Rad et al.

, J Spine Neurosurg 2013, 2:4

http://dx.doi.org/10.4172/2325-9701.1000119

Case Report

Journal of Spine &

Neurosurgery
a SciTechnol journal

A Case of Avascular Necrosis of

a Lumbar Vertebral Body after
Sport Injury
Mohamad Faraji Rad1*, Amirshahriar Ariamanesh1, Hamidreza
Eghbalee1 and Elnaz Farajirad1

Abstract
Avascular necrosis of vertebral body is not common. There are
some radiologic findings that imply avascular necrosis however
they are not characteristic. It is due to obliteration of blood supply
of bone after trauma and non traumatic events.
The accurate diagnosis is based on pathological examination of
the pathologic vertebra. Treatment is based on the neurological
symptoms and spinal stability. A case of avascular necrosis of
a vertebral body in a young man who had it after sport injury is
reported in this case study with the review of the progression of
disease and treatment plan.

months before worsening the pain showed no pathology (Figure

1). Lumbosacral MRI was not advised because the patient was
neurologically intact and plain X-Rays were normal .Evidences of
osteoporosis, fracture, infiltration or congenital abnormalities were
not observed.
A course of medical and physical therapy was prescribed. The
patient started to intake Ibuprofen 1200 mg and Baclofen 30 mg per
day for two weeks. Physiotherapy exercises were performed for two
weeks subsequently. During history taking, no risk factor including
malnutrition, malabsorption, drug intake, drug abuse and familial
diseases were observed. In general physical examination the only
symptom was chronic low back pain and neurological examination
was normal. Standard laboratory studies included a complete blood
count, electrolyte panel, glucose, and coagulation panel which were
found to be normal. The erythrocyte sedimentation rate (ESR) and
C-reactive protein (CRP) level were normal according to age and
gender of the patient (12 and negative respectively). Metabolic studies

Keywords
Avascular necrosis; Vertebral body; Sport

Introduction
Ischemic necrosis of bone like infarction in other organs is
because of significant reduction or obliteration of blood supply in
affected areas [1].
Vertebral osteonecrosis is a rare disease and is thought to be the
consequence of an insult to anterior segment of the vertebral body,
with either traumatic or non traumatic mechanism.
The first mechanism is called Kmmell disease and represents
delayed vertebral collapse after major trauma [2]. The second
mechanism involves repeated microtrabecular fractures in a vertebral
body that is weakened because of osteoporosis, replacement of marrow
by abnormal cells, or long-term administration of glucocorticoids
[3]. This case report is about an avascular necrosis of the 5th lumbar
vertebra after sport injury in a healthy young adult.

Figure 1: Initial antero-posterior and lateral lumbosacral radiographies of

the patient shows normal bone density without evidences of fracture or
abnormality.

Case Report
A healthy 29-year-old man with no previous problem referred
with severe low back pain after a sudden slip and fall in a soccer
match. He experienced such a severe back pain that could not drive
home that day. The pain subsided gradually but dull chronic low back
pain remained after a week.
The early lumbosacral radiographs which had been taken 4
*Corresponding author: Mohamad Faraji Rad, Mashad University of Medical
Sciences 48 Mollasadra 4 Ahmadabad BLVD Mashad 9176563378, Iran, E-mail:
farajirad@yahoo.com
Received: December 12, 2012 Accepted: August 29, 2013 Published:
Spetember 04, 2013

International Publisher of Science,

Technology and Medicine

Figure 2: Lateral Lumbosacral radiography of the patient after 4 months

shows collapse of the 5th lumbar vertebral.

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Citation: Rad MF, Ariamanesh A, Eghbalee H, Farajirad E (2013) A Case of Avascular Necrosis of a Lumbar Vertebral Body after Sport Injury. J Spine
Neurosurg 2:4.

doi:http://dx.doi.org/10.4172/2325-9701.1000119
included serum calcium (10.1 mg/dl), inorganic phosphate (3.9 mg/
dl) and 25-hydroxyvitamin D (49 ng/ml) which were normal. After
a period of nearly 4 months inspite of medical therapy (included
NSAIDs, rest and physical therapy) the patient still had low back pain
so another lumbosacral radiography was done.
The second lumbosacral imaging showed a collapsed L5 vertebra
(Figure 2). CT scan of the affected vertebra showed nonspecific areas
of sclerosis and lysis in the body of L5 vertebra (Figure 3). In MRI
examination no specific changes in soft tissue or thecal sac adjacent
to the collapsed vertebra was not found (Figure 4). Whole body bone
scan was negative for multiple or disseminated lesions (Figure 5).

