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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

Arun K. Gupta MBBS MA FRCA


Director of Neuro-critical care and Consultant in Anaesthesia
Associate Lecturer
Addenbrooke’s Hospital
Cambridge

Andrew C. Summors BSC (HONS) MBBS (HONS) FRCA


Formerly Specialist Registrar and Fellow in Neuroanaesthesia
Addenbrooke’s Hospital
Cambridge
Consultant in Anaesthesia and Critical Care
Nevill Hall Hospital
Abergavenny
Wales
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© 2001

GREENWICH MEDICAL MEDIA LTD


137 Euston Road
London
NW1 2AA

ISBN 1 84110 035 8

First published 2001

Apart from any fair dealing for the purposes of research or private study,
or criticism or review, as permitted under the UK Copyright Designs
and Patents Act 1988, this publication may not be reproduced, stored,
or transmitted, in any form or by any means, without the prior permis-
sion in writing of the publishers, or in the case of reprographic repro-
duction only in accordance with the terms of the licenses issued by the
appropriate Reproduction Rights Organisation outside the UK.
Enquires concerning reproduction outside the terms stated here should
be sent to the publishers at the London address printed above.

The right of Arun K. Gupta and Andy Summors to be identified as


editors of this work has been asserted by them in accordance with the
Copyright Designs and Patents Act 1988.

The publisher makes no representation, express or implied, with regard


to the accuracy of the information contained in this book and cannot
accept any legal responsibility or liability for any errors or omissions that
may be made.

A catalogue record for this book is available from the British Library.

Distributed worldwide by
Plymbridge Distributors Ltd

Typeset by Phoenix Photosetting, Chatham, Kent


Printed by Ashford Colour Press Ltd, Hants

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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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NOTES IN NEUROANAESTHESIA AND CRITICAL CARE

Neuroanaesthesia

12. Craniotomy for space occupying lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47


C. Duffy
13. Craniotomy for vascular lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 51
C. Duffy
14. Posterior fossa surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 57
C. Goldsack
15. Air embolism . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
C.Goldsack
16. Acoustic neuroma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65
A. Swami
17. Epilepsy surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 69
M. Smith
18. Awake craniotomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 73
M. Smith
19. Microvascular decompression . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77
K. Grixti
20. Transsphenoidal hypophysectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 81
R. Erskine,A. Summors
21. Stereotactic surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 85
A. Summors
22. Anaesthesia for head injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 89
C. Duffy
23. Complex cervical spine surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
I. Calder
24. Fibreoptic intubation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97
I. Calder
25. Thoraco-lumbar surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103
C.Williams
26. Carotid endarterectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107
A.K. Gupta
27. Anaesthesia for interventional neuroradiology . . . . . . . . . . . . . . . . . . . . . . . . . . 111
J. M.Turner
28. Anaesthesia and sedation for magnetic resonance imaging . . . . . . . . . . . . . . . . . . 115
D. K. Menon
29. Shunt surgery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 121
A. Summors
30. Anaesthesia for paediatric intracranial procedures . . . . . . . . . . . . . . . . . . . . . . . . 125
J. M.Turner
31. Congenital craniofacial procedures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129
J. Shapiro
32. Congenital spinal lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 133
J. Shapiro

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CONTENTS

33. Paediatric craniospinal trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 137


C. Duffy
34. Recovery: general considerations . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 141
S. Gupta

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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NOTES IN NEUROANAESTHESIA AND CRITICAL CARE

53. Jugular venous oximetry . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 225


A.K. Gupta
54. Near infrared spectroscopy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 229
A.K. Gupta
55. Measurement of tissue oxygenation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 233
A.K. Gupta
56. Microdialysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237
P. J.A. Hutchinson
57. Evoked potential and peripheral neurophysiology . . . . . . . . . . . . . . . . . . . . . . . . 241
B. McNamara
58. Electroencephalography and cerebral function monitoring . . . . . . . . . . . . . . . . 247
B. McNamara
59. Transcranial Doppler ultrasonography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 253
B. Matta
60. Application of multimodal monitoring. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 259
A.K. Gupta

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

Rowan Burnstein Richard Erskine


FRCA FRCA
Specialist Registrar Consultant Anaesthetist
University of Cambridge Addenbrooke’s Hospital,
Cambridge
Ian Calder
DRCOG FRCA
Consultant Anaesthetist Jonathan H. Gillard
The National Hospital for Neurology and BSc, MD FRCR
Neurosurgery, and The Royal Free Hospital Clinical Lecturer
Queen Square, London Univ Dept of Radiology
Addenbrooke’s Hospital,
Alisdair Coles
Cambridge
BA BM BCh MRCP PhD
Wellcome Advanced Fellow, Neurology
Cambridge University
Craig Goldsack
Jonathan Coles BSc MRCP FRCA
FRCA Consultant Anaesthetist
Addenbrooke’s Hospital, University College London Hospitals
Cambridge London

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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NOTES IN NEUROANAESTHESIA AND CRITICAL CARE

Sanjeeva Gupta Quentin J. W. Milner


FRCA FRCA
Consultant in Chronic Pain Consultant Anaesthetist
Bradford Hospital, Portsmouth Hospitals,
Yorkshire Hants

Nicholas P. Hirsch Joseph Monteiro


FRCA MD
Consultant Neuroanaesthetist Consultant Anesthesiologist
Harris Neurorespiratory Intensive Care Unit Hinduja National Hospital and
The National Hospital for Neurology and Medical Research Centre,
Neurosurgery, Bombay, India
Queen Square, London
Ivan Ng
P. J. A. Hutchinson FRCS
FRCS Co-Director of Neurosciences ICU
Specialist Registrar National Neuroscience Institute
Addenbrooke’s Hospital, Singapore
Cambridge
Phil Popham
MD FRCA
Rodney Laing
Chairman
MA MD FRCS (SN)
Dept of Anaesthesia
Consultant Neurosurgeon
Addenbrooke’s Hospital,
Addenbrooke’s Hospital,
Cambridge
Cambridge
Mahesh Prabhu
Tim Leary FRCA
FRCA
Specialist Registrar
Specialist Registrar
Addenbrooke’s Hospital,
Addenbrooke’s Hospital, Cambridge
Cambridge

Brian McNamara Sandra Rees-Pedlar


MRCP BSc (Hons) PG Cert
Specialist Registrar Sister, Neurointensive Care
Addenbrooke’s Hospital, Addenbrooke’s Hospital,
Cambridge Cambridge

Basil Matta Siva Senthuran


FRCA FRCA
Director of Perioperative Services Specialist Registrar
Addenbrooke’s Hospital, Addenbrooke’s Hospital,
Cambridge Cambridge

David K. Menon Ravi Shankar


MD PhD FRCP FRCA F Med Sci Specialist Registrar
Professor of Anaesthesia Addenbrooke’s Hospital,
University of Cambridge Cambridge

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CONTRIBUTORS

Jay Shapiro John M. Turner


MD MA FRCA
Associate Professor Consultant in Anaesthesia and Neurointensive Care
Director of Pediatric Anaesthesia Addenbrooke’s Hospital,
Medical College of Virginia, Cambridge
Richmond, VA
USA
John Ulatowski
Martin Smith
MD PhD MBA
FRCA
Vice Chairman, Clinical Affairs
Consultant Neuroanaesthetist and Honorary
Associate Professor, Anesthesiology/
Lecturer in Anaesthesia
Critical Care Medicine
The National Hospital for Neurology and
Johns Hopkins Medical Institutions,
Neurosurgery,
Baltimore, MD
University College London Hospitals
USA
Queen Square, London

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

xiii
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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

ACA anterior cerebral artery EEG electroencephalogram


ACh acetylcholine EMG electromyogram
AChR acetylcholine receptor ETT endotracheal tube
ACTH adrenocorticotropic hormone GBS Guillain–Barré syndrome
ADH antidiuretic hormone GCS Glasgow coma scale
AJDO2 arterio-jugular differences in O2 GCSC generalised convulsive status
content epilepticus
ANF atrial natriuretic factor GTN glyceral trinitrate
AVM arteriovenous malformation GH growth hormone
BAEP brainstem auditory evoked Hb haemoglobin
potential HbO2 oxygenated Hb
BBB blood–brain barrier HI head injury
BP blood pressure ICA internal carotid artery
BSR burst suppression ratio ICH intracranial haemorrhage
CBF cerebral blood flow ICP intracranial pressure
CBV cerebral blood volume IHD ischaemic heart disease
CEA carotid endarterectomy IJV internal jugular vein
CFM cerebral function monitoring LDF laser Doppler flowmetry
CMAP compound motor action potential MAP mean arterial pressure
CMR/CMRO2 cerebral metabolic rate of oxygen MABP mean arterial blood pressure
CN cranial nerve MCA middle cerebral artery
CNS central nervous system MCAFvx middle cerebral artery flow velocity
CPP cerebral perfusion pressure MMC myelomeningocele
CSF cerebrospinal fluid MRI magnetic resonance imaging
CT computed tomography MRS magnetic resonance spectroscopy
CTG cardiotocography NIRS near infrared spectroscopy
CVP central venous pressure NO nitric oxide
CVR cerebrovascular resistance N2O nitrous oxide
DAI diffuse axonal injury PaO2 arterial oxygen tension
DI diabetes insipidus PaCO2 arterial carbon dioxide tension
DIC disseminated intravascular PbO2 brain tissue oxygen tension
coagulation PCA posterior cerebral artery
ECA external carotid artery PCoA posterior communicating artery
ECG electrocardiogram PEG percutaneous gastrostomy
ECoG electrocorticogram PEEP positive end-expiratory pressure
EDH extradural haematoma PICA posterior-inferior cerebellar artery

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1
ANATOMY OF THE BRAIN
AND SPINAL CORD

