Professional Documents
Culture Documents
NOTES IN NEUROANAESTHESIA
AND CRITICAL CARE
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Dedication
To our families whose understanding, patience and support has made this book possible.
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NOTES IN NEUROANAESTHESIA
AND CRITICAL CARE
Edited by
© 2001
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Contents
Contributors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ix
Preface . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiv
Abbreviations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xv
Anatomy
1. Anatomy of the brain and spinal cord . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1
C.Williams
2. Cerebral circulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
R. Burnstein
3. Anatomy of the posterior fossa . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
A. Swami
4. Nerves: anatomy and function . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
S. Gupta
Physiology
5. Cerebral blood flow . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 19
M. Prabhu,A.K. Gupta
6. Intracranial pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23
M. Prabhu,A.K. Gupta
7. Cerebrospinal fluid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 27
J. Coles
Pharmacology
8. Intravenous anaesthetic agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 31
J. Coles,A.K. Gupta
9. Inhalation anaesthetic agents . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 35
J. Coles,A. Summors
10. Opioids and adjuvant drugs . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 39
K. Grixti,A.K.Gupta
11. Anticonvulsants . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 43
J. Monteiro
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Neuroanaesthesia
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CONTENTS
Neurointensive care
35. Management of spinal cord injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 145
I. Ng, R. J. C. Laing
36. Glasgow Coma Scale . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149
A. Summors
37. Severe head injury: initial resuscitation and transfer . . . . . . . . . . . . . . . . . . . . . . . 151
B. Matta
38. Intensive care management of acute head injury . . . . . . . . . . . . . . . . . . . . . . . . . 155
D. K. Menon
39. Management of subarachnoid haemorrhage . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163
J. Ulatowski
40. Neuroprotection in ICU . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 169
A. Summors, P. Doyle,A. K. Gupta
41. Inotropes in neuro-critical care . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175
R. Shankar
42. Electrolyte disorders in the neurointensive care unit . . . . . . . . . . . . . . . . . . . . . . 179
J. Ulatowski
43. Fluid management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 183
J. Monteiro
44. Sedation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 187
J. Monteiro
45. Coagulation disorders . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 191
P. Doyle
46. Status epilepticus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195
N. Hirsch
47. Guillan-Barré syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 199
N. Hirsch
48. Tracheostomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203
Q. Milner
49. Brainstem death . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 207
Q. Milner
50. Nutrition in the neurocritical care unit . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
Q. Milner
51. Nursing issues . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 215
S. Rees-Pedlar, S.Walters
Monitoring
52. Intracranial pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 219
M. Czosnyka
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Miscellaneous
61. Anaesthesia and muscular dystrophy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 263
T. Leary
62. Myasthenia gravis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 267
S. Senthuran
63. Autonomic hyperreflexia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 271
T. Leary
64. Management of patients for multi-organ donation . . . . . . . . . . . . . . . . . . . . . . . 275
Q. Milner
65. Basic concepts of neuroimaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 279
J. H. Gillard
66. Neuroanaesthesia in pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285
P. Popham
67. Thrombolysis in acute stroke . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 289
A. Coles
Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 293
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Contributors
Marek Czosnyka
PhD Ken Grixti
Snr Research Scientist FRCA
University of Cambridge Specialist Registrar
Addenbrooke’s Hospital,
Patrick Doyle
Cambridge
Specialist Registrar
FRCA
Addenbrooke’s Hospital,
Cambridge Arun K. Gupta
MA FRCA
Cathy Duffy Director of Neuro-critical care
FRCA Associate Lecturer
Consultant Anaesthetist University of Cambridge
Addenbrooke’s Hospital, Addenbrooke’s Hospital,
Cambridge Cambridge
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CONTRIBUTORS
Andrew C. Summors
BSc FRCA Sally Walters
Formerly Specialist Registrar and Fellow in BSc
Neuroanaesthesia Senior Sister
Addenbrooke’s Hospital, Neurointensive Care
Cambridge Addenbrooke’s Hospital,
Cambridge
Consultant in Anaesthesia and Critical Care
Nevill Hall Hospital
Abergavenny
Wales Charles Williams
MD
Atul Swami Assistant Professor
MRCP FRCA Director of Neuroanesthesiology
Consultant Anaesthetist Medical College of Virginia,
Addenbrooke’s Hospital, Richmond, VA
Cambridge USA
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Preface
Anaesthetists in training are expected to acquire an that further detailed information can be found if
extensive knowledge of a number of diverse required. In this way we hope that that the book will
specialities in a short period of time. During their be a useful practical guide to clinical practice.
period of training in neuroanaesthesia and neuro-
Although this book is aimed at trainee anaesthetists
critical care, they are expected to remind themselves
preparing for their final FRCA exam, it may be of
of many basic principles including neuroanatomy,
value as a revision aid for all practising anaesthetists,
neurophysiology and pharmacology. In addition they
medical and nursing staff in Intensive Care Units,
need to understand new concepts to a sufficient
junior doctors in neurology and neurosurgery as well
depth to be able to apply them in the clinical setting.
as medical students. Staff in non-neurosurgical
In our experience, few trainees will contemplate centres who manage neurologically injured patients
reading a detailed textbook and we are frequently in their units or who have to transfer patients to other
asked to recommend a more appropriate text on the units will also find this book valuable.
subject. We therefore decided to collate short notes
Contributors have come from both trainee and
on specific topics in neuroanaesthesia and critical care
faculty grades in an attempt to convey the essential
for use by anaesthetists working toward their profes-
information as succinctly as possible. The key points
sional examinations and to stimulate discussion and
at the end of each chapter should help as a quick ‘aide
teaching between trainees and faculty. This book is a
memoire’.
compilation of these short notes.
The book is not intended to be a complete reference A. K. G.
text, of which there are many, but primarily to A. S.
provide essential information and key references so February 2001
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Acknowledgements
We are indebted to all our colleagues who have con- grateful to the authors, publishers and editors for
tributed their knowledge and expertise in preparing permission to reproduce or modify various tables and
this book, in particular Philip Ball, Senior Medical figures used.
Artist at Addenbrooke’s Hospital for his skill in
preparing many of the illustrations. We are also Cover image courtesy of Philips Medical System
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Abbreviations
xv
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1
ANATOMY OF THE BRAIN
AND SPINAL CORD
C. Williams
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2 ANATOMY
I Olfactory Smell
II Optic Vision
III Oculomotor Moves eyes, constricts
pupils, opens eyelids
IV Trochlear Moves eyes
V Trigeminal Sensory to face, chews
VI Abducens Moves eyes
VII Facial Motor to face, taste,
closes eyelids
VIII Vestibulocochlear Hears, regulates balance
IX Glossopharyngeal Swallows, sensory to
posterior pharynx,
controls salivation
X Vagus Sensory to airway and
abdominal viscera,
parasympathetic to heart
XI Accessory Lifts shoulders, rotates
head
XII Hypoglossal Motor to tongue
Figure 1.1 Anatomy of the brainstem
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4 ANATOMY
2
CEREBRAL CIRCULATION
R. Burnstein
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8 ANATOMY
(b)
A.C.A (A1)
A.Com.A.
I.C.A.
M.C.A.
P.Com.A.
P.C.A. P.C.A.
(P2) (P1)
S.C.A.
Basilar A.
Figure 2.1a & b (a) Anatomy of the Circle of Willis. The classic polygonal ring is found in less than 50% of brains. ICA, inter-
nal carotid artery, ACA, anterior cerebral artery, MCA, middle cerebral artery, PCA, posterior cerebral artery, ACoA, anterior
communicating artery, PCoA, posterior communicating artery, SCA, superior cerebellar artery. (b) Relationship of Circle of
Willis and branches to the base of the brain
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CEREBRAL CIRCULATION 9
The vertebral arteries arise from the subclavian arteries at cerebellar arteries. However, the presence of
the base of the neck. They fuse to form the basilar anatomical variations may substantially modify
artery at the level of the pontomedullary junction. patterns of infarction following large vessel occlusion.
The basilar artery lies on the ventral surface of the Figure 2.2 demonstrates the areas supplied by the
brainstem and supplies blood to the pons, midbrain cerebral arteries.
and cerebellum. At the level of the midbrain the
The majority of intracranial aneurysms may be found
artery bifurcates to form two large posterior cerebral
in the following sites:
arteries (PCAs), from which several small branches
arise including the small PCoAs. • Anterior communicating (25%);
• Internal carotid (22%);
The anastomoses between the internal carotid system
• Middle cerebral (25%);
and the vertebrobasilar systems form the Circle of
• Internal carotid bifurcation (4%);
Willis (Fig. 2.1). It is located in the interpenduncular
• Basilar bifurcation (7%).
cistern and encloses the optic chiasm, pituitary stalk
and mamillary bodies. The ‘classic’ polygonal anasto-
motic ring (Fig. 2.1a), however, is found in less than VENOUS DRAINAGE
50% of brains. The vessels of the Circle send branches
Venous drainage (Fig. 2.3) comprises a series of
supplying superficial tissue as well as long penetrating
external and internal veins, which drain into the
branches supplying deep grey matter structures.
venous sinuses. The venous sinuses are endothelialised
These deep penetrating branches are functional end
channels, continuous with the endothelial surface of
arteries and although there are anastomoses between
the veins, but which lie between folds of dura mater.
distal branches of cerebral and cerebellar arteries, the
They have no valves and their walls are devoid of
concept of boundary zone (i.e. watershed) ischaemia
muscular tissue. The sinuses drain into the internal
is important. Global cerebral ischaemia with systemic
jugular vein (IJV), which are continuous with the
hypotension (e.g. cardiac arrest), typically produces
sigmoid sinus at the jugular foramen. The IJV has a
lesions in areas where the zones of blood supply from
‘bulb’ at its upper end, which is an enlargement in the
two vessels meet – between the cortical areas of dis-
wall of the vein. At the level of the jugular bulb the
tribution of the ACA, MCA and PCA and between
IJVs receive minimal venous return from extracranial
the superior cerebellar and posterior inferior
tissue and measurement of oxygen saturation (SjvO2)
at this level can be used as a measure of cerebral oxy-
genation. Current evidence suggests that about 70%
of the flow to each vein are from ipsilateral tissue, 3%
from extracranial tissue and the remainder from the
contralateral hemisphere.
Many clinicians are concerned that internal jugular
central lines will impair venous drainage from the
Figure 2.2 Areas supplied by the cerebral arteries Figure 2.3 Venous drainage of the brain
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10 ANATOMY
brain and that this impairment may lead to increased The BBB maintains tight control of ionic distribution
bleeding into the surgical site or increased intracranial in the extracellular fluid of the brain. Four areas, the
pressure in the intact skull of a susceptible patient. circumventricular organs, which include the poste-
The evidence to support this as being clinically rior pituitary gland, lie outside the blood–brain
relevant is weak. barrier.
MICROCIRCULATION
The architecture of the cerebral microvasculature is KEY POINTS
highly organised. Pial vessels on the surface of the • The brain has the highest metabolic requirement
brain give rise to arterioles that penetrate the brain at of any organ.
right angles. These give rise to capillaries at all lami- • The arterial supply is from the carotid arteries and
nar levels. Each arteriole supplies a hexagonal column the vertebrobasilar system.
of tissue with overlapping boundary zones resulting • The arteries anatomose in the Circle of Willis.
in columnar patterns of local blood flow. This paral- • Venous drainage occurs through epithelialised
lels the columnar arrangement seen within neuronal venous sinuses draining into the internal jugular
groups and physiological functional units. Capillary veins.
density in the adult is related to the number of • The microcirculation is highly organised with
synapses and can be closely correlated with the capillary density correlated with functional activ-
regional level of oxidative metabolism. ity.
• The blood–brain barrier is maintained by the cap-
BLOOD–BRAIN BARRIER illary endothelium and is highly impermeable.
Endothelial cells in cerebral capillaries contain spe-
cialised tight junctions. As a result the cerebral capil- FURTHER READING
lary endothelium has a high electrical resistance and is
relatively impermeable. Passage of substances across Williams PL (ed). Gray’s Anatomy, 38th Edn. Edinburgh:
the intact blood–brain barrier (BBB) is predomi- Churchill Livingstone, 1995
nantly a function of lipid solubility and the presence Menon DK. Cerebral circulation. In: Cardiovascular
of active transport systems. physiology. London: BMJ Publishing Group, 1999
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3
ANATOMY OF THE
POSTERIOR FOSSA
A. Swami
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12 ANATOMY
Sella
Oculomotor
Nerve
Posterior
Clinoid Trigeminal
Process Nerve
Basilar
Artery Facial
Nerve
Vertebral
Artery Sigmoid
Sinus
Foramen
Magnum
Posterior
Fossa
Transverse
Tentorium Sinus
Cerebelli
Straight
Sinus
Anterior
Fossa
Posterior
fossa
Anterior and
middle fossa
ANATOMY OF THE P O S T E R I O R F O S S A 13
Inferior Colliculus
Cerebral Aqueduct
Anterior
medullary
Vellum
Fourth
Ventricle
Basilar Pons
Cerebellum
Pontine
Tegmentum
Medulla
fourth ventricle the pons contains the nuclei of CN V rootlets of the hypoglossal nerve and the upper
(sensory and motor), VI, VII and part of VIII. Blood rootlets of the first cervical nerve. It gives off the
supply is from the pontine branches of the basilar anterior spinal artery and the posterior inferior
artery. cerebellar artery and spirals up to meet its opposite
fellow at the lower border of the pons to form the
The medulla oblongata is piriform in shape and extends
basilar artery.
from the lower margin of the pons to a transverse
plane passing above the first pair of cervical nerves. It The basilar artery runs up the front of the pons and
contains the nuclei of CN IX, X, XI and XII. Blood ends at the upper border of the pons by branching on
supply anteriorly is via the vertebral and basilar arter- each side into superior cerebellar and posterior cere-
ies and laterally and posteriorly by posterior inferior bral arteries.
cerebellar arteries.
The fourth ventricle – the substance of the midbrain sur- The veins of the posterior fossa drain the cerebellum
rounds the cerebral aqueduct and the substance of the and brainstem. The major venous structures include:
lower medulla surrounds the central canal. Between 1. the venous sinuses (straight, lateral, occipital, supe-
the two, however, the substance of the pons and the rior petrosal, left and right transverse)
upper medulla lies anteriorly and the central canal is 2. great vein of Galen
expanded as the fourth ventricle. It is tent-shaped and 3. petrosal vein.
situated anterior to the cerebellum. It has three aper-
tures, one median (foramen of Magendie) and two The posterior fossa contains four foraminae:
lateral (foramina of Luschka) through which CSF
escapes from the ventricular system into subarachnoid 1. The foramen magnum contains the medulla oblon-
space for absorption by the arachnoid villi. gata, which becomes the spinal cord
2. The hypoglossal canal which contains CN XII
The arteries in the posterior cranial fossa comprise the
3. The jugular foramen contains the sigmoid sinus,
two vertebral and the basilar arteries with their
which becomes the internal jugular vein, CN IX,
branches (Fig. 3.1).
X, XI
The vertebral artery runs forward in front of the 4. The internal auditory meatus transmits CN VII, VIII
ligamentum denticulatum between the lower and the nervus intermedius.
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14 ANATOMY
4
NERVES: ANATOMY
AND FUNCTION
S. Gupta
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16 ANATOMY
INTRODUCTION
Neurones are the basic building blocks of the nervous
system and are involved in the integration and trans-
mission of nerve impulses. A typical motor neurone
and sensory neurone are shown in Figure 4.1 and 4.2
respectively. The axon acquires a sheath of myelin, a
protein-lipid complex made up of many layers of the
cell membranes of Schwann cells. In the CNS of
mammals, more neurones are myelinated, but the
cells that form the myelin are oligodendrocytes rather
than Schwann cells.
From the functional point of view the neurones gener-
ally have four important zones (Fig. 4.1).
1. A receptor or dendritic zone where multiple local
potential changes generated by the synaptic con-
nections are integrated.
2. A site where propagated action potentials are gen-
erated (the initial segment in the spinal motor
N E RV E S : A N A T O M Y A N D F U N C T I O N 17
Na+/K+ATPase and this maintains membrane polari- • The cell body maintains the functional and
sation. During maximal activity, the energy require- anatomical integrity of the neurone.
ment rate is doubled. • A neurone may be divided into four zones:
receptor zone, zone where conducted impulses
Nerve cells are stimulated by electrical, chemical and
originate, axonal zone and the nerve endings
mechanical stimuli. When an adequate stimulus is
where synaptic transmitters are released.
applied, the propagated nerve impulse is known as an
action potential which is normally conducted along
the axon to its termination. The action potential is an
‘all or none’ phenomena (Fig. 4.3). If the stimulus is
subthreshold in intensity, no action potential is gen-
erated. With adequate stimulus, the action potential
occurs with a constant amplitude and form regardless
of the strength of the stimulus.
Saltatory conduction occurs in faster conducting
myelinated nerves where depolarisation jumps from
one node of Ranvier to the next. Nerve fibres are
classified (see Table 4.1) depending on diameter and
conduction velocity. The relative susceptibility of
mammalian A, B and C nerve fibres to conduction
block produced by various agents is shown in Table
4.1.
KEY POINTS
• Neurones are the building blocks of the nervous
system. The motor and sensory neurones are dif- Figure 4.3 A typical action potential in a neurone
ferent as shown in Figures 4.1 and 4.2.
Table 4.1 Mammalian nerve fibre types and their susceptibility to conduction blockade
by hypoxia, pressure and local anaesthetics
A and B fibres are myelinated; C fibres are unmyelinated; LA = local anaesthetic; + = least susceptible;
++ = intermediate susceptibility; +++ = most susceptible
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18 ANATOMY
5
CEREBRAL BLOOD FLOW
20 PHYSIOLOGY
22 PHYSIOLOGY
6
INTRACRANIAL PRESSURE
24 PHYSIOLOGY
Intracranial pressure is the pressure inside the cranial in volume cause a slight rise in ICP. As volume
vault relative to atmospheric pressure. increases, there is a steady decline in compliance
which increases the ICP even more (point 3) until a
small rise in volume is associated with a marked rise
PATHOPHYSIOLOGY in ICP causing a fall in the perfusion pressure and
ultimately cerebral ischaemia (between points 3
The rigid cranium surrounding the brain creates a and 4).
unique protective space. As brain tissue is nearly
incompressible, any rise in pressure will cause CSF CSF
and blood to be expressed out of the cranium. Thus
change in volume of one compartment is accompa- The reduction of the volume from one compartment
nied by a reciprocal change in another compartment. as a result of an increase in another compartment is
known as ‘spatial compensation’. CSF plays the
The intracranial contents can be divided into four biggest role in spatial compensation. As a space-occu-
compartments: pying lesion expands, it will cause progressive reduc-
• Solid material ≈ 10%; tion of the CSF space (reduced size of the ventricles/
• Tissue water ≈ 75%; basal cisterns). Rapidly growing masses (e.g.
• CSF (150 ml) ≈ 10%; haematoma) exhaust spatial compensation quickly
• Blood (50–75 ml) ≈ 5%. resulting in a rapid rise of ICP.
INTRACRANIAL PRESSURE 25
intracranial volume will have a significant reduc- pineal gland, bony erosion and abnormal
tion in ICP in the presence of intracranial hyper- calcification may indicate chronic intracranial
tension because the system operates on the steep hypertension.
part of the pressure volume curve (see Fig. 6.1). 2. CT
• PaO2 – Cerebral vasodilatation occurs with • A CT scan may show a mass (e.g. haematoma
hypoxia resulting in a rise in CBV. There is or tumour), hydrocephalus or brain swelling.
evidence that hyperoxia causes vasoconstriction The signs of raised ICP include midline shift,
although there is no human evidence to suggest obliteration of the CSF cisterns around the
this is clinically significant. brainstem, effacement of the ventricles and
• Flow-metabolism coupling (see Chapter 5) – cortical sulci.
Increased metabolic demand increases CBF, CBV 3. MRI
and ICP. • MRI is useful in demonstrating midline and
• Autoregulation (see Chapter 5) – A fall in MAP can posterior fossa structures. MRI is more
lead to a decrease in cerebrovascular tone causing expensive, slower and requires more patient
cerebral vasodilatation and increase in CBV within cooperation.
limits.
7
CEREBROSPINAL FLUID
J. Coles
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28 PHYSIOLOGY
CEREBROSPINAL FLUID 29
cytes), and even one granulocyte is considered abnor- • Production and absorption can be affected by
mal. To the naked eye the normally clear CSF will many factors.
appear cloudy when there are greater than 200 white • Examination of CSF can aid in diagnosis of certain
blood cells per mm3 or 400 red blood cells per mm3. conditions.
The typical changes in CSF microscopy in meningi-
tis and neuromuscular conditions such as multiple
sclerosis are displayed in Table 7.2. FURTHER READING
In subarachnoid haemorrhage a yellow discoloura- Artu AA. Isoflurane does not increase the rate of CSF pro-
duction in the dog. Anesthesiology 1984; 60: 193–197
tion of CSF following centrifugation is a diagnostic
sign. This xanthochromia, appears several hours Artu AA. Effects of enflurane and isoflurane on resistance to
following an acute bleed and is due to haemolysis of reabsorption of cerebrospinal fluid in dogs. Anesthesiology
red blood cells. It is maximal at 1 week and usually 1984; 61: 529–533
disappears after 3 weeks. It can be distinguished from Artu AA. Propofol combined with halothane or with
a ‘bloody tap’, which does not clear as the CSF drains fentanyl/halothane does not alter the rate of CSF formation
from the puncture needle. A CT scan is the diag- or resistance to reabsorption of CSF in rabbits. Journal of
nostic tool of choice for identifying subarachnoid Neurosurgical Anesthesiology 1993; 5(4): 250–257
haemorrhage. Dougherty JM, Roth RM. Cerebral spinal fluid.
Emergency medicine clinics of North America 1986; 4(2):
281–297
KEY POINTS Kazemi H, Johnson DC. Regulation of cerebrospinal fluid
• CSF is an ultrafiltrate of plasma. acid-base balance. Physiological Reviews 1986; 66(4):
• Approx 150 ml circulates around the CNS in 953–1037
adults. Segal MB. Extracellular and cerebrospinal fluids. Journal of
• Normal pressure < 10 mmHg. Inherited Metabolic Disease 1993; 16: 617–638
Meningitis
CSF Normal Bacterial Viral Tuberculous Multiple sclerosis
8
INTRAVENOUS ANAESTHETIC
AGENTS
32 PHARMACOLOGY
Propofol provides smooth induction of anaesthesia Methohexitone has epileptogenic properties and may
with few excitatory side-effects. It produces a be useful for augmenting abnormal EEG activity dur-
progressive reduction in CBF coupled with global ing surgical treatment of focal epilepsy.
metabolic suppression with up to 60% reduction in
CMRO2. Intracranial pressure may be reduced, par-
ticularly in patients with an elevated baseline ICP. ETOMIDATE
However, it can cause a dose-dependent reduction in Etomidate depresses the cardiovascular system mini-
arterial pressure and compromise CPP. The respon- mally and is the agent of choice when preservation of
siveness of the cerebral circulation to CO2 and CPP is crucial. The effect on CMRO2 and CBF is
autoregulation is maintained with propofol. As well as similar to the barbiturates. It is a potent suppressant of
these beneficial effects on cerebral haemodynamics corticosteroid synthesis which is evident after one
propofol has free radical scavanging properties which induction dose. The clinical relevance of this is
are greater than thiopentone, and in vitro has calcium uncertain. Seizures can be elicited in susceptible
channel blocking and glutamate antagonist properties. patients with low-dose etomidate and it has been
The effects on the electroencephalogram (EEG) used to unmask seizure foci during operative EEG
include a dose-related suppression of activity in the b- mapping for epilepsy surgery.
frequency range and increases in the d range, followed The effects on the EEG are similar to those of the
by an isoelectric EEG. It is an anticonvulsant, however barbiturates although an isoelectric EEG may be pre-
seizure activity has been anecdotally reported. The ceded by intermittent spike activity which may be
effect on electrically stimulated motor evoked associated with myoclonus. Etomidate has minimal
potentials and somatosensory evoked potentials is dose- effects on evoked potentials and may increase
dependent and low dose infusions are useful during somatosensory evoked potentials.
procedures requiring intraoperative neurophysio-
logical monitoring. Propofol has been used successfully
for conscious sedation during awake craniotomy. KETAMINE
Ketamine increases global MAP, CBF and ICP with
BARBITURATES specific increases in regional CBF and CMRO2 in
limbic structures. These effects are partially reversible
Thiopentone is the only drug with evidence of protec- using induced hypocapnia and/or the administration
tion in focal ischaemia, and is also of proven cerebral of thiopentone or benzodiazepines.
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I N T R AV E N O U S A N A E S T H E T I C A G E N T S 33
Midazolam produces a dose-related increase in high Ravussin P, Tempelhoff R, Modica P, Bayer-Merger MM.
