,
422f, 425
mass, 3-D scan, 15f
medical disease of
acute interstitial nephritis, 432
acute renal cortical necrosis, 432
acute tubular necrosis, 431f
glomerulonephrosis, 430
hemolytic uremic disease, 430431,
431f
Henoch-Schnlein purpura, 431
sonographic findings, 430432
stasis nephropathy, 430, 431f
medullary pyramids, 385f, 386, 386f,
409410
multicystic dysplastic, 411412, 412f
neonatal anatomy, 386f
obstruction, acquired, 405
palpable, 401
parenchymal vessels, 15f
pulmonary hypoplasia and, 401
renal fracture, 439f
renal pelvis, dilated, 401f
renal vascular disease, 432437, 433f, 434f,
436f, 437f
right, 5f, 384, 403f
sonography, developmental changes, 386,
386f
subcapsular hematoma, 28f
transplanted, 39f (see also Renal
transplantation)
with trapezoidal array, 7f
traumatic injury, 438440
tubular necrosis, 442
twinkle artifacts, 40f
vascular anatomy, 386387, 387f, 388f
Klinefelter syndrome, 156, 560
Klippel-Trenaunay syndrome, 193, 619
Klippel-Trenaunay-Weber syndrome, 313
Knee
genu recurvatum, 616
normal anatomy of, 605606, 605f
L
Lactating adenoma, 208209, 209f
Lactobezoar, 348
Lacunar skull, 8687, 88f
Ladd bands, 353
Lambdoid suture, normal, 111f
Langerhans histiocytosis, 143, 146, 317
Lateral plantar artery, 640
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718 INDEX
Lateral ventricles
asymmetric, 51f
body of, 44f, 46f
coarctation, 52, 52f
frontal horns, 44f, 45, 45f
normal, 51f
occipital horn, 44f, 46f, 63f
size of, 5152
temporal horn, 44f
Leg
major veins, 637f
vascular imaging, 639
Legg-Calve-Perthes disease, 636
Leiomyomas, 347, 487, 542
Leiomyomatous hamartoma, 422423
Leiomyosarcomas
hepatic, 230
ovarian, 522
paratesticular, 568
renal, 422
retroperitoneal, 501
small bowel, 365
urinary bladder, 452
Lemierre syndrome, 144
Lentriculostriate vasculopathy, 103, 103f
Lesch-Nyhan syndrome, 437
Lesser omentum, thickened, 253f
Lesser saphenous veins, 637
Leukemias
hepatosplenomegaly, 232
ovaries as sanctuary for, 527
paratesticular, 568, 569f
renal involvement, 420, 420f
spleen and, 317
testicular sonogram in, 567f, 568f
Leydig cell hyperplasia, 566
Leydig cell tumors, 563, 565, 565f
Ligaments, anatomy, 603604
Ligamentum teres, 215, 217f, 224
Ligamentum venosum, 215, 217f, 224
Limb enlargement, 636
Linear array transducers, 47, 6f
Lingual thyroid, 149, 150f
Lipoblastomas, 331, 501, 502, 622
Lipoblastomatosis, peritoneal, 331f
Lipoid adrenal hyperplasia, 476477
Lipomas
chest wall, 193195, 193f
corpus callosum, 92, 93f
gastric, 347
hepatic, 239
intradural, 662
pancreatic, 487
peritoneal cavity, 331
retroperitoneal, 502
sonographic findings, 622f
Lipomyeloceles, 658, 659f
Lipomyelomeningocele, 658, 659f
Liposarcomas, 331, 487
Lissencephaly, 9798, 99f
Littoral cell angioma, 313, 314f
Liver, 214274. see also Hepatic entries
abscesses, drainage of, 694f
adenoma, 238
anatomic variations, 225226
arteriovenous malformations, 257259
biopsy of, 678f, 684, 684f
Budd-Chiari syndrome, 256257
cavernous hemangioma, 233234
color Doppler pulsation artifact, 39f
cysts, 239240
cysts, reverberation artifacts, 27f
diffuse parenchymal diseases, 244248
duplication of, 21, 25f
fatty infiltration, 245f
focal nodular hyperplasia, 237
hepatic fibrosis, 405
hepatic infarction, 260 Lympholiferative disorders, 447, 447f
hepatic trauma, 262264 Lymphomas
hepatic veno-occlusive disease, 257 calcifications, 332f
hepatic vessel disorders, 249261 chest wall, 195
infections, 240244 cutaneous, 625f
mesenchymal hamartoma, 234237 GI tract, 348
metabolic diseases, 248 liver involvement, 232
neoplasms, 226240 mediastinum, 184f
benign, 232233 mesenteric, 331332, 331f
malignant, 226230 neck, 138139, 139f
nodular regenerative hyperplasia, paratesticular, 568
238239 renal involvement, 419420, 419f, 420f
normal anatomy, 214226 retroperitoneal lymphadenopathy, 500f
Doppler sonographic, 220222 small bowel, 365
fissures, 214215 spleen and, 317, 317f
hepatic artery, 219, 224 Lysosomal acid lipase deficiency, 477478
ligaments, 215
lobar, 214215
parenchyma, 224 M
portal veins, 220222 Macromastia, 203
segmental, 214215, 215f, 216f Magille syndromes, 294
vascular, 215218 Male genital tract, 554601. see also Specific
veins, 218, 220223 organs; Specific tissues
venous, 216f acute epididymitis, 580583
passive venous congestion, 261 edema, vasculitis and, 584
peliosis hepatis, 261 fluid collections, 587590
portal hypertension, 248, 252253 hydroceles, 587590
portal vein thrombosis, 255257 inflammatory diseases, 580583
portal venous gas, 261 inguinal hernias, 590591
posttransplantation lymphoproliferative penis, 594597
disorder, 231232 prostate, 594
radiation effects, 262 scrotal calcifications, 591593
scanning technique, 214 seminal vesicles, 594
sonographic artifacts, 224225 traumatic injuries, 584587
surgical portosystemic shunts, 253254 urethra, 594597
transjugular intrahepatic portosystemic shunts, varicocele, 590
254255 Malffucci syndrome, 619
transplantation, 475 Malignant invasive moles, 544
imaging guidelines, 264269 Mammary duct ectasia, 203204
Lower extremities. see also Leg Marfan disease, 493, 494495, 495f
anatomy Margins, of breast lesions, 203
arteries, 641f Mastitis, 206207, 206f
peripheral veins, 637 Mastoid fontanelle, 4344, 44f, 50f
sonographic techniques, 638 Maximum systolic velocity (PSV), 58, 387
Lckenschdel, 8687, 88f Mayer-Rokitansky-Kster-Hauser syndrome,