C. Williams
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2 ANATOMY

GENERAL ORGANISATION Firstly, it is a conduit for transmitting signals back and


forth from the cerebrum and cerebellum to the spinal
The central nervous system (CNS) can be divided cord, e.g. the long motor fibres (corticospinal tracts)
into brainstem, cerebellum, cerebrum and spinal run along the anterior aspect of the brainstem in the
cord. cerebral peduncles, cross the midline in the pyramids,
A fibrous membrane surrounds the entire CNS and and enter the top of the spinal cord. Sensory path-
its cerebrospinal fluid (CSF), and is composed of ways pursue similar courses, although most do not
three layers, collectively known as the meninges. The cross the midline here. Secondly, the 12 cranial
outermost layer is the dura, which adheres to the nerves (CN) and their nuclei are found in the brain-
inner surface of the skull and continues down to the stem. These nerves control the motor and sensory
tip of the spinal cord (filum terminale). While neural functions of the head, face and most of the neck
tissue itself does not generally sense pain, the dura Table 1.1. The vagus nerve (CN X) also communi-
does, and the sympathetic discharge from dural inci- cates with the chest, heart and abdomen, and if
sion can lead to unwanted rises in blood pressure and compressed in the carotid sheath during carotid
heart rate if not anticipated. The innermost layer is endarterectomy or anterior cervical fusion, can cause
the pia, which is in contact with the neural tissues of bradycardia. Since these nerves and nuclei are so
the CNS. The middle layer is called the arachnoid, closely located in and around the brainstem, problems
and the trabeculated space between the arachnoid and in this area rarely affect only one cranial nerve.
pia membranes contains CSF. Blood vessels on the Compression of the facial nerve (CN VII) by an
outside of the dura service the meninges itself, and acoustic neuroma (on CN VIII) is common, so
disruption of these vessels causes epidural hematomas. during surgical resection of this tumour, both facial
The pia supports blood vessels that service the meta- electromyogram (EMG) and evoked brainstem
bolically active neural tissues, and disruption of these auditory monitoring may be required. Even simple
vessels cause subdural hematomas. Around the base of manipulation of the trigeminal nerve (CN V) easily
the brain, these subdural (pial) vessels form a network affects the nearby nucleus ambiguus (of CN X),
called the Circle of Willis that, in most patients, causing bradycardia. Lastly, management of the
assures a collateral supply of blood (see Chapter 2 for essential involuntary functions of heart rate, blood
blood supply to the brain). pressure and respiratory rate occurs in the reticular
networks of the brainstem, with input from the
hypothalamus. Considering the overall importance of
ANATOMY OF THE BRAINSTEM
(FIG. 1.1)
The brainstem is a small but extremely important Table 1.1 The cranial nerves and
structure, and has primarily three functions. their functions

Cranial Nerve Function

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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ANATOMY OF BRAIN AND SPINAL CORD 3


brainstem function, it is easy to see why strokes or called the central sulcus, and the strip of frontal cor-
injury to the brainstem have such devastating effects tex running just anterior to the sulcus is the primary
to the patient. motor control centre. Control of the contralateral
lower extremity is more rostral on this strip (supplied
by the anterior cerebral artery), and control of the
ANATOMY OF THE CEREBELLUM AND contralateral upper extremity and face is more caudal
DEEP STRUCTURES OF THE BRAIN (supplied by the middle cerebral artery). The primary
sensory cortex exists in a similar arrangement on the
Sitting atop the brainstem are the deep brain struc-
strip of parietal cortex just posterior to the sulcus, and
tures of the hypothalamus, thalamus and basal ganglia.
is responsible for discerning fine touch, determining
These are primarily relay and control stations for the
proprioception, and for recognising the source, qual-
autonomic and endocrine nervous systems and
ity and severity of pain and temperature. The area
receive enormous amounts of sensory input.
around the most posterior tip of the brain (occipital
Pathology here is seldom surgically correctable, with
lobe) is the visual cortex and is used for the interpre-
the notable exceptions of thalamotomies for tremors
tation of sight and for high-level control of the occu-
(usually Parkinsonian), or pituitary surgery.
lomotor complex. Extending forward and laterally is
The cerebellum, which lies posterior to the brain- the temporal lobe, whose deeper structures form the
stem, functions primarily in the regulation of fine limbic systems that play important roles in memory
motor control. Dysfunction is generally characterised and learning.
by awkwardness of intentional movements or
Although the cerebrum is bilaterally symmetrical in
tremors. Together with the brainstem it sits at the
appearance, its function is not. Almost all right-
bottom of the skull in the posterior fossa and is
handed people are left-brain dominant, but only
covered by a dural sheet (the tentorum) that separates
60–70% of left-handed people are right-brain domi-
it from the cerebrum. Compared to the cerebral
nant. Dominance can be determined by a WADA
vault, the posterior fossa is small, and a small increase
test (selectively anaesthetising each temporal lobe),
in volume here can quickly compress the brainstem.
and can be especially important for temporal lobe
Postoperative blood pressure elevation may lead to
resections since language interpretation (Wernicke’s
haematoma following surgery in this area.
area) and motor speech centres (Broca’s area) are
found primarily in the fronto-temporal regions of the
ANATOMY OF THE CEREBRUM dominant hemisphere.
(FIG. 1.2)
The hemispheres of the cerebrum can each be
divided into four major areas called lobes. The frontal ANATOMY OF THE SPINAL CORD
lobes lie over the orbital bones and are responsible for (FIG. 1.3)
abstract thinking, voluntary eye movements, mature
judgements and self-control. They are separated from Although there are many identifiable ascending and
the more posterior parietal lobes by a vertical groove descending neuronal tracts in the spinal cord, only
three hold major clinical significance.
The only important descending tract is the corti-
cospinal tract, which runs from the brain’s motor cor-
tex (precentral gyrus), through the internal capsule
and cerebral peduncles, across to the contralateral side
via the pyramidal decussation, and down the lateral
columns of the spinal cord. Motor nerve roots come
off of the spinal cord periodically and are bundled
together as peripheral nerves that pass through each
spinal foramina as they continue on to the body’s
muscles. Although there are 30 vertebral bones, there
are actually 31 pairs of spinal nerves. Since the top
seven cervical nerves exit over their corresponding
seven vertebrae, and all of the nerves below the top-
most thoracic level exit under their corresponding
vertebrae, an extra cervical nerve (C8) exists between
Figure 1.2 Gross anatomy of the cerebrum the C7 and T1 vertebrae.
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4 ANATOMY

passing through the thalamus. While in the thoracic


and cervical spinal cord, the lateral spinothalamic
tract maintains a somatotopic organisation, as nerve
fibres originating in the lowermost levels are pushed
laterally by fibres entering from successively higher
levels. This organisation allows neurosurgeons to
sometimes perform very selective cordotomies to
treat intractable pelvic or leg pain, and to help localise
lateral spinal cord lesions. Furthermore, expanding
central cord lesions will compress the medial fibres
from higher levels first, often sparing the more lateral
fibres from the sacrum.
The second of the two major ascending neuronal tracts,
the dorsal column-medial leminiscal system, carries
information about two-point discrimination, joint
position and vibration up the ipsilateral dorsal
columns to a contralateral crossover point in the
medulla. From there, the signal is relayed through the
thalamus to the brain’s primary sensory cortex (post-
central gyrus).
The anterior and central portions of the spinal cord
(including the corticospinal and lateral spinothalamic
tracts) are supplied with blood from the anterior
spinal artery, which arises from the vertebral arteries
at the base of the brain rostrally and the arteria magna
of Adamkewicz (a low-thoracic branch of the aorta)
caudally. Paired, poorly defined posterior spinal arter-
Figure 1.3 Major spinal cord pathways of clinical signifi- ies, however, service the dorsal columns. This
cance arrangement can lead to differential ischaemia of the
spinal cord, if only one of the arterial systems is dis-
rupted. Anterior cord syndromes, for example, are
For any given muscle target, this entire pathway seen in cervical spine hyperflexion injuries, displaced
comprises only two cells: the upper motor neurone spinal fractures, posteriorly herniated disks or
runs from the brain to the appropriate spinal cord ischaemia from anterior spinal artery occlusion. It
level, and the lower motor neurone runs from the produces injury to the lateral spinothalamic and cor-
spinal cord to the muscle. Injury or disease affecting ticospinal tracts while sparing the dorsal columns and
the lower motor neurone results in a focal weakness, typically causes immediate paralysis with loss of pain
fasciculation, wasting and hyporeflexia, while pathol- and temperature sensation below the level of the
ogy affecting the upper motor neurones of the lesion; light touch and vibration and joint position
spinothalamic tract produces spasticity and hyper- senses are preserved throughout. Radicular branches
reflexia to all muscles serviced by neurones below the from the posterior spinal arteries (arising from the
level of injury. It is however, clinically difficult to posterior inferior cerebellar arteries or the vertebral
correlate spinal cord levels with specific motor inner- arteries) service the posterior one-third of the spinal
vation of the trunk, so sensory losses may be a more cord. As they are so much more widely anastamosed
valuable localising tool when the lesion is above the than their anterior counterparts, injury to any one of
first lumbar level. them will not necessarily result in cord ischaemia.
Spinal cord blood flow is autoregulated in similar
The first of the two major ascending neuronal tracts is fashion to cerebral blood flow.
the lateral spinothalamic tract. Information about
pain, temperature and crude touch from peripheral Complete and incomplete sectioning of the spinal
nerves enters the posterior horn of the spinal cord, cord produces characteristic clinical pictures based
crosses to the contralateral side of the cord one or two upon the extent of damage done to these three major
levels above where it entered, and is sent rostrally to neuronal tracts. Traumatic complete sectioning of the
the brain’s sensory cortex (postcentral gyrus) after cord produces immediate loss of voluntary move-
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ANATOMY OF BRAIN AND SPINAL CORD 5


ment and sensation below the level of the injury fol- 4. The sympathetic system is commonly also dam-
lowed by distal hyperreflexia and muscular spasticity aged in high hemisections, producing an ipsilateral
after several weeks. A hemisection of the cord pro- Horner’s syndrome (miosis and ptosis).
duces the Brown–Séquard syndrome, which has four
parts:
FURTHER READING
1. Corticospinal tract injury produces ipsilateral
motor loss below the lesion. Goldberg S. Clinical neuroanatomy made ridiculously
2. Dorsal column injury produces ipsilateral sensory simple. Miami, Florida: MedMaster, 1997
loss to joint position, two-point discrimination, Pansky B, Allen DJ. Review of neuroscience. New York:
and vibration below the lesion. Macmillan, 1980
3. Lateral spinothalamic tract injury produces con- Rowland LP. Clinical syndromes of the spinal cord and
tralateral loss of pain, temperature and crude touch brain stem. In: Kandel ER, Schwartz JH, Jessell TM (eds)
below a point one to two levels above the Principles of neural science, 3rd Edn. Norwalk,
lesion. Connecticut: Appleton & Lange, 1991, pp. 711–720
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2
CEREBRAL CIRCULATION