Propofol vs thiopental – isoflurane for neurosurgical anes-
amplitude EEG activity below 8 Hz. Burst suppres-
thesia: comparison of hemodynamics, CSF pressure and
sion does not occur, and the EEG does not appear to recovery. J Neurosurg Anesthesiol 1991; 3: 85
become isoelectric.
Todd MM, Warner DS, Sokoll MD, et al. A prospective com-
Prolonged sedation precludes these drugs as induc- parative trial of three anesthetics for elective supratentorial
tion agents for neuroanaesthesia, although the short craniotomy. Propofol/fentanyl, isoflurane/nitrous oxide and
acting drugs are appropriate as premedicant agents. fentanyl/nitrous oxide. Anesthesiology 1993; 78: 1005–1020
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9
INHALATIONAL
ANAESTHETIC AGENTS
J. Coles, A. Summors
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36 PHARMACOLOGY
GENERAL PRINCIPLES CMRO2 and CBF decreases in low doses and there is
greater cortical metabolic suppression than halothane.
All the fluorinated agents have effects on CBF, CBV At higher concentrations (≥ 2 MAC), an isoelectric
and CMRO2. EEG is achieved with a 50% decrease in CMRO2.
• CBF increases with all agents by a direct intrinsic Autoregulation is disrupted ≥ 1.5 MAC and a dose-
effect which reduces arterial wall tension and dependent rise in CBF and ICP occurs. These effects
results in cerebral vasodilatation. The magnitude can be attenuated by hypocapnia commenced when
of the increase in CBF depends on the balance isoflurane is introduced or modified by baseline phys-
between this intrinsic vasodilatory action and the iology and other pharmacological agents. Isoflurane
reduction in blood flow secondary to a dose- may decrease CSF production and decreases its resist-
related decrease in CMRO2. ance to absorption.
• The order of rise in CBF is approximately
halothane > enflurane > isoflurane ≥ sevoflurane.
Desflurane has similar effects to isoflurane. SEVOFLURANE
• CBV increases as a consequence of vasodilatation, Although similar to isoflurane in its cerebral vascular
which in turn increases brain volume and possibly effects in animals, there is some evidence to suggest
ICP. that it produces less intrinsic vasodilation of cerebral
• The gradient of the flow-metabolism coupling rela- vessels and allows cerebral autoregulation to occur at
tionship increases in clinically used doses (see Fig. higher anaesthetic concentrations compared with
9.1). These changes are attenuated by hypocapnia. other agents. Up to 1.5 MAC sevoflurane anaesthesia
• CO2 reduction attenuates the increase in CBF. causes little increase in ICP. The responsiveness of
The normal CO2 vs CBF curve is shifted to the CBF to changes in PaCO2 is also maintained. The
left. Hypercapnia causes a more rapid increase in lower blood:gas solubility coefficient (0.6) allows a
CBF with these agents. rapid induction and recovery from anaesthesia and
• Autoregulation of CBF is impaired in a dose- this combined with lower airway irritability has
dependent manner until CBF becomes dependent favoured its use for inhalation induction especially in
on mean arterial pressure. children. The EEG is activated in some animal mod-
• Progressive slowing of the EEG at concentrations els and decreased in others.
> 1 MAC.
HALOTHANE
ISOFLURANE
Halothane has a potent vasodilatory action and pro-
Isoflurane produces less cerebral vasodilatation than duces a dose-related decrease in CMRO2. However,
the other agents except possibly sevoflurane. Global the effect on CMRO2 is less than with other agents
and global CBF increases more than with equipotent
concentrations of other inhalational agents. Unlike
isoflurane, this rise in CBF can only be attenuated by
hypocapnia if induced before addition of halothane.
In concentrations above 2.5% there is evidence that it
may be directly toxic on oxidative phosphorylation.
DESFLURANE
Cerebral effects are similar to isoflurane with a dose-
dependent decrease in CMRO2, CBF and loss of
cerebral autoregulation. Under conditions of maxi-
mal metabolic suppression (high dose), intrinsic
vasodilatation is also similar to isoflurane. Again these
changes can be attenuated by hypocapnia induced at
Figure 9.1 Changes in gradient of flow-metabolism the time desflurane is commenced. During prolonged
coupling in an animal model exposed to 1 and 2 MAC isoflu- desflurane administration a slow increase in ICP is
rane. CMRGlu = cerebral metabolic rate of glucose reflecting
metabolic rate, CBF = cerebral blood flow. (Adapted from observed, possibly due to an increase in CSF produc-
Todd MM, Warner DS. Neuroanesthesia. In: Principles and tion. EEG burst suppression is attenuated over time
practice of anesthesia, 1993.) in some animal models.
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FURTHER READING
NITROUS OXIDE
Amorim P. Nitrous oxide in neuroanaesthesia: an appraisal.
N2O alone causes an increase in CBF without a Curr Opin Anaesthiol 1999; 12: 511–515
decrease in CMRO2 . This increase is unaffected by Artru AA, Lam AM, Johnson JO, Sperry RJ. Intracranial
hypocapnia alone but is modified when hypocapnia is pressure, middle cerebral artery flow velocity, and plasma
combined with other inhalational agents or barbitu- inorganic fluoride concentrations in neurosurgical patients
rates. This may be of concern in cerebral ischaemia receiving sevoflurane or isoflurane. Anesth Analg 1997; 85:
and should be used with care if ICP is raised. 587–592
Work in humans has shown N2O to cause a signifi- Gosslight K, Foster R, Colohan AR, Bedford RF.
cant increase in cerebral blood flow acting synergisti- Isoflurane for neuroanesthesia: risk factors for increase in
cally with inhalational agents. More importantly, the intracranial pressure. Anesthesiology 1985; 63: 533
increase in CBF due to a combination of isoflurane Matta BF, Heath KJ, Tipping K, Summors AC. Direct
and N2O is greater than equipotent concentrations of cerebral vasodilatory effects of sevoflurane and isoflurane.
the inhalational agent alone. Increases in ICP have Anesthesiology 1999; 91: 677–680
been demonstrated when N2O is used for patients Ostapkovich ND, Baker K, Fogarty-Mack P, Sisti M,
with intracranial tumours. However one study Young ML. Cerebral blood flow and CO2 reactivity is sim-
addressing short-term outcome found no difference ilar during remifentanyl/N2O and fentanyl/N2O anesthesia.
when N2O was used. Anesthesiology 1998; 89: 358–363
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10
OPIOIDS AND ADJUVANT
DRUGS
40 PHARMACOLOGY
11
ANTICONVULSANTS
J. Monteiro
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44 PHARMACOLOGY
MECHANISMS OF ANTICONVULSANT
ACTION DOSING SCHEDULES AND
SIDE-EFFECTS
The mechanisms of action of anticonvulsants can be
divided into three major categories: Usual daily doses and therapeutic serum concentra-
tions are shown in Table 11.2. Side-effect profiles of
1. Action on sodium channels Carbamazepine, the more common anticonvulsants are shown in
phenytoin, lamotrigine and valproate all limit Table 11.3. Dose regimes used in the management of
sustained repetitive neuronal firing by prolong- status epilepticus are outlined in Chapter 46.
ing the inactivation of sodium ion channels. Ventilatory support is usually required in status and
This reduces the ability of neurones to fire at drug dose can be titrated to desired effect on EEG.
high frequencies. The inactivated channel itself
remains open but is blocked by the inactivation
gate.
COMBINATION THERAPY
2. Action on GABAergic neurones
AND INTERACTIONS
a. Reduced GABA metabolism: Valproate, viga-
batrim and gabapentin all inhibit the enzyme Combinations of anticonvulsants are sometimes used
GABA transaminase responsible for GABA on the basis that therapeutic effects are additive while
metabolism. Increased levels of available individual toxicity is reduced. Toxicity, however, may
GABA result in hyperpolarisation of neurones. be enhanced with combination therapy. A second drug
A. Partial seizures
(confined to local areas of brain):
1. Simple partial (no Carbamazepine, phenytoin, Gabapentin, lamotrigine
alteration to consciousness) phenobarbitone
2. Complex partial As above
(altered consciousness)
3. Partial with secondarily Carbamazepine, phenytoin Primidone, valproate
generalised tonic clonic seizures
B. Generalised seizures
Absence seizure Ethosuximide, valproate Clonazepam, lamotrigine
Myoclonic atonic Valproate Clonazepam
Tonic clonic seizure (grand mal) Phenytoin, carbamazepine, Phenobarbitone, primidone
valproate
Status epilepticus Diazepam, phenytoin Phenobarbitone, thiopentone
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ANTICONVULSANTS 45
Table 11.2 Therapeutic serum levels and dosing schedules of common anticonvulsants
Therapeutic serum
Drug Dose in adults (mg) Dose in children (mg/kg) concentration (µg/ml)
12
CRANIOTOMY FOR SPACE
OCCUPYING LESIONS
C. Duffy
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48 NEUROANAESTHESIA
INTRAOPERATIVE MANAGEMENT
TUMOURS
The aims of anaesthetic management are:
Primary Lesions 1. Smooth induction.
Most primary lesions (55–60%) are supratentorial. 2. Haemodynamic stability (hypotension can lead to
Gliomas are the most common primary brain tumour ischaemia in areas of impaired autoregulation;
and range from relatively benign pilocytic and well- hypertension increases the risk of haemorrhage
differentiated astrocytomas to aggressive anaplastic and vasogenic oedema).
astrocytomas and glioblastoma multiforme. On CT 3. Relaxed brain (for optimal surgical access,
or MRI, malignant lesions have a contrast-enhancing decreasing the risks of retractor injury).
rim with surrounding oedema. Gliomas are treated 4. Cerebral protection if required.
with varying combinations of chemotherapy, radio- 5. Rapid and smooth emergence.
therapy and surgery.
Induction
Meningiomas are extraparenchymal lesions and may be
very vascular. The surgical goal is complete excision. Invasive blood pressure monitoring may be estab-
Colloid cysts of third ventricle usually present with lished prior to induction. Induction is performed
obstructive hydrocephalus. using an intravenous anaesthetic agent of choice
(Chapter 8), together with a non-depolarising muscle
Secondary Lesions relaxant and an opiate (fentanyl, alfentanil, sufentanil
and remifentanil have all been used successfully).
These comprise 40–45% of supratentorial tumours Normotension should be maintained by anticipating
arising mostly from the lung (50%) and breast (10%). stimuli and preventing haemodynamic responses.
Excision of solitary lesions is justified in those whose The hypertensive response to laryngoscopy and intu-
underlying disease is well controlled. Abscesses may bation can be obtunded with an additional bolus of
extend from local sinus or ear infections especially in intravenous induction agent, a short-acting opioid
immunocompromised patients, or are blood-borne in β-blocker or intravenous lidocaine.
those with right-to-left cardiac shunts and intra-
venous drug abusers. After induction, a nasopharyngeal temperature probe
and urinary catheter should be inserted. A central
venous line should be inserted if there is an indication
PREOPERATIVE MANAGEMENT (e.g. cardiorespiratory disease, anticipated blood loss).
A pulmonary artery catheter may be further required
Specific preoperative information to obtain includes
in severe cardiac disease. Further neuromonitoring,
an accurate assessment of the acute neurological con-
e.g. EEG, somatosensory evoked potentials (SSEPs)
dition together with preoperative Glasgow coma
and jugular bulb catheter (SjvO2) can also be estab-
scale (GCS), an examination of radiological images
lished if required.
and an evaluation of concurrent disease (e.g. under-
lying chronic respiratory disease in those with lung Insertion of skull-pin head-holder is a potent stimulus
metastases). Preoperative examination of CT and/or and the hypertensive response should be pre-empted
MRI scan provides information about lesion size, either by local anaesthetic infiltration, an additional
ease of surgical access, positioning of the patient and dose of induction agent or a supplemental dose of
indirect information regarding likelihood of blood opiate. A CSF drainage device may also be inserted
loss and ICP, remembering that patients may have prior to surgery.
raised ICP even if not evident clinically on CT or
MRI. Maintenance
Premedication is only given if the patient is particu- The patient’s head should be positioned so that
larly anxious, provided there is no evidence of venous drainage is not obstructed. The choice of
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13
CRANIOTOMY FOR
VASCULAR LESIONS
C. Duffy
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52 NEUROANAESTHESIA
CEREBRAL ANEURYSM
Table 13.1 Hunt and Hess classification
A cerebral aneurysm is a diverticulum arising from of intracranial aneurysms
vessels of the circle of Willis, usually at a bifurcation.
They occur in 2–5% of the population and are three Category Criteria
times as common in females as males. Over 90% of
0 Unruptured aneurysm
all aneurysms involve the anterior circulation and
about 10% involve the posterior circulation (see I Asymptomatic or minimal headache and
Chapter 2). slight nuchal rigidity
II Moderate to severe headache, nuchal
rigidity, ± cranial nerve palsy
PREDISPOSING FACTORS
III Drowsiness, confusion, or mild focal
Aneurysm formation is predisposed in hypertension, deficit
pregnancy and a number of genetic and collagen
abnormalities including those with a family history of IV Stupor, moderate to severe hemiparesis,
possibly early decerebrate rigidity and
cerebral aneurysm, coarctation of the aorta, fibro-
vegetative disturbances
muscular dysplasia, polycystic kidney disease and type
III collagen deficiency. V Deep coma, decerebrate rigidity,
moribund appearance
CLASSIFICATION
Hydrocephalus
Aneurysms are classified as small (< 12 mm diameter
– 78% of all aneurysms); large (12–24 mm – 20% of This may occur if blood enters the ventricles and
aneurysms) or giant (> 24 mm – 2% of aneurysms) obstructs the flow of CSF. Absence of CSF flow is
and most present as a haemorrhage into the subarach- associated with vasospasm (see below) and a further
noid space (SAH). disruption of the blood–brain barrier.
Re-bleeding
NATURAL HISTORY
Thirty per cent of ruptured cerebral aneurysms re-
The risk of rupture is estimated at 0.05–6%. Factors bleed within 2 weeks with half of these occurring
associated with an increased risk of rupture include: within the first 24 hours.
larger sized aneurysms, previous SAH, aneurysm
location (especially basilar tip aneurysms) and Cardiac Dysfunction
increased patient age. Rupture occurs more fre-
quently in the 40 to 60-year age group. When rup- This is frequently associated with SAH and probably
ture occurs, it is related to hypertensive episodes. In mediated by a variety of mechanisms including
the event of SAH, one-third of patients do not reach catecholamine release triggered by SAH, direct
hospital, one-third have a poor outcome and one- trauma to cerebral autonomic control mechanisms
third are functional survivors. The risk of periopera- and a hypothalamic neurogenic mechanism. This may
tive mortality increases with worsening neurological lead to hypertension, dysrhythmias (especially ventric-
grade at presentation (see below). ular ectopics that may progress to life-threatening
ventricular dysrhythmias) and pulmonary oedema.
PRESENTATION
Table 13.2 World Federation of
Subarachnoid Haemorrhage Neurological Surgeons (WFNS) SAH Scale
Headache is the presenting symptom in 85–95% of WFNS grade GCS score Motor deficit
patients. Other symptoms are brief loss of conscious-
ness, nausea, vomiting, photophobia or neurological I 15 Absent
deficits (see Tables 13.1 and 13.2). Bleeding increases II 14–13 Absent
ICP and leads to reduced CPP. The subsequent
III 14–13 Present
reduction in CBF stops bleeding. If CBF recovers,
reactive hyperaemia allows function to improve. IV 12–7 Present or absent
Non-survivors are those in whom CBF does not V 6–3 Present or absent
recover.
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54 NEUROANAESTHESIA
vessel or the anaesthetist may induce systemic and controlled pharmacologically if required.
hypotension using short-acting vasodilators or β- Hypertension is frequently seen as a response to restore
blockers. The minimum MAP to prevent ischaemia CPP and CBF. Systolic pressures over 240 mmHg
has never been established. (MAP > 150 mmHg) can lead to vasogenic oedema.
Temporary clips are applied more frequently and the
risk of ischaemia is high if occlusion is prolonged (>
10–15 minutes). Ideally, electrophysiological moni- ARTERIOVENOUS
toring should be used as a guide to the safe duration MALFORMATIONS
of temporary clipping. Use of pharmacological neu-
An arteriovenous malformation (AVM) is a congeni-
roprotection, e.g. bolus doses of intravenous anaes-
tal intraparenchymal cluster of arterial-venous com-
thetic agents together with hypothermia may allow
munications. Over 70–90% are supratentorial and
the safe duration of temporary clipping to be
10% are infratentorial with 10–15% involving the
extended but controlled trials are lacking. Induced
dura. They present usually at age 20–40 years.
hypertension at this time may help improve collateral
Untreated, the risk of haemorrhage is 1–3% per year
blood flow.
and the annual rate of death and disability is 4%.
Following permanent clip application, cerebral perfu-
The majority of patients (50–75%) present with
sion may be improved by allowing blood pressure to
intracerebral haemorrhage (ICH). Unlike aneurysms,
increase. This should be weighed against the potential
haemorrhage is not related to hypertension and is
for myocardial ischaemia. In the presence of known
usually venous in origin. Vasospasm and acute re-
unclipped aneurysms, normotension should be con-
bleeding tend not to occur.
tinued.
Other presenting symptoms include seizures,
migraine-like headaches and a steal syndrome mani-
MANAGEMENT OF INTRAOPERATIVE
festing as a progressive neurological deficit.
ANEURYSM RUPTURE
Surgical risk of AVM excision is graded according to
This may be suspected before aneurysm exposure by
size, anatomy of feeding arteries and venous drainage,
a Cushing’s reflex with hypertension ± bradycardia
and location and eloquence of adjacent brain areas.
and treatment is outlined in Table 13.3.
Other therapeutic options are considered if surgical
Controlled hypotension, to a MAP of 50 mmHg, is risk is high, i.e. endovascular embolisation or radio-
reserved for situations where intraoperative aneurysm surgery.
rupture has occurred and the rate of blood loss needs
to be slowed in order to achieve surgical control.
PATHOPHYSIOLOGY
AVMs are high-flow, low-resistance shunts and, if
POSTOPERATIVE MANAGEMENT
large, may steal normal perfusion from the surround-
A fast, smooth emergence enables early clinical assess- ing brain. Up to 10% are associated with aneurysms,
ment and a diagnostic CT or angiogram should be which probably develop because of increased flow
performed if the neurological assessment is not satis- through the AVM. These often resolve following
factory. Blood pressure should be closely monitored AVM resection.
100% inspired O2
Fluid resuscitation
Controlled hypotension: MAP of 50 mmHg reduces the rate of blood loss aiding surgical control. MAP is
normalised after bleeding is controlled.
Neuroprotection strategies: Boluses of thiopentone, etomidate or propofol to produce burst suppression or
an isoelectric EEG;
Mild hypothermia (35–36°C); Mannitol (0.25–1 g/kg) if significant brain
swelling;
For prolonged temporary clipping or uncontrolled bleeding: cool to 33°C and
commence infusions of thiopentone (1 g/h) or propofol (100–200 mg/h)
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14
POSTERIOR FOSSA SURGERY
C. Goldsack
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58 NEUROANAESTHESIA
KEY POINTS
• The conduct of anaesthesia is similar to supraten-
COMPLICATIONS torial surgery.
• The facial and peripheral nerves can be injured in
AIR EMBOLISM
the prone and lateral position.
See Chapter 15. • The sitting position has risks of venous air
embolism and cerebral ischaemia.
• Haemodynamic instability occurs if the brainstem
ARRHYTHMIAS is manipulated.
These are often due to manipulation of the brain- • Extubation should be delayed if there are concerns
stem. Bradycardia can occur when the periventricular of brainstem or cranial nerve injury.
grey matter and the reticular formation are stimu-
lated. Most arrhythmias occur during surgery near the
pons and the roots of nerves V, IX and X. Severe FURTHER READING
hypertension can result from stimulation of the Black S, Ockert DB, Oliver WC, et al. Outcome following
trigeminal nerve. posterior fossa craniectomy in the sitting or the horizontal
positions. Anesthesiology 1988; 69: 49
AIRWAY PROBLEMS McAlpine FS, Seckel BR. Complications of positioning.
The peripheral nervous system. In: Martin TJ (ed.)
Macroglossia and upper airway swelling can occur Positioning in anesthesia and surgery. Philadelphia: WB
following prolonged surgery in the prone position. Saunders, 1987
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60 NEUROANAESTHESIA
Marshall WK, Bedford RF, Miller ED. Cardiovascular Matjasko J, Petrozza P, Cohen M, et al. Anesthesia and
responses in the seated position–impact of four anesthetic surgery in the seated position: analysis of 554 cases.
techniques. Anesth Analg 1983; 62: 648 Neurosurgery 1985; 17: 695
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15
AIR EMBOLISM
C. Goldsack
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62 NEUROANAESTHESIA
INTRODUCTION Capnography
A vein cut during surgery will normally collapse, A continuous capnograph will show a fall in end-
which prevents air being sucked into the circulation. tidal carbon dioxide concentration as air enters the
In posterior fossa surgery cut veins may not collapse: pulmonary circulation. It is less sensitive than the
veins in the skull are held open by the surrounding Doppler but is much easier to use. However, other
bone, suboccipital veins are held open by cervical causes of a fall in end-tidal carbon dioxide ten-
fascia, and the large venous sinuses are held open by sions, such as reduced cardiac output can cause
the dura. Air can thus readily enter the circulation if confusion.
these veins are opened. The incidence of air
embolism is usually reported at between 25 and 40%. End-tidal Nitrogen
However, recent use of transoesophageal echocardio-
When air enters the pulmonary circulation there is a
graphy has reported an incidence as high as 75%. In
rise in end-tidal nitrogen, which mirrors the decrease
most cases the amount of air entering the circulation
in end-tidal carbon dioxide. However, nitrogen
is small and may have little clinical importance.
increase is more specific than end-tidal carbon
dioxide and is not influenced by other cardiovascular
PATHOPHYSIOLOGY changes.
Air enters the venous system if the cut vein is posi- Pulmonary Artery Pressure
tioned significantly above the level of the heart. It
enters the right side of the heart and reduces cardiac Air embolism will increase the pulmonary artery
output leading to systemic hypotension. Air also pressure proportionally to the size of the embolism.
passes into the pulmonary arterial circulation, leading
to a rise in pulmonary vascular resistance and an Pulse Oximetry
increase in pulmonary artery pressure. The ECG
Oximetry will detect air embolism in the way that
show signs of right ventricular strain and right ven-
capnography does but it is an indicator of the magni-
tricular failure may occur. Physiological dead space
tude of circulatory disturbance and provides an index
increases as air blocks the pulmonary circulation with
of the progress of treatment.
many alveoli ventilated but not perfused. This in turn
leads to a decrease in carbon dioxide excretion and a
fall in end-tidal carbon dioxide tension. Central Transoesophageal Echocardiography
venous pressure (CVP) will rise as a result of obstruc- A highly sensitive method of detecting intracardiac
tion to right ventricular outflow. This increase in air and of diagnosing atrial septal defects.
CVP together with arrhythmias and the classical mill-
wheel murmur on auscultation, however, are late
signs. PREVENTION OF AIR EMBOLISM
If the patient has a patent foramen ovale there is If N2O is used during anaesthesia when an air
potential for air to pass from the right atrium to the embolism occurs, then N2O will diffuse into the
left atrium and thus into the systemic arterial circula- embolic bubbles and increase their size. If there is a
tion. This leads to emboli in any organ but has most significant air embolism, N2O should be discontin-
serious consequences in the cerebral and coronary ued.
arteries.
Volume loading patients to raise their CVPs will
reduce the hydrostatic pressure gradient and reduce
DETECTION OF AIR EMBOLISM the likelihood of air embolism. Similarly, raising end-
expiratory pressure may reduce the negative pressure
Precordial Doppler Device in an open vein in the posterior fossa. However,
PEEP will reduce venous return and may cause sys-
The altered reflection of ultrasonic beams from an
temic hypotension.
air–gas interface means that precordial Doppler
probes can detect bubbles of air in the circulation and Anti-gravity suits and medical anti-shock trousers
can indicate air emboli as small as 1 ml; some critics help to reduce venous pooling in the lower limbs.
claim that the device is oversensitive. An experienced The increase in venous pressure reduces postural
observer is required. Diathermy machines will inter- hypotension and decreases the negative hydrostatic
fere with probe function. pressure in the posterior fossa.
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AIR EMBOLISM 63
A central venous catheter is a useful cardiovascular KEY POINTS
monitor and is a helpful diagnostic tool if air enters
the circulation. It also provides a useful method of • Venous air embolism is more common with open
attempting to aspirate air from the right atrium. skull veins, particularly in the posterior fossa.
• Intravascular air increases cardiac work and
reduces cardiac output and gas exchange.
MANAGEMENT OF AIR EMBOLISM • Reducing hydrostatic pressure differences in open
veins helps prevent air entry.