Sections showed trabecular bone without osteocytes, and bone

marrow showed necrotic cells (Figure 8).

Discussion
As previously described, ischemic necrosis of bone like infarction
in other systems of body is because of a significant reduction or
obliteration of the blood supply in affected areas [1]. One of the
following phenomena can usually be proposed or inferred as an
impending blood flow:
(1) Intraluminal obstruction (e.g: thromboembolic disorders,
sludging of blood cells or stasis)

We decided to take a needle biopsy specimen from L5 vertebra.

Under GA and fluoroscopy guide from transcutaneus-transpedicular
approach, a specimen of L5 vertebral body was obtained (Figure 6).

(2) Vascular compression ( e.g: external mechanical pressure or

vasospasm)

The pathology report emphasized that the specimen is formed

from fibro- connective and osseous tissues without any remarkable
finding. Because of chronic low back pain and onset of paresthesias
in right lower limb, we decided to plan L5 corpectomy and fusion
procedure. In a transperitoneal approach, corpectomy of L5 vertebra
and L4-5, L5-S1 discectomy and fusion with IMPLANT lumbar
expandable cage were done (Figure 7). Anterior approach to address
the anterior pathology was offered to the patient. Iliac bone of the
patient was not used to avoid the graft site morbidity and also because
of the patient preference.

The production of ischemic injury or necrosis and the rapidity with

which cell death occurs depends on the sensitivity of the individual
cell type. It is generally believed that hematopoietic elements are the
first to undergo anoxic death (in 6 to 12 hours), followed by bone
cells (osteocytes, osteoblasts, and osteoblasts; in 12 to 48 hours) and,
subsequently, marrow fat cells (48 hours to 5 days) [5].

Pain and paresthesias subsided after procedure. Pathology report

was compatible with avascular necrosis of L5 vertebral body. Biopsy

(3) Physical disruption of the vessel (e.g: trauma). These factors

can act alone or in combination [4].

In 1891, Kmmel described a post traumatic osteitis in which

painful kyphosis developed in several patients after a symptom-free
period of months to years following an injury [6]. Subsequently,
Schmorl and Janghanns [7] provided pathological observations

Figure 3: CT scan of the lumbosacral area shows collapse and sclerosis of the 5th lumbar vertebral body without evidence of paraspinal mass. Posterior arc is
intact.

Figure 4: Lumbosacral MRI demonstrates signal change in the 5thlumbar vertebral body and vacuum cleft sign. Soft tissue is not involved and other vertebral
bodies have normal shape and signal intensity.

Volume 2 Issue 4 1000119

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Citation: Rad MF, Ariamanesh A, Eghbalee H, Farajirad E (2013) A Case of Avascular Necrosis of a Lumbar Vertebral Body after Sport Injury. J Spine
Neurosurg 2:4.

doi:http://dx.doi.org/10.4172/2325-9701.1000119
The traumatic event might be a minor injury, and osteoporosis is
not a consistent finding.
A single vertebra or more rarely multiple vertebrae are affected.
Aseptic necrosis begins as a painless bone abnormality and it can
remain painless. The involved bone often later becomes painful,
especially in activities.
In a new study vertebral bodies at T12 and L1 were most often
involved and together accounted for about two thirds of all affected
vertebral bodies [4].
Figure 5: Bone scan of the patient after vertebral collapse did not show
multiple lesions.

Conditions that are associated with aseptic necrosis include

alcoholism, cortisone medications, Cushings syndrome, radiation
exposure, Sickle cell disease, pancreatitis, gaucher disease, systemic
lupus erythematosus, and malignancy [9].
Clinical presentation is typically a middle aged man with backache
after trauma. Asymptomatic period is usually followed.
After weeks to months, osteonecrosis of the vertebral body
predictably causes a collapse and consequently severe pain. Then,
kyphotic deformity and neurologic symptoms may occur [10].
In this case, the patient had no risk factor for aseptic necrosis.
He was young and not osteoporotic. He experienced a mild to
moderate trauma and had pain from the beginning. The affected
vertebra was unusual site for traumatic osteonecrosis. According to
medical history and physical examination, the patient had no risk
factor for osteoporosis. The laboratory tests were normal and plain
radiographies did not suggest osteoporosis, so we did not perform
bone densitometry.