R. Burnstein
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8 ANATOMY

INTRODUCTION Just above the bifurcation, the ECA passes between


the ICA and the pharyngeal wall. It supplies the soft
The brain has the highest metabolic requirements of tissues of the neck, eye, face and scalp. The ICA
any organ in the body. It receives 14% of the resting continues to pass vertically upwards in the neck
cardiac output in the adult (approximately 700 within the carotid sheath giving off no branches. It is
ml/min) and accounts for 20% of basal oxygen con- superficial at first in the carotid triangle, but then
sumption (about 50 ml/min). Blood flow within the passes deeper, medial to the posterior belly of the
brain is variable with flow in the grey matter (110 digastric muscle. At its origin is a fusiform dilatation
ml/100 g tissue/min) on average 5 times that in white known as the carotid sinus. The walls of the sinus
matter (22 ml/100 g/min). contain baroreceptors that are stimulated by changes
in blood pressure. The ICA enters the skull through
the foramen lacerum and turns anteriorly through the
ARTERIAL BLOOD SUPPLY cavernous sinus in the carotid groove on the side of
The arterial supply to the brain is from both right and the sphenoid body.
left internal carotid arteries (ICAs) supplying the
Each ICA gives rise to a posterior communicating artery
anterior two-thirds of the cerebral hemispheres and
(PCoA) before ending by dividing into the anterior
the vertebrobasilar system, which supplies the
cerebral artery (ACA) and middle cerebral artery (MCA).
brainstem and the posterior regions of the hemi-
The ACA runs medially then superiorly, supplying
spheres.
the undersurface of the frontal lobe and the medial
The common carotid artery lies in the neck within the neostriatum. The MCA turns laterally from its origin,
carotid sheath medial to the internal jugular vein (IJV) immediately giving rise to a series of small penetrating
with the vagus nerve posteriorly between them. The branches, the lenticulostriate arteries. These arteries are
sympathetic trunk runs behind the artery but outside the only supply to the lateral part of the striatum. The
the sheath. At approximately the level of the thyroid MCA continues to run laterally where it divides into
cartilage the common carotid artery bifurcates into several major branches carrying blood to the lateral
ICA and external carotid artery (ECA). surfaces of the frontal, temporal and parietal lobes.

(b)

(a) A.C.A (A2)

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

INTRODUCTION • The fossa is covered superiorly by the tentorium


cerebelli.
The posterior cranial fossa is almost circular in outline
and is the largest and deepest of the three cranial
fossae (Fig. 3.1) (the others being anterior and middle CONTENTS
fossae). It contains the cerebellum and brainstem,
which are covered by a dural sheet (the tentorium The cerebellum lies posterior to the brainstem and
cerebelli) which separates it from the cerebrum. consists of two hemispheres united in the midline by
cerebellar vermis (Fig. 3.2). Three peduncles connect
The boundaries of the posterior fossa are as follows: each hemisphere to the three parts of the brainstem.
• Anteriorly lies the dorsum sellae, the clivus, the The superior peduncle enters the midbrain, the mid-
posterior part of sphenoid and the basilar part of dle peduncle consists of transverse fibres of the pons
the occipital bone. and the inferior peduncle arises from the medulla.
• Posteriorly lies the squamous part of the occipital Blood supply is from:
bone, the transverse sinus and the superior sagittal 1. posterior inferior cerebellar artery
sinus. 2. anterior inferior cerebellar artery
• Laterally lies the petrosal and mastoid part of 3. superior cerebellar artery.
temporal bone, the internal auditory meatus, the
jugular foramen and the sigmoid sinus. The pons lies anterior to the cerebellum and is con-
• Inferiorly lies the occipital bone, foramen mag- tinuous with the midbrain superiorly and with the
num and hypoglossal canal. medulla oblongata inferiorly. Beneath the floor of the

Sella

Posterior part of Olfactory


Lesser Wing of Nerve
Sphenoid
Optic
Nerve

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

Figure 3.1 Relationship of posterior fossa with other intracranial landmarks


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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

Figure 3.2 Saggital view of contents of the posterior fossa

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

KEY POINTS • Increased volume in the posterior fossa may lead


to brainstem ischaemia.
• The posterior fossa contains the cerebellum and
brainstem
• The fourth ventricle lies between the cerebellum
and brainstem FURTHER READING
• Cranial nerves IV–XII are either transmitted or
contained within the posterior fossa Neurology. In: Gray’s Anatomy, 35th edn. Warwick R,
• The veins in the posterior fossa may contribute to Williams P (eds). Longman, Edinburgh 1973, pp. 260–278
intraoperative complications such as haemorrhage, Last RJ. Anatomy: regional and applied. Churchill
haematoma or venous air embolism Livingstone, London 1972, pp. 760–763
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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

Figure 4.2 A sensory neurone with cell body, bifurcating


axon and peripheral and central connections

neurone, the initial node of Ranvier in the


cutaneous sensory neurone).
3. An axonal process that transmits propagated
impulses to the nerve endings.
4. The nerve endings, where action potentials cause
the release of synaptic transmitters. The cell body is
often located in the dendritic zone end of the axon.
All necessary proteins are synthesised in the endoplas-
mic reticulum and Golgi apparatus of the cell body
and then transported along the axon to the synaptic
knobs by the process of axoplasmic flow. Thus, the cell
body maintains the functional and anatomic integrity
of the axon; if the axon is cut, the part distal to the cut
Figure 4.1 A motor neurone with myelinated axon. The degenerates (Wallerian degeneration). Most of the
four functional zones of the neurone are labelled to the left energy requirement of a neurone is supplied by the
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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

Fibre type Function Fibre Conduction Hypoxia Pressure LA


diameter velocity
(mm) (m/s)

Aa Proprioception; 12–20 70–120 ++ +++ +


Somatic motor
Ab Touch, pressure 2–12 30–70
Ag Motor to muscle 3–6 15–30
spindle
Ad Pain, cold, touch 2–5 12–30
B Preganglionic <3 3–15 +++ ++ +
autonomic
C Pain, temperature, 0.4–1.2 0.5–2 ++ ++ +++
Dorsal root mechanoreception,
reflex response
C Postganglionic 0.3–1.3 0.7–2.3
Sympathetic sympathetics

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

• A minimum threshold stimulus is necessary to ini- FURTHER READING


tiate a propagated action potential (Fig. 4.3) which
Ganong WF. Review of medical physiology. Excitable tis-
is an ‘all or none’ phenomena.
sue: nerve. Stamford, Connecticut: Appleton & Lange,
1997, pp. 47–59
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5
CEREBRAL BLOOD FLOW

M. Prabhu, A.K. Gupta


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20 PHYSIOLOGY

INTRODUCTION Autoregulation changes in the presence of intra-


cranial pathology and volatile anaesthetic agents (see
Although the adult brain constitutes only 2% of body Chapter 9). Chronic hypertension or sympathetic
mass, it accounts for 20% of basal oxygen consump- activation shifts the autoregulatory curve to the right.
tion (50 ml/min). Mean resting cerebral blood flow
(CBF) in adults is about 50 ml/100 g/min. The
anatomy of the cerebral circulation is described in Flow-Metabolism Coupling
Chapter 2. Increased neuronal activity causes an increase in cere-
The whole brain oxygen consumption is approxi- bral metabolic rate (CMR), resulting in a well
mately 3.5 ml of oxygen/100 g of brain tissue/min. matched increase in CBF. The parallel change in
The substantial demands for both oxygen and glucose CBF with CMR is known as ‘flow-metabolism cou-
are met by maintaining CBF. CBF is related to pling’. Acetylcholine, nitric oxide, serotonin and
cerebral perfusion pressure (CPP) and cerebrovascu- substance P have been described as mediators but the
lar resistance (CVR) as follows: precise mechanism of this coupling is still unknown.
There is evidence to suggest that CBF may be mod-
CBF = CPP / CVR where ulated by changes in glucose consumption rather than
CPP = Mean arterial pressure (MAP) – Intra- O2 consumption.
cranial pressure (ICP) – venous pressure (VP).
Chemical Regulation
REGULATION OF CBF Arterial carbon dioxide tension (PaCO2)
Factors affecting CBF are shown in Figure 5.1. CO2 is a potent vasodilator. CBF changes by 1–2
ml/100 g/min for each 1 mmHg change in PaCO2
Myogenic Regulation (Autoregulation) within physiological limits. These changes are
Autoregulation is defined as the maintenance of a believed to be driven by changes in extracellular or
constant level of CBF in the presence of alterations in interstitial H+ concentration. However, after 6–8
the perfusion pressure. The normal physiological hours, the CBF returns to baseline values because
limits of autoregulation are approximately 50 mmHg CSF pH gradually normalises as a result of the extru-
and 150 mmHg (mean arterial pressure). These limits sion of bicarbonate.
are in reality less distinct than shown in Figure 5.1.
Autoregulation is brought about by changes in CVR Arterial oxygen tension
caused by myogenic reflexes in the resistance vessels
probably due to changes in transmural tension. Although arterial oxygen was previously not thought
to effect CBF unless PaO2 fell below 50 mmHg
recent evidence from studies in human volunteers
have demonstrated the threshold for hypoxic vasodi-
latation exists at arterial saturations of 90–92%.
Localised hypoxia may cause vasodilatation and an
increase in CBF.