• Flood the operative field with saline and cover the
wound with wet swabs to prevent further air
entrainment. FURTHER READING
• Ventilate with 100% oxygen, discontinue N2O. Cucchiara RF, Black S, Steinkeler JA. Anaesthesia for
• Raise the venous pressure at the operative site, intracranial procedures. In: Barash P, Cullen B, Stoelting R
which can be done by squeezing the veins in the (eds) Clinical anesthesia. Philadelphia: JB Lippincott, 1989,
neck. p. 849
• Aspirate from the CVP catheter to try to aspirate Young ML, Smith DS, Murtagh F, et al. Comparison of
air from the right atrium. surgical and anesthetic complications in neurosurgical
• If cardiovascular collapse occurs, standard resusci- patients experiencing venous air embolism in the sitting
tative measures should be employed. position. Neurosurgery 1986; 18: 157
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16
ANAESTHESIA FOR
ACOUSTIC NEUROMAS
A. Swami
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66 NEUROANAESTHESIA
ACOUSTIC NEUROMA 67
17
EPILEPSY SURGERY
M. Smith
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70 NEUROANAESTHESIA
Epilepsy may be longstanding or develop de novo The pattern, type and frequency of seizures should be
secondary to another pathology (e.g. brain tumour). noted. Co-existing medical problems are frequently
Under normal circumstances electrical activity is well encountered. Anticonvulsant levels should be mea-
controlled within the brain, but in epileptic patients sured and attention given to the potential side-effects
regulatory functions are altered. A group of neurones of therapy. Drugs should be continued into the peri-
develop the capacity to produce spontaneous burst operative period and doses adjusted to ensure ade-
discharges which are recognised as inter-ictal spikes quate plasma levels.
on the EEG. Failure of normal inhibitory processes Premedication with a benzodiazepine is acceptable in
allows spread of these discharges to surrounding areas, most patients but should be avoided if intraoperative
resulting in uncontrolled neuronal firing and seizure recording of inter-ictal spike activity is planned. A
activity. Changes in membrane flux, impaired sympathetic visit from the anaesthetist reduces the
GABA-mediated synaptic inhibition and alterations need for pharmacological premedication under such
in local neurotransmitter levels are implicated in this circumstances.
process.
The epilepsies may usefully be classified into gener- INTRAOPERATIVE MANAGEMENT
alised and partial types (Table 17.1). Generalised
seizures involve both hemispheres and are charac- Specific requirements for the management of a
terised by an initial loss of consciousness. Partial patient undergoing epilepsy surgery include the
epilepsies occur when the initial discharge is limited recording of intraoperative cerebral electrical activity
to one area of the brain. Simple partial seizures are and/or activation of the epileptic focus. Knowledge
caused by a localised discharge and there is no impair- of the effects of anaesthetic agents on the EEG allows
ment of consciousness. In complex partial seizures the a rational choice of technique to be made (see
initial focal discharge spreads widely and secondary Chapter 58).
loss of consciousness occurs. This is the most com- Neurosurgery for medically intractable epilepsy may
mon seizure disorder and includes temporal lobe be carried out under general anaesthesia or with local
epilepsy. High quality MRI has demonstrated that a anaesthesia and sedation. General anaesthesia is pre-
ferred in the UK but in patients in whom resection
margins might impinge upon eloquent areas an
Table 17.1 Classification of the awake procedure is preferable (see Chapter 18). In
epilepsies some patients, it is necessary to map EEG spike activ-
ity intraoperatively, to allow mapping of the epileptic
Generalised epilepsy focus and aid planning of the surgical resection mar-
Generalised absence – petit mal gins. After dural opening, a small electrode grid is
Generalised tonic-clonic – grand mal
placed on the brain surface and allows the underlying
Myoclonic
Tonic/atonic – drop attacks cortical activity (the electrocorticogram – ECoG) to
be recorded.
Partial epilepsy
Complex partial – temporal lobe epilepsy The anaesthetic techniques employed during epilepsy
Simple partial surgery are similar to those for any intracranial proce-
dure with special attention given to the choice of
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EPILEPSY SURGERY 71
anaesthetic agent if intraoperative ECoG recording is
indicated. Careful titration of end-tidal concentration Table 17.2 Factors which predispose
of a volatile agent in combination with moderate to seizures
doses of a short-acting opioid allows a depth of anaes- Anaesthetic factors
thesia to be maintained which does not interfere with Proconvulsant anaesthetic agents (e.g. methohexi-
ECoG recording whilst minimising the risk of aware- tone, enflurane)
ness. Alternatively, anaesthesia may be maintained by Light anaesthesia
propofol infusion, although the effect on the ECoG is Hypocarbia/hypercarbia
not yet fully characterised. Neuromuscular blockade Hypoxaemia
should be maintained during the lighter stages of Metabolic factors
anaesthesia necessary for ECoG recording and moni- Hypoglycaemia
toring of neuromuscular function is essential because Hyponatraemia/hypernatraemia
of interactions between muscle relaxant and anticon- Hypocalcaemia
vulsants. Blood pressure may be controlled by incre- Hypomagnesaemia
mental opioid and labetolol infusion. In patients in Uraemia
whom intraoperative spike activity is not observed, it Neurosurgical
may be necessary for the anaesthetist to administer Mass lesion in ‘epileptogenic’ area
proconvulsant anaesthetic drugs. Small doses of Post-craniotomy haematoma
methohexitone, thiopentone, propofol, fentanyl and Head injury
alfentanil have all been successfully used for this pur- Previous uncontrolled epilepsy
pose.
Intraoperative seizures during general anaesthesia are
rare but may be masked by neuromuscular blockade.
Unexpected tachycardia, hypertension or increases in KEY POINTS
end-tidal CO2 are suspicious warning signs. ECoG • Side-effects/interactions and plasma levels of anti-
can confirm the diagnosis. An intravenous bolus of convulsant medication are important features.
propofol or thiopentone, followed by deepening of • Careful choice of anaesthetic agents will allow
anaesthesia is usually sufficient to bring seizures under intraoperative recording of spike activity.
control. • Risk of intraoperative and postoperative seizures.
18
AWAKE CRANIOTOMY
M. Smith
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74 NEUROANAESTHESIA
AWAKE CRANIOTOMY 75
trigeminal nerve and cervical plexus are blocked. lesions causing a mass effect, brain swelling can be
Although the skull has minimal sensation, raising the problematic.
craniotomy flap can be an unpleasant experience
because of noise from the power tools and incomplete POSTOPERATIVE CARE
anaesthesia. Sedation should therefore be continued
until the dura is exposed. At this stage the dura is anaes- This is determined by the neurosurgical procedure
thetised with plain lidocaine 1% by blocking the nerve and there are no special requirements from the anaes-
trunk which runs with the middle meningeal artery thetic technique itself. Patients are fully alert and
and providing a field block around the edges of the cooperative in the immediate postoperative period.
craniotomy. The sedation should then be discon- Adequate analgesia should be provided before the
tinued and the patient will rapidly regain conscious- effect of the local anaesthetic wears off.
ness and be able to participate in cortical stimulation
testing. Furthermore, during epilepsy surgery, the
EEG can be recorded awake without interference KEY POINTS
from anaesthetic agents (see Chapter 17). • Patient cooperation is essential.
Stimulation testing involves the application of a small • Airway control during sedation phase is required.
electrical current to the cortex adjacent to the area of • Sedation should continue until the dura is
surgical interest. The resulting motor and sensory exposed.
responses are used to map the cortical representation • Seizures may occur, particularly with cortical
in that area, thereby allowing the neurosurgeon to stimulation.
determine the safe limits of the surgical resection. • BP and PaCO2 control may be difficult.
Despite cortical testing, many neurosurgeons prefer • Patients are fully alert and cooperative in the
to complete the resection with the patient awake so immediate postoperative period.
that any infringement upon eloquent areas is immedi-
ately recognised. Following resection it is usually FURTHER READING
appropriate to re-sedate the patient during closure of
the craniotomy. Herrick IA, Craen RA, Gelb AW, et al. Propofol sedation
during awake craniotomy for seizures: electrocortico-
graphic and epileptogenic effects. Anesth Analg 1997; 84:
INTRAOPERATIVE PROBLEMS 1280
Huggins NJ. ‘Diprifusor’ for neurosurgical procedures.
Although airway management is generally unevent- Anaesthesia 1998; 53 (suppl 1): 13
ful, sedation carries the risk of airway obstruction and
apnoea. Facilities for emergency airway control Johnson KB, Egan TD. Remifentanil and propofol combi-
should be available. The possibility of seizures also nation for awake craniotomy: case report with pharmacoki-
exists, particularly during cortical stimulation. netic simulations. J Neurosurg Anesthesiol 1998; 10: 25
Seizures should be terminated rapidly and a small Manninen P, Contreras J. Anesthetic considerations for
bolus of propofol is usually adequate. The disadvan- craniotomy in awake patients. Int Anesthesiol Clin 1986;
tages of awake techniques include nausea, vomiting 24: 157
and difficulty in controlling blood pressure and Smith M. Anaesthesia for epilepsy surgery. In: Shorvon SD,
PaCO2. In patients undergoing epilepsy or functional Dreifuss FE, Fish DF, Thomas DGT (eds). The treatment
surgery this is rarely a problem but, in patients with of epilepsy. Oxford: Blackwell Scientific, 1996
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19
MICROVASCULAR
DECOMPRESSION
K. Grixti
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78 NEUROANAESTHESIA
MICROVASCULAR DECOMPRESSION 79
nerve function. In most cases the preoperative abnor- • Separating the vessel and root entry zone by
mality corrects itself during surgery, sometimes at the Teflon sponge is the most common surgical
opening of the dura but mostly during dissection of treatment.
the aberrant vessel. This gives a good indication of • Complications include immediate cranial nerve
the likelihood of success of surgery. neuropathies caused by surgical encroachment on
the brainstem and delayed neuropathy caused by
Facial electromyography is used intraoperatively
fibrosis around the sponge.
during CN VII decompression. This allows identifi-
• Anaesthesia is the same as for posterior fossa
cation of aberrant vessels and correlates well with the
surgery.
success of surgery. The lateral spread response in facial
• Electrophysiological monitoring can be used to
EMG (i.e. the antidromic impulse in one facial nerve
monitor surgical effectiveness and encroachment
branch generated in response to a stimulus in another
on neighbouring cranial nerves.
branch) resolves during decompression. Muscle
relaxants are either not used or the twitch height kept
at 30–40% of control. Caution must be exercised as
surgical stimulation of motor centres at the brainstem FURTHER READING
may cause facial and shoulder movements.
Brainstem auditory evoked potenials involve record- Gieger H, Naraghi R, Schobel HP, Frank H, Sterzel RB,
ings from scalp electrodes of the response to auditory Fahlbusch R. Decrease of blood pressure by ventro-
medullary decompression in essential hypertension. Lancet
clicks. An averaging technique involving over 2000
1988; 352: 446
clicks eliminates background electrical activity of the
scalp. This gives a typical 7 waveform response num- Mcaney JF, Eldridge PR, Dunn LT, Nixon TE,
bered from I to VII. Loss of amplitude of wave V is Whitehouse GT, Miles JB. Demonstration of neuro-
specific and has a high sensitivity in preventing vascular compression with MNR imaging. Comparison
surgical damage if measures to restore the wave are with surgical findings in 52 consecutive cases. J Neurosurg
taken promptly. Concomitant direct compound 1995; 83: 799
action potentials on the exposed VIIIth nerve can Resnick DK, Levy EI, Janetta PJ. Microvascular decom-
help differentiate between damage to the acoustic pression for paediatric onset trigeminal neuralgia.
nerve and cochlear nucleus. Neurosurgery 1998; 32: 804
Hatayan T, Moeller AR. Correlation between latency and
amplitude of peak V in the brain stem evoked potentials:
KEY POINTS intraoperative recording in microvascular decompression
• Microvascular decompression treats a range of cra- operation. Acta Neurosurg 1998; 140: 7
nial nerve neuropathies. Moeller AR, Janetta PJ. Monitoring facial EMG responses
• These are mainly due to atherosclerotic vessels during microvascular decompression operation for hemifa-
impinging on root entry zones in the brainstem. cial spasm. J Neurosurg 1987; 66: 681
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20
TRANSSPHENOIDAL
HYPOPHYSECTOMY
R. Erskine, A. Summors
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82 NEUROANAESTHESIA
INTRODUCTION PHYSIOLOGY
Tumours of the pituitary region are common, The gland has two distinct components. The anterior
accounting for 10–15% of intracranial neoplasms. An pituitary (adenohypophysis) releases hormones (Table
understanding of the anatomy, physiology and patho- 20.1) in pulsatile fashion that regulate growth and
physiology of the gland and its immediate relations is development, thyroid function, the adrenal cortex,
important in the management of patients for breast and gonads. The secretion of these hormones
transsphenoidal surgery. are directed by releasing hormones formed in the
hypothalamus and conveyed to the gland by the pitu-
itary portal vessels.
ANATOMY
The posterior pituitary (neurohypophysis) is responsible
The pituitary gland is situated in the upper aspect of for the release of vasopressin, oxytocin and antidi-
the body of the sphenoid bone within the sella tur- uretic hormone. These octapeptides are carried down
cica. The bony floor of the sella consists of the roof of to the pituitary from the hypothalamus in secretory
the sphenoid sinuses. The anterior tuberculum and granules along nervous tissue within the pituitary
the posterior dorsal wall are also sphenoid bone. stalk by an active transport mechanism.
Laterally on each side are the cavernous sinuses and
their contents, the cranial nerves and the ICA (the
PATHOPHYSIOLOGY
arteries may indent the gland on each side). The roof
of the sella (sella diaphragma) has dura mata attached Functioning tumours derived from the adenohypo-
to the anterior and posterior clinoid processes on each physis may secrete excess hormone to impinge on
side. The hypophyseal stalk acting as a conduit for anaesthetic management of the patient undergoing
nerves and the vessels of the portal system descending surgical resection. Excesses of adrenocorticotropic
from the hypothalamus, pierces this dura. A wide hormone (ACTH) and growth hormone (GH) only,
dural opening may lead to transmission of CSF present management problems (see below). Prolactin
pressure giving rise eventually to the empty sella hypersecretion is present in 60% of all cases due to the
syndrome. The optic nerves converge above the sella failure of the normal hypothalamic suppression of
to form the optic chiasm. prolactin secretion. Prolactinomas are usually first
Table 20.1 Hypothalamic release and inhibiting hormones controlling anterior pituitary
hormone release
ACTH Corticoliberin*
(corticotrophin releasing factor)
GH Somatoliberin*
(GH releasing factor) Somatostatin*
(GH release inhibiting hormone)
PRL Thyroliberin*
(thyrotropin releasing hormone) Prolactostatin*
(prolactin release inhibiting hormone)
TSH Thyroliberin* Somatostatin*
LH Folliberin*
(gonadotrophin releasing hormone)
FSH Folliberin*
MSH Melanoliberin* Melanostatin*
(melanotropin releasing hormone) (melanotropin release inhibiting hormone)
TRANSSPHENOIDAL HYPOPHYSECTOMY 83
treated medically with bromocriptine. Up to 30% of PITUITARY APOPLEXY
pituitary adenomas are endocrinologically silent and
present with symptoms secondary to mass effects Tumours of the pituitary may suddenly enlarge as a
(headache, visual field disturbance) or pituitary hypo- result of bleeding with consequent infarction and
function secondary to destruction of normal gland. necrosis of the tumour and possibly the whole pitu-
Parasellar tumours may also present this way. The itary. The signs are those of meningism with or
most common are craniopharyngiomas formed from without sudden blindness. SAH may be a feature.
the embryonic remains of Rathke’s pouch (the origin This constitutes a surgical emergency and surgery
of the anterior pituitary). Other tumours in this area must take place within hours. Patients should be sup-
include meningiomas and gliomas of the optic plemented with steroids intraoperatively. Panhypo-
chiasma. pituitarism may be a feature.
Increasing tumour pressure produces failure of
hormone secretion in a typical order, i.e. gonado-
DIABETES INSIPIDUS
trophins first, followed by GH, ACTH and thyroid-
stimulating hormone (TSH). A patient presenting for Diabetes insipidus (DI) may be a feature of patients
surgery with normal gonadal function will conse- presenting for transsphenoidal surgery. Polyuria results
quently not be deficient in any other pituitary from insufficient synthesis or release of antidiuretic
hormone. hormone (ADH). In addition, surgery in this region
often (in about 50% of cases) results in a temporary state
of DI postoperatively. Glucocorticoids and mineralo-
GH AND ACROMEGALY corticoids are necessary for the control of fluid balance.
DI may not manifest in anterior pituitary insufficiency
Acromegaly commonly gives rise to diabetes mellitus until the patient is supplemented with steroids. Section
and all patients exhibit an abnormal glucose toler- of the pituitary stalk produces temporary DI that resolves
ance. Hypertension and coronary artery disease is with time as ADH is released into the blood directly
usually present. Patients may present with a car- from the median eminence. In the postoperative period,
diomyopathy leading to cardiomegaly and failure. close attention should be paid to fluid balance and
The most notable changes are in the bones and soft osmolality. Supplementation with the synthetic ADH
tissues of the face with enlargement and thickening analogue Desmopressin (DDAVP) should be cautious
within these structures. Airway difficulties are pro- anticipating a return of endogenous ADH.
duced by an enlarged tongue and soft tissue hypertro-
phy within the pharynx. Narcolepsy and sleep apnoea
are common. The degree of airway compromise may PREOPERATIVE MANAGEMENT
require an awake fibreoptic intubation to avoid the Anaesthetic management of patients for trans-
need for tracheostomy. sphenoidal surgery is similar to transcranial surgery.
The patient should undergo appropriate preoperative
investigation and preparation, including baseline
endocrine function tests and investigation of anatom-
ACTH AND CUSHING’S ical manifestations (e.g. changes in airway). The pre-
DISEASE operative visit ascertains the general patient condition
with particular attention to anatomical or metabolic
Most of these tumours are ACTH-secreting
consequences of pituitary pathology. An enlarged
microadenomas (less than 10 mm diameter). Features
tongue in acromegaly may make intubation more
of the disease result from secondary adrenal hyper-
difficult. Any medical treatment is continued into the
plasia. These features are both physical and physio-
postoperative period. Assessment of the hypothalmic–
logical. Physical features include truncal obesity,
pituitary axis will establish the requirement for gluco-
osteoporosis and kyphosis (the so-called buffalo
corticoid replacement. Thyroid function should be
hump). Hypertension and glucose intolerance nearly
controlled and diabetes stabilised. Antibiotic prophy-
always features, although frank diabetes is unusual.
laxis is commonly given especially for at risk patients
Depression is also common. Patients may receive
(those with nasal or sinus infections, previous pituitary
metyrapone, a metabolic inhibitor of cortisol
surgery and Cushing’s syndrome).
synthesis prior to surgery. These patients need cortisol
supplementation perioperatively. Postoperatively a Explanations are given for mouthbreathing postoper-
synacthen test is performed to test for residual atively, intensive care admission, or awake fibreoptic
deficiency of cortisol response. intubation if required.
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84 NEUROANAESTHESIA
A short-acting benzodiazepine is sufficient for pre- At the end of surgery the nose is comprehensively
medication if required. packed to prevent bleeding and the patient is
woken ensuring the throat pack is removed. Fluid
balance is observed closely in the postoperative
INTRAOPERATIVE MANAGEMENT
period. Opioid analgesia may be required postoper-
The patient is positioned either supine with the head atively although care must be taken to avoid respi-
extended or semi-recumbent with the head slightly ratory depression.
to the right. The guiding C arm of the image intensi-
fier is positioned for a lateral view to guide the sur-
geon. The anaesthetist and their equipment are KEY POINTS
positioned along one side of the patient. • An understanding of the anatomy and patho-
Anaesthetic aims are a smooth induction, stable main- physiology of pituitary tumours is essential for
tenance and recovery with appropriate monitoring their management.
and fluid management with control of ICP but it is • Tumours may produce hormones or be non-
rare to have raised ICP without suprasellar extension. functioning and produce mass effects or destroy
Anaesthesia is routinely induced using an intravenous normal pituitary tissue.
induction agent, opioid analgesic and non-depolaris- • Excess GH or ACTH requires careful anaesthetic
ing muscle relaxant of choice. Invasive arterial moni- management.
toring is recommended. An oral armoured • DI may be a significant problem in the periopera-
endotracheal tube is taped securely out of the left-hand tive period.
side of the mouth and a throat pack inserted.
Good venous access is important. Bleeding is usually FURTHER READING
minimal but when it occurs, it may be catastrophic. Matjasko MJ. Anesthetic considerations in patients with
Central venous access is not usually required unless endocrine disease. In: Cottrell JE, Smith DS (eds)
indicated for the patient’s medical condition. Anesthesia and neurosurgery. St Louis: Mosby, 1994, pp.
604–624
Maintenance of anaesthesia can be achieved with a
total intravenous technique or with inhalational Jewkes D. Anaesthesia for pituitary surgery. Curr Anaes
agents with or without N2O. Dissection and drilling Crit Care 1993; 4: 8–12
to the sella can be highly stimulating and an infusion Drury PL. Endocrinology. In: Kumar P, Clark (eds)
of remifentanil at this stage has proven helpful. Clinical medicine, 3rd Edn. London: Bailliére-Tindall,
Valsava manoeuvres on occasion may be required to 1994, pp. 769–824
prolapse the gland down, or check for leaks of CSF at Landolt AM, Schiller Z. Surgical technique: transsphe-
the end of surgery. A mean BP between 60 and 80 noidal approach. In: Landolt AM, Vance ML, Reilly PL
mmHg at the highest point of the skull maintains (eds) Pituitary adenomas. London: Churchill-Livingstone,
CPP and minimises blood in the surgical field. 1966, p. 315
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21
STEREOTACTIC SURGERY
A. Summors
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86 NEUROANAESTHESIA
STEREOTACTIC SURGERY 87
22
ANAESTHESIA FOR HEAD
INJURY
C. Duffy
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90 NEUROANAESTHESIA
ANAESTHESIA FOR H E A D I N J U R Y 91
(90%) are associated with skull fractures and due to be used in concentrations < 1 MAC, and nitrous
injury of the middle meningeal artery and there- oxide is best avoided. CMRO2 should be min-
fore affect the parietal and parieto-temporal areas. imised and an infusion of propofol is often useful.
The remainder is due to venous sinus laceration. The use of mild hypothermia (33–35°C) is con-
Underlying brain contusion is less common than troversial but frequently used.
with SDH. Outcome depends on the level of con-
sciousness at the time of surgery with mortality Normovolaemia, an appropriate haematocrit for the
approaching 20% if unconscious. patient’s age and underlying medical condition and a
5. Diffuse axonal injury (DAI) occurs in 50–60% of normal blood sugar should be maintained. Hypotonic
severe head injuries and is characterised by small and glucose-containing solutions should be avoided
bilateral non-haemorrhagic lesions affecting the and there is some evidence in favour of using hyper-
lobar white matter, corpus callosum and upper tonic solutions.
brainstem. They are classified as mild (coma for
6–24 hours), moderate (> 24 hours coma without
decerebrate posturing) and severe (> 24 hours COMPLICATIONS
coma with decerebrate posturing). Outcome is Up to 20% of patients with acute SDH develop sud-
usually poor with the mortality for severe DAI den and massive brain swelling at the time of clot
approaching 50%. removal. This should be treated with increased venti-
6. Traumatic arterial and venous injuries (e.g. dissection, lation (ensuring SjvO2 > 50%), diuretics (mannitol or
fistula formation, pseudoaneurysm) are diagnosed furosemide) and removal of CSF. Administration of
by angiography. These injuries may be associated thiopentone or propofol to achieve EEG burst sup-
with subarachnoid haemorrhage and secondary pression should be considered. Swollen brain tissue
vasospasm. may need to be retracted (leading to further injury) or
resected.
PREOPERATIVE MANAGEMENT Penetrating brain injuries may be associated with
profuse bleeding, usually from venous sinuses. Post-
History traumatic seizures occur in 15% of severe head
An accurate account of the acute injury is important injuries and are treated with phenytoin for up to 1
in assessment. Progressive loss of consciousness sug- week post-injury.
gests an expanding intracranial mass. If the patient has
been unconscious from the time of accident, DAI is POSTOPERATIVE MANAGEMENT
likely.
Continued sedation and ventilation with ICP mon-
itoring is required for low preoperative GCS and
Resuscitation
for multiple associated injuries. Extubated patients
The initial resuscitation and transfer is described in need to be monitored closely in a dependent set-
Chapter 37. ting for neurological deterioration. Postoperative
rises in ICP may be due to local swelling or devel-
opment of a new lesion and occurs more com-
INTRAOPERATIVE MANAGEMENT
monly following evacuation of intracerebral
Monitoring should include ECG, pulse oximetry, haematoma.
capnography, invasive pressure monitoring, arterial
blood gases, SjvO2, glucose, electrolytes, haematocrit
and coagulation. The aims of intraoperative manage- KEY POINTS
ment are similar to those for elective craniotomy
• Hypotension must be avoided by adequate fluid
(Chapter 12), with some notable additions:
resuscitation.