Lumbar punctures, 669f, 697, 697f 536537, 537f
Lumbosacral cutaneous stigmata, 656 Mayer-Rokitansky-Kster syndrome, 541
Lung McCune-Albright syndrome, 157, 547, 549
abscess, 176177, 177f Meckel diverticulum, 358f, 372f, 373
congenital anomalies, 177182 Meckel-Gruber syndrome, 85, 92, 246
necrosis, 176177 Meckel syndrome, 410
pleural mass biopsy, 685f Meconium ileus, 351352, 351f
primary neoplasms, 182183 Meconium periorchitis, 593, 593f
Lupus erythematosus, 156, 304 Meconium peritonitis, 352, 352f
Lymph nodes Meconium pseudocyst, 352, 352f
intramammary, 211 Mediastinal views, chest, 166f
retroperitoneal, 500501, 501f Mediastinum, 183, 184185, 184f, 185f
sonographic findings, 621f masses, 685686
Lymphadenitis, inflammatory, 141f normal anatomy, 183
Lymphadenopathy. see also Adenopathy Mediastinum testis, 555
cervical node enlargement, 143 Medullary carcinoma, 152
mesenteric, 366f Medullary cystic disease, 410f
retroperitoneal, 500f Medullary nephrocalcinosis, 437f
sonographic findings, 621 Medullary pyramids, kidney, 386
tumor spread and, 414 Medullary sponge kidney, 409, 410f
Lymphangiectasia, small bowel, 363, 364f Medullary tubular ectasia, 409
Lymphangiomas, 129130, 130f, 327328, 486, Medulloepitheliomas, 110
486f. see also Mesenteric cysts Mega-cisterna magna, 88, 90
chest wall, 193f Megacystitis, congenital, 451
cystic (see Multilocular cystic renal tumors) Megacystitis-megaureter syndrome, 451
description, 121 Megalencephaly, unilateral, 97
retroperitoneal, 501, 502503, 503f Megaureter, 395397, 397f, 398f
splenic, 314, 314f, 315f Meigs syndrome, 526
Lymphatic malformations Melanoma, metastatic, 212f, 231f
neck, 129136 Menetrier disease, 345, 345f
slow flow, 619 Meningiomas, in infants, 110
Lymphoceles, 444445, 590 Meningitis, 103106
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INDEX 719
bacterial, 105f, 106f Murphy sign, 285f, 286 Neu-Laxova syndrome, 97
sonographic findings Muscles Neural placode, 657
brain abscess, 106 herniated, 623, 623f Neural tube, 8592, 647
cerebral edema, 105, 105f injuries, 636 Neurenteric cysts, 650
cortical infarct, 106f Muscular dystrophy, 636 Neuroblastomas
extra-axial fluid, 104105 Musculoskeletal system, anatomy, 603605 adrenal, 465470, 469f
hydrocephalus and, 106 Mycobacterium avium intracellulare, 244, 319, cystic, 468f
vasculitis, 105f 428 description, 139140
venous thrombosis, 106 Mycobacterium tuberculosis, 142, 319 extra-adrenal, 467f
subdural effusion, 104f Myelocele, 649, 649f, 657658 hepatic, 226
subdural empyema, 104f Myelocystoceles, terminal, 659660, 660f intra-abdominal spread, 468470
Meningoceles, 658659, 659f Myelolipoma, adrenal, 473, 473f mediastinal, 186f
Meningococcus, 476 Myelomeningocele, 649, 649f, 657658, 658f mediastinal masses, 185
Meningoencephalitis, fetal, 102 Mylohyoid muscle, 120f metastatic, 231f, 568
Meningoencephalocele, 85 Myoblastoma tumors, 209210 ovarian metastases, 527
Meniscal cysts, 623 Myoclonic encephalopathy of infancy, 465 prognosis, 465466
Menkes syndrome, 449 Myofibroblastic tumors, 501 renal cell carcinoma and, 418
Menstrual cycle, 511513, 535f Myofibromatosis, gastric, 347 retroperitoneal, 501
6-mercaptopurine, 261 Myositis ossificans, 633 sonographic findings, 139f, 466, 468
Mesenchymal hamartoma, 195, 196f staging system, 465t
hepatic, 226, 234237 suprarenal, 466f, 467f
liver, 233237 N Neurofibromas, 122, 139140, 347, 487,
renal, 422423 Narcotics, for interventional procedures, 621622
solid, benign, 237f 676677 Neurofibromatosis, 432, 470471, 547, 621
Mesenteric adenitis, 365366 National Wilms Tumor Study Group Staging Neurogenic bladder, 451452, 452f
Mesenteric cysts, 327328, 328f, 329f System, 414t Neurogenic tumors, neck, 139140
Mesenteric lymphadenitis, 335, 335f Neck Neurulation, primary, 660662
Mesenteric lymphadenopathy, 366f benign noncystic masses, 136138 Neutropenic colitis, 375376
Mesentery, 323, 685f cervical adenitis, 141142 Neutropenic typhlitis, 375
Mesoblastic nephroma, 422423, 423f congenital masses, 129 Niemann-Pick disease, 248, 311, 321
Mesothelial cysts, hepatic, 240f cystic masses, 129 Nodular regenerative hyperplasia, 238239,
Mesothelioma, mesenchymal, 332 great vessels, 143144 239f
Metanephric adenomas, 424 inflammatory masses, 141143 Non-Hodgkin lymphoma, 138
Metastatic disease lymphatic malformations, 129136 abdominal, 365f
breast, 212 malignant masses, 138, 139141, 139f chest, 195f
in children, 140141 normal anatomy, 127129, 128f liver involvement, 232
malignant melanoma, 212f sonographic techniques, 127 lymphoma of testes and, 567568
peritoneal, 332333 thymic extension, 167f mesenteric, 331
pleural, 174f, 175 thyroglossal duct cysts, 132, 133f pancreatic, 486487
splenic, 317318 vascular lesions, 129 renal involvement, 419420
Methotrexate, 261 vascular malformations, 131132 splenic involvement, 317
Methysergide, 304 Necrotizing enterocolitis (NEC), 261, 261f, 374f, uterine, 544
Metopic synostosis, isolated, 111 583 Nonfamilial aniridia, 416
Microgastria, 341 Necrotizing fasciitis, 583, 627628 Noonan syndrome, 129, 549
Microlithiasis, testicular, 593594, 594f Necrotizing pneumonia, 176177 Norman-Roberts syndrome, 97
Midaortic syndrome, 432 Needle biopsies, 682f Notocord splitting, abnormal, 650f
Midazolam, 676 Needle guidance, 678680, 678f, 679f
Middle cerebral arteries, 55, 57f Needles