Potassium and adenosine


Both potassium and adenosine are potent vasodila-
tors. Increased concentrations are detected during
seizures, direct cortical stimulation and hypoxia
which causes an increase in CBF.
Calcium is a potent vasoconstrictor in high concentra-
tions. Some calcium antagonists blunt hypoxic
vasodilatation and prevent adenosine release.
Recent evidence suggests that nitric oxide (NO)
plays an important role in cerebral vasodilatation
Figure 5.1 Factors affecting CBF: PP = perfusion pressure
caused by hypercapnia, ischaemia, increased cerebral
(mmHg), PaCO2 = arterial carbon dioxide tension (mmHg), metabolic rate, excitatory amino acids and volatile
PaO2 = arterial oxygen tension (mmHg) anaesthetic agents.
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CEREBRAL BLOOD FLOW 21


Neurogenic regulation neuromuscular blockers have little effect on CBF and
CMR. Succinylcholine can produce ICP increases,
The autonomic nervous system mainly affects the
probably secondary to rise in CBF. However, these
larger cerebral vessels. b-1 adrenergic stimulation
changes are transient and mild.
results in vasodilatation, whereas a-2 adrenergic
stimulation causes vasoconstriction. Significant vaso-
constriction can be produced by extremely high MEASUREMENT OF CBF
concentration of catecholamines as in haemorrhagic
Methods of measuring CBF can be regional or global.
shock.
All methods that provide an absolute estimate of CBF
use one of two principles. They either measure the
Blood viscosity
distribution of a tracer or estimate regional CBF
CBF can be influenced by blood viscosity, of which (rCBF) from a washin or washout curve of an indica-
haematocrit is the single most important determinant. tor. Other techniques measure a related flow variable
Studies suggest that a haematocrit of 30–34% may (arterial flow velocity) or infer changes in flow from
result in optimal oxygen delivery. However, if maxi- changes in metabolic parameters.
mum vasodilatation already exists, O2 delivery may
decrease with haemodilution. Kety Schmidt Technique
Nitrous oxide (10–15%) is inhaled and arterial and
EFFECT OF ANAESTHETIC AGENTS jugular venous samples are obtained at rapid intervals
O N C B F (see also Chapters 8–10) for measurement of N2O levels. Plotting concentra-
tion against time produces a rapid rise in arterial N2O
Inhalational Agents concentration and a slower venous rise. The rate of
equilibration of the two curves measured reflects the
All volatile anaesthetic agents produce a dose-related
rate at which N2O is being delivered thereby giving
decrease in CMR while causing an increase in CBF.
an estimate of global CBF. Actual CBF is propor-
Flow and metabolism is not actually uncoupled, but
tional to the area between the arterial and venous
the gradient of the slope is increased with higher
curves.
doses of agent. Nitrous oxide (N2O) may cause an
increase in CBF without a decrease in CMR. This
Xenon-133 Washout Technique
increase is unaffected by hypocapnia.
This technique measures regional CBF. Radioactive
Intravenous Agents Xenon is inhaled or injected into the carotid artery or
the aorta and a washout curve is obtained. Individual
Thiopentone, etomidate and propofol all cause a
washout curves can be separated into high and slow
reduction in global CMR and CBF. Even high doses
washout components which may represent flow in
of thiopentone or propofol do not affect autoregula-
grey and white matter. This method primarily esti-
tion, flow-metabolism coupling or CO2 responsive-
mates cortical blood flow.
ness.
Tomographic rCBF Measurement
Opiates
Dynamic CT
The general pattern is one of modest reduction in
both CMR and CBF. High doses of morphine (3 Rapid sequential computed tomography (CT) may
mg/kg) and moderate doses of fentanyl (15 µg/kg) be used to quantify the washout of a radioactive con-
have little effect on CBF and CMR. High doses of trast agent.
fentanyl (50–100 µg/kg) and sufentanyl (10 µg/kg)
depress CMR and CBF. Alfentanil (0.3 µg/kg) shows Single photon emission computed tomography (SPECT)
no reduction in CBF.
This technique uses gamma emitting and positron
emitting isotopes respectively, to produce tomo-
OTHER DRUGS graphic images of regional CBF.
Benzodiazepines cause reduction in CMR and
Functional magnetic resonance imaging (f MRI)
CBF by about 20–25%. Ketamine increases in CMR,
CBF and ICP. These changes can be partially An intravenous MR contrast agent can give a
attenuated by hypocapnia. Lidocaine produces a dose- reflection of CBF. Changes in MR signal intensity
related reduction in CMRO2. Non-depolarising produced by decreases in regional deoxyhaemoglobin
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22 PHYSIOLOGY

levels can give tomographic images of changes in KEY POINTS


regional CBF.
• The brain is highly metabolic and has a high blood
Indirect or Non-quantitative Measures flow.
• Five major factors control CBF: PaCO2, auto-
1. Doppler ultrasonography: Provides an indirect regulation, PaO2 flow-metabolism coupling and
measure of arterial flow velocity. the autonomic nervous system.
2. Magnetic resonance spectroscopy (MRS): Pro- • Similar factors control CBF and CBV.
vides information regarding intracellular pH and • Inhalational agents are potent vasodilators.
tissue levels of adenosine triphosphate and lactate. • By decreasing CMR, intravenous anaesthetic
3. Near infrared spectroscopy (NIRS): measures agents reduce CBF and CBV.
regional haemoglobin oxygenation and cyto-
chrome redox state (see Chapter 54).
4. Laser Doppler flowmetry (LDF): An investi-
gational technique measuring the Doppler shift of FURTHER READING
reflected laser light induced by movement of red
blood cells within the microcirculation. Provides a Menon DK. Cerebral circulation. In: Cardiovascular phys-
non-quantitative measurement of microvascular iology. London: BMJ Publishing Group, 1995
blood flow in a small area of tissue. Strong A, Pollay M. Cerebral blood flow. In: The practice
5. Thermal dilution flow probes: These are also of neurosurgery, Vol 1. Baltimore: Williams & Wilkins,
investigational and consist of a flexible cortical 1996
strip electrode for placement on the brain at cran- Todd MM, Warner DS. Neuroanesthesia: a critical review.
iotomy which provides information on relative, In: Rogers MC, Tinker JH, Covino BG, Longnecker DE
not absolute, changes in CBF in a relatively small (eds) Principles and practice of anesthesiology. Chicago:
(20–30 mm3) volume of brain. Mosby-Year Book, 1993, pp. 1599–1648
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6
INTRACRANIAL PRESSURE

M. Prabhu, A.K. Gupta


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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.

Cerebral blood volume (CBV)


MONRO KELLY DOCTRINE
Most of the intracranial blood volume is contained in
Raised ICP causes brain damage by reducing CPP or the venous sinuses and pial veins. This acts as a buffer
by focal compression of brain tissue due to distortion in the event of raised ICP. Factors affecting CBV
and herniation of intracranial contents. include:
• Venous distension – from jugular venous obstruc-
tion, increased intrathoracic pressure, raised
CONTROL OF ICP
central venous pressure, head down tilt, vaso-
dilators.
VOLUME BUFFERING
• PaCO2 – Both CBF and CBV increase with raised
(PRESSURE–VOLUME RELATIONSHIP)
PaCO2, but the CBV response curve is flatter than
The pressure–volume relationship is given in Figure the CBF curve (Fig. 6.2). A reduction in PaCO2
6.1. During initial compensation, between points 1 from 40–20 mmHg (5.3–2.7 kPa) results in a 65%
and 2, there is hardly any rise in ICP with changes reduction in CBF but only a 28% reduction in
in intracranial volume. At point 2, further increases CBV (2.8 ml/100 g). This small change in

Figure 6.2 Relationship of cerebral blood flow and blood


volume with changes in arterial carbon dioxide. (Adapted
with permission from Todd MM, Warner DS. Neuro-
Figure 6.1 Intracranial pressure volume curve anesthesia: a critical review.)
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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.