• Brain swelling is likely and a target CPP > 70 • Consider associated injuries. Chest injuries may
mmHg should be maintained. Commencement of cause hypoxia which must be avoided.
inotropes may be required. • A stable anaesthetic is required, with manipulation
• Hyperventilation below PaCO2 of 4 kPa should of intracranial physiology in order to maintain
be avoided and SjvO2 should remain above 50%. CPP > 70 mmHg.
Patients should be paralysed and have adequate • Neuroprotective strategies such as EEG burst sup-
analgesia. The choice of anaesthetic agent is not a pression with intravenous anaesthetic agents, may
crucial factor, although inhalational agents should be required.
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92 NEUROANAESTHESIA
• Postoperative high dependency or intensive care Gopinath SP, Robertson CS. Management of severe head
with ICP monitoring is essential. injury. In: Cottrell JE, Smith DS (eds) Anesthesia and neu-
rosurgery. St Louis: Mosby, 1994, pp. 661–684
FURTHER READING The Royal College of Surgeons of England. Report of the
working party on the management of patients with head
Polin RS, Shaffrey ME, Bogaev CA, et al. Decompressive
injuries. London: RCSE, 1999
bifrontal craniectomy in the treatment of severe refractory
posttraumatic cerebral edema. Neurosurgery 1997; 41: McGrath BJ, Matjasko J. Anaesthesia and head trauma.
84–94 New Horizons 1995; 3: 523–533
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23
COMPLEX CERVICAL SPINE
SURGERY
I. Calder
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94 NEUROANAESTHESIA
96 NEUROANAESTHESIA
24
FIBREOPTIC INTUBATION
I. Calder
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98 NEUROANAESTHESIA
ORIENTATION
IDENTIFICATION OF PATIENTS
REQUIRING FLEXIBLE The commonest cause of difficulty is that the endo-
scopist loses their orientation. If a television system
FIBREOPTIC INTUBATION is used it is essential to establish that the screen view
corresponds to the eyepiece view. It will be helpful
It is easy to identify patients that obviously require to know where the top, bottom and sides of the
fibreoptic intubation. Identifying the less obvious airway are to be found as the endoscope is
patient remains more of an art than a science. advanced, as identification of anatomy (particularly
abnormal anatomy) is then much more likely. Loss
of orientation is nearly always the result of failing to
RHEUMATOID ARTHRITIS identify the hard palate (nasal approach) or tongue
(oral approach). With the nasal approach, it is useful
Patients suffering from cervical rheumatoid disease are to identify the hard palate before entering the nostril. It
frequently difficult to laryngoscope directly. Glottic is sensible to examine both nostrils and choose the
involvement is common (patients will often admit to more patent. Once the palate is identified, it is sim-
intermittent hoarseness and stridor). Fibreoptic intuba- ple to follow it, turn over or under the soft palate
tion has been shown to reduce the incidence of post- (depending on the position of the endoscopist),
extubation stridor in these patients. enter the oro-pharynx and identify glottic struc-
tures. With an oral approach, the fibreoptic laryn-
goscope is kept in the midline with the tongue at
UNSTABLE CERVICAL SPINE the top or bottom of the field.
The advantage of fibreoptic intubation over direct
laryngoscopy with regards to neurological safety is VISION
unproven. No convincing report of cervical spinal
cord injury due to direct laryngoscopy has appeared. Adequate vision depends on an air space and minimal
However, the lack of published evidence of direct secretions. Provision of an air space and minimisation
laryngoscopy-induced cord injury can not be taken as of secretions are the objectives. An awake patient has
proof that the procedure is without hazard; difficult the most patent airway. Artificial airways such as the
direct laryngoscopy is hazardous for normal patients, Ovassapian or COPA can be helpful, whilst the LMA
and cervical disease should militate against any nearly always provides a satisfactory view.
24-GUPTA-24-cpp 6/2/01 11:56 am Page 99
FIBREOPTIC INTUBATION 99
The administration of drying agents is not usually glycopyrrolate should be given, preferably at least 30
necessary, but is essential if topical anaesthesia is to be minutes before the start. Lidocaine is relatively free
effective. Secretions can be ‘blown away’ by insuffla- from toxic complications when applied to the naso-
tion of oxygen through the suction channel, but rupture pharynx and glottis but is distinctly irritant. Minor
of the stomach has been reported. In the awake patient degrees of stridor are not uncommon and complete
asking for a deep breath is usually very helpful. The airway obstruction has been reported. Doses up to
LMA (or ILMA) is particularly useful when there are 10 mg/kg of lidocaine are acceptable, but hypo-
copious secretions, since they help to isolate the glottis tension is sometimes seen following intubation. The
from secretions. The suction channel in fibreoptic use of the oral route in awake patients is compli-
laryngoscopes is ineffective; a normal suction catheter cated by the gag reflex, which follows stimulation of
is better. the base of the tongue. Blockade of the lingual
branch of the glossopharyngeal nerve may partially
obtund this reflex, but needle insertion is difficult if
VENTILATION the patient cannot open their mouth adequately, as
is usual. Topical 10% lidocaine spray directed to the
Anxiety about ventilation of the anaesthetised patient distal paraglossal gutter may be more reliable than a
will distract the endoscopist. Relative inexperience in needle blockade of the nerve. The use of a dental
endoscopy (of both operator and assistants) should be prop is recommended if the oral route is used in an
regarded as reasons to consider an awake endoscopy. awake patient.
There are two options:
The nasal route avoids the gag reflex and provides a
1. Apnoea: The experienced endoscopist will be able better angle of attack. In preparation, 2% lidocaine
to intubate an apnoeic patient in much the same gel should be instilled into the nasal cavity, followed
time as is required with direct laryngoscopy. by 10% spray into the oropharynx. Vasoconstrictors
2. Ventilation systems: Artificial aids to ventilation in such as xylometazoline and phenylephrine or 4%
anaesthetised patients include special face masks, cocaine can also be used and endoscopy can begin
nasal airways, modified Guedel airways and the almost at once, since the passage of the endoscope
COPA. The LMA and ILMA provide the most is not painful. Topical anaesthesia of the glottis will
satisfactory solution to the problem of ventilation be partially achieved by the lidocaine already
during endoscopy. Ventilation of the patient’s administered. Further anaesthesia can be obtained
lungs can continue whilst the endoscope is by either a crico-thyroid injection or injection of
inserted through a bronchoscopic catheter lidocaine through the endoscope. The advantage of
mount. The endoscope is withdrawn when the a crico-thyroid injection is that the endoscopist can
operator is confident of entry to the trachea, the proceed immediately to enter the glottis once seen.
catheter mount is removed and the endoscope The disadvantage is that coughing at the time of
re-inserted. injection is sometimes florid. Injection of lidocaine
A crico-thyroid cannula can provide a means of through the suction port requires a skilled assistant.
ventilation, and be placed before induction of It is wise to practice this beforehand, or use an
anaesthesia. It is essential that intra-tracheal place- epidural catheter (end cut off) passed down the
ment is confirmed before insufflation with high suction channel, as a conduit. The injection need
airway pressures. not be accurate, 5 ml of 4% lidocaine in the direc-
tion of the glottis will be satisfactory. Vision is often
lost, but will be restored by asking the patient to
SUPPRESSION OF REFLEXES take deep breaths.
100 NEUROANAESTHESIA
there is an element of airway obstruction. This guidewire is introduced into the oral cavity through a
advice needs to be qualified, because in some cases crico-thyroid needle; the guidewire is then passed
of serious airway obstruction where direct laryn- through the endoscope’s suction channel (a 2 metre
goscopy is certain to be difficult and endoscopy is wire is required – a suitable retrograde kit is available
also difficult because of swelling and secretions, the from Cook™). The endoscope is advanced until the
endoscopist may only have one chance of seeing and entry point of the wire into the trachea is seen. The
entering the glottis. In such dire circumstances it wire is withdrawn through the mouth and the endo-
may be necessary to give intravenous anaesthesia and scope advanced further into the trachea.
suxamethonium as soon as the endoscope is in the
trachea.
TEACHING FIBREOPTIC
POSITION OF PATIENT AND INTUBATION
TELEVISION SCREEN
A television system is desirable, and it is difficult to
If a television is used it is helpful to position it so that sustain a training programme without one.
the endoscopist need not turn their head to see it.
The position of the endoscopist is generally at the It is important to ensure that ventilation of the
patient’s head in anaesthetised patients and beside the patient’s lungs is not interrupted whilst trainees
patient when the patient is awake. Awake patients become familiar with endoscopic appearances. The
feel less threatened if allowed to sit up. most satisfactory solution is to place a tracheal tube by
direct laryngoscopy in uncomplicated patients. The
pupil can then perform endoscopy in an unhurried
ROTATION fashion. The LMA is also useful in instruction, both
to allow endoscopic inspection of the glottis via the
Stiles et al published an account of 100 fibreoptic mask and to facilitate ventilation whilst nasendoscopy
intubations in 1972. They concluded that the best is performed. The mask can be removed after
tubes to use were flexible, reinforced, ‘armoured’ nasendoscopy to permit the endoscopist to see the
tubes and it was essential to rotate them constantly as glottis.
they were passed. This advice is still entirely correct.
It is particularly important to use this ‘drilling’ tech-
nique when attempting to pass tubes through the
nose or LMA. Failure to rotate is a very common KEY POINTS
cause of failure. If an armoured tube is not available,
it is useful to soften a plastic tube by warming in ster- • Identifying patients that require fibreoptic intuba-
ile water. It is foolish to attempt to pass tubes larger tion is sometimes difficult.
than 7.0 mm over a fibreoptic laryngoscope and it is • An awake endoscopy should be performed if there
rarely necessary to use a tube larger than 7.0 mm for is concern regarding ventilation during the
anaesthesia. Lubricating jelly on the endoscope or procedure.
tube should be used only at the moment of passing • Suppression of the cough reflex and sedation is
the tube. Jelly on the fingers seriously hampers the recommended.
operator’s ability to manipulate the endoscope and • It is important to rotate the tracheal tube over the
tube. The position of the tube should be checked endoscope during insertion.
both endoscopically and by ausculation. It is easy to
confuse the carina and the divisions of the right main
FURTHER READING
bronchus.
Caplan RA, Posner KL. Medical-Legal considerations: the
ASA closed claims project. In: Benumof JL (ed) Airway
RETROGRADE FIBREOPTIC management. New York: Mosby, 1996, pp. 944–955
INTUBATION Koh KF, Hare JD, Calder I. Small tubes revisited.
Anaesthesia 1998; 53: 46–49
Problems of swelling, distorted anatomy displacing Lechman MJ, Donahoo JS, MacVaugh H III. Endotracheal
the glottis from the midline and secretions can pre- intubation using percutaneous retrograde guide wire
vent successful endoscopy. Retrograde fibreoptic insertion followed by antegrade fiberoptic bronchoscopy.
intubation can be successful in these situations. A Crit Care Med 1986; 14: 589–590
24-GUPTA-24-cpp 6/2/01 11:56 am Page 101
25
THORACO-LUMBAR SURGERY
C. Williams
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104 NEUROANAESTHESIA
26
CAROTID ENDARTERECTOMY
A.K. Gupta
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108 NEUROANAESTHESIA
27
ANAESTHESIA FOR
INTERVENTIONAL
NEURORADIOLOGY
J. M. Turner
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112 NEUROANAESTHESIA
28
ANAESTHESIA AND
SEDATION FOR MAGNETIC
RESONANCE IMAGING
D.K. Menon
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116 NEUROANAESTHESIA
118 NEUROANAESTHESIA
systems. The availability of commercial systems for employed for sedation of children include ketamine,
safe monitoring makes such home made solutions barbiturates, benzodiazepines, high dose chloral
completely unacceptable (Table 28.2). A typical MR hydrate (50–150 mg/kg) and low dose propofol infu-
system costs in excess of one million pounds, and sions. Sedation can only be safely employed for MRI
there seems little justification to avoid spending in children provided they are accompanied by trained
£30,000 to ensure safe anaesthesia in this context. personnel and are adequately monitored. Supple-
mentary oxygen should be given to all patients.
Laryngeal mask airways (LMA) reinforced with a
SEDATION AND ANAESTHESIA metal spiral are ferromagnetic and produce substantial
FOR MRI imaging artefacts; however, newer reinforced LMAs
containing plastic spirals can be used during MR stud-
PREANAESTHETIC PREPARATION ies. When intubation is undertaken, use of a pre-
formed endotracheal tube is preferable. After the head
It is essential to determine contraindications to MRI
coils are in place there may be little room for anything
prior to induction of anaesthesia. The anaesthetist
protruding from the mouth. Unless there is a specific
must also ensure that they are familiar with the MR
indication, it is not absolutely necessary to ventilate
installation, particularly the extent of fringe fields and
patients for MRI. Both inhalational anaesthesia using
the location of resuscitation equipment. The use of
halothane or isoflurane, and total intravenous anaes-
earplugs or other auditory protection can substantially
thesia with propofol, have been used successfully for
reduce the stimulation associated with imaging, and
spontaneously breathing and ventilated patients. A
permit the use of lower doses of sedatives or anaes-
suitable recovery area, equipped with monitoring
thetic agents. Anaesthetic equipment may be posi-
equipment, suction apparatus, oxygen and trained staff
tioned within the MRI suite, or outside it. The
should be located outside the 50 G line.
former solution will mean that the anaesthetist will be
unable to leave the room without interrupting the Although a number of infusion devices do function
scan, the latter will limit access to the patient to inter- accurately, most are ferromagnetic, malfunction or
scan intervals, except in an emergency are inaccurate in fringe fields. Pumps must be sup-
ported on non-ferromagnetic poles. Needles and
intravenous cannulae are usually non-ferromagnetic
CONDUCT OF ANAESTHESIA
but should be tested before use. The surface of trol-
Induction of anaesthesia should ideally take place out- leys used for MRI is very firm and should be suitably
side the 50 G line with dedicated equipment. Standard padded to prevent the development of pressure sores,
Macintosh laryngoscopes are not ferromagnetic but do especially in critically ill patients.
undergo a degree of torque in a strong magnetic field.
Standard laryngoscope batteries are highly magnetic.
STRATEGIC ISSUES
Fibreoptic light sources or plastic laryngoscopes
powered by paper- or plastic-jacketed lithium batter-
Perhaps the most common continuing problems in
ies are available. Standard hospital trolleys are highly connection with anaesthesia in the MRI environ-
ferromagnetic and special trolleys should be available ment pertain to a lack of strategic thinking when such
for use in the MRI suite.
facilities are being constructed. The provision of
While sedation is commonly used, particularly in chil- filtered AC power, piped anaesthetic gases and ports
dren, it must be undertaken with care. Techniques in the RF shield costs relatively little at the time of
29
SHUNT SURGERY
A. Summors
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122 PHYSIOLOGY
30
ANAESTHESIA FOR
PAEDIATRIC NEUROSURGERY
J.M. Turner
30-GUPTA-30-cpp 6/2/01 11:57 am Page 126
126 NEUROANAESTHESIA
THE CHILD FROM 2 TO 7 surgery the need to expose head, chest and abdomen
YEARS means that warming blankets covering the child can-
not be used. The child should therefore lie on a
Space-occupying lesions (SOL) and head trauma are heated mattress and warm air using tubes around the
more frequent in this age group. Indeed, intracranial child but under the surgical drapes are valuable. With
tumours are the second most common neoplasms such problems, accurate temperature measurement is
occuring in childhood. About 70% of SOL are situ- particularly important.
ated in the posterior fossa. Some arteriovenous mal-
formations present in childhood, but large AVMs are Monitoring should be comprehensive. All patients
rare.2 Anaesthesia may be required for imaging tech- require oximetry, blood pressure, ECG and end-tidal
niques (angiography and CT or MRI scanning); CO2. Children with space-occupying lesions require
sedation for such procedures is often unreliable. direct intra-arterial monitoring of arterial pressure and
if the tumour is vascular, central venous pressure mea-
As in the adult, the extent of intracranial space-occu- surements are of value. Estimation of blood loss may
pation needs to be assessed as well as the degree of be difficult, because a common practice is to moisten
oedema formation and whether or not CSF obstruc- the surgical swabs, so that swab weighing gives an
tion is present. The likely vascularity of the SOL must inaccurate estimate of blood loss. Oesophageal mea-
be considered, taking into account the probable his- surements of temperature are reliable and an
tology. oesophageal stethoscope is often recommended.
31
CONGENITAL CRANIOFACIAL
PROCEDURES
J. Shapiro
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130 NEUROANAESTHESIA
CLINICAL PROBLEMS
CONDUCT OF ANAESTHESIA
INCREASED ICP Most of these patients will arrive in the operating
Most of the infants with craniofacial anomalies will theatre with no i.v. access and inhalational induction
have some degree of increased ICP. This may be is often the method of choice. Prior to induction,
most pronounced in infants with premature closure minimal monitoring should include pulse oximetry
of major suture lines. and a precordial stethoscope. As the inhalation
induction proceeds (usually with sevoflurane or
halothane in oxygen/nitrous oxide) an assistant
DIFFICULT AIRWAY ACCESS should place additional monitors, as tolerated,
Difficulty in laryngoscopic visualisation of the glottic including ECG, non-invasive BP cuff, and tempera-
structures varies with the syndrome. Isolated cranial ture probe. If ICP concerns exist, the patient should
vault anomalies do not usually present with airway be moderately hyperventilated. Intravenous access
difficulties. However, many of the congenital syn- should be obtained with a large-bore cannula as is
dromes which have major facial involvement (e.g. reasonable based on the patient’s size. Note that the
Pierre-Robin, Goldenhar) can present as significant saphenous vein is usually quite large and a 22 g or
intubation challenges. larger cannula can usually be placed for later volume
resuscitation even in infants. If not previously
obtained, a sample should be sent to the blood bank
BLOOD LOSS for cross-match of two ‘adult’ units of packed red
Significant blood loss may be expected in any of the cells. Following securing of the airway with an
surgical repairs for craniofacial anomalies. Procedures endotracheal tube, a second i.v. should be obtained
involving reshaping of the cranial vault and/or fore- as well as arterial access for continuous monitoring
head and upper face, in particular, may result in losses of BP. At the time of skin incision, mannitol (1
of one-third to one-half of the patient’s estimated g/kg) is administered. A brisk diuresis usually ensues
blood volume. shortly after administration and it is important to
closely monitor haemodynamic parameters to main-
tain adequate intravascular volume. Once the
craniectomies are started, furosemide (0.5–1 mg/kg)
ANAESTHETIC MANAGEMENT may be administered if the dura looks ‘tight’, but
this is rarely required after mannitol administration.
ASSESSMENT AND PREMEDICATION If subcutaneous/intradermal local anaesthetic solu-
tions are utilised by the surgeons prior to incision,
A survey of other organ systems, principally the car-
opiate requirements are reduced.
diovascular and renal systems, should be made to
assess for other significant congenital defects. A his- Continuous assessment of blood loss is required,
tory of nausea, vomiting, or ataxia suggests significant keeping in mind that most of the blood lost will be
ICP. A careful assessment of the upper airway includ- hidden in the surgical drapes. Most patients will
ing the relative size of the mandible, tongue and oral require replacement with red blood cells. It is best to
opening should be made. Evaluation of possible wait until the haemoglobin drops to about 8 g/dl
venous and arterial access may suggest the need to before transfusing unless the infant has heart disease
have special paediatric central line equipment avail- or other co-existing pathology requiring a greater
able prior to induction. oxygen carrying capacity. At that point, a continuous
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32
CONGENITAL SPINE
LESIONS
J. Shapiro
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134 NEUROANAESTHESIA
33
PAEDIATRIC CRANIOSPINAL
TRAUMA
C. Duffy
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138 NEUROANAESTHESIA
140 NEUROANAESTHESIA
Bracken MB, Shepherd MJ, Collins WF, et al. A random- American Heart Association. Pediatric Advanced Life
ized, controlled trial of methylprednisolone or naloxone in Support. Trauma Resus 1997: 8–3
the treatment of acute spinal-cord injury. N Engl J Med
Ward JD. Pediatric issues in head trauma. New Horizons
1990: 322: 1405–1411
1995; 3: 539–545
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34
RECOVERY:
GENERAL CONSIDERATIONS
S. Gupta
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142 NEUROANAESTHESIA
The airway may be compressed by haematoma after Postoperative nausea and vomiting may increase BP
cervical spine or carotid surgey causing stridor and and ICP. Droperidol, 0.625–2.5 mg intravenously,
hypoxia. promethazine 12.5–25 mg i.v. or intramuscularly
Cyclizine 50 mg i.v. or Ondansatron 4–8 mg i.v. may
be used to control nausea and vomiting. Refractory
CENTRAL NERVOUS SYSTEM nausea may suggest development of acute hydro-
cephalus or increased ICP secondary to brain oedema
or haematoma.
Postoperatively, altered level of consciousness could
be either due to residual effects of anaesthetic drugs or
more commonly cerebral pathology. Close observa-
FLUID AND ELECTROLYTE BALANCE
tion of GCS is necessary to detect any changes that
may occur in the postoperative period. Focal signs Fluid loss and intake are carefully noted with the aim
such as change in pupillary size are a good indicator of maintaining normovolaemia except in patient’s
of an evolving postoperative complication, e.g. following aneurysm clipping in whom hyper-
intracranial haematoma. Haemodynamic changes volaemic haemodilution is preferred.
such as hypertension and bradycardia (Cushing’s
Electrolytes should be measured early in the postop-
response) or altered ventilatory pattern are also
erative period to monitor changes in serum sodium
important signs of possible postoperative complica-
and potassium, particularly if diuretics have been
tions. If a complication is suspected then immediate
administered. If a suprasellar mass has been resected
CT scanning is indicated to rapidly diagnose a
or the patient has experienced severe head injury, the
reversible problem which may be resolved surgically.
onset of diabetes insipidus should be considered if
If seizures occur postoperatively control should be urinary output exceeds 200–400 ml/h and if specific
obtained with small doses of benzodiazipines while gravity is less than 1.005 and be treated by adminis-
ensuring an adequate airway. A CT scan should be tering vasopressin or DDAVP (1 µg). The syndrome
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35
MANAGEMENT OF SPINAL
CORD INJURY
I. Ng, R. J. C. Laing
35-GUPTA-35-cpp 7/2/01 1:25 pm Page 146
PATHOPHYSIOLOGY
DIAGNOSIS
The primary injury is the immediate damage inflicted
on the spinal cord and is due to either impact with The diagnosis of spinal cord injury requires a high
compression (e.g. disc rupture, burst fracture or index of suspicion on the part of the attending physi-
fracture dislocation), impact without compression cian. These patients often have other more life-
(hyperextension injuries), distraction (burst fracture) threatening conditions that divert attention away
or cord laceration. Any loss of neuronal tissue is likely from the spinal cord injury. All patients with head
to be permanent. injury are assumed to have a cervical injury until
proven otherwise. A cervical collar should be fitted
The secondary injury comprises all damage that occurs until definitive investigation has taken place. The
to the cord following the initial impact and is mechanism of injury may give a clue to the likely
potentially preventable by prompt resuscitation and presence of a spinal injury, for example the associa-
good intensive care. tion between rear seat lap strap restraint and thoraco-
lumbar burst fractures.
Systemic Effects of Spinal Cord Injury
Careful neurological examination should include an
Neurogenic or spinal shock (see below) results in the assessment of tone, reflexes, motor power and sensa-
secondary loss of sympathetic tone, and together with tion if possible. The anal tone should be checked and
unopposed vagotonia leads to a state of systemic patients should be log-rolled to allow examination of
hypotension that is related to the level and severity of the back. The presence of bruising or a palpable step
injury. This state of hypoperfusion leads to cord in the spine may indicate an underlying spinal injury.
ischaemia which will compound the injury already In the conscious trauma patient, the complaint of
sustained. pain in any part of the spine must be taken seriously
and if plain X-rays are normal further radiological
Local Effects assessment is necessary. Spinal shock refers to the
Vascular changes complete loss of motor, tone, sensory and reflex
activity below the affected spinal segment. It may last
Damage to the microvasculature including both as long as 6 weeks. The end of spinal shock is her-
capillaries and venules, results in microhaemorrhages alded by the return of spinal reflexes.
and thrombosis. The spinal cord at the level of the
injury undergoes infarction as the neurones at the Computed axial tomography is very sensitive to the
epicentre of the injury become ischaemic. presence of bony injury but further investigation with
MRI may be required to diagnose ligamentous injury
Biochemical changes and soft tissue encroachment into the spinal canal.
Flexion and extension cervical spine films will diag-
With the disruption of the integrity of the neural nose the presence of ligamentous instability.
tissue, the Na+/K+ pump fails with accumulation of Although usually safe in the conscious patient they
intracellular sodium and resultant cytotoxic oedema. should only be ordered by experienced doctors
35-GUPTA-35-cpp 7/2/01 1:25 pm Page 147
MANAGEMENT OF S P I N A L C O R D I N J U R Y 147
following full assessment of the mechanism of injury prevent bladder distension and allows accurate moni-
and the static radiological images. tor ing of fluid output.