Midgut malrotation, 352355, 354f for aspiration and drainage, 686 O
Midgut volvulus, 355f echogenicity, 680f Obesity, cholesterol gallstones and, 281
Migrational defects, 85 selection of, 681682, 686 Oblique positioning artifacts, 681f
Milk of calcium bile, 285 Neisseria meningitidis, 475, 528, 580 Obliterative arachnoiditis, 67
Miller-Dieker syndrome, 97 Neonatal arterial occlusive disease, 7778 Occipital lobe, 46
Mineralizing vasculopathy, 103 Neonates. see also Infants, term; Occult spinal dysraphism, 656,
Mirizzi syndrome, 301 Premature infants 660666
Mirror-image artifacts functional ovarian cysts, 514516 Oligohydraminos, maternal, 401
carotid artery, 38f gallbladder size, 277 Omentum, 190, 323, 324f
internal mammary artery, 38f osteomyelitis and, 629630 Oral contraceptives, 261
pleura-lung interface, 21, 22f, 37, 168f sonography Oral-facial-digital syndrome, 408, 410
Mixed gonadal dysgenesis, 549 brain, 4344 Orchiopexy, 561562
Mononucleosis, 143 urinary tract anatomy, 385386, 385f Orchitis
Morgagni hernia, 188189, 190f spinal sonography, 650651 acute, 580583, 581f
Morison pouch, 325 spinal tumors, 666 acute scrotum and, 571
Moyamoya, 432 Neoplasms. see Specific neoplasms; Specific chronic, 583
Mucoepidermoid carcinomas, 122 organs; Specific tissues focal, 580, 581f
Mucopolysaccharidoses, 321 Nephroblastoma. see Wilms tumor primary, 583
Mucus retention cysts, 123124 Nephroblastomatosis, 417418, 417f, Organogenesis, stages of, 81
Mllerian ducts, 536, 537f, 538f, 594 418f Ortolani maneuver, 607
Multicystic dysplastic kidney, 411412, 412f Nephrocalcinosis, 437, 437f Osgood-Schlatter disease, 637
Multilocular cystic nephroma. see Multilocular Nephrogenic adenofibroma, 424 Ossifying renal tumor of infancy, 424,
cystic renal tumors Nephromegaly, 416417 424f
Multilocular cystic renal tumors, 412413, 413f Nephropathies, drug-induced, 442 Osteomyelitis, 195f, 629630, 630
Multinodular goiter, 157158, 158f Nephrostomy tube placement, 694 Osteosarcoma, 174f, 422
Multiplanar needle display, 678f Nephrotoxicity, drug-related, 442 Ovarian cyst, hemorrhagic, 10f
Multiple-element array transducers, 34, 310, 4f Nerve sheath tumors, 501f, 621622, 621f Ovaries
Multiple endocrine neoplasia (MEN), 152, Nerves, sonographic anatomy, 604 adnexal torsion, 530533
470471 Nesidioblastosis, 482 benign neoplasms, 519521, 522
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720 INDEX
Ovaries (continued)
cancer, 527
cystic teratoma, 520f, 521f
edema of, 533
malignant lesions
Doppler imaging, 527528
dysgerminoma, 523, 524f
ectodermal sinus tumor, 523, 525f, 526
epithelial cancer, 527f
germ cell tumors, 522526, 523t
granulosa cell tumors, 526
mixed germ cell tumors, 525f
Sertoli-Leydig tumors, 526, 527f
sex cordstromal tumors, 526527
teratomas, 523, 524f
neonatal, functional cysts, 515f
nonneoplastic lesions, 514517
normal anatomy
blood flow, 513514, 514f
sonogram, 510f
vasculature, 513f
phases, menstrual cycle, 511513
physiology, 511513
postmenarcheal
functional cysts, 516517, 516f
parovarian cysts, 518519, 518f
peritoneal inclusion cysts, 519, 519f
sonographic anatomy, 511, 512f
theca lutein cysts, 517518
volume, 511, 511t
prepubertal, 510511, 511f, 511t
secondary neoplasms, 527
torsion, 532f
P Parovarian cysts, 518519, 518f
P fimbriae, 425
Pampiniform plexus, 556
Pancreas, 478491. see also Pancreatitis
acute pancreatitis, 488491, 489f
chronic pancreatitis, 490491, 491f
congenital anomalies, 480, 481
congenital systemic diseases
autosomal dominant polycystic disease, 482,
483f
congenital hyperinsulinism, 482483
cystic fibrosis, 481482
Johanson-Blizzard syndrome, 482
lipomatosis, 482
Shwachman-Diamond syndrome, 482
von Hippel-Lindau disease, 482
cystic masses, congenital, 487, 487f
embryology, 480
endocrine tumors, 485, 485f
exocrine tumors, 483485, 484f
islet cell carcinoma, 230
metastatic lesions, 488
necrosis, 490f
nonepithelial neoplasms, 486487, 486f
normal gross anatomy, 478, 478f
pediatric, 479f
pseudocyst formation, 489490
scanning technique, 478
sonographic anatomy, 478480
artifacts, 480
dimensions, 479480
pancreatic duct, 479
pancreatic echotexture, 478479, 479f
pitfalls, 480
Pancreatic duct, normal, 479f, 480f
Pancreatic fluid drainage, 692
Pancreaticobiliary ductal anomalies, 490
Pancreaticoblastoma, 483, 484f
Pancreatitis
acute, 488491, 488f
autoimmune, 490491
chronic, 490491, 491f
splenic involvement, 319320 occlusion, 641642
traumatic, 491 sonographic technique, 641
Papillary epithelial neoplasms, 484f stenosis, 641642
Papillary process, 224 Peripheral precocity, 547, 548f
Papillary thyroid carcinoma, 152, 153f Peripherally inserted central catheters (PICCs),
Papillomas, choroid plexus, 110 695
Paracentesis, 687f Peritoneal cavity, 323325, 326f
Paraneoplastic syndromes, 465 Peritoneal compartments, 324325
Paraneumonic effusion, 171 Peritoneal fluid pathways, 325, 325f, 326f
Parasternal views, chest, 165 Peritoneal inclusion cysts, 327, 519
Paratesticular dermoid, 570f Peritoneum, 226, 324f
Paratesticular tumors, malignant, 568569 Peritonitis, 325, 334335, 352, 352f, 369,
Parathyroid glands 370f
adenoma, 159, 159f Perivascular tissue vibration, 39f
function, 158 Periventricular halo, 46, 54f
hyperplasia, 159f Periventricular leukomalacia (PVL), 7375, 73f,
hyperthryoidism, 159 74f, 75f
indications for ultrasonography, 158159 Perlman syndrome, 413
normal anatomy, 158 Peroneal vein, 637