M O N I T O R I N G I C P (see Chapter 52)


CLINICAL FEATURES OF
RAISED ICP KEY POINTS
There are no pathognomonic signs or symptoms of • The intracranial contents are enclosed in a rigid
raised ICP. Most of them are related to traction and cranial vault.
distortion of pain-sensitive cerebral blood vessels and • Raised ICP causes secondary brain injury.
dura mater. Pressure headaches seen on waking up • Changes to the CSF space is a major compen-
and relieved by vomiting, papilloedema, amaurosis satory factor with raised ICP.
fugax (intermittent loss of vision), unilateral pupillary • Manipulation of CBV can rapidly reduce ICP if
dilation, oculomotor or abducent nerve palsy and intracranial hypertension exists.
finally loss of consciousness and respiratory depres- • CBV does not change in parallel with CBF.
sion all feature with increasing pressure.
The oval pupil is an important sign and represents a FURTHER READING
transitional stage between the normal and fixed,
unreactive pupil. Lee KR, Hoff JT. Intracranial pressure. In: Youmans neu-
rological surgery. London: WB Saunders, 1996, pp.
491–519
R A D I O L O G I C A L S I G N S (see Chapter Shalmon E, Caron M, Becker D. Intracranial pathology
and pathophysiology. In: Tindall GT, Cooper PR, Barrow
65)
DL (eds) The practice of neurosurgery. Baltimore:
1. Skull X-rays Williams & Wilkins, 1996, pp. 45–70
• In children up to the age of 8–9 years, diastasis Todd MM, Warner DS. Neuroanesthesia: a critical review.
of sutures, erosion of the dorsum sellae and In: Rogers MC, Tinker JH, Covino BG, Longnecker DE
thinning of the vault may be present. (eds) Principles and practice of anesthesiology. St Louis:
• In adults, erosion of the dorsum sellae, displaced Mosby-Year Book, 1993, pp. 1599–1648
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7
CEREBROSPINAL FLUID

J. Coles
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28 PHYSIOLOGY

INTRODUCTION gravity of 1.004–1.007. The normal pressure which


may be expressed using Davson’s equation: (resistance
Cerebrospinal fluid is contained within the sub- to csf outflow) × (CSF formation rate) + (pressure in sagittal
arachnoid space, surrounding the brain and spinal sinus) ranges from 80 to 180 mm of CSF (< 10 mmHg).
cord, lying between the pia mater (which is closely It has a composition similar to plasma (Table 7.1).
adherent to the underlying neural tissue) and the
arachnoid mater. Hypocapnia, hypothermia, high serum osmolality
and alkalosis (metabolic or respiratory) can all
reduce CSF production. Many agents acting as
STRUCTURE AND FUNCTION inhibitors of ion transport, including acetazolamide,
The majority of the 450–500 ml of CSF produced digoxin, amiloride, furosemide, bumetanide,
daily is formed in the choroid plexus of the ventricles. omeprazole, cholera toxin, norepinephrine,
The CSF circulates around the brain and spinal cord angiotensin II, 5-hydroxytryptamine and some
through the ventricular system and subarachnoid vasoactive peptides have also been shown to inhibit
space (Fig. 7.1). The two lateral ventricles communi- CSF formation.
cate with the third ventricle through the foramen of
Munro, which communicates with the fourth ventri- Anaesthetic agents have varying effects on CSF
cle via the aqueduct of Sylvius. From here fluid is free production and reabsorption. The intravenous anaes-
to circulate around the brainstem and spinal cord, thetic agents propofol, thiopentone and etomidate and
cerebellum and cerebral hemispheres. There is about fentanyl have no significant effect on the rate of CSF
150 ml of fluid circulating around the adult central formation or absorption. The volatile agents, in con-
nervous system, which is constantly produced by the trast, have varied but more significant effects. Isoflurane
choroid plexus and absorbed through the arachnoid is the only agent which reduces CSF production and
villi into the dural venous sinus network. CSF acts facilitates reabsorption. Desflurane induces an increase
both as a supporting fluid cushion for the intracranial in CSF production, whilst enflurane combines the
contents and as an important pathway for nutrients deleterious effects of increasing production and
and chemical mediators. reducing absorption. The other inhalational agents,
halothane and sevoflurane, decrease CSF production
SECRETION AND COMPOSITION but may also decrease its absorption.
CSF is a clear colourless fluid formed as an ultrafiltrate The total white blood cell (WBC) count in normal
of plasma and is composed of 99% water with a specific adult CSF is 0–5 per mm3 (lymphocytes and mono-

Table 7.1 Comparison of CSF and Plasma


(Modified and reproduced, with
permission, from Ganong WF.

Substance CSF Plasma

Na+ (meq/Kg H2O) 147 150


K (meq/Kg H2O)
+
2.9 4.6
Mg (meq/Kg H2O)
2+
2.2 1.6
Ca2+ (meq/Kg H2O) 2.3 4.7
-
Cl (meq/Kg H2O) 113 99
-
HCO3 (meq/Kg H2O) 25.1 24.8
pCO2 (kPa) 6.6 5.3
pH 7.33 7.4
Figure 7.1 Circulation of cerebral spinal fluid. (Modified Osmolality (mosm/Kg H2O) 289 289
and reproduced, with permission, from Meyer FB. Protein (g/l) 0.2 60
Cerebrospinal fluid physiology and the management of
increased intracranial pressure. Mayo Clin Pro 1990; 65: Glucose (mmol/l) 3.6 5.6
687.)
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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

Table 7.2 Cerebrospinal fluid findings in some common disorders.


Traumatic tap correction: For every 1000 red cells/mm3 subtract one white cell/mm3.

Meningitis
CSF Normal Bacterial Viral Tuberculous Multiple sclerosis

Appearance Clear and Turbid Clear to turbid Turbid Clear


colourless
Cell count/mm3 0–5 > 1000 < 500 < 500 5–60
Cell type Lymphocytes Polymorphs Lymphocytes Lymphocytes Monocytes
Protein concentration 0.15–0.45 > 1.5 0.5–1.0 1–5 0.4–1.0
(g/L)
CSF glucose At least 50% Less than 50% At least 50% Less than 50% At least 50%
of blood level of blood level of blood level of blood level of blood level
Ig < 15% of protein > 15% of protein
Oligoclonal IgG None Bands present in
80%
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8
INTRAVENOUS ANAESTHETIC
AGENTS

J. Coles, A.K. Gupta


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32 PHARMACOLOGY

INTRODUCTION protection during cardiac surgery. It may be useful


during periods of temporary intraoperative ischaemia
There are certain properties that the ‘ideal’ intra- (dose ≥ 5 mg/kg) if hypotension can be avoided. It is
venous agent for use during neuroanaesthesia and less protective in global compared to focal ischaemia. It
neurocritical care should possess: also has significant free radical scavenging properties,
• Rapid recovery of consciousness to enable early reduces calcium influx, and may block sodium
neurological assessment. channels. A coupled decrease in CBF occurs with
• Easily and rapidly titratable. CMRO2. If coupling is disrupted, CBF may increase.
• Minimal effects on other systems, e.g. cardiovas- EEG effects include initial fast activity anteriorly fol-
cular, respiratory, renal, hepatic. lowed by slowing leading to burst suppression with
• Analgesia. infusions doses up to 15 mg/kg/h after an initial
• Favourable effect on cerebral haemodynamics: loading dose. When CMRO2 is reduced by 50%, the
• A reduction in CMR coupled with CBF. EEG becomes isoelectric and increasing the dose has
• No increase in CBV. no further effect on CMRO2 or CBF. The effect on
• Vasoreactivity to CO2 maintained. evoked potentials is also dose-dependent (≠ latency, Ø
• Cerebrovascular autoregulation maintained. amplitude).
• Does not predispose to seizures.
Prolonged infusion is useful in status epilepticus and
Propofol, thiopentone, and etomidate are the agents refractory intracranial hypertension, and can be
most commonly used for intravenous induction of titrated to burst suppression. After prolonged infu-
anaesthesia for neurosurgery. sion, thiopentone is associated with dilated pupils, a
protracted recovery period and depression of con-
PROPOFOL sciousness.

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

Ketamine produces hypersynchronous d waves in the KEY POINTS


EEG, but has little effect on somatosensory or motor
evoked potentials. • Propofol, thiopentone and etomidate have similar
effects on cerebral haemodynamics and metabolism.
Although ketamine may offer theoretical cerebral • All three agents reduce CMRO2 and CBF and main-
protection via NMDA antagonism, its use in tain responsiveness to CO2 and autoregulation.
neuroanaesthesia is limited by its ability to increase • These agents cause dose-dependent suppression of
ICP. EEG. Burst suppression and isoelectric EEG can
be achieved.
• Ketamine causes increased CBF and ICP,
although it is an NMDA antagonist.
BENZODIAZEPINES • Benzodiazepines have a small effect on blood flow
and metabolism. They are anticonvulsant drugs
All produce a small reduction in CBF, CMRO2 and
but EEG burst suppression cannot be achieved.
ICP whilst preserving cerebral autoregulation and
vasoreactivity to CO2. This effect is inconsistent
and much less marked than the intravenous induction FURTHER READING
agents. A ceiling effect occurs whereby increasing Michenfelder JD. The interdependency of cerebral func-
doses do not produce greater reductions in these tion and metabolic effects following maximum doses of
variables. thiopental in the dog. Anesthesiology 1974; 41: 231
All are anticonvulsant and increase seizure threshold. Ravussin P, Guinard JP, Ralley F, Thorin D. Effect of
All effects, including any reduction in ICP, are propofol on cerebrospinal fluid pressure and cerebral
reversible using the competitive antagonist flumaze- perfusion pressure in patients undergoing craniotomy.
nil, the use of which may precipitate seizures. Anaesthesia 1988; 43(suppl): 37–41

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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INHALATIONAL ANAESTHETIC AGENTS 37

ENFLURANE KEY POINTS


Low concentrations decrease CMRO2, CBF and • All inhalational anaesthetic agents cause cerebral
cerebral autoregulation. Concentrations > 1.5 MAC vasodilatation.
produce spike and wave EEG appearances especially • All agents effect cerebral autoregulation.
with concomitant hypocapnia (< 4.0 kPa). The rate • All agents decrease CMRO2.
of production and resistance to reabsorption of CSF • These effects are dose-dependent and modified by
are also increased by enflurane, thereby exacerbating hypocapnia.
any increase in ICP. • Flow metabolism coupling is maintained in low
doses.