• The management of spinal cord injury requires Frisbie JH, Sarkarati M, Sharma GV, Rossier AB. Venous
early aggressive resuscitation to prevent systemic thrombosis and pulmonary embolism occurring at close
hypotension. intervals in spinal cord injury patients. Paraplegia 1983; 21:
• The use of methylprednisolone in patients who 270–271
arrive within the 8-hour therapeutic window Grahm TW, Zadrozny DB, Harrington T. The benefits of
should be considered. early jejunal hyperalimentation in the head-injured patient.
• Delayed surgical decompression and stabilisation Neurosurgery 1989; 25: 729–735
should be considered in suitable candidates. Marshall LF, Knowlton S, Garfin SR, et al. Deterioration
following spinal cord injury. A multicenter study. J
Neurosurg 1987; 66: 400–404
FURTHER READING
Geisler WO, Jousee AT, Wynne-Jones M. Survival in trau- REFERENCE
matic transverse myelitis. Paraplegia 1977; 14: 262
1. Bracken MB, Shepard MJ, Holford TR, et al.
Tator CH. Pathophysiology and pathology of spinal cord Methylprednisolone or tirilazad mesylate administration
injury. In: Wilkins RH, Rengachary SS (eds) Neuro- after acute spinal cord injury: 1-year follow up. Results
surgery, Vol 2. New York: McGraw Hill, 1996, pp. of the third National Acute Spinal Cord Injury random-
2847–2859 ized controlled trial. J Neurosurg 1998; 89: 699–706
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36
GLASGOW COMA SCALE
A. Summors
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37
SEVERE HEAD INJURY: INITIAL
RESUSCITATION AND
TRANSFER
B. Matta
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38
INTENSIVE CARE
MANAGEMENT OF ACUTE
HEAD INJURY
D.K. Menon
38-GUPTA-38-cpp 6/2/01 11:59 am Page 156
Table 38.1 Physiological insults following head injury and their relation to outcome
All patients with or at risk of intracranial hypertension must have invasive arterial
monitoring, CVP line, ICP monitor and Rt SjO2 catheter at admission to NCCU.
Efforts must be made to attach TCD and multimodality monitoring computer within the first six hours of NCCU
stay.
Check whether the patient is or may be a candidate for research protocols.
Guidelines may be modified at the discretion of the consultant in charge.
Treatment grades III and IV should only be initiated after express approval of the
Consultant in charge of NCCU.
I
• 10–15° head up, no venous obstruction yes
• CPP ≥ 70 (CVP 6–10; ± PAC)
• SPO2 ≥ 97%; PaO2 ≥ 11 kPa, PaCO2 ⯝ 4.5 kPa
• Temp ≤ 37°C; SjO2 > 55%; blood sugar 4–7 mmol/l
• Propofol 3–5 mg/kg/hr (midazolam ⯝ 0.1 mg/kg/hr from day 2) ICP < 20
• Fentanyl 1–2 µg/kg/hr; atracurium 0.5 mg/kg/hr CPP > 70
• Sucralfate 1g Po 6 hrly (Ranitidine 50 mg 8 hrly iv if no OGT or
aspirate >200 ml/6 hrs)
• Phenytoin 15 mg/kg if indicated (fits, depressed #) no
yes – recent CT
– low risk of
II surgical lesion
IV
Trial of bolus i.v. anaesthetic (e.g. Propofol 50–200 mg), yes
– maintain CPP with fluids and vasoactive agents
If favorable effect on ICP and CPP start thiopentone
– 250 mg boluses up to 3–5 g + infusion 4–8 mg/kg/hr to
achieve and maintain burst suppression surgery
39
MANAGEMENT OF
SUBARACHNOID
HAEMORRHAGE
J. Ulatowski
39-GUPTA-39-cpp 6/2/01 12:00 pm Page 164
Preoperative
Syncope CT scan
intracerebral clot Evacuation, treat oedema
hydrocephalus ventricular CSF drainage
Cardiovascular
Arrhythmia ECG Anti-arrhythmic, correct electrolytes
Hypotension Myocardial enzymes, ECG, ECHO Intravascular volume and inotropic support
Hypertension ECG, assess blood volume Prevent rebleeding, anti-hypertensive
therapy, sedation, pain control
Pulmonary
Pneumonia Chest X-ray Oxygen, antibiotics, intubation,
mechanical ventilation
Pulmonary oedema Chest X-ray Oxygen, intubation, PEEP, mechanical
ventilation
Seizures Electroencephalogram (EEG) Anticonvulsants
Postoperative
Delayed cerebral CT scan
ischaemia (vasospasm) Surgical retraction injury Maintain MAP, treat oedema
Hydrocephalus CSF drainage
No lesion Calcium channel blockers,
TCD blood flow velocity increases HHH therapy, angioplasty,
at stenosis papaverine infusion
Congestive heart failure ECG, ECHO, chest X-ray Diuresis, inotropic support,
and pulmonary oedema Pulmonary artery catheter PEEP
Electrolyte disturbance Blood sampling Repletion
(hyponatremia)
Cerebral salt wasting Assess volume Sodium & blood volume repletion
Syndrome of inappropriate
ADH secretion Plasma & urine osmolality Free water intake restriction
Nutrition Caloric intake Enteral, parenteral supplementation,
gastrostomy
Prolonged ventilation Weaning trials, assess airway Trial of extubation, tracheostomy
competency
Deep venous thrombosis Doppler ultrasound of extremities Heparin, coumadin, vena cava filter
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MANAGEMENT OF S U B A R A C H N O I D H A E M O R R H A G E 165
For further information on the presentation and nat- require intubation, supported ventilation and seda-
ural history of SAH see Chapter 13. tion with full monitoring.
CARDIAC FUNCTION
INTENSIVE CARE
Cardiac arrhythmias and changes in cardiac function
MANAGEMENT occur in approximately 50% of patients. The most
Patients presenting with significant neurological common are electrocardiographic abnormalities,
deficit from SAH usually have substantial parenchy- many of which are non-specific (sinus tachycardia,
mal injury due to intracerebral extension of clot, mass T-wave inversion, U waves, QT interval prolonga-
effect, hydrocephalus (raised ICP) and seizures. tion). However, others may be more ominous
Decreased level of consciousness and arrhythmia including variable states of heart block, premature
must be treated to prevent aspiration pneumonia or atrial and ventricular ectopy that may lead to tachy-
respiratory failure and haemodynamic decline while cardia, ST segment depression, and elevated cardiac
surgical options (evacuation of clot or external ven- enzymes associated with echocardiographic ventricu-
tricular drainage of CSF) are addressed. This simulta- lar wall abnormalities. Most of these occur immedi-
neous team effort involving intensive care physicians, ately after SAH and are probably due to transient
neurologists and neurosurgeons, requires coordina- catecholamine release. As a result, beta blocker med-
tion that usually occurs in the ICU. ications are a first choice for treating cardiac compli-
cations in these patients. Further cardiovascular
testing and therapy may be necessary to rule out
BLOOD PRESSURE CONTROL ongoing myocardial ischaemia prior to surgery.
Preoperative ICU management concentrates on nor-
malisation of blood pressure to reduce the risk of
rebleeding. Caution is advised not to reduce MAP SEIZURES
quickly. Blood pressure management should be Seizures can occur at various points after SAH, but
guided by changes in neurological exam (ischaemic are generally thought to be infrequent. Abnormal
symptoms), maintaining CPP between 70 and motor posturing is witnessed with onset of SAH.
90 mmHg and/or ensuring adequate cerebral perfu- This may be as a result of overall depression of the
sion by measuring cerebral oximetry with a jugular nervous system (herniation) or generalised seizures,
venous catheter, indwelling oximetric probe or both due to transient ischaemia caused by the initial
transcutaneous oximetry for patients in stupor or increase in ICP. Seizures in the first 1–2 weeks after
coma. Blood pressure should be reduced (SBP < 180 aneurysm rupture and surgery occur in approxi-
mmHg) within the first 2 hours followed by normal- mately 1–3% of patients. Prophylactic phenytoin
isation of BP if tolerated within 4–8 hours. Calcium treatment is routine in many centres during the
channel blockers used for neuroprotection (nimodip- period prior to aneurysm clipping and, although still
ine, nicardipine) may be supplemented with other controversial, proponents argue that seizure preven-
drugs such as labetalol or captopril. Direct-acting tion lessens the chance of rebleeding, hypertension
vasodilators (nitrates, hydralazine) may increase and transient hypoxaemia. Prolonged postoperative
cerebral blood volume causing raised ICP and are a seizure prophylaxis has no proven benefit, therefore
last resort. anticonvulsants are most commonly used during the
Preventive measures to reduce elevations in blood first 7–14 days after SAH and only continued in
pressure are also invoked. This may include keeping patients with witnessed seizures. Further therapy is
the patient sedated and analgesed using short-acting guided by improvement in neurological status and
sedative and narcotic medications. Bedside activities EEG studies.
are kept to a minimum to prevent agitation. For good
grade patients (Hunt and Hess grade I–II), invasive
HYDROCEPHALUS
cardiovascular monitoring and other testing is post-
poned until the time of surgery. The diet is kept Hydrocephalus occurs in two forms after SAH.
simple and avoids caffeinated products. A laxative Communicating hydrocephalus is due to block-
may be used to prevent straining during bowel age of CSF outflow at the arachnoid granulations.
movements. Finally, the patient should be reassured Non-communicating (obstructive) hydro-
that they are in a safe environment and that there is a cephalus is due to the obstruction of CSF outflow
therapy for their disease. Patients with grades III–V from the ventricular system either by large clots
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leading to external compression or to bleeding into prophylactic gastrointestinal antacid therapy (espe-
the ventricles. Intraventricular haemorrhage is more cially in patients treated with steroids), pre-emptive
common with anterior cerebral artery and vertebro- treatment of constipation that can occur in bedridden
basilar artery aneurysms. Hydrocephalus can be part patients, facilitated early nutrition and prevention of
of the initial presentation of SAH or can occur at deep venous thrombosis and bedsores in immobilised
any time in the postoperative period presenting as a patients. Normothermia should be maintained, by
decline in level of consciousness. Early after SAH, active cooling if necessary.
hydrocephalus can make the initial neurological
exam appear more grave than actual parenchymal
SURGERY
damage would indicate. Later it can mimic global
ischaemia from vasospasm. Timing of surgery can either be early (1–3 days after
SAH) or late (10–14 days). Early surgery reduces the
Hydrocephalus (communicating and non-communi-
risk of rebleed, and early removal of the blood clot
cating) is usually treated with external ventricular
may reduce the risk of vasospasm. Late surgery is
drainage using a temporary indwelling catheter,
technically easier. Although there is still debate as to
which also allows measurement of ICP. CSF can be
optimal timing, in many institutions surgery is
drained to reduce pressure and maintain adequate
performed within 4 days after SAH.
cerebral perfusion pressure. Slow drainage of CSF in
patients with untreated aneurysms is recommended Onset of global or focal ischaemia due to cerebral
to avoid rapid changes in transmural forces across vasospasm is delayed ranging from day 4 to day 21
the aneurysm wall or settling of the brain thereby following aneurysmal rupture, with a peak incidence
compressing the aneurysm and leading to rebleed- on days 5–10. Best evidence supports the presence of
ing. Most patients with obstructive hydrocephalus blood products around the large arteries at the base of
eventually clear the blood from the ventricular the brain as a cause for the segmental narrowing of
system but may have persistent hydrocephalus due the blood vessels. Not surprisingly the best predictor
to continued interruption of CSF outflow at the of vasospasm is the amount of the subarachnoid blood
arachnoid granulations. Should this condition detected by CT scan. Angiographic studies have
become more chronic, the intraventricular catheter demonstrated cerebral vasospasm to occur in 60–75%
can be changed to lessen risk of infection or sub- of patients. However, with current therapy, one-
stituted with lumbar CSF drainage. Alternatively, third of SAH patients develop clinical symptoms of
frequent spinal taps are used for communicating delayed ischaemia. Serial neurological examinations
hydrocephalus before determining the need for supplemented by TCD is used for monitoring onset
permanent shunting. of vasospasm. Vasospasm is frequently treated
prophylactically with calcium channel blockers
(nimodipine or nicardipine). Angiographic studies
PULMONARY COMPLICATIONS have not confirmed reversal of vasospasm in larger
arteries implying that the effect is of calcium channel
Pulmonary complications are more rare after SAH; blockers on small distal vessels or a direct neuropro-
however, they account for 50% of the medical mor- tective effect in brain tissue. This treatment continues
tality. Pneumonia occurs due to aspiration in for 21 days.
patients with a decreased level of consciousness with
or without an endotracheal tube. Neurogenic pul- Hypervolaemia, hypertension, haemodilution (HHH)
monary oedema can occur in approximately 2% of therapy is thought to improve neurological status and
patients who present in coma. Treatment includes decrease the incidence of neurological deficits and
endotracheal intubation and mechanical ventilatory death due to vasospasm. However, evidence of long
support using positive end-expiratory pressure and term benefit is scarce and there is the potential for
supplemental oxygen. A pulmonary artery catheter is many complications. Increasing blood volume with
sometimes inserted to differentiate cardiac from crystalloid or colloid solutions to achieve a haemato-
pulmonary oedema, both of which can occur after crit of 30% after aneurysmal repair facilitates
SAH. haemodilution and spontaneous hypertension. The
combination of a reduced blood viscosity and higher
blood pressure proximal to the stenosis is believed to
increase cerebral perfusion. If symptoms persist with
GENERAL CARE
only moderate increases in blood pressure (MAP
General medical care includes attention to electrolyte 90–110 mmHg) further haemodynamic augmenta-
disturbances (sodium and potassium predominantly), tion with inotropes (e.g. dopamine 2.5–15
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MANAGEMENT OF S U B A R A C H N O I D H A E M O R R H A G E 167
µg/kg/min) or vasoconstrictors is commenced and KEY POINTS
guided by use of a pulmonary artery catheter. Care
must be taken to maintain systolic blood pressure • Intensive care management of patients with SAH
below 150 mmHg in patients with unclipped begins early in the course of therapy and continues
aneurysms. If neurological improvement is not throughout a variable period
achieved using this therapy, more aggressive treat- • Hydrocephalus and vasospasm may complicate
ments are tried (see below). recovery despite successful ablation of the aneurysm
• Systemic complications need to be treated pre-
operatively
Balloon angioplasty to directly dilate accessible ves- • Vasospasm can be treated with HHH therapy in
sels has shown good results in cases of refractory ICU, or angiographically using papaverine or bal-
vasospasm. Mechanical dilatation of the intracerebral loon angioplasty.
vessels has been shown to increase distal perfusion
and the effect appears to be long-lasting. Intra-arter-
REFERENCES
ial injection of papavarine, (a vasodilator), alone or
in addition to angioplasty, is also believed to 1. Sacco RL et al. Subarachnoid and intracerebral hemor-
improve brain blood flow. The effect of these two rhage: natural history, prognosis, and precursive factors in
therapies may be delayed as late as 12–36 hours. the Framingham Study. Neurology 1984; 34(7): 847–854
2. Rinkel GJ, Djibuti M and van Gijn J. Prevalence and
Lack of controlled trials demonstrating effect on risk of rupture of intracranial aneurysms: a systematic
outcome, as well as limited technical expertise, has review. Stroke 1998; 29(1): 251–256
relegated this treatment to large academic centres 3. Mayberg MR et al. Guidelines for the management of
with ongoing studies. aneurysmal subarachnoid hemorrhage. A statement for
healthcare professionals from a special writing group of
the Stroke Council, American Heart Association.
Improvements in neurological symptoms and nor- Stroke 1994; 25(11): 2315–2328
malisation of TCD velocities guide the intensity and 4. Weir B. Subarachnoid hemorrhage: causes and cures.
duration of therapy for cerebral vasospasm. HHH CNS: Contemporary Neurology Series, Vol. 52.
therapy is weaned slowly over hours to days while Oxford University Press, New York, 1998
observing for recurrence of symptoms. Calcium 5. Hunt WE, Hess RM. Surgical risk as related to time of
channel blockers are stopped after 3 weeks of ther- intervention in the repair of intracranial aneurysms. J
apy and replaced by long-term anti-hypertensive Neurosurg 1968; 28(1): 14–20
therapy if indicated. If prolonged intubation 6. Solenski NJ et al. Medical complications of aneurysmal
(beyond 10 days) is anticipated, an elective tra- subarachnoid hemorrhage: a report of the multicenter,
cooperative aneurysm study. Participants of the
cheostomy is performed. Patients unable to main-
Multicenter Cooperative Aneurysm Study [see com-
tain nutritional intake sufficient to sustain recovery ments]. Crit Care Med 1995; 23(6): 1007–1017
undergo gastrostomy tube placement. Once these 7. McKhann GM II, Le Roux PD. Perioperative and
and other general medical conditions have been sta- intensive care unit care of patients with aneurysmal sub-
bilised, patients can be transferred from intensive arachnoid hemorrhage. Neurosurg Clin N Am 1998;
care. 9(3): 595–613
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40
NEUROPROTECTION IN ICU
PRINCIPLES OF Hyperventilation
NEUROPROTECTION Hypocapnia causes cerebral vasoconstriction thereby
Current strategies for brain protection focus around reducing CBV and hence ICP. Whilst hyperventila-
prevention of secondary injury (Table 40.1). tion may help reduce ICP, two issues need consider-
ation:
The pathophysiological mechanisms of secondary
injury are complex, but have common manifestations 1. Hyperventilation causes a reduction in both global
such as reduced CBF or raised ICP. Laboratory and regional CBF which may fall below ischaemic
studies have identified many potential therapeutic thresholds. This is most commonly detected by
interventions that might have clinical application jugular bulb desaturation (< 50%) and is associated
following brain injury (e.g. antagonism of inflam- with a poor outcome. In our unit, PaCO2 is kept
matory mediators, hypothermia, gene therapy and above 4 kPa in an attempt to maintain an adequate
neural transplantation). Many of these therapies have CBF.
progressed into completed clinical trials, and others 2. The effects of hyperventilation on ICP are often
have been prematurely terminated or are in various temporary due to pH compensation in the brain
phases of testing. The results of completed phase III and CSF, and may lead to a rebound rise in cere-
drug trials have been generally disappointing com- bral blood volume and ICP when arterial CO2 is
pared with the success in animal laboratory studies, normalised.
with few, if any, drug treatments proving to improve
outcome. Normoglycaemia
Neuroprotection strategies can be categorised into The brain is dependent on exogenous glucose for its
optimising physiology, pharmacological methods and cellular energy requirements. During ischaemia,
non-pharmacological interventions. anaerobic glycolysis produces lactate which is
regarded as neurotoxic per se. The amount of lactate
formed depends on the duration and severity of
ischaemia and the pre-existing stores of glucose and
OPTIMISING PHYSIOLOGY glycogen. The higher the concentration of glucose,
the more lactate is formed, thereby aggravating brain
Maintenance of CBF and oxygenation injury. Tight glucose control is essential with routine
measurement of blood glucose levels and avoidance
Chestnut et al demonstrated that hypotension (sys-
of glucose containing fluids. Insulin infusions may be
tolic blood pressure < 90 mmHg) and hypoxia (PaO2
needed.
< 60 mmHg) after head injury were independent
predictors of poor outcome.1 Careful fluid manage-
ment and the use of inotropes should ensure an ade- PHARMACOLOGICAL THERAPY
quate CPP. Adequate sedation reduces agitation and
may help control ICP (see Chapter 44). Low dose Anaesthetic agents
propofol has been shown to be superior to morphine
at controlling ICP but gives no improvement in neu- The primary mechanism by which the anaesthetic
rological outcome. agents confer neuroprotective effects involves a
Nitric oxide Variable success with both inhibitors of NO synthesis and NO donors
Calpain Protease acting on structural and regulatory proteins involved in injury; inhibition
provides protection
Immunophilins e.g. Cyclosporin A & FK506 inhibit calcineurin and NO synthesis, modulate
neurotransmitter release & cytosolic Ca++ increases and mediate nerve growth
PARP/Caspases (Poly (ADP-ribose) polymerase) a DNA repair enzyme activated on injury and
depleting energy stores at a time when they are critical; Caspases involved in
PARP activation and inhibition is protective
Matrix metalloproteases Released in injury and disrupts BBB; inhibition is protective
Adenosine Improves microvascular flow, inhibits platelet aggregation, role in ischaemic
preconditioning; but action on some receptor subtypes may worsen injury
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41
INOTROPES IN
NEURO-CRITICAL CARE
R. Shankar
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42
ELECTROLYTE DISORDERS
IN THE NEUROINTENSIVE
CARE UNIT
J. Ulatowski
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INTRODUCTION PATHOLOGY
Electrolyte imbalance can lead to a wide variety of Hypernatraemia
symptoms affecting many cell types and organs.
These disturbances can occur because of reduced or The most common causes of hypernatraemia in the
excess intake of electrolytes, diseases of the endocrine neurointensive care unit are neurogenic diabetes
organs controlling electrolyte concentrations insipidus (DI), mannitol induced diuresis, water
(absorption and excretion), or iatrogenic changes in dehydration from lack of intake in neurologically
the fluid and electrolyte balance (such as admini- impaired individuals and, more recently, the admini-
stration of incorrect electrolyte concentrations or stration of large volumes of hypertonic saline for the
inappropriate fluid volume). Furthermore, endocrine treatment of cerebral oedema and raised intracranial
function may be disturbed and fluid and electrolyte pressure. Acute elevations in sodium concentration
concentrations may be deregulated as part of multi- due to excessive free water losses which occur rapidly
system failure in ICU patients. Finally, certain from DI are corrected by the administration of
diseases involve or require treatment (such as massive hypotonic fluids (e.g. 0.45% saline) and intravenous
fluid resuscitation) which significantly affects the fluid vasopressin (0.5–1 mg desmopressin). More chronic
balance within the body. hypernatraemic states due to prolonged dehydration
or administration of hypertonic saline infusions over
Fluid and electrolyte imbalances can lead to a variety periods of days should be reversed more slowly. Brain
of symptoms in the intensive care population. cells exposed to chronically high concentrations of
Disturbances of calcium, magnesium and potassium sodium will form what has been termed ‘ideogenic
can lead to cardiovascular changes including osmoles’. These osmoles act as a strong osmotic force
hypotension and arrhythmia. Disturbances in these drawing water into brain cells when plasma fluid
same electrolytes can cause irritability in nerve and suddenly becomes isotonic. Brain oedema can ensue.
muscle function. Hypophosphataemia can lead to
muscle weakness of the limbs and diaphragm. Diagnosing the cause of hypernatraemia is not diffi-
However, the most common conditions seen in the cult if an evaluation of intravascular volume can be
neurointensive care unit involve disturbances in performed. Dehydration, and DI result in decreases
sodium and water balance. in plasma volume and can be diagnosed by decreased
skin turgor, orthostatic blood pressure changes and
reduction in central venous pressure. A low urine
SODIUM AND WATER BALANCE osmolality and high plasma osmolality is seen in DI
The measured concentration of any ion must be (Fig. 42.1), with a urine specific gravity of < 1.005,
interpreted in the context of circulating or total body and high urine output. In neurologically impaired
fluid volume because ion concentrations can be individuals who cannot maintain intake of water,
affected by changes in the solute (e.g. sodium) or the
solvent (i.e. water).