normal development, 158 Perrault syndrome, 549
parathyroid cysts, 159160 Peutz-Jeghers syndrome, 365, 563
Paraumbilical vein, recanalized, 250, 252f Phakomatoses, 8485
Paraurethral cysts, 546547, 547f Phased array transducers, 5f
Parenchyma, parasagittal scan, 49f Pheochromocytoma, 470471, 471f
Parenchymal disease, 175176 Phleboliths, 193
Parenchymal hemorrhage, 71, 72f Phlegmon, 360, 368
Parietal lobes, 46 Phrenic nerve injury, 190191
Parkes-Weber syndrome, 619 Phrygian cap, 277
Parotid gland Phyllodes tumor, breast, 211
bacterial infection, 124126, 126f Phytobezoar, 348
color flow sonography, 120f Piezoelectric crystals, 2
hemangiomas, 122f Pilonidal cyst, 662f
location, 119f Pilonidal sinus, 662, 662f
normal anatomy, 118120, 119f Placode, 657
Parotitis, acute bacterial, 124126, 125f, 126f Plagiocephaly, 111
Plasma cell granuloma, 346
Partial volume artifacts, 681f Pleomorphic adenomas, 122, 123f
Partially cystic kidney. see Multilocular cystic Pleural effusion
renal tumors aspiration of, 174f
Passive venous congestion, 261 chylous, 171
Patella, congenital anomalies, 616, 617f drainage, 693f
Patellar tendon, 604f, 605 exudates, 172f
Patent ductus venosus, 218f hemorrhagic, 171
Patient preparation, for procedures, 675 nonloculated, 173
Pavlik harness, 611 paraneumonic, 171
Peliosis, splenic, 313314 percutaneous drainage, 173
Peliosis hepatis, 261 quantification of fluid, 173, 173f
Pelvic inflammatory disease (PID), 528530, 528f sonography, indications, 171173
Pelvic kidney, 391f thoracocentesis, 692
Pelvicaliceal dilatation, 393 transudate, 172f
Pelviectasis, megaureter and, 395 Pleuralung interface, 166168, 167f, 168f
Pelvis Pleuropulmonary blastoma, 182183
female, 509553 Pneumocystis carnii, 244, 319, 428, 476
3-D untrasonography, 510 Pneumonia, necrotizing, 176177
Doppler imaging, 510 Pneumoperitoneum, 336
sonohysterography, 510 Pneumothorax, 175
transabdominal sonography, 509510 Poland syndrome, 203
transvaginal sonography, 509510 Polycystic ovarian disease, 548549, 548f
reverberation artifacts, 2627, 28f Polyembryoma, ovarian, 522
Penis, 594597, 596f Polymastia, 203
Penoscrotal hypospadias, 595f Polymicrogyria, 100
Pentobarbital, 676 Polyorchidism, 559560, 559f
Percutaneous biopsy, ultrasound-guided, 680686 Polyps
Percutaneous nephrostomy, 694, 695f gallbladder, 289f
Perfluoroctylbromide (PFOB), 19 gastric, 347
Periappendiceal abscess, 369f renal obstruction and, 405
Pericallosal artery, 57f small bowel, 365, 365f
Pericardial cysts, 187f Polysplenia, 308309, 309f
Perimysium, 603 Polysplenia syndromes, 496
Perinatal asphyxia, 59f, 77f Polytetrafluoroethylene (PTFE), 429
Perinephric fluid collections, 444445 Polythelia, 203
Perineum, Fournier gangrene, 583 Popliteal artery, anatomy, 640
Peripancreatic fluid, 489f Popliteal cysts, 622, 623f
Peripheral arteries Popliteal vein, 637
anatomy, 640641 Porencephaly, 102
normal appearance, 641 Port wine stains, 193
normal waveforms, 641f Portal hypertension, 252253
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INDEX 721
clinical signs, 248 Pyelonephrosis, 427, 428f Retinocerebellar angiomatosis, 84. see also Von
nonvascular findings, 252253 Pyeloplasty, dismembered, 395 Hippel-Lindau disease
sonographic findings, 248f, 249f Pylephlebitis, 370, 371f Retroaerolar cysts, 204205
types of shunts, 250f Pyloric atresia, 341 Retrocaval ureter, 405
Portal veins Pyloric muscle, thickened, 342 Retromandibular vein, 119
anatomy, 215, 218f, 220 Pyloric stenosis, 343f, 344f Retroperitoneal anatomy
blood flow, 223f Pyloromyotomy, 344 fibrosis, 304
cavernous transformation, 256f, 290f Pylorospasm, 344, 344f great vessels, 491492
fistula, 259f Pyomyositis, 628629, 629f hemorrhage, 503
intrahepatic, 219, 219f Pyosalpinx, 528, 528f muscles, normal, 499f
normal Doppler anatomy, 221f, 222f Pyourachus, 450451, 451f normal, 461
portal hypertension, 248 Pyrocele, scrotal, 583, 583f primary tumors, 501503
stenosis, 266f Retroperitoneal hemangioma, 667f
thrombosis, 255257, 255f, Retroperitoneal lymphadenopathy, 500f
265266 Q Reverberation artifacts, 2527, 26f, 27f,
Portal venous gas, 261, 268 Quadratus lumborum muscle, 498499 28f
Portosystemic shunts, 253 Quadriceps muscle, 605 Rhabdoid medullary tumors, 420421, 421f
Posterior fontanelle, 4344, 44f, 58 Quadrigeminal cistern, 46, 46f Rhabdomyolysis, 634
Posterior fossa, 46f, 50f Rhabdomyosarcoma
Posterior fossa vallecula, 55 abdominal, 333f
Posterior tibial artery, 640 R bladder wall, 453, 453f
Posteriorparaspinal approach, chest, 165 Radial artery, 9f, 640 cervical, 140f
Postsinusoidal hypertension, 256 Radiation exposure, 154, 262 chest wall, 195
Posttransplantation lymphoproliferative disorder, Ranulas, 123124, 124f color Doppler imaging, 624f
231232 Real-time compounding, 1213, 13f description, 140
Power mode Doppler, 15f, 1718, 55 Real-time imaging, 310, 1011 embryonal, 568
Precocious puberty, 547 Rectal duplication cyst, 377f gray-scale imaging, 624f
Pregnancy-related abnormalities, 544 Rectus femoris muscle, 636f hepatic, 230
Premature infants. see also Infants, term Rectus muscle, 24, 24f mesenchymal, 332
brain, 4951, 50f Red blood cells, 17 metastatic, 140f
fontanelle, 43 Reduction mammoplasty, 203 pancreatic, 487
intracranial hemorrhage, 6068 Reflection, causes of, 2 paratesticular, 569f
kidney, 386f Refraction artifacts, 2125, 24f porta hepaticus, 302f