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

K. Grixti, A.K. Gupta


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40 PHARMACOLOGY

OPIOIDS CSF CIRCULATION


The opioid analgesics most frequently used in neuro- At low doses, fentanyl, sufentanil and alfentanil
anaesthesia in the UK are morphine, fentanyl and increase CSF absorption at the arachnoid villi.
alfentanil. Outside the UK, sufentanil has been used Fentanyl at high doses decreases the rate of CSF
successfully for elective intracranial procedures. More secretion and, along with sufentanil, may increase
recently, remifentanil is being used as a substitute to resistance to absorption.
these agents. The effects of these agents on cerebral
physiology are similar.
OTHER EFFECTS
The responsiveness to carbon dioxide is decreased
CEREBRAL HAEMODYNAMICS although hypoxic stimulation is preserved. The
Although opioids have little effect in low doses, in hypercapnic vasodilatation that can occur from
high doses reduction in CMR and CBF have been opioid-induced respiratory depression may increase
reported. Remifentanil decreases cerebral blood flow ICP if ventilation is not supported. This, together
in a regionally selective fashion. A rise in ICP has with hypoxia, can cause problems post-craniotomy
been reported with some agents (alfentanil in especially in the elderly, diabetics and the obese.
patients with tumours, morphine due to histamine Stimulation of the 5HT3 and dopamine receptors in
release, sufentanil in head-injured patients). the chemoreceptor trigger zone causes nausea and
However, none of these reports demonstrated any vomiting. Depression of the cough reflex caused may
clinical significance or effect on outcome. All be detrimental postoperatively if brainstem reflexes
opioids maintain autoregulation and CO2 reactivity are already impaired.
of the cerebral circulation.

EEG ACTIVITY NALOXONE


Opioid drugs generally slow down the EEG into the It has been shown that naloxone alone probably has
theta and delta wave activity though isoelectricity and no important effect on CBF/CMR, and in narcotised
burst suppression is not seen. However, high-dose patients these parameters are normalised with careful
opiates such as fentanyl at 200 µg/kg are known to titration. However, abrupt naloxone reversal has
cause convulsions in animals. It is also reported that resulted in hypertension, arrhythmias, myocardial
opioids may trigger limbic system epileptiform ischaemia and intracranial haemorrhage.
activity in known epileptics. This does not preclude
using opioids for epilepsy surgery. These drugs have
no significant effect on somatosensory, motor and
auditory evoked potentials. NEUROMUSCULAR BLOCKING
AGENTS
SEDATION AND EMERGENCE Coughing, straining and intolerance of the endotra-
POSTOPERATIVELY cheal tube can cause substantial increases in ICP,
which can be avoided by the administration of
When combined with N2O or propofol, opioids
neuromuscular blocking agents.
allow for more rapid emergence from anaesthesia
than inhalational anaesthetics as sole agents. Remi- Suxamethonium can increase ICP and CBF due to
fentanil in turn allows an even more rapid emergence muscle spindle activation. These increases are
when compared with fentanyl and alfentanil due transient, clinically insignificant and can be avoided
to a short half-life with plasma cholinesterase by ‘precurarisation’ if deemed necessary. Suxa-
metabolism. methonium is not contraindicated in neurosurgical
patients, particularly when the airway needs to be
Hypocapnia-induced cerebral vasoconstriction may
secured rapidly.
cause prolonged emergence due to an increased vol-
ume of distribution and a longer elimination. This is All non-depolarising agents have little effect on CBF or
secondary to decreased cerebral blood flow causing a CMR. Only d-tubocurarine through the release of
decrease in washout of the drug. A change in the histamine can increase CBV and ICP. Atracurium has
drug lipid/plasma distribution coefficient due to a no significant effect and its level of histamine release
higher pH may also contribute. is significantly less than d-tubocurarine. Atracurium
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OPOIDS AND ADJUVANT DRUGS 41


does not accumulate and is suitable for use as a pro- administration of nifedipine is well recognised in the
longed infusion. Laudanosine, a metabolite of recovery period. Long-term blood pressure control is
atracurium, can cross the blood–brain barrier and more appropriate with these drugs. The use of
predispose to seizures. However, even after pro- nimodipine and nicardipine in patients with sub-
longed infusion the serum levels of laudanosine are arachnoid haemorrhage is discussed elsewhere.
not clinically relevant.
Interactions with anticonvulsants, particularly phenytoin, KEY POINTS
shifts the dose–response curve for most relaxants to
the right, thereby increasing dose requirements. The • Opioids in low doses have little effect on CMR,
exception to this is atracurium which is independent CBF and ICP.
of liver metabolism. • Abrupt use of naloxone is detrimental.
• Non-depolarising muscle relaxants have little
effect on cerebral physiology.
• Suxemethonium is not contraindicated in neu-
ANTIHYPERTENSIVES roanaesthesia.
SNP, GTN, hydralazine – Direct smooth muscle • Vasodilator drugs increase CBV and ICP but not
relaxation of the cerebral vasculature causes an necessarily CBF.
increase in CBV and consequent rise in ICP. This • α- and β-blockers appear to have little or no effect
change is independent of CBF which appears not to on ICP/CBF.
rise. The rise in CBV and ICP may be related to
speed of infusion and the ability of compensatory
FURTHER READING
mechanisms to take effect. This is demonstrated by
the observation that hydralazine, which has a gradual Coles JP, Monteiro JN, Brazier P, et al. Propofol anesthe-
onset of activity thus allowing spatial compensation, sia for craniotomy: a double-blind comparison of remifen-
has least effect on ICP. tanil, alfentanil and fenatanyl. J Neurosurg Anesthesiol
2000; 12(1): 15–20
α and β blockers appear to have little or no effect on
Dahl A, Russell D, Nyberg-Hansen R, et al. Effect of
ICP/CBF. Labetolol has been extensively studied nitroglycerin on cerebral circulation measured by transcra-
and is useful for control of hypertension periopera- nial doppler and SPECT. Stroke 1989; 20: 1733
tively.
Muzzi DA, Black S, Losasso TJ, et al. Labetalol and esmolol
Calcium channel blockers are of little use for the acute in the control of hypertension after intracranial surgery.
management of hypertension, although sublingual Anesth Analg 1990; 70: 68
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11
ANTICONVULSANTS

J. Monteiro
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44 PHARMACOLOGY

INTRODUCTION b. Increased GABA response: Benzodiazepines


and barbiturates act at the GABA receptor to
The term seizure refers to a transient alteration in enhance chloride ion influx in response to
behaviour due to disorganised synchronous and GABA and produce a hyperpolarisation of the
rhythmic firing of populations of neurones. Epilepsy nerve membrane.
refers to a disorder of brain function characterised by 3. Calcium channel blockade: Valproate, ethosuximide
the periodic and unpredictable occurrence of and dimethadione reduce calcium ion flow
seizures. Seizure classification and treatments are through T type calcium ion channels and reduce
shown in Table 11.1. the pacemaker current known as the T current.

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

Table 11.1 Classification of seizures and treatment

Seizure type Usual anticonvulsant Alternative treatment

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)

Phenytoin 300–400 4–7 10–20


Carbamazepine 600–1200 20–30 6–12
Valproate 1000–3000 15–60 50–100
Clonazepam 1500–2000 0.01–0.2 0.013–0.072
Phenobarbitone 60–180 5–8 0.06–0.18

Table 11.3 Side-effect (S/E) profile of common anticonvulsants

Drug Dose related S/E Idiosyncratic S/E Long term S/E

Phenytoin Ataxia, tremor, nystagmus, Rashes, lymphadenopathy, Gingival hyperplasia,


lethargy, dystonia, blood dyscrasias, liver hirsuitism, neuropathy,
confusion damage, SLE folate deficiency,
osteomalacia
Carbamazepine Drowsiness, ataxia, Stevens-Johnson syndrome, Gynaecomastia,
diplopia, hyponatremia Rashes, dyspepsia, blood galactorrhoea,
dyscrasias, cholestatic thromboembolism,
jaundice, acute renal impotence, aggression
failure
Valproate Nausea, anorexia, tremors, Rashes, sedation, alopecia, Hearing loss, vasculitis,
ataxia, drowsiness hepatic necrosis, menstrual irregularities,
thrombocytopenia weight gain
Phenobarbitone Drowsiness, nystagmus, Rashes, SLE, paradoxical Folate deficiency,
ataxia excitement neuropathy,
osteomalacia

should be added to the dosing regime only if seizures FURTHER READING


persist despite therapeutic serum drug levels or intoler-
Commission on the classification and terminology of the
able side-effects of the first-line drug. Interactions
International league against epilepsy. Proposal for revised
between anticonvulsants are complex, highly variable classification of epilepsies and epileptic syndromes.
and unpredictable and may enhance toxicity without Epilepsia 1989; 30: 389–399
corresponding increases in anti-epileptic effect. The
mechanism of interaction is usually due to hepatic McDonald RL, Kelly KM. Antiepileptic drug mechanisms
microsomal enzyme induction or inhibition. Dis- of action Epilepsia 1993; 34 (supplement 5): S1–S8
placement of drugs from protein binding sites is usually McNamara JO. Drugs effective in the management of epilep-
not a contributory factor. Monitoring of serum drug sies. In: Molinoff PB, Ruddon RW, Gilman AG (eds) Good-
levels is therefore mandatory with combination man and Gilman’s The pharmacological basis of therapeutics,
therapy. 9th Edn. New York: McGraw Hill, 1996; pp. 461–486
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12
CRANIOTOMY FOR SPACE
OCCUPYING LESIONS

C. Duffy
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48 NEUROANAESTHESIA

CLASSIFICATION raised ICP. In this case, consider a short-acting


benzodiazepine. Medications such as anticonvulsants
Space occupying lesions comprise tumours, vascular and steroids are continued in the perioperative
lesions (Chapter 13), abscesses and haematomas period. Steroids may reduce oedema and improve
(spontaneous or traumatic). Presenting symptoms are symptoms in patients with malignant lesions and
commonly those of raised ICP, seizures or neuro- abscesses.
logical deficit.