Although sodium and water homeostasis is controlled
by separate hormone systems within the body, the
trigger for initiating changes in sodium and water
control may be shared. For instance, significant
intravascular volume loss will stimulate both sodium
and water retention and is initiated through a baro-
receptor response in the atria of the heart and the
aorta. The effector of sodium retention is mainly
through the action of aldosterone via the
renin–angiotensin system. Water retention is con-
trolled by antidiuretic hormone (ADH) secreted from
the neurohypophysis. In addition to responding to
gross changes in intravascular volume there are more
delicate controls to fine-tune sodium and water
balance. Osmo-receptors in the periventricular
organs of the brain are extremely sensitive to small Figure 42.1 Relationship of plasma to urinary osmolality
changes in serum osmolarity and result in more under normal and polyuric conditions. Adapted from Moses,
minor secretion of ADH. with permission from the publisher
42-GUPTA-42-cpp 6/2/01 12:03 pm Page 181
The syndrome of inappropriate ADH secretion Magnesium is another important ion for contractility
(SIADH) occurs when ADH is secreted without an of the heart and at the neuromuscular junction. The
osmotic trigger. Neurological disease is a common central nervous system effects are less prominent.
cause of SIADH, because the osmostatic cells in the Patients with impaired renal function are susceptible
brain are involved with the offending process. to hypermagnesaemia as elimination is primarily
Patients with SIADH have normal intravascular through the kidney. Hypermagnesaemia can be
volume and the urine is less than maximally dilute treated with administration of calcium in the acute
given the degree of relative water excess within the phase. Fluid loading and diuresis is used in patients
plasma. In order to make a diagnosis of SIADH, the with competent renal function; however, dialysis
patient must be normovolemic and have no evidence may be necessary.
of adrenal or thyroid insufficiency, or excessive renal Hypomagnesaemia can occur from malabsorption
losses of fluid. Treatment is to restrict free water syndromes including alcoholism and in gastrointestinal
administration, and in severe states with addition of disorders involving diarrhoea and vomiting. Patients
furosemide to induce a diuresis greater than natri- with hypomagnesaemia present with hyperreflexia,
uresis or democlocycline which impairs the effect of muscle spasm and seizures. Cardiac irritability and an
ADH on the kidney. increased risk of digoxin-induced cardiac dysrhythmias
may occur. Hypomagnesaemia can be treated by
OTHER ELECTROLYTES administration of intravenous magnesium sulphate
1–2 g over 30–60 min to reverse the cardiovascular and
Hyperkalaemia neurologic side-effects. Magnesium sulphate admini-
stration can be monitored at the bedside by evaluating
Hyperkalaemia from iatrogenic administration, or depression in the tendon reflexes.
reduced excretion of potassium due to renal failure
can cause life-threatening arrhythmia. Particular to Phosphate
the neurological patient, hyperkalaemia can occur
after the administration of succinylcholine to patients Neurologically impaired individuals may have
who have severe burns, peripheral neuropathy or inadequate nutrition leading to hypophosphataemia.
spinal cord injury all associated with significant Re-administration of nutritional supplement to these
denervation of muscle. patients induces severe hypophosphataemia, as part of
42-GUPTA-42-cpp 6/2/01 12:03 pm Page 182
a refeeding syndrome. Phosphate levels in the blood malities are seen at a frequency similar to the
can drop precipitously causing a variety of central general ICU patient population.
nervous system effects including decreased level of
consciousness. Most frequently, however, hypophos-
phataemia presents with diffuse neuromuscular weak- Diabetes SIADH Salt
Insipidus Wasting
ness which may also affect muscles of respiration
requiring mechanical ventilation. Phosphate should Serum Sodium ↑ or ↔ ↓ ↓
be repleted in large doses orally during refeeding, and Urine Sodium ↔ ↔ ↑
should a severe refeeding syndrome occur, intra- Urine Osmolality ↓ ↑ ↔ or ↓
venous sodium or potassium phosphate should be
Vascular Volume ↓ or ↔ ↔ or ↑ ↓
administered slowly over 2–4 h.
Body Weight ↓ ↔ or ↑ ↓
Blood Pressure ↓ or ↔ ↔ or ↑ ↔
CVP ↓ ↔ ↓
KEY POINTS
Figure 42.2 Common clinical syndromes in the neuro-
∑ The importance of monitoring and evaluating intensive care unit
electrolyte and water disturbances in neurologic
disease cannot be understated. FURTHER READING
∑ Brain injury affects sodium and water homeostasis
within the body. Shifts in electrolyte and water Andrews B 1994 Fluid and electrolyte disorders in neuro-
can affect brain function and worsen cerebral intensive care. Neurosurg Clin N Am W B Saunders,
oedema regardless of the cause. Philadelphia, pp. 707–724.
∑ Understanding the pathological mechanisms Bhardwaj A, Ulatowski JA 1999 Cerebral edema: hyper-
behind these abnormal concentrations requires an tonic saline solutions. Curr Treatment Options Neurol. 1:
understanding of the complex interaction of 179–199.
neuroendocrine hormones controlling water and Diringer M 1995 Neuroendocrine regulation of sodium
sodium balance. and volume following subarachnoid hemorrhage. Clin
∑ The initial evaluation of these syndromes is made Neuropharmacol. 18(2): 114–126.
easier by first evaluating intravascular volume (Fig. Moses AM, Blumenthal SA, Streeten DH 1985 Acid-base
42.2). and electrolyte disorders associated with endocrine disease:
∑ While neurointensive care patients can experience pituitary and thyroid: In: Arief A, De Fronzo RA (eds)
a variety of electrolyte abnormalities beyond Fluid, electrolyte and acid-base disorders. Churchill
sodium and water, these other electrolyte abnor- Livingstone. New York pp. 851–892.
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43
FLUID MANAGEMENT
J. Monteiro
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HYPERTONIC FLUIDS
Table 43.1 Osmolality of replacement
fluids
Hypertonic Saline
Fluid Osmolality mosm/l Saline (3%, 10% and 23.4%) has been shown to be
effective in reducing ICP in patients with resistant
7.5% NaCl 2400 intracranial hypertension by decreasing brain water
25% Mannitol 1100 content by osmosis. It also increases cardiac output,
0.9% NaCl 308
6% Hetastarch 310
decreases peripheral and cerebrovascular resistance
Plasma 285 thereby decreasing intracranial pressure. Its use is
Lactated ringers 250–260 economical and free from infectious risk, although it
5% Dextrose 252 is associated with increases in plasma osmolarity,
sodium and chloride levels and hypokalemia. Cerebral
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44
SEDATION
J. Monteiro
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MUSCLE RELAXANTS
Table 44.1 Indications for sedation in
neurointensive care Neuromuscular blocking drugs are frequently used to
synchronise ventilation, manipulate PaCO2 and min-
• Control intracranial pressure imise increases in ICP. Atracurium is commonly
• Decrease cerebral metabolism given, tolerated well haemodynamically and has few
• Facilitate mechanical ventilation drug interactions. Laudanosine, a metabolite pro-
• Provide amnesia during paralysis with muscle
relaxants
duced by Hoffman elimination is not a clinical prob-
• Treat status epilepticus lem in humans. Pancuronium boluses are
• Relieve anxiety and fear; facilitate sleep occasionally used, guided by a peripheral nerve stim-
• Provide haemodynamic stability ulator. Generally, the steroid-based agents are best
avoided in critical illness.
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SEDATION 189
45
COAGULATION DISORDERS
P. Doyle
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46
STATUS EPILEPTICUS
N. Hirsch
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KEY POINTS
DRUG THERAPY (see Table 46.2) • Overall mortality and morbidity is high and
directly related to duration of seizures.
GCSE is often heralded by an increase in the intensity
• Neurological and systemic complications may occur.
or frequency of seizures (the so-called premonitory
• Cardiorespiratory support is the first step in man-
stage). Treatment at this stage may abort evolution
agement of this condition.
into true status. The drugs of choice at this stage are
• Benzodiazepines may initially help prevent evolu-
diazepam, midazolam or paraldehyde.
tion of established status.
Early GCSE (within first 30 minutes) is best treated • Therapeutic doses of phenytoin or phenobarbi-
with diazepam or lorazepam. Repeated doses of tone should be given in established status.
Dosage
Premonitory stage:
Diazepam 10–20 mg i.v. or rectally repeated once after 15 minutes if necessary
Midazolam 5–10 mg i.m. or rectally repeated once after 15 minutes if necessary
Paraldehyde 10–20 ml 50% rectally or i.v. repeated once after 15–30 minutes if necessary
Early status:
Lorazepam 0.07 mg/kg i.v.
Established status:
Phenytoin 15–18 mg/kg i.v. at rate < 50 mg/min
Phenobarbitone 10–15 mg/kg i.v. at rate < 100 mg/min
Refractory status:
Thiopentone 250 mg bolus then 2–5 mg/kg/h
Propofol 2 mg/kg bolus then 5–10 mg/kg/h
46-GUPTA-46-cpp 6/2/01 12:04 pm Page 198
• Refractory status should be treated with anaesthetic Shorvon S. Status epilepticus: its clinical features and treat-
agents with EEG monitoring in a neurointensive ment in children and adults. Cambridge: Cambridge
care unit. University Press, 1994
Walker MC, Howard RS, Smith SJ, Miller DH, Shorvon
FURTHER READING
SD, Hirsch NP. Diagnosis and treatment of status epilepti-
Lowenstein DH, Alldredge BK. Status epilepticus. N Engl cus on a neurological intensive care unit. Quart J Med
J Med 1998; 338: 970–976 1996; 89: 913–920
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47
GUILLAIN–BARRÉ SYNDROME
N. Hirsch
47-GUPTA-47-cpp 6/2/01 12:04 pm Page 200
Specific therapy
patients. More dangerous are the bradyarrhythmias Plasma exchange (PE) has been shown in a number of
that may occur with even trivial vagal stimulation. large, well-conducted trials to accelerate recovery.
Other autonomic features include postural hypoten- Patients likely to benefit most are those who are
sion, excessive sweating and urinary retention. exchanged within 1 week of the onset of symptoms
and those with rapid deterioration of limb power; no
benefit is seen if the exchange is performed after 2
MANAGEMENT
weeks of onset. Typically, the exchange consists of
The management of GBS consists of supportive treat- replacing 250 ml/kg body weight of the patient’s
ment and specific therapy. plasma with 4.5% human albumin solution.
Morbidity relates to exacerbation of co-existing
Supportive treatment infection and infective and thromboembolic compli-
cations of the large-bore cannula used.
Good general medical and nursing care are essential
in the treatment of GBS. Patients must be carefully Intravenous normal immunoglobulin (IvIg) is as effective
monitored during the acute and progressing phases as PE in speeding up the rate of recovery in GBS. It
and early tracheal intubation should be performed if has now become the treatment of choice for GBS as
vital capacity falls below 15 ml/kg. If bulbar weakness it does not require the manpower demanded by PE
co-exists, intubation should be carried out earlier. and has a lower complication rate. A recent study has
Tracheostomy should be performed early if it is obvi- suggested that the combination of IvIg and methyl-
ous that a prolonged period of ventilation will be prednisolone may be more effective than IvIg alone.
needed.
Sedation is usually given for the first 24 hours fol- PROGNOSIS
lowing intubation but is not appropriate after this
Mortality of GBS varies between 2 and 13%. Typical
period.
mortality for patients requiring respiratory support
The cardiovascular system must be monitored care- and nursed in a specialised unit is approximately 5%.
fully and persistent tachycardia and hypertension In general, 25% of patients will be left with a degree
treated with small doses of a β-blocker (e.g. propra- of disability 1 year after the onset of GBS.
nolol 5–15 mg daily). Severe episodes of bradycardia
warrant temporary or permanent cardiac pacing.
Enteral feeding should be started as soon as possible; KEY POINTS
however, ileus is common in the acute stages of GBS • Triggering agents may be bacterial or viral.
and may require the use of prokinetic agents such as • The disease causes neurological and other systemic
metoclopramide. Rarely parenteral nutrition may be effects.
needed. • As well as supportive therapy, the preferred spe-
Regular turning of the patient with GBS is essential cific treatment includes intravenous immunoglob-
to help prevent pressure sores; passive physiotherapy ulin therapy.
and the use of limb splints helps to prevent tendon
contractures. FURTHER READING
Thromboembolic complications remain a major Hughes RA. Guillain–Barré syndrome. London: Springer-
cause of morbidity and mortality in this group and all Verlag, 1990
47-GUPTA-47-cpp 6/2/01 12:04 pm Page 202
Ng KKP, Howard RS, Fish D, Hirsch NP, et al. Winer JB. Guillain-Barré syndrome. In: Miller DH, Raps
Management and outcome of severe Guillain–Barré syn- EC (eds) Critical care neurology. Boston: Butterworth-
drome. Quart J Med 1995; 88: 243–250 Heinemann, 1999, 33–49
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48
TRACHEOSTOMY
Q. Milner
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TRACHEOSTOMY 205
49
BRAINSTEM DEATH
Q. Milner
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KEY POINTS
CHILDREN
• An irreversible intracranial event causing apnoea
The British Paediatric Association (1991) have stated must be identified.
that for children over the age of 2 months, brainstem • Patients need to satisfy all brainstem death criteria.
death criteria should be the same as for adults. • Brainstem death criteria should be carried out on
two occasions by qualified medical staff.
PERSISTENT VEGETATIVE STATE (PVS) • Time of death is noted after the first set of tests.
Patients in PVS have suffered cortical damage and do
not meet the basic criteria for brainstem death testing; FURTHER READING
these two conditions should not be confused. Department of Health. A Code of Practice for the diagno-
sis of Brain Stem Death. Health Service Circular, 1998
SUBSEQUENT MANAGEMENT Jennett B. Brain death. Intens Care Med 1982; 8: 1–3
Organ donation should only be discussed with Milner QJW, Vuylsteke A, Ismail F, Ismail-Zade I, Latimer
patient’s relatives after the diagnosis of brainstem RD. ICU resuscitation of the multi-organ donor. Br J
death has been made. The family should be clear that Intens Care 1997; 2: 49–54
despite the presence of a beating heart, the patient is Wijdicks EFM. Determining brain death in adults.
dead and ventilation may legally be ceased. If organ Neurology 1995; 45: 1003–1011
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50
NUTRITION IN THE
NEUROCRITICAL CARE UNIT
Q. Milner
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51
NURSING ISSUES
S. Rees-Pedlar, S. Walters
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52
INTRACRANIAL PRESSURE
M. Czosnyka
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220 MONITORING
Figure 52.3 Example of regular (30 second) vasogenic ICP Figure 52.5 Example of a dramatic onset of refractory
B-waves with amplitude 5 mmHg. This pattern is a reflection intracranial hypertension in a patient after severe HI who ini-
of the vasocycling often seen in the ABP tracing. tially presented with only moderately elevated ICP. After 3
hours of monitoring, ICP increased to above 60 mmHg. The
Cushing reflex causing an increase in ABP has been
Figure 52.3 shows Vasogenic B waves. Plateau waves recorded, which ended during the fourth hour with brainstem
are shown in Figure 52.4. Figure 52.5 shows refrac- herniation (demonstrated by a sudden drop in ABP and ICP)
tory intracranial hypertension (poor prognostic sign).
pulse transmission. If this relationship is disturbed the
PULSE WAVEFORM ANALYSIS cerebral vessels are no longer pressure-reactive.
OF ICP A moving linear correlation coefficient between
mean ICP and ICP pulse amplitude values termed the
In order to identify adequate CPPs in individual RAP index (R = symbol of correlation, A = ampli-
patients, an analysis of the amplitude of ICP wave- tude, P = pressure) calculated over a 3- to 5-minute
forms can be used. The pulse waveform of ICP pro- time-window is used for continuous detection of the
vides information about the transmission of arterial amplitude:pressure relationship. The advantage is that
pulse pressure through the arterial walls to the CSF the coefficient has a normalised value from –1 to +1
space. As CPP decreases, the wall tension in reactive allowing comparison between patients. The relation
brain vessels decreases. This in turn increases trans- of RAP and ICP or CPP in a pooled analysis of
mission of the arterial pulse to ICP. Therefore when patients with HI show a RAP close to +1. This is
cerebral vessels are normally reactive, a decrease in expected in head-injured patients with a moderately
CPP should provoke an increase in the ABP to ICP raised ICP (> 15 mmHg) and CPP > 50 mmHg indi-
cating decreased compensatory reserve with pre-
served cerebrovascular reactivity. A decrease in RAP
to 0 or negative values is found with very high ICP
and very low CPP and indicates a loss of cerebrovas-
cular reactivity with a risk of brain ischaemia and is
also predictive of a poor outcome (Fig. 52.6).
CHANGES IN ICP IN
RESPONSE TO VARYING ABP
The correlation between spontaneous waves in ABP
and ICP is dependent on the ability of cerebral vessels
to autoregulate. With intact autoregulation, a rise in
ABP produces vasoconstriction, a decrease in cerebral
blood volume, and a fall in ICP. With disturbed
Figure 52.4 Example of a high vasogenic elevation of ICP autoregulation, changes in ABP are transmitted to the
(plateau wave) caused by a vasodilatation provoked by an intracranial compartment resulting in a pressure-
initial short-term decrease in ABP passive effect.
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222 MONITORING
The correlation coefficient between changes in mean transducer or transducer tipped intraparenchymal
ABP and ICP (termed the PRx index = pressure- sensors.
reactivity index) is either negative or near to 0 when • The PRx reflects autoregulatory reserve of cere-
cerebral vessels are pressure-reactive. A positive cor- bral blood vessels.
relation coefficient indicates disturbed cerebrovascu- • Analysis of the ICP pulse waveform gives useful
lar pressure-reactivity. This index may fluctuate with information regarding adequacy of CPP.
time as ICP and CPP varies (Fig. 52.6), but on aver-
age it is predictive of outcome.
FURTHER READING
Narayan RK, Kishore PR, Becker DP, et al. Intracranial
ICP AND OUTCOME pressure: to monitor or not to monitor? A review of our
experience with severe head injury. J Neurosurg 1982;
FOLLOWING SEVERE HI 56(5): 650–659
In severe HI, an average ICP above 25 mmHg is Czosnyka M, Czosnyka Z, Pickard JD. Laboratory testing
associated with a twofold-increased risk of death. In of three intracranial pressure microtransducers: technical
addition, RAP and PRx indices are strong predictors report. Neurosurgery; 1996, 38: 219–224
of death, and may be stronger than mean ICP. Good
Ghajar J. Intracranial pressure monitoring techniques. New
vascular reactivity is an important element of brain Horiz 1995; 3(3): 395–399
homeostasis, enabling the brain to protect itself
against uncontrollable rises in intracerebral volume. Bruder N, N’Zoghe P, Graziani N, Pelissier D, Grisoli F,
Francois G. A comparison of extradural and intraparenchy-
matous intracranial pressures in head injured patients.
Intens Care Med 1995; 21(10): 850–852
KEY POINTS
Portnoy HD, Chopp M, Branch C, Shannon M.
• Measurement of ICP allows us to estimate CPP. Cerebrospinal fluid pulse waveform as an indicator of cere-
• The two commonly used methods of measuring bral autoregulation. J Neurol Neurosurg Psychiatry 1997;
ICP are intraventricular catheters with an external 63: 721–731
Figure 52.6 Long-term (6 days) monitoring of ICP, ABP, CPP, PRx and
correlation coefficient between mean ICP and its pulse amplitude (RAP)
in a patient who died following severe HI. Initial ICP was moderately ele-
vated (25 mmHg) with a good compensatory reserve (RAP around 0)
and good vascular reactivity (PRx also around 0). On day 2 ICP started
to oscillate slowly from 20 to 60 mmHg, RAP increased indicating
decrease in cerebrospinal compensatory reserve but PRx remained
around 0 indicating good cerebrovascular reactivity. On day 4, PRx
increased to positive values (loss of cerebrovascular reactivity) and RAP
decreased at a mean ICP of around 50 mmHg (indicating terminal
derangement of cerebrovascular responses). Brainstem death was con-
firmed on day 6
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53
JUGULAR VENOUS OXIMETRY
A.K. Gupta
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226 MONITORING
Jugular venous oximetry (SjvO2) is a method of esti- lactate and glucose which is technically easy and
mating global cerebral oxygenation and metabolism. cheap. However, this method will only give a ‘snap-
shot’ of the state of cerebral oxygenation and
metabolism at the time of sampling, and samples may
INSERTION TECHNIQUE be contaminated by factors such as extracranial
venous blood, especially if catheter placement is too
A catheter is inserted into the internal jugular vein low, against the petrosal veins, or if blood sampling is
using a Seldinger technique and advanced cephalad too rapid.
beyond the outlet of the common facial vein into the
jugular bulb at the base of the skull (Fig. 53.1). Insertion of fibreoptic catheters enable continuous
Correct placement is confirmed when the catheter tip monitoring of SjvO2 with normal values ranging from
is level with the mastoid air cells on a lateral neck 60 to 75%. No blood samples need to be taken except
radiograph. for initial calibration. The advantages of a continuous
on-line display of SjvO2 are easily apparent. This
technique, however, does have its disadvantages.
SITE OF PLACEMENT Calibration drift may occur and frequent in vivo
It was previously thought that the superior saggital recalibration may be required. Inaccurate readings
sinus drained into the right IJV and jugular bulb can be obtained if the sensor is impacted against the
catheters were generally placed on the right to sample vessel wall or if there is a decrease in intensity of the
the most representative side of the brain. However, near infrared light in the fibreoptic sensor which
more recent data suggest that the venous drainage is occurs with thrombus formation on the catheter tip,
less lateralised, and the dominant side of venous changes in head position or blood flow characteristics
drainage can be determined by sequential manual in the vein.
compression of the IJV on each side. The side with the
largest rise in ICP is the dominant side and should be
FACTORS AFFECTING SjvO2
cannulated. If the dominant side is not easily detected,
the side of the brain with the most pathology is used. Although SjvO2 does not give quantitative informa-
In many centres, however, it is still common practice tion about either CBF or CMRO2, it reflects the bal-
to cannulate the right side, which is usually the domi- ance between the two variables. Reductions in SjvO2
nant IJV. Contraindications and complications are or increases in AJDO2 below 9 ml/dl provide useful
similar to those of an internal jugular CVP line. markers for inadequate CBF. Causes of altered SjvO2
are given in Figure 53.2.
The threshold of SjvO2 below which cerebral
METHODS OF MEASUREMENT ischaemia occurs may vary with the individual and
Serial samples can be taken to estimate SjvO2, arterio- the pathology. The two most common causes of
jugular differences in oxygen content (AJDO2 ), jugular bulb desaturation (SjvO2 < 55%) are:
1. Decreased CPP due to raised ICP or systemic
hypotension.
2. Hypocapnia: In head-injured patients, SjvO2 values
less than 50% have been shown to increase mortal-
ity.1 In patients undergoing cardiopulmonary
bypass for cardiac surgery, cerebral venous desatu-
ration below 50% correlated with worse postoper-
ative cognitive function.2
CLINICAL APPLICATIONS
A rise in ICP associated with a normal or low SjvO2
would suggest that oedema is the predominant cause.
If ICP and SjvO2 were both high, hyperaemia would
Figure 53.1 Placement of the jugular bulb catheter in the be implicated and hyperventilation the appropriate
IJV. Note the tip of the sensor should be above the common therapy SjvO2 may therefore help target appropriate
facial vein therapy.
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Vasospasm Pain
LIMITATIONS
Hypotension Light anaesthesia
The main limitation of this form of monitoring is that
Hypoxia
it is a global measure and a regional change in cerebral
Cardio-respiratory insufficiency oxygenation will not be detected unless it is of suffi-
Anaemia
cient magnitude to affect overall brain saturation. It is,
however, the most widely used monitor for cerebral
Haemorrhage oxygenation in neuroanaesthesia and intensive care.
Hb abnormalities
Sepsis
KEY POINTS
SjvO2 • SjvO2 is a global measure of the balance of CBF
and CMRO2.
• Insertion technique and complications are similar
to an internal jugular central venous line.
• Measurement can be intermittent or continuous.
• Measurement of SjvO2 is useful in monitoring
interventions such as hyperventilation therapy.
• Lack of sensitivity to regional changes is a major
Oxygen delivery Oxygen consumption
limitation.
228 MONITORING
of jugular venous oxygen saturation in head-injured Glower DD, Reeves JG, Newman MF. Jugular bulb
patients. J Neurosurg 1992; 76: 212–271 saturation and mixed venous saturation during car-
2. Croughwell ND, White WD, Smith LR, Davis RD, diopulmonary bypass. J Card Surg 1995; 10: 503–508
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54
NEAR INFRARED
SPECTROSCOPY
A.K. Gupta
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230 MONITORING
EQUIPMENT
Near infrared instruments are made for clinical use by Figure 54.1 Principle of NIRS. (Reproduced with permis-
a number of manufacturers. Light is generated at up sion from Al-Rawi.)
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232 MONITORING
Germon TJ, Young AER, Alexander R, Manara AR, monitored by near infrared spectroscopy. J Neurol
Nelson RJ. Extracerebral absorption of near infrared light Neurosurg Psychiatry 1995; 58: 477–479
influences the detection of increased cerebral oxygenation
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55
MEASUREMENT OF TISSUE
OXYGENATION
A.K. Gupta
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234 MONITORING
Figure 55.1 Diagrammatic representation of a cross section of the NeurotrendTM sensor. (Reproduced
with permission from Codman UK.)
55-GUPTA-55-cpp 6/2/01 12:06 pm Page 235
MEASUREMENT OF T I S S U E O Y G E N A T I O N 235
care and in the operating room. Tissue PO2 (PbO2) is effects of temporary clipping on brain tissue parame-
normally lower than arterial PaO2 due to the extra- ters of O2, CO2 tension and pH is shown in Figure
vascular sensor placement and high metabolic activity 55.2.
of the brain (range 15–50 mmHg); PbCO2 is normally
higher than PaCO2 and is directly related, reflecting
RESPONSE TO PHYSIOLOGICAL
the high diffusibility of CO2 (range 40–70 mmHg);
VARIABLES
pH is normally lower in brain tissue (pHb), also
reflecting high brain metabolism (range 7.05–7.25). Reduction in PbO2 as a result of arterial desaturation
has been demonstrated by numerous authors. In
Head injury head-injured patients a rise in PbO2 occurs in
response to increased inspired O2. A correlation
PbO2 tension is generally lower in HI, with reported
between PbO2 and regional CBF has been reported.
values < 10 mmHg. Demonstrable rises in PbCO2
Tissue CO2 and pH seem to change in parallel with
and concomitant falls PbO2 and pHb occur during
arterial CO2 and pH except in ischaemia when
brain death. Changes in these parameters have been
PbCO2 increases and pHb decreases.
shown to be different in normal and abnormal areas
of brain. These sensors are useful in monitoring
changes in trends of cerebral oxygenation, detecting
secondary insults and guiding specific therapy such as SAFETY AND VALIDATION
hyperventilation and induced hypothermia.