subarachnoid spaces, 68f Rejection, 441442, 442f prostatic, 594, 595f
Prenatal hemorrhage, 72 Renal agenesis, 390391, 390f, 464f renal, 422
Prepatellar bursa, 606 Renal arteries retroperitoneal, 501
Primary aldosteronism, 473 infarction, 433434, 443 urinary bladder, 452
Primitive neuroectodermal tumors (PNET), 110, normal, 386387 vaginal, 544546, 545f
422, 487 stenosis, 432433, 432f, 433f, 443, 443f Rheumatoid arthritis, 156
Probst bundles, 90 thrombosis, 433434, 434f, 442, 443, Ribs, fractures, 197
Propofol, 676677 443f Riedel lobe, 225
Prostaglandin E, 345 Renal candidiasis, 428f Ring-down artifacts, 2728, 28f
Prostate gland, 448f, 450, 451, 594 Renal cell carcinoma, 418419, 419f Robert syndrome, 129
Proteus spp., 106, 425, 452 inferior vena cava extension of, 489f Rokitansky-Aschoff sinuses, 288
Proteus syndrome, 619 Renal cystic disease, 405413 Rotator cuff, 13f, 606f
Proximal femoral focal deficiency (PFFD), acquired, 411
613614, 613f, 614f bilateral, 405408, 406f, 407f, 408f,
Prune belly syndrome, 393, 403405, 404f 409410, 409f S
Pseudoaneurysms complications of, 411 Sacral dimples, 656, 662f
after renal transplants, 442, 444, 445f multisystem disorder-associated, 410f Sacrococcygeal teratomas, 664666
description, 642643, 642f unilateral, 411413, 412f benign, 666f, 667f
hepatic, 263 Renal dysplasia, 392, 392f classification of, 664, 665f
hepatic artery, 266 Renal fracture, 439f malignant, 665f, 666f
mycotic, 494f Renal hypoplasia, 391 Sagittal sinus, 8081
pancreatic, 490 Renal medullary carcinoma, 421422 Salivary glands
renal, 435, 435f Renal-retinal dysplasia, 408 acute infections, 124126
Pseudoangiomatous stromal hyperplasia (PASH), Renal transplantation, 440f benign epithelial neoplasms, 122
310, 310f allograft calcification, 447f calculi, 127
Pseudocysts, 489490, 489f biopsies, 683684, 683f infection/inflammation, 126127
Pseudohermaphrodites, 549 Doppler waveforms, 441f nonsuppurative viral inflammation,
Pseudomass, spinal cord, 654655 lymphocele, 444445 124126
Pseudomenbranous colitis, 375, 375f normal morphology, 440441, 440f sonographic findings, 118121
Pseudomonas aeruginosa, 425 parenchymal complications, 441442 Salmonella typhosa, 361
Pseudopapillary tumor, 484485 pathology, 441 Salt-wasting crisis, 476
Pseudosexual precocity, 547 perinephric fluid collections, 444445 Sarcoidosis, 143, 322
Psoas muscles, 498500, 500f posttransplant lymphoproliferative disease, Sarcomas
Puberty, disorders of, 547548 447f hepatic, 226
Pulsality artifacts, 37 vascular complications, 442 renal, 422
Pulsation artifact, liver, 39f vascular imaging, 440441 thyroid, 152
Pulsed Doppler, 16 Renal tubular acidosis (RTA), 437 Saw-tooth pattern, 60
aliasing, 36f Renal vein thrombosis, 435437, 436f, 437f, 442, Scaphocephaly, 111
peripheral arteries, 641f 444 Schistosomiasis, 243
Pyelocaliectasis, 394 Renal veins, normal anatomy, 387 Schizencephaly, 9899, 100f
Pyelonephritis Resistive index (RI), 58, 58t, 59 Schwann cells, 310
acute bacterial, 425, 425f, 426f arterial resistance and, 385 Schwannomas, 139140, 487, 621
chronic, 428429, 429f renal arteries, 388 Scimitar syndrome, 180, 182f
xanthogranulomatous, 429 testes, 558f Scrotal sonography, 554
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722 INDEX
Scrotoliths, 588f, 593f
Scrotum
abscesses, 583, 583f
acute swelling and pain, 571
cystic masses, 569570
extratesticular calcifications, 591594
Fournier gangrene, 583
idiopathic edema, 584f
with linear array transducer, 6f
normal anatomy, 554559, 555f
normal arterial anatomy, 556f
vascular anatomy, 555556
Sedation
discharge monitoring, 677
for interventional procedures, 675677
monitoring during, 677
parenteral drugs for, 676677
presedation preparation, 676
recovery from, 677
Sedatives, 676677
Segmental artery, 387f
Segmental omental infarction, 335, 335f
Seldinger technique, 687
Seminal vesicles, 448f, 594, 595f
Seminomas, 563, 565f
Septate uterus, 538f, 540, 540f
Septic arthritis, 624625, 625
Septic bursitis, 631
Septic shock, pyelonephrosis and, 427
Septo-optic dysplasia, 9697
Septum pellucidum, absent, 96f, 97, 97f
Sequenced array transducers, 47
Serratia marcescens, 106
Sertoli cell tumors, 563, 566f
Sertoli-Leydig tumors, 526, 527f
Sex cordstromal tumors, 526527
Sexually transmitted diseases, 528, 580
Shadowing, 3031
artifacts, 24
bezoar, 349f
gallstone, 31f
ligamentum teres and, 224
ligamentum venosum and, 224
partial, 32f
teratomas and, 519
testicular cysts, 26f
Shoulder, normal anatomy, 606
Shwachman-Diamond syndrome, 482
Sialadenitis, recurrent, 126
Sialolithiasis, 127, 127f
Sickle cell disease, 7980, 79f, 304, 320f
Side-lobe artifacts, 2830, 29f, 30f
Sinding-Larsen disease, 637
Sinus histiocytosis, 143
Sinus pericranii, 112, 112f
Sinus thrombosis, 80f
Situs inversus, 225, 225f, 310
Sjgren syndrome, 126127
Skeletal muscle
general sonographic anatomy, 603, 603f
heterotopic ossification, 633
Skin, 554, 603, 603f
Slice-thickness artifacts, 3133
Slipped capital femoral epiphysis, 636f
Small, round blue cell tumors, 332
Small bowel
benign masses, 364365
enteric duplication cysts, 364365
hemorrhage, 362363
intussusception, 355358, 356f, 357f, 358f
lymphoma, 365
malignant masses, 365
normal anatomy, 349350, 349f, 350f
obstruction, 350359, 359f
polyps, 365
scanning technique, 349350
wall thickening, 359364