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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CRANIOTOMY FOR SPACE OCCUPYING LESIONS 49


anaesthetic drugs is largely at the discretion of the POSTOPERATIVE MANAGEMENT
anaesthetist. Total intravenous anaesthesia (using
propofol) and/or inhalational agents (using isoflurane Patients with a depressed level of consciousness pre-
or sevoflurane) can be used. Most anaesthetists operatively usually require postoperative ventilation
choose a technique allowing for control of ICP and and monitoring in intensive care, otherwise, pro-
rapid emergence at the completion of surgery. The vided the intraoperative course is uneventful, patients
lungs are ventilated aiming for a PaCO2 between 4.0 with a preoperative GCS of 13–15 can be extubated
and 4.5kPa. Mannitol 0.5–1 g/kg is given approxi- once they open eyes to command and have demon-
mately 30–60 minutes prior to dura opening. Many strated a gag reflex. The overall aim is to achieve a
anaesthetists allow body temperature to drift to smooth emergence with minimal coughing and
34–36ºC, although there is no good evidence that straining which may be reduced by intravenous lido-
this is beneficial. Rewarming is commenced as soon caine (1.5 mg/kg) a few minutes prior to extubation.
as the dura is closed. One of the intraoperative com- Hypertension at this stage can be treated with a bolus
plications is acute cerebral oedema, the management of β-blocker (esmolol 0.5 mg/kg or labetalol 10–20
of which is given in Table 12.1. mg). Direct vasodilators may increase CBF and ICP
and should be avoided. In patients with delayed
Fluid management emergence in whom a drug or metabolic cause has
been excluded, a neurosurgical complication should
CVP is used as a guide to maintain normovolaemia. be suspected and an immediate CT scan should be
Dextrose-containing fluids should be avoided, as arranged.
there is an increased incidence of neurological
deficit associated with hyperglycaemia and focal After routine craniotomy, analgesic requirements are
cerebral oedema in experimental models. Blood usually satisfied by mild opiates such as codeine phos-
products should be available in the event of major phate or non-steroidal analgesics (if not contraindi-
bleeding aiming for resuscitation to a haematocrit cated). Potent opiates are often not required and may
of 0.30. Thromboplastin release causing dissemi- cause some degree of respiratory depression.
nated intravascular coagulation (DIC) may occur
and appropriate clotting factors should be given
early.
KEY POINTS
• Preoperatively assess neurological state, determine
the presence of raised ICP and optimise under-
lying disease.
Table 12.1 Management of • A total intravenous and/or inhalational anaesthesia
intraoperative cerebral oedema technique may be used.
• Maintain normotension, normovolaemia and a
• Optimise ventilation and blood gases relaxed brain intraoperatively.
• Maximise venous drainage • Aim for smooth, rapid emergence postoperatively.
• Deepen anaesthesia: bolus intravenous • Potent postoperative opioid analgesics are usually
anaesthetic agent, adjust inhalational agent not required. Avoid sedative drugs.
concentration
• Diuretics: Mannitol (0.25–1.0 g/kg) ± FURTHER READING
furosemide (0.25–0.5 mg/kg)
McDonald JD, Rosenblum ML. Gliomas. In: Rengachary
• CSF drainage SS, Wilkins RH (eds) Principles of neurosurgery. London:
• Minimise CMRO2: bolus lidocaine; thiopentone Wolfe 1994; 26.2–26.32
or propofol infusion Todd MM, Warner DS. Neuroanesthesia: a critical review.
• Consider further doses of diuretic and CSF In: Rogers MC, Tinker JH, Covino BG, Longnecker DE
drainage. (eds) Principles and practice of anesthesiology. St Louis:
Mosby-Year Book 1993, pp. 1599–1648
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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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CRANIOTOMY FOR VASCULAR LESIONS 53


Ventricular wall function is depressed in 30% of ischaemia in areas of vasospasm. Hyponatraemia may
patients. A diffuse myocardial ischaemia occurs in 50% be present from either a true SIADH or a central salt
of patients with widespread ST segment and T wave wasting syndrome. Previous medical history should
changes on ECG. The ECG abnormalities probably be noted. Avoid premedication unless the patient has
reflect the severity of neurologic dysfunction. grade I SAH and is particularly anxious. Nimodipine
should be continued throughout the perioperative
Vasospasm period. This is best administered through a central
venous catheter.
This occurs in 30–40% of patients admitted to hospi-
tal, typically 4–9 days post-SAH. It rarely occurs Early surgery soon after aneurysm rupture reduces the
within the first 3 days, peaks in 7–10 days and risk of re-bleeding but does not affect the incidence
resolves over 10–14 days. The diagnosis rests on clin- of vasospasm. Early surgery is also technically difficult
ical signs of a new neurological deficit and decreased due to oedema but facilitates medical and neuroradi-
level of consciousness. Other causes need to be ological treatment of vasospasm if it occurs later.
excluded such as re-bleed, hydrocephalus, seizures,
oedema, electrolyte abnormalities, drug effects and INTRAOPERATIVE MANAGEMENT
other medical complications. Angiography is the
‘gold standard’ investigation to confirm diagnosis and Monitoring
may be abnormal even in the absence of clinical evi-
dence of vasospasm. Vasospasm can also be suggested Direct arterial blood pressure, central venous pressure
by trends in transcranial Doppler ultrasonography of monitoring and a urinary catheter are mandatory.
cerebral blood flow velocity . The cause of vasospasm Pulmonary arterial pressure monitoring should be used
is uncertain, however the amount of subarachnoid if impaired myocardial function is suspected. More
blood correlates with its occurrence and severity, as specialised intraoperative monitoring may include
does the degree of abnormality in CBF autoregula- jugular bulb oximetry, transcranial Doppler, EEG or
tion and CO2 reactivity. The microscopic appearance evoked potentials.
is suggestive of a vasculopathy triggered by inflamma-
tory mediators released from blood and its break- Induction
down products. These include oxyhaemoglobin, Aneurysmal rupture is related to transmural pressure
bilirubin, endothelin and superoxide radicals, which across the wall of the aneurysm (MAP–ICP).
in turn affect nitric oxide production, calcium release Rupture occurs in 1–2% of anaesthetic inductions
and prostaglandin synthesis. All of these cause vaso- with a mortality rate approaching 75%. Hypertension
constriction of cerebral arteries. The occurrence of increases the risk of aneurysm rupture as does aggres-
vasospasm doubles the risk of mortality. Nimodipine sive hyperventilation and hypocapnia. In addition,
has been shown to improve outcome for SAH despite hypotension can lead to ischaemia in areas of
not preventing vasospasm. It should be started on impaired autoregulation. Accordingly, the objective
admission with an oral or nasogastric dose of 60 mg should be normotension during the induction and
every 4 hours, or a reduced intravenous dose if maintenance phases of anaesthesia and large changes
hypotension is a problem. The reason for improved in transmural pressure should be avoided. Invasive
outcome remains uncertain. blood pressure monitoring should commence prior
to induction and supplemental doses of induction
PREOPERATIVE MANAGEMENT agent or high dose opiate may be required to avoid
pressor responses of laryngoscopy and intubation.
The patient’s acute condition is assessed and graded
according to Hunt and Hess (Table 13.1) or World
Maintenance
Federation of Neurological Surgeons (Table 13.2)
scales. With worsening grades, CBF autoregulation and A technique allowing for titration of blood pressure is
CO2 response also deteriorate. Grades I and II (Hunt important. A propofol infusion and/or inhalational
and Hess scale) often have near normal ICP values. technique are acceptable. Mannitol and mild hyper-
ventilation after dura opening may be required to
Cardiac function must be assessed and optimised.
reduce brain swelling permitting better exposure.
Serious dysrhythmias need to be treated. Fluid resus-
citation with invasive monitoring may be required
Temporary Clipping/Induced Hypotension
preoperatively especially in poor grade patients as
they are often intravascularly depleted. Hypo- During dissection, the surgeon may reduce tension in
volaemia should be avoided to help prevent further the aneurysm using a temporary clip on a feeding
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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.

Table 13.3 Treatment guidelines for ruptured intraoperative aneurysm

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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CRANIOTOMY FOR VASCULAR LESIONS 55

PREOPERATIVE MANAGEMENT ventilated postoperatively with ICP monitoring.


Blood pressure should be maintained in the low nor-
The presence of cerebral aneurysms should be noted. mal range. Continuation of muscle paralysis min-
imises the risk of venous congestion due to coughing
INTRAOPERATIVE MANAGEMENT and straining and other neuroprotective strategies
should be considered (Chapter 40).
Bleeding from AVMs can be large, rapid and sus-
tained. Blood products must be readily available. As
haemorrhage is usually venous in origin, avoid KEY POINTS
increases in jugular venous pressure that can be trans-
mitted to the cerebral circulation (i.e. care with inter- Aneurysms
nal jugular lines, ETT fixation tapes, avoiding head
• SAH is associated with cardiac dysfunction and
down, PEEP). Management of acute brain swelling
fluid and electrolyte imbalance.
intraoperatively is described in Chapter 12.
• Vasospasm and further bleeding are complications
Deliberate hypotension may assist the surgeon in the of aneurysm rupture.
visualisation and ligation of arterial feeders. However, • Avoid large changes in transmural pressure (MAP-
it carries the risk of causing ischaemia in non- ICP) across the wall of unclipped aneurysms.
autoregulating surrounding brain and may lead to • CPP should be optimal at the time of temporary
venous thrombosis. A decision about blood pressure clip application.
management should be made on an individual basis • Maintain normovolaemia if intraoperative rupture
after discussion with the surgical team. occurs.