There have been many reports of the use of these
sensors in both animal and human studies with no
Subarachnoid haemorrhage
reports of any major complications to date. Stable and
Profound changes in all parameters have been shown reproducible results have been published which cor-
in various studies with prolonged temporary clipping relate with in vitro methods. Changes in PbO2 have
of feeder vessels during surgery. This has correlated been shown to correlate well with changes in SjvO2
well with changes in brain chemistry using microdial- and end capillary PO2 measured by positron emission
ysis (see Chapter 56, Fig. 56.2). An example of the tomography.
Figure 55.2 Tracing from a Neurotrend TM monitor showing changes in brain tissue PO2, PCO2 and pH as a
result of temporary clip application of an artery feeding an MCA aneurysm shown by the arrows. (Reproduced
with permission from R. Kett-White.) PbO2 decreases to 0 after both episodes of temporary clipping. Tissue CO2
rises and pH falls after the first episode of clipping. Tissue O2 recovers when the clip is removed
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236 MONITORING
56
MICRODIALYSIS
P. J. A. Hutchinson
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238 MONITORING
CLINICAL APPLICATIONS
Cerebral microdialysis has been applied to patients in
intensive care and the operating room.
Head injury
Figure 56.1 Diagram of a concentric microdialysis catheter
consisting of two tubes. Physiological solution is pumped Derangements in metabolism associated with reduc-
between the space of the outer tube of dialysis membrane tions in brain glucose and elevation of the
and the inner tube. Molecules diffuse across the membrane
from extracellular fluid into the physiological solution and on lactate:pyruvate ratio have been demonstrated during
reaching the tip of the catheter, pass up the inner tube into periods of intracranial hypertension and cerebral
collecting vials for analysis ischaemia. Wide variations in the concentration of
56-GUPTA-56-cpp 6/2/01 12:07 pm Page 239
MICRODIALYSIS 239
the excitatory amino acids glutamate and aspartate Epilepsy
have also been detected, with extremely high levels
Epileptic foci in the temporal lobe are associated with
in secondary ischaemia and contusions.
elevated glutamate and reduced g-amino-butyric acid
levels prior to seizures and increases in both amino
Subarachnoid Haemorrhage
acids during seizures.
During aneurysm surgery, changes in concentration
of glucose, lactate, pyruvate and glutamate have been Tumours
demonstrated during CSF drainage, brain retraction
By implanting the microdialysis catheter directly into
and temporary clipping. The combination of micro-
gliomas, chemotherapeutic agents can be added to
dialysis and multiparameter sensors can monitor the
the perfusion fluid and delivered to the centre of the
effect of clinical events on brain metabolism (Fig.
tumour.
56.2). The chemistry of ventilated patients with poor
grade SAH on the intensive care unit can also be
assessed.
KEY POINTS
• Microdialysis directly measures the concentration
of substrates and metabolites in the extracellular
space including substances such as glucose, pyru-
vate, lactate and neurotransmitters.
• It is presently used as a research technique to mon-
itor the progress of the injured brain and to
increase understanding of disease processes.
FURTHER READING
Editorial: Microdialysis. Lancet 1992; 339: 1326–1327
Hutchinson PJA, Al-Rawi PG, O’Connell MT, et al.
Monitoring of brain metabolism during aneurysm surgery
using microdialysis and brain multiparameter sensors.
Neurol Res 1999; 21: 352–358
Mendelowitsch A, Sekhar LN, Wright DC, et al. An
increase in extracellular glutamate is a sensitive method of
detecting ischaemic neuronal damage during cranial base
and cerebrovascular surgery. An in vivo microdialysis study.
Acta Neurochir Wien 1998; 140: 349–355
Persson L, Valtysson J, Enblad P, et al. Neurochemical
monitoring using intracerebral microdialysis in patients
with subarachnoid haemorrhage. J Neurosurg 1996; 84:
606–616
Robertson CS, Gopinath SP, Uzura M, Valadka AB,
Goodman JC. Metabolic changes in the brain during tran-
sient ischemia measured with microdialysis. Neurol Res
1998; 20 (Suppl 1): S91–S94
Ungerstedt U. Microdialysis-principles and applications for
Figure 56.2 Perioperative mean arterial blood pressure studies in animals and man. J Intern Med 1991; 230:
(MAP), arterial oxygen (pO2a), brain oxygen (pO2b), and 365–373
microdialysis parameters in a patient undergoing aneurysm
clipping. Arrow 1 indicates a decrease in (pO2b) associated Vespa P, Prins M, Ronne-Engstrom E, et al. Increase in
with mild hypotension (measured using an intraparenchymal extracellular glutamate caused by reduced cerebral perfu-
multiparameter sensor – Paratrend“). This was accompanied sion pressure and seizures after traumatic brain injury: a
by decreases in glucose and pyruvate and increases in lac- microdialysis study. J Neurosurg 1998; 89: 971–982
tate and glutamate. Arrow 2 indicates a second decrease in
(pO2b) due to hydrocephalus which recovered on re-opening Whittle IR. Intracerebral microdialysis: a new method in
the dura (arrow 3). (Reproduced with permission from applied clinical neuroscience research. Br J Neurosurg
Hutchinson et al. Neurosurgery 2000; 46: 201–206.) 1990; 4: 459–462
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57
EVOKED POTENTIAL
AND PERIPHERAL
NEUROPHYSIOLOGY
B. McNamara
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242 MONITORING
INTRODUCTION
Evoked potentials are the electrical response of the
cerebral cortex, subcortical nuclei, brainstem and
spinal cord to a peripheral sensory stimulus. Nerve
conduction studies (NCS) and EMG are used to
examine the peripheral nervous system.
EVOKED POTENTIALS
The most commonly used are the visual evoked
potential (VEP) which is the response of the occipital
cortex to a visual stimulus (normally a flash or a
reversing checkerboard), the brainstem auditory
evoked potential (BAEP) which is the response of
brainstem nuclei to a simple auditory stimulus and the
somatosensory evoked potential (SEP) which is the
response of the cerebral cortex and spinal cord to
peripheral sensory stimulation (normally electrical
stimulation of a sensory or mixed peripheral nerve).
These responses are quite small when compared with
background electrical activity and to improve resolu-
tion of the response the average response to a large
number of stimuli is produced.
SOMATOSENSORY EVOKED
POTENTIALS (SEP)
The upper limb SEP is produced by electrical stimula-
tion of the median or ulnar nerve. The lower limb SEP
is produced by electrical stimulation of the posterior
tibial nerve. The cortical and spinal cord responses are
summarised in Figure 57.1. The spinal recorded
response is generated by dorsal horn interneurones
(P15), the first cortical recorded response (N20) is Figure 57.1 The cortical (A) and spinal SEP (B). The princi-
generated by the posterior bank of the rolandic fissure. pal cortical components (N20/P22) are generated by the pri-
mary somatosensory cortex. The N9 component of the spinal
Clinical Applications SEP is generated in the brachial plexus while the N13 is gen-
erated in the dorsal column and dorsal horn
Measurement of peak latency and peak-to-peak
amplitude of the SEP is a particularly useful means of
monitoring spinal cord and brain function during the SEP is a useful alternative to EEG monitoring in
surgery. carotid surgery.
244 MONITORING
Table 57.1 Some neuromuscular conditions causing respiratory failure and the findings
found on nerve conduction studies and EMG
58
ELECTROENCEPHALOGRAPHY
AND CEREBRAL FUNCTION
MONITORING
B. McNamara
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248 MONITORING
100 Awake
Light to moderate sedation
70 Light hypnotic state
Low probability of explicit recall < 70
60 Moderate hypnotic state
Low probability of consciousness < 60
40 Deep hypnotic state
0 EEG suppression
CLINICAL APPLICATIONS
The commonest application of EEG is in the investi-
gation and management of epilepsy. Although up to
50% of patients with epilepsy may have a normal
Figure 58.4 Burst suppression, this characteristic pattern
EEG; the EEG can help confirm the diagnosis, clas- consists of bursts of EEG activity which alternate with periods
sify the seizure disorder and identify a focal or later- when the EEG is virtually isoelectric. This is also associated
alised epileptogenic source. with a characteristic pattern on CFM monitoring
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250 MONITORING
within an epoch of ≥ 0.5 seconds during which EEG but is not a depth of anaesthesia monitor or a pre-
voltage is ≤ 0.5 mV) by the epoch length. dictor of movement under anaesthesia. The
advantages of BIS may include a reduction in the
Other i.v. induction agents with the exception of amount of anaesthetic agent used intraoperatively,
ketamine, produce a similar pattern with loss of α and a faster wake-up and extubation with more alert
varying degrees of β, θ or δ activity. Ketamine acti- and oriented patients in PACU.
vates the EEG at low doses and synchronisation
(lower frequency and higher amplitude) at higher
doses. Opioids produce an excess of δ and θ activity EEG IN THE ICU
at high concentrations. Norpethidine (a metabolite of
pethidine) is proconvulsant after accumulation. EEG can be easily performed during intensive care
without moving the patient. It is particularly useful in
All inhalational agents activate the EEG at very low the following circumstances:
concentrations with α activity recorded over the
entire cortex, especially the frontal leads. Higher con- 1. Seizure management: To confirm the diagnosis and
centrations synchronise the EEG with lower frequen- detecting subclinical seizures.
cies predominating until burst suppression is reached, 2. Diagnosis of certain neurological disorders (Table
followed by an isoelectric EEG when there is maxi- 58.2).
mally suppressed cortical electrical activity. The con-
centration required to do this varies between agents.
This occurs at around 2 MAC for isoflurane, sevoflu- Table 58.2 Neurological conditions with
specific EEG changes
rane and desflurane, and ≥ 4 MAC for halothane.
Enflurane produces seizures above 1.5 MAC depen- Diagnosis EEG feature
dent on pCO2 levels (see Chapter 9). N2O produces a
decrease in α amplitude and frontal high frequency Creutzfeldt-Jakob disease Periodic sharp wave
activity. complexes
Herpes Simplex Temporal periodic
encephalitis lateralized epileptiform
INTRAOPERATIVE EEG MONITORING discharges
Continuous EEG monitoring (normally facilitated by Subacute sclerosing Paroxysmal bursts of
some form of EEG processing such as CFAM) is use- panencephalitis 2–3 Hz
ful in the following circumstances:
1. CEA: EEG patterns correlate with CBF and aid 3. Outcome prediction: Certain EEG features are asso-
the decision to shunt during cross-clamping. ciated with a poor outcome and in some cases may
Hypoxaemia produces an acute increase in ampli- be useful in predicting eventual survival. Various
tude of the EEG initially followed by a reduction grading systems have been developed based on the
in amplitude and the appearance of slow waves but presence or absence of these features (Table 58.3).
may be masked by deep anaesthesia. Persistent Grades I and II are associated with a good outcome,
EEG changes may predict neurological deficit. grade III an intermediate prognosis, grades IV and
2. Cardiac surgery: EEG may be used to detect cere- V are associated with a very poor outcome.
bral ischaemia during extra-corporeal circulation
or monitor barbiturates given to provide neuro-
protection (see Chapter 40). Table 58.3 Grading system for outcome
3. Other surgery: Sphenoidal or foramen ovale elec- prediction by EEG
trodes and electrocorticography (direct recording
from the cortical surface during surgery) are also Grade I Dominant a, reactive
useful for epilepsy surgery and evaluation of effects Grade II Dominant q-d, reactive
of temporary occlusion of blood flow.
4. Assessing depth of anaesthesia? Almost all anaesthetic Grade III Dominant d-q, no a
agents produce a discernible evolution of the EEG Grade IV Burst Suppression
as depth of anaesthesia increases. However, the Low voltage d, unreactive,
pattern of evolution of the EEG with increasing periodic general phenomena
anaesthetic depth shows a great deal of variation Grade V Very low voltage EEG
between individual patients and this is not used Isoelectric EEG
clinically. BIS correlates with hypnotic endpoints
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59
TRANSCRANIAL DOPPLER
ULTRASONOGRAPHY
B. Matta
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254 MONITORING
M1CA, M2CA, segments of middle cerebral artery; ACA, anterior cerebral artery; P1CA, P2CA, segments of
posterior cerebral artery; VA, vertebral artery; BA, basilar artery; OA, ophthalmic artery, ICS, internal carotid
syphon. N.B. flow velocity decreases with age.
CEREBRAL AUTOREGULATION
Autoregulation of CBF is a complex process composed
of at least two mechanisms operating at different rates;
a rapid response sensitive to pressure pulsations
(dynamic autoregulation) followed by a slow response
to changes in mean pressure (static autoregulation).
Both of these processes can be tested using TCD.
The static rate of autoregulation or the index of
autoregulation (IOR) is the ratio of percentage
change in estimated cerebral vascular resistance
(CVRe) to percentage change in mean blood pres-
Figure 59.2 Method of determining systolic (Vs), diastolic
sure (MBP). An IOR of one implies perfect autoreg-
(Vd) and time averaged mean flow velocity (Vmean) from the ulation and an IOR of zero complete disruption of
spectral outline autoregulation.
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256 MONITORING
SAH
TCD is an unreliable measure of CBF in patients
with SAH because of vasospasm-associated changes
in vessel diameter. However, for a given blood flow,
a reduction in vessel diameter is associated with an
increase in FV. Therefore, cerebral vasospasm is con-
sidered present when FVmca > 120 cm.sec-1 or the ratio
between the FVmca and FV in the internal carotid
artery (the Lindegaard ratio) exceeds 3.
Figure 59.3 Typical middle cerebral artery blood flow
velocity response to short compression of the common carotid TCD can also be used during test occlusion on ICA
artery in a healthy volunteer (A), and a patient with impaired in patients with giant aneurysms.
autoregulation (B)
60
APPLICATION OF
MULTIMODAL MONITORING
A.K. Gupta
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260 MONITORING
INTRODUCTION
Secondary brain injury may result from raised ICP,
inadequate oxygenation or CBF which occur by
mechanisms which are complex and multiple. These
processes occur frequently and are transient in nature.
The purpose of monitoring the brain either in the
operating room or ICU is to minimise secondary
injury by:
• Detecting harmful pathophysiological events before
they cause irreversible damage to the brain.
• Diagnosing and effectively treating these harmful
pathophysiological processes.
• Providing ‘on-line’ feedback to guide therapy
directed at these processes.
METHODS OF MONITORING
Continuous cerebral monitoring requires a combina-
tion of routine systemic methods and specialised
techniques specific for the brain:
• Systemic methods: These detect systemic changes,
which may contribute to secondary brain injury
Figure 60.1 Changes in oxyhaemoglobin (HbO2), deoxy-
such as hypoxia, hypotension or profound haemoglobin (Hb), SjvO2 CPP and SjO2 with arterial desatu-
hypocarbia. These methods include measurements ration (SaO2). See text for explanation. (Reproduced with
of arterial BP, central venous ± pulmonary artery permission from M Czosnyka.)
occlusion pressure, arterial blood gases, tempera-
ture, pulse oximetry and capnography. oximetry is not detected by SjvO2, whereas it is
• Brain-specific methods: These enable observations to reflected by the rise in deoxyhaemoglobin and
be made of different variables reflecting changes in reciprocal fall in oxyhaemoglobin. A rise in CPP
cerebral haemodynamics, brain oxygenation and and cerebral blood FV is also seen.
metabolism. Current techniques include con- 2. Although monitoring of a single modality will
tinuous ICP measurements, TCD, NIRS, jugular yield useful information, it is possible that the
venous oxygen saturation (SjvO2), laser Doppler observed changes may lead to misinterpretation of
flowmetry and electrophysiology (EEG, CFM). events. The addition of other modalities will help
More recently, continuous on-line estimation of to correctly interpret the acquired data and
brain tissue oxygenation using tissue sensors and thereby make the right diagnosis. This is demon-
brain tissue chemistry using microdialysis have strated in Figures 60.2 and 60.3. In Figure 60.2 the
been used. The principles behind these specific rise in ICP is accompanied by a fall in SjvO2, laser
methods and their clinical utility are detailed in Doppler flow (LDF), CPP and FV. This indicates
their individual chapters. that the rise in ICP was a primary event causing a
reduction in CBF. Figure 60.3 shows FV, LDF
and total haemoglobin (tHb) rising with an
APPLICATION OF increase in ICP indicating that this was due to
cerebral hyperaemia. The ability to differentiate
MULTIMODAL MONITORING between the two causes of raised ICP has major
1. While each of the methods has definite advantages, implications for the direction of treatment.
the drawbacks and limitations of each method are 3. The multimodal monitoring systems allow more
different and do not usually coincide. An example reliable decisions to be made intraoperatively. For
of this is demonstrated in the monitoring of a head- example brain tissue oxygen sensors in combina-
injured patient shown in Figure 60.1. NIRS and tion with microdialysis has been shown to help
SjvO2 are both measures of cerebral oxygenation determine safe duration of temporary clipping
but the systemic desaturation shown by pulse during cerebral aneurysm surgery (see Chapter 56).
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KEY POINTS
• Monitoring single variables is useful but has signif-
icant limitations.
• Multimodal monitoring gives greater versatility
and power of diagnosis.
• Secondary insults of short duration are less likely
to be missed.
• General systemic monitoring is part of the multi-
modal approach.
• Computer support is essential for data acquisition
and analysis.
FURTHER READING
Czosnyka M, Kirkpatrick PJ, Pickard JD. Multimodal
monitoring and assessment of cerebral haemodynamic
reserve after severe head injury. Cerebrovasc Brain Metab
Rev 1996; 8: 273–295
Figure 60.3 Secondary rise in ICP due to cerebral hyper- Kirkpatrick PJ, Czosnyka M, Pickard JD. Multimodal
aemia demonstrated by a rise in FV, LDF, SjvO2 and HbO2. monitoring in neurointensive care. J Neurol Neurosurg
(Reproduced with permission from M Czosnyka.) Psychiatry 1996; 60: 131–139
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262 MONITORING
Hutchinson PJ, Al-Rawi P, O’Connel MT, et al. Kirkpatrick PJ, Lam J, Al-Rawi P, Smielewski P, Czosnyka
Monitoring of brain metabolism during aneurysm surgery M. Defining thresholds for critical ischemia by using near
using microdialysis and brain multiparameter sensors. infrared spectroscopy in the adult brain. J Neurosurg 1998;
Neurol Res 1999; 21: 352–358 89: 389–394
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61
ANAESTHESIA AND
MUSCULAR DYSTROPHY
T. Leary
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INTRAOPERATIVE MANAGEMENT
KEY POINTS
Induction agents should be used carefully due to
enhanced cardiovascular and respiratory depressant • Muscular dystrophies are characterised by muscle
effects. Propofol has been implicated in the genera- weakness and wasting, without evidence of den-
tion of myotonia. A balanced technique using opioids ervation.
and inhalation agents is thought to be safe. • There is often cardiac and respiratory involve-
Ventilation using a cuffed endotracheal tube, should ment. Anaesthesia and postoperative care should
be assisted even for short procedures. Intubation of be aimed at reducing complications within these
the trachea may not require neuromuscular blockade, systems.
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62
MYASTHENIA GRAVIS
S. Senthuran
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63
AUTONOMIC HYPERREFLEXIA
T. Leary
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272 MISCELLANEOUS
INTRODUCTION TREATMENT
The best management of this condition is prevention.
Autonomic hyperreflexia may be seen in patients However, should an attack occur, the first stage in
with spinal cord injury following resolution of spinal treatment involves removal of the stimulus and treat-
shock and in association with return of the spinal cord ing the afferent limb of the response. This may
reflexes. It is characterised by acute generalised auto- include providing further analgesia, deepening the
nomic overactivity, in response to stimuli below the depth of general anaesthesia or raising the level of
level of the spinal cord lesion. regional anaesthesia. Attempts should also be made to
reduce the efferent limb of the reflex using ganglion-
blocking drugs (trimethaphan), α1 adrenergic
PATHOPHYSIOLOGY receptor antagonists (phentolamine or phenoxy-
benzamine), or direct-acting vasodilators (nitro-
Autonomic hyperreflexia may occur in up to 85% of prusside). Central-acting antihypertensives such as
patients with spinal cord transection above T6 (the clonidine are not predictably effective in treating the
splanchnic outflow). The response is rarely seen in hypertension associated with autonomic hyper-
those with transection below T10. The trigger to this reflexia.
instability or mass reflex involving sympathetic and
motor hypertonus can be cutaneous, proprioceptive
or visceral (such as a distended bladder). Such CONDUCT OF ANAESTHESIA
impulses elicit spinal cord reflexes over the splanchnic Surgery is a potent stimulus to autonomic hyper-
outflow tract. In the presence of cord transection, the reflexia and even patients with no previous history of
descending modulation of these responses is lost, pro- this response may be at risk during operative proce-
ducing persistent vasoconstriction and hypertension. dures. Autonomic hyperreflexia may be seen even in
Subsequent stimulation of the carotid sinus and aortic the presence of general or spinal anaesthesia. A 20%
arch is manifest as parasympathetic activity. Such perioperative mortality rate for patients with spinal
activity may produce bradycardia and vasodilatation cord transection has been reported. Appropriate vaso-
above the level of the spinal cord lesion. constrictors, vasodilators, as well as drugs that increase
or reduce heart rate should be immediately available.
Preoperative intravenous hydration is helpful in pre-
SIGNS AND SYMPTOMS venting hypotension during induction of anaesthesia.
Clinical features of autonomic hyperreflexia include Prior to surgery, a thorough assessment of renal,
vasoconstriction below, and vasodilatation above the cardiac and respiratory (FEV1:FVC ratio) function
level of the spinal cord lesion. Effects of vasodilatation should be undertaken to enable planning of both
above the level of the spinal lesion may manifest in intraoperative and postoperative care.
many ways, nasal congestion for example. Typically,
vasodilatation in the intact portion of the body is General Anaesthesia
insufficient to offset the effects of vasoconstriction, as A smooth induction of anaesthesia is appropriate in
reflected by persistent hypertension. Severe head- these patients in whom sympathetic function is
ache, loss of consciousness and seizures may occur. A unpredictable. Where muscle relaxation is required
precipitous rise in BP may lead to cerebral, retinal, or to facilitate surgery or intubation of the trachea, non-
subarachnoid haemorrhage, as well as increased depolarising muscle relaxants should be used.
operative blood loss. Bradycardia, ventricular Between 48 hours and 6 months following the den-
ectopics and heart block may result from increased ervation injury, suxamethonium should be avoided.
parasympathetic activity. Left ventricular failure and During this time, there may be a fatal hyperkalaemic
dysrhythmias may reflect the effect on a heart work- response reflecting the proliferation of extrajunc-
ing against increasing peripheral vascular resistance. tional cholinergic receptors.
These responses may be fatal.
Local Anaesthesia
Other problems to consider in patients with spinal
cord injury include a tendency to renal failure sec- Regional techniques may be used alone or as a useful
ondary to recurrent urinary tract infection, respira- adjunct to a general technique. Both spinal and
tory insufficiency, muscle spasm and contractures, epidural blockade may be effective at preventing the
poor temperature regulation, gastric haemorrhage mass response. However, control of block height may
and stasis. not be easy to attain. Epidural anaesthesia has been
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64
MANAGEMENT OF PATIENTS
FOR MULTI-ORGAN
DONATION
Q. Milner
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65
BASIC CONCEPTS OF
NEUROIMAGING
J.H. Gillard
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280 MISCELLANEOUS
INTRODUCTION
Imaging for patients requiring neurocritical care who
have not had surgery is usually performed in trauma
and SAH. The primary objectives of imaging focus
on clearing the cervical spine and defining the extent
and prognosis of any intracranial injury. This involves
the use of plain films and CT. Postoperative imaging
is primarily performed to assess haemorrhage, mass
effect and cerebral oedema.
SPINAL TRAUMA
There is a high incidence of cervical spine injury
associated with cases of multiple trauma. A lateral
cervical spine radiograph is invariably obtained in the
Accident and Emergency Department on admission.