Soft tissue
foreign bodies, 535f, 636
masses
abscesses, 628, 628f
chest wall, 191197, 195
congenital vascular lesions, 618620, 618f
hemangiomas, 618
imaging approach, 617618
malignant tumors, 624
vascular malformations, 618620
Soleus muscle, 606
Somatostatinoma, 485
Sonographic air bronchogram, 176, 176f
Sonographic fluid bronchogram, 176, 176f
Sonography equipment, 677678
Sound, propagation of, 2
Spectral Doppler imaging, 5560, 58f
Spermatic cord, 555556, 568, 571, 574f, 590
Spermatic fascia, 554555
Spermatoceles, 569570, 570f
Spina bifida aperta, 655, 656
Spinal canal tumors, 666668
Spinal cord
disruption, 668f
epidural fluid collection, 669f
normal longitudinal anatomy, 651f
normal motion, 655f
normal transverse anatomy, 652f
split cord malformation, 660661, 661f
traumatic injuries to, 668669
Spinal dysraphism, 655657, 658666
Spine
embryology, 647650, 648f, 649f
epidural veins, 650f
extradural tumors, 668f
normal anatomy, 651654
normal newborns, 650f
rod-related infections, 670f
sonographic technique, 650651
tumors, 666668
ultrasonography of, 647674
Spleen
accessory, 308, 308f
anatomic variants, 307
benign masses, 313f
congenital anomalies, 307308
function, 305
fungal abscess, 318319
gross anatomy, 305
hematomas, 322f
infarction, 308, 308f, 320f
lacerations, 322f
lengths by age, 307t
leukemic infiltration, 371f
malignant tumors, 317318
normal anatomy, 306f
pancreatitis and, 319320
pyogenic abscess, 318
sonographic anatomy, 305307
sonographic technique, 305
storage diseases, 321322
subcapsular hematoma, 323f
torsion, 307308
traumatic injury, 322323
wandering, 307308
Splenic artery, 221f
Splenic cysts, 311313, 312f
Splenic varices, 253f
Splenic vein, 252253, 319f, 320
Splenogonadal fusion, 570f
Splenomegaly, 310311, 311f
Splenorenal collateral pathway, 251, 252f
Splenorenal ligament, 306f, 307
Splenosis, 308
Split cord malformation, 660661, 661f
Split notocord syndrome, 660661
Squamosal sutures, 44
Squamous cell carcinomas, 123
Standard array transducers, 8f
Staphylococcus aureus
aortic aneurysms and, 493
bacteremia, 493
breast infections, 204
cellulitis and, 626627
cervical adenitis and, 141
chronic granulomatous disease and,
243
hepatic pyogenic abscess, 241, 241f
infectious tenosynovitis, 630631
osteomyelitis and, 629630
parotid infection, 126
pyomyositis and, 628629
septic arthritis and, 625
septic bursitis, 631
Staphylococus saprophyticus, 425
Stasis nephropathy, 430, 431f
Steatosis, hepatic, 244245
Stein-Leventhal syndrome, 548549
Stenosis, duodenal, 350351
Stensen duct, 118
Sternocleidomastoid muscle, 137, 137f
Stomach, 341
Storage diseases, splenic, 321322
Straight sinus, 55
Streptococcus spp., 126
-hemolytic, 630
group A, 141, 584, 625, 627
group B, 103, 625
S. pneumoniae, 103
S. pyrogenes, 626627, 630631
Stroke, 7778, 79
Stroke Prevention Trial in Sickle Cell Anemia
(STOP), 79
Stromal tumors, testicular, 563565
Sturge-Weber syndrome, 193, 470471
Subarachnoid fluid, 71f, 104105
Subarachnoid hemorrhage, 68, 71
Subarachnoid spaces, normal, 68f
Subclavian artery, 640
Subdeltoid bursa, 606
Subdiaphragmatic views, chest, 165
Subdural effusion, meningitis and, 104f
Subdural empyema, meningitis and, 104f
Subdural fluid, 71f
Subdural hematoma, infratentorial,
69f, 70t
Subdural hemorrhage, 6971, 71
Subependymal hamartomas, 85
Subependymal hemorrhage, 72
Subhyoid cysts, 133f
Sublingual glands, 119f, 121, 121f
Submandibular glands, 119f, 120121,
120f
Subscapularis muscle, 606
Subxiphoid views, chest, 165
Sunburst appearance, 91, 92
Superficial femoral artery, 640
Superior mesenteric artery (SMA), 353
Superior vena cava, stenosis, 187f
Supernumery nipple, 203
Supraclivicular views, chest, 164
Suprahyoid cysts, 133f
Supraspinatus muscle, 606
Suprasternal views, chest, 164165
Sutures
evaluation of, 111112
normal, 111f
Sylvian fissure, 49f, 99f
Synostosis, coronal sutures, 112f
Synovial sheaths, 603
Synovitis, 631, 632f
Syringomyelia, 668, 670
Syrnix, 671f
Systolic peak velocity increase, 4041
LWBK505-Ind_711_726.qxd 09/07/2010 06:58 PM Page 723 Aptara

INDEX 723
T intravaginal, 571573, 573f, 574f dimensions, 149t
T4 (thyroxine), 147, 149 partial, 575f, 576f, 577f dysgenesis, 148149
T3 (triodothyronine), 147, 149 types of, 571572, 572f dyshormonogenesis, 149
Takayasu aortitis, 493 tumors of, 562568 ectopic tissue, 149, 150f
Takayasu arteritis, 432 clinical staging, 563 elastography scan, 18f
Takayasu disease, 146, 146f metastases, 563 function, 147
Talipes equinovarus, 616617 primary testicular germ cell neoplasms, hemorrhagic cysts, 152
Tamoxifen, 203 562563 nodules, 18f, 149154
Tanner stages, 200201, 201f seminomas, 563 benign vs. malignant, 154, 154t
Tapeworm, 242 sonographic findings, 563 biopsies, 685
Temporal bone, 44, 58 stromal tumors, 563565 cancer and, 154
Tendon-joint inflammation, 631 teratomas, 563 malignant, 152154
Tendonitis, tenosynovitis and, 631 treatment options, 563 thyroid adenomas, 150151, 151f
Tendons, 603604, 604f, 636 undescended, 561562 normal anatomy, 147148, 147f, 148f
Tenosynovitis, tendonitis and, 631, 632f vascular anatomy, 558f normal development, 147
Teratocarcinomas, 563, 564f Testicles. see Testes simple cysts, 152
Teratomas, 563 Testicular appendages, 556f size of, 149t
atypical, 520f normal anatomy, 556, 578f thyroid cysts, 151152
cervical, 134 torsion of, 571, 577580, 579f, 580f ultrasonography, 148