Figure 6: Needle biopsy of the 5th vertebrae was done to take a biopsy
specimen .Under fluoroscopy guide and prone position from transcutaneustranspedicular approach we obtained bone tissue.

MR imaging has been used to study the intravertebral vacuum

phenomenon [11]. In reported cases, decreased signal intensity in
the area of the vacuum cleft has been observed on T1- weighted spin
echo images and hyper intensity in this region (probably reflecting
the presence of fluids) has been evident on T2- weighted images [12].
However low signal intensity, probably related to the gas itself, may be
seen on T2 weighted images as well. The linear or band like pattern
of abnormal signal intensity assumes diagnostic importance [13].
Gas within a vertebral body is even not diagnostic for osteonecrosis,
osteoporotic fractures or neoplasm. We should differentiate between
spinal infection, degenerative cysts and Shmorls nodes.

Figure 7: Post operative lumbosacral imaging of the patient shows L5

corpectomy and anterior fusion .The operation performed via transperitoneal
approach with the assistance of general surgery team .The cage is in
appropriate location and spinal column maintained sagittal stability.

Collection of intravertebral fluid has been described in cases

of vertebral osteonecrosis, mainly on MR imaging [14]. In a study
vertebral collapse was significantly more severe in those having only
intravertebral air than in those having intravertebral fluid with or
without air.

supporting the concept of delayed post traumatic collapse of vertebral

bodies, although the nature of the underlying disease process was not
clear.
The prevalence of Kmmells disease is not known clearly,
although it is probably not uncommon. The patients are generally
middle aged or elderly men or women, the interval between
formations of collapse varies from days to years, and the lower
thoracic and upper lumbar vertebral bodies are principally involved.
Chronic back pain is a characteristic clinical finding [8].
Volume 2 Issue 4 1000119

Figure 8: Pathology exam is compatible with aseptic or ischemic vertebral

necrosis. X=400 .Section shows trabecular bone without osteocytes and
bone marrow shows necrotic cells.

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Citation: Rad MF, Ariamanesh A, Eghbalee H, Farajirad E (2013) A Case of Avascular Necrosis of a Lumbar Vertebral Body after Sport Injury. J Spine
Neurosurg 2:4.

doi:http://dx.doi.org/10.4172/2325-9701.1000119
Collapse was also significantly more severe when air was present
than when fluid was present [15]. In our case the MRI shows low
intensity signal in both T1 and T2- weighted images probably due to
air in the collapsed vertebrae.
Although relatively non-specific, a bone scan shows early
activity [16].
Kummells disease is a post traumatic vertebral fracture that is
initially asymptomatic and radiographically negative, but finally
vertebral body collapse occurs [17]. One way to establish the diagnosis
of avascular necrosis is performing spinal angiography.
Because of rare but significant side effects of angiography we
decided not to perform it. Only few reports are presented which
have done angiography [18]. Ideally Kummells disease is diagnosed
on the basis of repetitive plain x-rays, in which initial films do not
demonstrate evidence of a fracture [16].

2. Osterhouse MD, Kettner NW (2002) Delayed post traumatic vertebral collapse

with intravertebral vacuum cleft. J Manipulative Physiol Ther 25: 270-275.
3. Panow C, Valavanis A (2002) A case of aseptic vertebral necrosis in the
context of metastatic lumbar disease. Neuroradiology 44: 249-252.
4. Donald Resnick (2002) Diagnosis of Bone and joint Disorders (4thedn) WB
Saunders, Philadelphia.
5. Johnson LC (1964) Histogenesis of avascular necrosis. In Proceedings of
the conference on Aseptic Necrosis of the Femoral Head. St Louis, National
Institutes of Health, p 55.
6. Stojanovic J, Kovac V (1981) Diagnosis of ischemic vertebral collapse using
skeletal spinal angiography. RoFo 135: 326.
7. Schmorl G, Junghanns H (1971) The human spine in health and disease
(2ndedn). American Ed, Grune & Stratton, New York.
8. Huang SL, Shi W, He XJ (2009) Avascular necrosis of a vertebral body.
Chinese Journal of Traumatology 12: 125-128.
9. Prakash, Prabhu LV, Saralaya VV, Pai MM, Ranade AV, et al. (2007) Vertebral
body integrity: a review of various anatomical factors involved in the lumbar
region. Osteoporos Int 18: 891-903.