Further views involve an antero-posterior (AP)
projection of the whole cervical spine as well as an open
mouth AP projection to demonstrate the C1/C2
articulation. Tracing curves connecting the anatomical
landmarks outlined in Table 65.1 is a simple and
essential part of interpretation (Fig. 65.1). The presence
of a step in one of these lines or soft tissue swelling
suggests a fracture or dislocation. It is important to
ensure that the C7/T1 junction is imaged; a dedicated
swimmer’s projection or oblique trauma projections
are sometimes necessary. CT, with two-dimensional
(2D) and three-dimensional (3D) reconstructions can
be very helpful in confirming or excluding an under-
lying fracture provided that it is used in a targeted Figure 65.1 Demonstrates the lines connecting the anterior
manner. Figure 65.2 demonstrates a unilateral facet dis- and posterior margins of the vertebral bodies, as well as the
location of C2 on C3 where the inferior facet of C2 has bases of the spinous processes. A further smooth curve can
be traced between the tips of the spinous processes. The
moved anteriorly, becoming perched on the anterior space between the odontoid peg and C1 should measure
border of the underlying superior facet of C3. 3 mm or less in an adult (arrows)
Normal soft tissue accounts for approximately one-
third of the width of the vertebral body from C1 to
282 MISCELLANEOUS
284 MISCELLANEOUS
aneurysms occur in up to 15–20% of cases. In patients Management is centred on preventing rebleeding and
with more than one aneurysm, the presence of an vasospasm.
irregular ‘nipple’ on one of them suggests recent rup-
ture. Not infrequently, no source of haemorrhage is
seen on the initial cerebral angiogram, which must RAISED ICP
include injection into the anterior circulation bilater-
The brain is vulnerable to swelling because it lies
ally, as well as the posterior circulation. If only one
within a rigid skull. Brain oedema will, therefore, result
vertebral artery injection is used, this must reflux into
in raised ICP and risks herniation. Herniation of brain
the contralateral vertebral artery to identify the origin
can take a number of forms: tonsillar or cerebellar her-
of the contralateral posterior inferior cerebellar artery.
niation through the foramen magnum, superior ver-
Repeat angiography approximately 5–7 days later
mian herniation, temporal lobe (uncal) herniation,
may identify an occult aneurysm that may have been
subfalcine herniation and transtentorial herniation.
tamponaded by local haemorrhage (a yield of
Mass effect can lead to associated hydrocephalus, e.g.
approximately 6%). A negative repeat conventional
effacement of the 4th ventricle, causing dilatation of
angiogram suggests non-aneurysmal SAH (occurring
the 3rd and lateral ventricles as well as uncal hernia-
in up to 15% of cases), which is frequently perimes-
tion causing contralateral temporal horn dilatation.
encephalic. Such haemorrhage is possibly venous in
Raised ICP itself causes effacement of the ventricles
origin and carries a good prognosis.
and CSF spaces (Figs 65.10 and 65.11). The diagnosis
SAH may be associated with cerebral oedema, raised of raised ICP can be difficult in young people as the
ICP, parenchymal haemorrhage (due to a jet effect) lateral and 3rd ventricles can be small in normal indi-
and intraventricular haemorrhage. Intraventricular viduals. A lack of sulcal effacement and the presence
haemorrhage frequently leads to hydrocephalus. of normal CSF cisterns makes raised ICP less likely.
Figures 65.10 & 65.11 These figures demonstrate features of raised intracranial pressure. There is almost complete efface-
ment of the basilar and suprasellar cisterns (Fig. 65.10). The 3rd ventricle is slit like (Fig. 65.11)
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NEUROANAESTHESIA IN
PREGNANCY
P. Popham
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67
THROMBOLYSIS IN ACUTE
STROKE
A. Coles
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290 MISCELLANEOUS
Index
Note: bold page numbers indicate figures and tables
abscesses 48 cerebrum 3
acoustic neuromas 2, 65–7 posterior fossa 11–14
anaesthesia 65–7 boundaries 12
monitoring 66 spinal cord 3–5
pre-, intra- and postoperative management 66–7 aneurysm see cerebral aneurysm
size and mortality 66 anticonvulsants 33, 43–5
surgical approaches 66 classification of seizures and treatment 44
acromegaly 83 combination therapy and interactions 44–5
ACTH, and Cushing’s disease 83 dosing schedules and side-effects 44
action potential, compound motor action potential (CMAP) 243 mechanisms of action 44
Adamkewicz, arteria magna 4 neuroprotection in ICU 171
Addenbrooke’s NCCU, ICP/CPP algorithm, head injury 159 side-effect (S/E) profile 45
adenosine therapeutic serum levels and dosing schedules 45
neuroprotection in ICU 172 antidiuretic hormone (ADH) 180
regulation of CBF 20 SIADH 185
air embolism 61–3 antihypertensives 41
detection 62 anxiolytics 188
capnography 62 apnoea testing 208
end-tidal nitrogen 62 Arnold–Chiari malformations 134
precordial Doppler device 62 arrhythmias, posterior fossa surgery 59
pulmonary artery preessure 62 arterial blood pressure see mean arterial pressure (MAP)
pulse oximetry 62 arterial identification, and flow velocities (TCD) 254
transoesophageal echocardiography 62 arteriovenous malformations
management 62 craniotomy 54–5
pathophysiology 62 pathophysiology 54
posterior fossa surgery 59 postoperative management and complications 55
prevention 62–3 preoperative and intraoperative management 55
airway management interventional neuroradiology 113
awake craniotomy 74 paediatrics 127
cervical spine surgery 95–6 astrocytomas 58
craniofacial surgery 130 atracurium 159
laryngeal mask airway (LMA) 99, 118 atrial natriuretic factor, salt wasting syndrome 185
post-anaesthesia recovery and PACU 142 auditory evoked potentials 79
posterior fossa surgery 59 autonomic hyperreflexia 272–3
alfentanil 40, 188 autoregulation see mean arterial pressure
alpha blockers 41 azathioprine, myasthenia gravis 268
anaesthesia
acoustic neuromas 65–7 balloon angioplasty, vasospasm 167
head injury 89–92 barbiturates 32
interventional radiology 111–13 neuroprotection in ICU 170–1, 171
paediatric neurosurgery 127 basal ganglia, anatomy 3
see also inhalational; intravenous anaesthetic agents basilar artery 13
analgesics 188 Becker muscular dystrophy, anaesthesia 264
anatomy 1–18 Beer—Lambert law, optical attenuation 230
brain and spinal cord 1–5 benzodiazepines 33, 188
brainstem 2–3 effect on CBF 21
cranial nerves and functions 2 status epilepticus 197
cerebellum and deep structures of brain 3 beta blockers 41
cerebral circulation 7–10 bispectral analysis (BIS) 249
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294 INDEX
blood pressure see mean arterial pressure (MAP) aneurysm rupture and treatment guidelines 52, 54
blood—brain barrier 10, 158, 184 induction of anaesthesia 53
bradycardia maintenance/monitoring 53
carotid endarterectomy 108 pre-, intra- and postoperative management 53–4
cranial nerve compression 2, 59 temporary clipping/induced hypotension 53–4
brain interventional neuroradiology, Guglielmi coils 112–13
anatomy 1–3 natural history and predisposing factors 52
cerebral circulation 7–10 presentation 52–3
brain injury cardiac dysfunction 52–3, 165
haemostatic response 192 hydrocephalus 52
oedema, intraoperative management 49 re-bleeding 52
secondary subarachnoid haemorrhage 52
initial trauma and ischaemia 170 TCD 256
systemic and intracranial causes 90 vasospasm 53
swelling 91, 284 SEPs 242
see also head injury sites 9
brain protection see neuroprotection in ICU vein of Galen, infant/premature infant 126
brainstem WFNS, SAH scale 52
anatomy 2–3 cerebral blood flow (CBF) 20–2
auditory evoked potentials 79 anatomy of circulation 7–10
function 2 blood viscosity 20–2
brainstem death 207–9 blood–brain barrier 10
children 209 carotid endarterectomy 108–9
diagnostic tests confirming 208–9 chemical 20
apnoea testing 208 calcium 20
caloric testing 208 PaCO2 20
corneal reflex 208 potassium and adenosine 20
facial sensation and motor responses 208 effect of anaesthetic agents on CBF 21
gag and cough reflexes 208 inhalational agents 21
oculocephalic reflex 208 intravenous agents 21
pupillary reflexes 208 opiates 21
and organ donation 275–7 flow–metabolism coupling 20
persistent vegetative state (PVS) 209 index of autoregulation (IOA) 255–6
physiology 276 inotropes 177
subsequent management 209 jugular venous oximetry 157
Brown–Séquard syndrome 5 maintenance 170
measurement 21
calcium, electrolyte disorders 181 dynamic CT 21
calcium channel blockade 41 functional magnetic resonance imaging (fMRI) 21–2
anticonvulsants 44 indirect or non-quantitative 22
neuroprotection in ICU 171 Kety Schmidt technique 21
caloric testing 208 MCAfvx 109, 157
calpain, neuroprotection in ICU 172 single photon emission computed tomography (SPECT) 21
capnography, detection of air embolism 62 tomographic rCBF 21
carbamazepine 44–5 xenon-133 washout technique 21
carbon dioxide, PaCO2 20 microcirculation 10
cardiac arrhythmias, subarachnoid haemorrhage (SAH) 52–3, 165 myogenic (autoregulation) 20, 157, 177, 255–6
cardiopulmonary bypass, NIRS 231 neurogenic 21
cardiovascular management 216 NIRS 231
brainstem death 276 transcranial Doppler (TCD) ultrasonography 253–7
carotid arteries 8–9 vasoconstriction, hypercapnia-induced 40
carotid artery disease venous drainage 9–10
angiography 283 cerebral blood volume (CBV) 24–5
TCD 256 and intracranial pressure 24–5
carotid endarterectomy 107–9 NIRS 109, 157, 229–32
monitoring 109 cerebral function
NIRS 230 analysing monitor (CFAM) 249
pre-, intra- and postoperative management 108–9 monitoring, electroencephalography (EEG) 247–51
regional anaesthesia 108 cerebral ischaemia, near infrared spectroscopy 109
somatosensory evoked potentials (SEPs) 242–3 cerebral metabolic rate: oxygen (CMRO2) 226–7
catecholamines 176 cerebral metabolic suppressants 159
cerebellopontine angle tumours 65–7 cerebral monitoring, continuous 260–1
cerebellum, anatomy 3, 12–13 cerebral oedema, intraoperative management 49
cerebral aneurysm 52–4 cerebral oxygenation measurement 233–6
classification 52 advantages and disadvantages 236
clips, MRI 116 near infrared spectroscopy (NIRS) 109, 157, 229–32
craniotomy 52–4 principles and equipment 234–5
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INDEX 295
clinical applications 234–5 increased ICP 130
head injury 235 congenital myasthenia 268
subarachnoid haemorrhage 235 congenital spinal lesions 133–5
response to physiological variables 235 anaesthetic management 134–5
safety and validation 235–6 assessment and premedication 134
see also cerebral blood flow; cerebral perfusion; jugular venous conduct 134–5
oximetry key problems 134
cerebral peduncles 2 postoperative considerations 135
cerebral perfusion pressure (CPP) 156–8 clinical features 134
Addenbrooke’s NCCU, ICP/CPP algorithm, management of corneal reflex 208
head injury 159 cortical stimulation testing 75
measurement 220 corticospinal tract 3, 4
monitoring 222 cranial nerves
TCD 256 compression, bradycardia 2, 59
target values 158, 176 functions 2
cerebral salt wasting syndrome 182, 185 microvascular decompression 77–9
cerebral vascular reactivity, TCD 255 cranial sutures, premature fusion 126, 130
cerebrospinal fluid 27–9 craniofacial surgery see congenital craniofacial anomalies
comparison of CSF and plasma 28 craniopharyngiomas 83
control of intracranial pressure 24–5 craniotomy, awake 73–5
findings in common disorders 29 background 74–5
secretion and composition 28–9 intraoperative management and problems 74–5
see also hydrocephalus postoperative care 75
cerebrospinal fluid obstruction, paediatrics 126 pre-, intra- and postoperative assessment 74
cervical magnetic stimulation, electromyography 244–5 suitable procedures 74
cervical spine injury 4–5 craniotomy for space-occupying lesions 47–9
instability, fibreoptic intubation 97–101 cerebral oedema 49
neuroimaging 280–1 classification 47–9
cervical spine surgery 93–6 fluid management 49
airway management 95–6 pre-, intra- and postoperative management 48–9
anterior cervical haematoma 95 tumours, primary and secondary lesions 47
extubation 95 craniotomy for vascular lesions 51–5
nutrition 96 arteriovenous malformations 54–5
surgery below C2 96 cerebral aneurysm 52–4
trans-oral, maxillotomy, mandibulotomy with tongue Cushing’s disease 83
split 96 cystoscopy, autonomic hyperreflexia 272–3
positioning for surgery 95–6
anterior and posterior approaches 95 Davson’s equations 28
lateral approaches 95–6 decubitus ulcers, spinal cord injury 147
tracheal intubation 95 degenerative disc disease 104
tracheostomy 95 demyelinating polyneuropathy 200
neurological damage during anaesthesia 94 desflurane 36
practical considerations 94–5 desmopressin (DDAVP) 83, 142, 185
direct laryngoscopy 94 dextrose, hypotonic replacement fluid 185
perfusion pressure 94 diabetes insipidus 83, 182, 185
positioning 94 and organ donation 275–7
spinal cord monitoring during anaesthesia 94–5 diffuse axonal injury (DAI) 91, 282
somatosensory evoked potentials 95, 242 disseminated intravascular coagulation (DIC) 192
cholinesterase inhibitors, myasthenia gravis 268 diuretics
choroid plexus 28 paediatric 138
circle of Willis 2, 8, 9 pregnancy 286
clonazepam 44–5 dopamine 176
coagulation disorders 191–3 droperidol 74, 142
management 192 Duchenne muscular dystrophy, anaesthesia 264
normal haemostatic response to brain injury 192
pathophysiology 192 edrophonium, myasthenia gravis 268
colloid cysts 48 electroencephalography (EEG) and cerebral function monitoring
compound motor action potential (CMAP) 243 247–51
computed tomography, rCBF measurement 21 automated EEG processing 248–51
congenital craniofacial anomalies 129–31 anaesthetic effects 249–50
anaesthetic management 130–1 BIS range guidelines 249
assessment and premedication 130 clinical applications 249
conduct 130–1 conditions with specific EEG changes 250
postoperative considerations 131 grading system, outcome prediction 250
clinical problems 130 ICU 250–1
blood loss 130 intraoperative EEG monitoring 250
difficult airway access 130 preoperative care 249
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296 INDEX
INDEX 297
TCD ultrasonography 157 hypothalamus, anatomy 3
therapeutic targets, selecting monitoring modalities 156–7 hypothermia, neuroprotection in ICU 172
multimodal monitoring 260–1 hypoxaemia, and organ donation 277
neuroimaging 281–2 hypoxia, and nerve fibre types 17
neuroprotection in ICU 169–73
novel neuroprotective interventions 159 image-guided stereotactic surgery 85–7
paediatrics 138 immunophilins, neuroprotection in ICU 172
pathophysiology 90–1 immunosuppressants, myasthenia gravis 268
physiological insults and relation to outcome 156 index of autoregulation (IOA), cerebral blood flow 255–6
pre-, intra- and postoperative management 91 inhalational anaesthetic agents 35–7
secondary brain injury, initial trauma and ischaemia 170 effect on CBF 21
sedation and neuromuscular blockade 158–9 electroencephalography (EEG) 249–50
sequential escalation vs targeted therapy 159–60 examples
target CPP values 158 desflurane 36
treatment 158–9 enflurane 37
ventilatory support, hypocapnia for ICP reduction 158 halothane 36
heart transplantation, organ donation 275–7 isoflurane 36
hemifacial spasm, microvascular decompression 77–9 nitrous oxide 37
HHH therapy (hypertension, hypervolaemia, haemodilution) sevoflurane 36
172, 173 paediatrics 130, 134–5
mean arterial pressure 166 pregnancy 286
Horner’s syndrome 5 inotropes 175–7
Hunt and Hess classification clinical application 176–7
intracranial aneurysms 52 cerebral blood flow maintenance 177
SAH 165 enhancement of blood flow 177
hydralazine 41 MAP pressure autoregulation 177
hydrocephalus indications 176
cerebral aneurysm 52 pharmacology 176
communicating, SAH 165–6 catecholamines 176
delayed 90 clinical effects 176
myelomeningocoele 134–5 dopamine 176
obstructing epinephrine 176
paediatrics 126 norepinephrine 176
SAH 165–6 side effects 176
post SAH 165–6 interventional neuroradiology 111–13
pregnancy 287 anaesthetic drugs and techniques 112
shunt surgery 121–3 aneurysm 112–13
hydroxyethyl starch 184 arteriovenous malformations 113
hygiene management 217 equipment 112
hyperaemia monitoring 113
arteriovenous malformations 55 movement 112
induced by ICP rise 261 safety 112
transient hyperaemic response test (THRT) 256 staff 112
hypercalcaemia 181 intracerebral aneurysm see cerebral aneurysm
hypercapnia, factors affecting SjvO2 226–7 intracerebral haematoma see haematoma
hypercapnia-induced cerebral vasoconstriction 40 intracranial haemorrhage
hyperkalaemia 181 pregnancy 287
hypermagnesaemia 181 stroke 290
hypernatraemia 180–1 intracranial mass lesions see space-occupying lesions
hyperosmolar therapy, head injury management 158 intracranial pressure (ICP) 23–5, 219–23
hyperphosphataemia 181–2 Addenbrooke’s NCCU, ICP/CPP algorithm, management of
hypertension, post-anaesthesia recovery 142 head injury 159
hypertonic fluids 184–5 clinical features of raised ICP 25
hyperventilation paediatrics 126–7, 130
in head injury 158 control 24–5
neuroprotection in ICU 170 cerebral blood volume (CBV) 24–5
hypocalcaemia 181 CSF volume buffering (pressure—volume relationship) 24–5
hypocapnia hydrocephalus 122
ICP reduction 170 factors affecting SjvO2 226–7
ventilatory support in intensive care 158 MAP, changes in ICP in response 221–2
measurement of SjvO2 226–7 measurement methods 220
hypokalaemia 181 intraventricular drains 220
hypomagnesaemia 181 transducer tipped systems 220
hyponatraemia 181 monitoring 25
hypophosphataemia 181–2 head injury management 157
hypophysectomy see transsphenoidal hypophysectomy typical events and trends 220–1
hypothalamic release and inhibiting hormones 82 neuroimaging 284
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myositis, nerve conduction study and EMG 244 psychosocial needs 217
myotonia congenita 265 respiratory management 216
myotonic muscular dystrophy 264 nutrition 211–13
enteral nutrition 212
naloxone 40 head injury management 158
nausea and vomiting 74, 142 management, nursing 216–17
near infrared spectroscopy (NIRS) 157, 229–32 post cervical spine surgery 96
advantages and disadvantages 231 prophylaxis against gastric ulcers in TPN 158
cerebral ischaemia 109 spinal cord injury 147
clinical application 230–1 total parenteral nutrition (TPN) 212–13
equipment 230
neostigmine, myasthenia gravis 268 oculocephalic reflex 208
nerve conduction studies 243–5 opiates, effect on cerebral blood flow (CBF) 21
compound motor action potential (CMAP) 243 opioids
nerves and adjuvant drugs 39–41
functions 15–18 antihypertensives 41
mammalian nerve fibre types 17 naloxone 40
pressure and hypoxia 17 neuromuscular blocking agents 40–1
neural tube defects see congenital spinal lesions cerebral haemodynamics 40
neuroimaging 279–84 CSF circulation 40
head injury 281–2 EEG activity 40
raised ICP 284 sedation and emergence postoperatively 40
SAH 283–4 optical attenuation, Beer—Lambert law 230
spinal cord injury 280–1 organ donation
neurointensive care 145–218 management 277
neurological management 216 transplantation 275–7
neuromuscular blockade oxygenation see cerebral oxygenation measurement
agents 40–1, 188
avoidance during spinal surgery 94 paediatric neurosurgery 125–40
head injury management 158–9 anaesthesia 127
neurones postoperative care 127
action potential 17 cerebrospinal fluid obstruction 126
motor and sensory 16–17 children from 2-7 years 127
neuroprotection in ICU 169–73 congenital craniofacial anomalies 129–31
brain injury mechanisms, initial trauma and ischaemia 170 congenital spinal lesions 133–5
HHH therapy (hypertension, hypervolaemia, haemodilution) head injuries 138
172, 173 pathophysiology 138
non-pharmacological methods 172 pre-, intra- and postoperative management 138
hypothermia 172 infant/premature infant 126
novel mechanisms and targets 172 aneurysm of vein of Galen 126
optimising physiology 170 myelomeningocoele and encephalocoele 126
hyperventilation 170 premature fusion of cranial sutures 126
maintenance of CBF and oxygenation 170 paediatric Glasgow Coma Scale (GCS) 150
normoglycaemia 170 spinal injuries 138–9
pharmacological therapy 170–2 pathophysiology 139
anaesthetic agents 170–1, 171 pre-, intra- and postoperative and intraoperative
calcium channel blockade 171 management 139
excitatory amino acid (EAA) antagonists 171 paramyotonia congenita 265
other novel therapies 172 parenteral nutrition see total parenteral nutrition
sodium channel blockade 171 PARP/caspases, neuroprotection in ICU 172
steroids 171 percutaneous gastrostomy, pre cervical spine surgery 96, 212
principles 170–2 peripheral neurophysiology 243–5
Neurotrend sensor 234–6 nerve conduction studies 243–5
NIRS see near infrared spectroscopy electromyography 243–4
nitric oxide, neuroprotection in ICU 172 persistent vegetative state (PVS) 209
nitrous oxide 37 pethidine, autonomic hyperreflexia 273
NMDA receptors 171 pH sensor 234
norepinephrine 176 pharmacology 31–45
NSAIDS, neuroprotection in ICU 172 anaesthetic agents 170–1, 171
nursing 215–18 anticonvulsants 33, 43–5
cardiovascular care 216 calcium channel blockade 41, 171
elimination 217 excitatory amino acid (EAA) antagonists 171
hygiene 217 inhalational anaesthetic agents 35–7
mobility 217 inotropes 176
neurological care 216 intravenous anaesthetic agents 31–3
nutrition 216–17 neuroprotection in ICU 170–2
pain and sedation 216 NSAIDS 172
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associated injuries 147 neuroprotection in ICU 170–1, 171
bladder 147 pregnancy 286
cardiovascular 147 thoraco-lumbar surgery 103–5
decubitus ulcers 147 degenerative disc disease 104
nutrition 147 general anaesthetic considerations 104–5
pulmonary function 147 position 104–5
during complex cervical spine surgery 94 scoliosis 104
methylprednisolone therapy 147 trauma 104
neuroimaging 280–1 thrombolysis
paediatrics 138–9 exclusions from 290
pathophysiology 146 stroke 289–91
local effects 146 thymectomy 268–9
systemic effects 146 tissue oxygenation see cerebral oxygenation measurement
surgical treatment 147 tissue plasminogen activator, recombinant (rtPA) 289–91
spinal stenosis 104 total parenteral nutrition (TPN) 212–13
spinal tumours 104 carbohydrates 213
spine electrolytes 213
congenital lesions 133–5 lipids 213
see also cervical spine; thoraco-lumbar surgery prophylaxis against gastric ulcers 158
spinothalamic tracts 3–5 proteins 213
spondylolisthesis 104 trace elements 213
status epilepticus 195–8 vitamins 213
definition and incidence 196 tracheal intubation, cervical spine surgery 95
aetiology 196 tracheostomy 203–5
clinical features 196 advantages 204
GCSE in adults 196 cervical spine surgery 95
pathophysiology 196 complications 204
management 196–7 delayed and late 204
stereotactic surgery 85–7 immediate procedural 204
anaesthesia 86 decannulation 205
criteria, anaesthesia 86 indications 204
steroids 147, 171 percutaneous 204
neuroprotection in ICU 171 transcranial Doppler (TCD) ultrasonography 157, 253–7
stroke arterial identification and flow velocities 254
monitoring, TCD 256 CBF 22
thrombolysis 289–91 detection of air embolism 62
subarachnoid haemorrhage (SAH) 163–7 FVmean and FVmax 255
cerebral oxygenation measurement 233–6 vs NIRS 231
delayed ischaemic neurologic deficits, vasospasm 166–7 transcranial/cervical magnetic stimulation, electromyography
management 165–6 244–5
blood pressure control 165 transfer of head-injured patient 153
cardiac function 52–3, 165 transoesophageal echocardiography, detection of air embolism 62
general care 166 transplantation, organ donation 275–7
hydrocephalus 165–6 transsphenoidal hypophysectomy 81–4
intervention 164 ACTH and Cushing’s disease 83
microdialysis 239 diabetes insipidus 83
in pregnancy 287 GH and acromegaly 83
pulmonary complications 166 pathophysiology 82–3
seizures 165 physiology 82
surgery 166 pituitary apoplexy 83
neuroimaging 283–4 pre-, intra- and postoperative management 83–4
presentation 52 trigeminal evoked potentials 78–9
signs 29 trigeminal neuralgia, clinical features 78
TCD 256 tumours
WFNS, SAH scale 52 interventional neuroradiology 112–13
subdural haematoma (SDH) 90–2 primary and secondary 47
neuroimaging 282 see also space-occupying lesions
SjvO2 226–7
suxamethonium 40 ultrasonography see Doppler US
muscular dystrophy 264
pregnancy 286 vagus nerve 2
valproate 44–5
temperature sensor 234 vascular lesions, craniotomy 51–5
tetra-hydro-aminomethane (THAM) 158 vasoconstrictors 20
thalamus, anatomy 3 vasodilators 20
thermal dilution, CBF 22 vasospasm
thiopentone 32, 197 balloon angioplasty 167
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