composition of, 519 Testicular artery, 555556 Thyroid-stimulating hormone (TSH), 147
cystic, 519521, 520f, 521f Testicular veins, 556 Thyroiditis, 154157, 155f, 156f
description, 134 Tethered cord Thyrotoxicosis. see Graves disease
gastrointestinal tract, 346, 347f embryology of, 649650 Thyrotropin-releasing hormone (TRH), 147
in infants, 110 sonographic findings, 657 Tibia, fragmented tubercle, 637
location of, 110 Tethered cord syndrome, 656, 657f Tibial heminelia, 615616, 615f
mediastinal, 183184, 183f Thalamic pseudolesion, 55 Tight filum terminale syndrome, 662663, 663f
ovarian, 523, 524f, 532f Thalamostriate arteries, 57f Time-averaged mean of the maximum velocity
retroperitoneal, 501, 502, 502f Thalamostriate vessels, 57f (TAMMX), 7980
sonographic findings, 135f, 519, 520f, 563, Theca lutein cysts, 517518, 518f Time gain compensation, 2
565f Thelarche, 200, 203, 547 Tip of iceberg sign, 520f
Teres minor muscle, 606 6-thioguanine, 261 Tissue harmonic sonography, 1112, 384385
Teritenon, 603 Third-spacing, ascites and, 325 Tissue vibration artifacts, 3739
Terminal myelocystoceles, 659660, 660f Third ventricle TORCH complex, 102
Testes coronal scan, 46f Torcular herophili, 84f
abscesses, 582f dilated, 107f Torticollis, fibromatosis colli and, 138f
acoustic shadowing, 32f mastoid fontanelle scan, 49 Toxic synovitis, 625626
agenesis, 559 sagittal scan, 47 Toxoplasmosis, 103
congenital anomalies, 559562 scanning planes, 44f Trachea, 21, 23f, 168, 168f
agenesis, 559 Thoracic kidney, 391 Tracheobroncial tree, 188
cryptorchidism, 561562, 562f Thoracocentesis, 692 Transducers, 23, 677678
cystic dysplasia, 561, 561f Thorax, drainage procedures, 692693 for chest sonography, 164
ectopia, 560 Three-dimensional ultrasound artifacts, 40 contact scanning, 679f
lymphatic, 570571 Three-dimensional ultrasound imaging, 1315, mechanical, 3
polyorchidism, 559560, 559f 15f multiple-element array, 310
size asymmetry, 560 Three-dimensional volume probes, 810, 10f needle guide and, 678f
torsion, 559f Three-dot sign, 46 pressure from, 59f
with cyst, 26f Threshold artifacts, 41f selection of, 1013
cystic dysplasia, 561 Thrombosis. see also Specific vessels Transitional cell carcinoma, 452
detorsion, sonogram after, 575f acute, 639640 Transjugular intrahepatic portosystemic shunt
ectopia, 560 chronic, 640 (TIPS), 254255, 254f
fracture, 585, 586f portal vein, 255257 Transmediastinal arteries, 556
gray-scale imaging, 557f splenic vein, 320 Transmembrane conductance regulator (DFTR),
hematomas, 584, 585f Thrombus, echogenic, 144145 481
infarction, 576 Thymic cysts, 136, 136f Transmitters, 2
ischemia, 582f Thymic extension, 137, 167f Transplantation. see also Liver, transplantation;
lobulated, 560f Thymopharyngeal duct, 134 Renal transplantation
lymphoma of, 567568 Thymus allograft resection site, 265
microlithiasis, 593594, 594f ectopic, 136137, 137f bone marrow transplantation, 258f
migration, 561 herniated mediastinal, 138f complications after, 265268, 266f, 444447,
neoplasms, secondary, 567568, 568f mediastinal window, 166f 446f
normal anatomy, 554555 normal, 165, 183, 183f imaging guidelines, 264265
prepubertal, 558f cervical extension of, 137, 167f lymphoproliferative disorder after, 231232
reverberation artifacts, 27f sonographic appearance, 165166 preoperative evaluation, 264
rupture of, 585, 587, 587f Thyroglobulin (TG), 147 pseudoaneurysms after, 442
simple cysts, 570, 571f Thyroglossal duct, 147 rejection, biopsies for, 683684
size asymmetry, 560f cysts, 132, 133f surgical anatomy, 264
size of, 556 Thyroid adenomas, 150151 Transrectal probes, 10
sonographic anatomy, 557f Thyroid-binding globulin (TBG), 147 Transsternal views, chest, 165
tissue covering, 554559 Thyroid-binding preglobulin, 147 Transtemporal scanning, 44, 58f
torsion, 559f Thyroid cancer, 152154, 157 Transtesticular arteries, 556
bell clapper deformity, 572f Thyroid cysts, 151152 Transvaginal probes, 10, 10f
chronic, 576, 576f Thyroid gland Trapezoidal array, 6f, 7f
delayed, 573f, 575f diffuse disease, 154158 Traumatic injuries
diagnosis of, 573576 De Quervain thyroiditis, 154155 gallbladder injury, 290
Doppler sonogram, 575f Graves disease, 157 intramural hemorrhage, 362363
extravaginal, 576577, 577f, 578f multinodular goiter, 157158 liver, 262264
infarction and, 571580 suppurative thyroiditis, 154 peritoneal, 335336
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724 INDEX

Traumatic injuries (continued) refluxing, 398f Doppler imaging, 536

renal, 438440 retrocaval, 405 endometrial development, 535f
small bowel, 362363 strictures, 446f fetal, normal anatomy, 533534
splenic injury, 322323 types of valves, 401 fluid-filled, 23f
Triangular cord, 292 ureteral jets, 388 hypoplastic, 540
Tributary collaterals, 249, 250f Ureteral reimplantation, 429, 454 myometrial tumors, 542544, 544f
Trichobezoar, 348 Ureterectasis, megaureter and, 395 neonatal, normal anatomy, 533f
Tricuspid regurgitation, 223, 223f Uretereral jets, 388f normal anatomy, 536f
Triglycerides, 244 Ureterocele, 400, 401f physiology, 535536
Trigones, 46, 47f Urethra postmenarchal, 534f, 535536
Trigonocephaly, 111 fibroepithelial polyps, 594 pregnancy-related abnormalities, 544
Trisomy 13 syndrome, 110f, 129, foreign bodies, 596f prepubertal, 533535, 533f, 534t
408 normal anatomy, 448 pubertal, normal anatomy, 534535,