Differential diagnosis includes neoplasms, chronic steroid

administration, infection, osteoporosis, radiotherapy, intraosseous
disc prolapse, and arteriosclerosis or alcohol abuse. Medical
conditions such as pancreatitis, cirrhosis and Erdheim Chester disease
also should be considered. Most of these diagnoses could be ruled out
by careful history taking and physical examination. Disk herniation
can be investigated with MRI study. Infection is an important
differential diagnosis. It can be pyogenic or nonpyogenic (tubercular
or fungal). MRI characteristics of infection and enhancement can
help to differentiate infection from necrosis. Again physical exam
and laboratory tests can aid in diagnosis. Sometimes, advanced
spondylosis can be confused with osteonecrosis like malignancies
(eg: myeloma, lymphoma) and metastasis. A definitive diagnosis can
usually be established by needle biopsy in such cases.

10. Van Eenenaam DP, el-Khoury GY (1993) Delayed post-traumatic vertebral

collapse (Kmmells disease): case report with serial radiographs. Computed
tomographic scans and bone scans. Spine 18: 1236-1241.

Erdheim Chester disease should be included in the differential

diagnosis in patients with lytic lesions of the spine. It is a systemic
disease with a broad spectrum of clinical manifestations. Bilateral
and symmetrical long bone involvement is almost universal in
ECD patients. Bone pain is the most frequent symptom associated
with ECD and mainly affects the lower limbs, knees and ankles.
Involvement of the axial skeleton is rare, occurring almost exclusively
with osteosclerosis of the extremities [19,20].

16. Young WF, Brown D, Kendler A, Clements D (2002) Delayed post Traumatic
osteonecrosis of a vertebral body (Kmmells disease). Acta Orthop Belg 68:
13-19.

Infarcts, including those in bone, are three dimensional and can

be sub- divided into four zones:

20. Veyssier-Belot C, Cacoub P, Caparros-Lefebvre D, Wechsler J, Brun B, et al.

(1996) Erdheim-Chester disease: Clinical and radiologic characteristics of 59
cases. Medicine 75: 157-169.

A central zone of cell death surrounded by successive zones of

ischemic injury, active hyperemia and finally normal tissue [1].
Histopathology demonstrates spongiosa with multiple hemorrhages,
atrophy of the bony frame work, multiple microscopic fractures,
inflammatory changes and paravertebral fibrosis [10,16].

Conclusion
Avascular necrosis of a vertebral body without trauma is rare.
This may be attributed to a wedge vertebra that causes repeated
microtrauma and resulting in avascular necrosis on the adjacent
vertebra due to insufficient blood supply. Surgical treatment is
required in avascular necrosis of a vertebral body with progressive
collapse and neurologic compromise secondary to fracture of a
wedge-shaped vertebra at the lumbar region.
References

11. Chevalier X, Wrona N, Avouac B, Larget-Piet B (1991) Thigh Pain and

multiple vertebral osteonecroses: value of magentic resonance imaging. J
Rheumatol 18: 1627-1630.
12. Bhalla S, Reinus WR (1998) The linear intravertebral vacuum: A sign of
benign vertebral collapse. AJR Am J Roentgenol 170: 1563-1569.
13. Hashimoto K, Yousi N, Yamagishi M, Kojimoto H, Mizuno K, et al. (1989)
Intravertebral column clef in the fifth lumbar vertebra .Spine 14: 351-354.
14. Baur A, Stbler A, Arbogast S, Duerr HR, Bartl R, et al. (2002) Acute
Osteoporotic and Neoplastic vertebral compression fractures: fluid sign at
MR imaging. Radiology 225: 730-735.
15. Yu CW, Hsu CY, Shih TT, Chen BB, Fu CJ (2007) Vertebral Osteonecrosis;
MR Imaging Findings and Related charges on adjacent levels. AJNR Am J
Neuroradiol 28: 42-47.

17. Li H, Liang CZ, Chen QX (2012) Kmmells disease, an uncommon and

complicated spinal disorder: A review. J Int Med Res 40: 406-414.
18. Swartz K, Fee D (2008) Kmmells disease: a case report and literature
review. Spine 33: E152-E155.
19. Resnick D, Greenway G, Genant H, Brower A, Haghighi P, et al. (1982)
Erdheim-Chester disease. Radiology 142: 289-295.

Author Affiliation

Top

Department of Neurosurgery, Mashad University of Medical sciences,

Mashad, Iran

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Philadelphia.

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