Trisomy 18 syndrome, 129 posterior urethral valve, 594, 596f 534t
Trisomy 21 syndrome, 129 scanning techniques, 448 tumors, 541544, 546
Trocar technique, 687, 690f sonographic findings, 594597 Uterus didelphys, 537539, 539f
Trophoblastic disease, 544 Urinary bladder Uterus duplex bicollis, 538f
TSC1 gene, 8485 augmentation, 449f, 452
TSC2 gene, 8485 benign lesions, 453, 453f
Tuberculosis, 142, 476 calculi, 452, 452f V
Tuberculous adenopathy, 142f congenital anomalies, 449450, 450f VACTERL syndrome, 654f
Tuberin, 85 congenital diverticula, 449f Vagina
Tuberous sclerosis cystitis, 454 anatomy, 536
genetics of, 8485 exstrophy, 452 congenital anomalies, 540, 541
hepatic cysts and, 239 malignant tumors, 452453 cysts, 546547
kidney, 410f neurogenic, 451452, 452f rhabdomyosarcoma, 545f
left sagittal scan, 85f normal, 448f tumors, 544546, 546f
origin of, 84 normal anatomy, 448 Vallecula, 56f
pheochromocytoma and, 470471 pathology, 449 Valsalva maneuver, 300, 591f
renal artery stenosis and, 432 rhabdomyosarcoma, 452, 453f Valvulae conniventes, 349
renal cell carcinoma in, 418 scanning techniques, 448 Vanillylmandelic acid (VMA), 465
renal lipomyolipoma and, 423 urethral polyps, 453454 Varicella zoster, 240
Tubo-ovarian complex, 529f, 530f volume of, 448 Varicoceles, 590, 591f
Tubular necrosis, 442 Urinary tract. see also Specific organs; Vas aberrans, 556
Tumor hyperemia, 565f Specific tissues Vascular access, 695696, 696f
Tunica albuginea, 555, 569f, 570 calcifications, 437438 Vascular occlusive disease, 7781
Tunica vaginalis, 554555, 570, 587 congenital hydronephros, 393 Vasculitis, 105, 105f, 571, 584
Turner syndrome, 549 extrarenal pelvis, 396f Vasculopathies, mineralizing, 103
cervical lymphangiomas and, 129 infections Vasoactive intestinal peptides (VIPs), 465,
Hashimoto thyroiditis and, 156 acute bacterial pyelonephritis, 425, 485
hepatic cysts and, 239 426f Vein of Galen, 55, 81, 82f, 83f, 85f
kidney, anechoic cysts, 410f chronic pyelonephritis, 428429, 429f Veins, normal compressibility, 638f
renal cysts and, 410 fungal, 427428, 428f Vendarterial cannulation, 7879
sonographic findings, 549f imaging guidelines, 425 Veno-occlusive disease, 257, 258f
Twinkle artifacts, 39, 40f pyelonephrosis, 427, 428f Venous malformations
Two-dimensional array transducers, 9f sonographic findings, 425426 neck, 131
Typhlitis, 378f xanthogranulomatous pyelonephritis, slow flow, 619
Tyrosinemia, 248 429 sonographic findings, 620f
juxtarenal processes, 438 Venous thrombosis, 8081. see also Deep vein
normal anatomy, 385386 thrombosis (DVT); Specific veins
U renal cystic disease, 405413 chronic, 145f
Ulcer disease, 345 renal transplant, 440447 clinical findings, 639
Ulcerative colitis, 375 sonography technique, 384385 intrathoracic vessels, 187, 187f
Ulnar artery, 640 term infants, 385386 meningitis and, 106
Umbilical artery catheters, 492f Urine pancreatic, 490
Umbilical vein, 263, 264f cortisol levels, 472 Ventricular shunts, 108f
Undifferentiated embryonal sarcoma, stasis, calculi and, 452 Ventricularis terminalis, 654655, 655f
230 Urinoma, 402, 403f, 445, 445f Ventriculomegaly, 107
Unicornuate uterus, 537, 538f Urolithiasis, 437, 438, 438f Ventriculoperitoneal shunts, 108f, 588f
Upper extremities Uterine artery, 513514 Vermian-cerebellar hypoplasia, 8790, 90f
anatomy, 637638 Uteropelvic junction (UPJ) obstruction, 392, 395f, Vertebral artery, 640
major veins, 637f 396f Vertebral body segmentation, 654f
peripheral arteries, 640641 Uterus Vesicoureteral reflux
sonographic techniques, 638 adenocarcinoma, 546 horseshoe kidney and, 392, 393f
Urachal anomalies, 450451, 450f, 451f congenital anomalies hydronephros and, 393, 397398
Uremic medullary cystic disease, 409 agenesis, 536537 megaureter and, 398f
Ureter arcuate uterus, 540 treatment procedures, 429, 429f
calculus, 405f bicornate uterus, 539540 Viral hepatititis, 240241
dilated, 395396 diethylstilbesterol exposure, 540 Voiding cystourethrogram (VCUG), 394
duplication, 399400, 399f, 400f embryology, 536 Volvulus, sonographic findings, 353354
ectopic, 400f hypoplasia, 536537 Von Hippel-Lindau disease
normal anatomy, 388 septate uterus, 538f, 540, 540f epididymal cystenadenomas in, 569
obstruction, 446447 unicornuate uterus, 537, 538f epididymal cysts, 569
polyps, 453454 uterus didelphys, 537539, 539f hepatic cysts and, 239
posterior urethral valves, 400403, 402f, uterus duplex bicollis, 538f, 539f pancreatic lesions, 482
403f uterus duplex unicollis, 538f pheochromocytoma and, 470471
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INDEX 725
renal cell carcinoma in, 418 Williams syndrome, 432, 437, 449 X
renal cysts and, 410 Wilms tumor, 413417, 414t Xanthogranulomatous disease, 476
Von Recklinghausen neurofibromatosis, 84. bilateral, 416f Xanthogranulomatous pyelonephritis, 429
see also Neurofibromatosis in children, 226 Xantomas, 122
cystic (see also Multilocular cystic renal
W tumors) Y
Walker-Warburg syndrome, 88, 97 pathology, 414 Yersinia enterocolitica, 335, 361, 362f, 365
Wall echo shadow (WES), 282, 282f sonographic features, 414, 415f, Yersinia pseudotuberculosis, 361
Warthin tumors, 122 416 Yolk sac tumors, 523, 562, 563, 564f
Wavelengths, ultrasound, 2 Wilson disease, 248
Weigert-Meyer rule, 399 Wolman disease, 477478 Z
Wharton duct, 120, 121 Wrist, 606, 686f Zellweger syndrome, 408, 410