POSTOPERATIVE MANAGEMENT AND AVMs


COMPLICATIONS • Intraoperative blood loss can be rapid and large.
Hyperaemia producing oedema or haemorrhage and • Onset of cerebral oedema can be rapid and occur
intracranial hypertension may occur in the postoper- intraoperatively soon after AVM resection.
ative period due to: • Postoperative hyperaemia worsens outcome.
• Postoperative blood pressure should be main-
1. ‘Normal perfusion pressure breakthrough’ (NPPB) tained in the low normal range.
where hypoperfused brain surrounding the AVM
theoretically loses the ability to autoregulate and
restoration of normal CBF after the AVM is FURTHER READING
removed leads to microhaemorrhages and diffuse The International Study of Unruptured Intracranial
swelling. Staged removal by excision or embolisa- Aneurysm investigators. Unruptured intracranial aneurysms
tion should theoretically allow the surrounding – risk of rupture and risks of surgical intervention. N Engl J
brain to regain autoregulatory mechanisms. Med 1998; 339: 1725–1733
2. Postoperative haemorrhage from residual AVM. Spetzler RF, Martin NA. A proposed grading system for arte-
3. ‘Occlusive hyperaemia’ where venous outflow riovenous malformations. J Neurosurg 1986; 65: 476–483
obstruction predisposes to haemorrhage if arterial
Guy J, McGrath BJ, Borel CO, Friedman AH, Warner DS.
feeders are not completely occluded. It is also Perioperative management of aneurysmal subarachnoid
possible that venous obstruction may result in hemorrhage: part 1. Operative management (review arti-
hypoperfusion due to stagnation of CBF. cle). Anesth Analg 1995; 81: 1060–1072
Hyperaemia is a major source of postoperative mor- McGrath BJ, Guy J, Borel CO, Friedman AH, Warner DS.
bidity/mortality. Perioperative management of aneurysmal subarachnoid
hemorrhage: part 2. Postoperative management (review
The risk of seizures following AVM resection article). Anesth Analg 1995; 81: 1295–1302
approaches 50%. If the intraoperative course has been
uneventful, the patient should be extubated at the Young WL, Kader A, Prohovnik I, et al. Pressure autoreg-
ulation is intact after arteriovenous malformation resection.
end of the procedure. Because of the risk of hyper-
Neurosurgery 1993; 32: 491–497
aemia, it is important to avoid hypertension at the
time of emergence. The use of β-blockers may Al-Rodhan NRF, Sundt TM, Piepgras DG, Nichols DA,
reduce blood pressure without delaying emergence. Rufenacht D, Stevens LN. Occlusive hyperemia: a theory
for the hemodynamic complications following resection of
If intraoperative bleeding has been excessive or there intracerebral arteriovenous malformations. J Neurosurg
is evidence of brain swelling, the patient should be 1993; 78: 167–175
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14
POSTERIOR FOSSA SURGERY

C. Goldsack
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58 NEUROANAESTHESIA

INTRODUCTION of deep venous thrombosis and improving emptying


of the epidural venous sinuses. The head is fixed in
The posterior fossa contains the cerebellum and the clamps in preference to a horseshoe in order to min-
brainstem. The major sensory and motor pathways imise pressure on the face and eyes.
between the cerebrum and the rest of the body run
through the posterior fossa. The brainstem also con-
tains the vital centres controlling cardiovascular and LATERAL POSITION
respiratory function. Failure of these centres is This is suitable for approaches to lesions not in the
incompatible with life. The anatomy of the posterior midline, particularly the cerebellopontine angle. A
fossa is given in Chapter 3. variation called the ‘park bench’ position is often used;
so-called because of the resemblance to a tramp sleep-
ing on a bench in the park. A pad should be placed
PATHOLOGY under the body in the axilla to minimise weight on
the lower arm and shoulder. The pelvis should be
TUMOURS fixed with supports in front and behind. The lower
leg is flexed at the hip and knee. The upper leg is kept
Primary brain tumours such as gliomas and astrocy- straight and slightly externally rotated to lock the knee
tomas are the commonest indication for posterior fossa with the foot on a firm support, which will prevent
surgery. Malignant tumours from elsewhere can the patient sliding down the table if significant head-
metastasise to the cerebellum. Benign tumours include up tilt is used. A pillow is placed between the legs.
meningiomas and also acoustic neuromas (Schwan- The lower arm is flexed across the body and the upper
nomas), which arise from the VIIIth cranial nerve, often arm is taped along the upper side of the body. The
in the cerebellopontine angle. Haemangioblastomas head is fixed in pins. Excessive flexion of the neck can
can develop in the cerebellum and frequently secrete obstruct the internal jugular veins. This can be
erythropoietin, resulting in polcythaemia. avoided by ensuring a two- or three-finger breadth
gap between chin and sternal notch.
VASCULAR LESIONS
These are uncommon in the posterior fossa. SITTING POSITION
Aneurysms tend to occur on the posterior-inferior This was widely used for posterior fossa surgery in the
cerebellar artery (PICA) which is an important supply past. It provides good surgical access to midline struc-
to the midbrain. Vasospasm will therefore have seri- tures, improves surgical orientation and allows good
ous consequences. Small vessels impinging on cranial drainage of blood and CSF. However, there are
nerves in the posterior fossa can result in symptoms increased risks of cord compression, pneumocephalus
such as trigeminal neuralgia. Surgical decompression and venous air embolism. Hypotensive techniques
has a good success rate. increase the risks of ischaemic damage. Many author-
ities now contend that with modern anaesthetic tech-
FORAMEN MAGNUM niques there is no place for the sitting position in
DECOMPRESSION neuroanaesthesia. However, excessive head-up tilt in
other positions exposes the patient to similar risks.
In the young this is usually for congenital abnormali-
ties such as Arnold–Chiari malformation; in the
elderly, degenerative changes can occur. ANAESTHETIC TECHNIQUE
The choice of particular agents is not critical but sta-
ble anaesthesia is paramount. The effects of a particu-
POSITIONING lar drug on blood pressure and neurophysiological
monitoring should be considered. Muscle relaxation
PRONE POSITION
is best provided by continuous infusion (e.g.
This position offers good access to midline structures atracurium). This helps ventilation and prevents
but bleeding can obscure the surgical field. Head-up movement in a relatively lightly anaesthetised patient.
tilt is employed to reduce haemorrhage but this If motor nerve function is monitored, such as the
increases the risk of air embolism. The chest and iliac facial nerve during acoustic neuroma surgery, muscle
crests should be well supported to ensure free move- relaxation must be discontinued and sufficient depth
ment of the abdomen during respiration. Pressure on of anaesthesia must be provided. A remifentanil infu-
the iliac vessels should be avoided, reducing the risk sion is ideal in this situation.
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POSTERIOR FOSSA SURGERY 59


A central venous line is usually required and access to This is due to obstruction of venous and lymphatic
the internal jugular veins may be difficult. Subclavian, drainage. Cranial nerve damage can also cause serious
antecubital fossa or femoral long lines are alternatives. airway problems.
A nasogastric tube should be inserted if there is any
risk of postoperative bulbar dysfunction.
NEUROLOGICAL COMPLICATIONS
Neurophysiological monitoring is used frequently.
Auditory evoked potentials are used for detecting dis- Extreme neck flexion can cause midcervical quadra-
section near the brainstem, particularly during plegia. Prolonged surgery and hypotension are con-
acoustic neuroma surgery. When somatosensory and tributory factors. Surgery near the roots of nerves
motor evoked potentials are monitored, they can be VII–X may lead to loss of airway reflexes, dysphagia
suppressed during deep anaesthesia. and dysphonia. Peripheral nerve damage can result
from faulty positioning. The brachial plexus, ulnar
Deliberate hypotension should be employed with nerve and common peroneal nerve are most vulnera-
caution if significant head-up tilt is used and because ble.
surgery near the brainstem can induce further
hypotension and bradycardia.
PNEUMOCEPHALUS
The anaesthetic technique and intraoperative man-
agement is otherwise similar to that required for Following a craniotomy, an air-filled space between
supratentorial craniotomy (Chapter 12). the dura and arachnoid remains after CSF has leaked
away during surgery and brain bulk is reduced. In the
POSTOPERATIVE MANAGEMENT recovery period brain bulk increases again as cerebral
oedema develops, arterial carbon dioxide concentra-
Extubation at the end of surgery should not occur if tions increase and CSF reaccumulates. The trapped
significant brainstem or cranial nerve injury has air then comes under increasing pressure. N2O will
occurred. This may manifest as repeated episodes of worsen the situation. Pneumocephalus presents as
intraoperative haemodynamic instability. Pulmonary delayed recovery or deteriorating neurological state
oedema may be precipitated by large venous air and should always be considered if this occurs.
embolism or after surgery to the floor of the fourth Pneumocephalus can be reduced by discontinuing
ventricle. Respiratory failure can occur suddenly, nitrous oxide 15 minutes before surgery finishes and
even when awake. Air may remain within the by allowing the PaCO2 to rise towards the end of the
cranium for 2 weeks postoperatively which may be operation.
relevant should return to theatre become necessary.

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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ANAESTHESIA FOR
ACOUSTIC NEUROMAS

A. Swami
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66 NEUROANAESTHESIA

INTRODUCTION tion is otherwise similar to that of posterior fossa lesions


(see Chapter 14). Premedication should be reserved
The term cerebellopontine angle (CPA) normally for those with small tumours and who are neuro-
means the space bounded anteromedially by the lower logically intact.
pons and medulla; posteromedially by the cerebellum;
and laterally by the petrous portion of the temporal
bone. An acoustic neuroma is a schwannoma arising INTRAOPERATIVE CONSIDERATIONS
from the vestibular portion of CN VIII, occurring in
the fifth and sixth decade of life with equal sex distri- Although these operations are usually prolonged, a
bution, and account for about 80% of all CPA tumours. smooth rapid wake up is still required to allow for
The primary presenting symptom is of hearing loss, neurological assessment. For patients with large
but hemifacial spasm and tic douloureux can also rarely tumours, total intravenous anaesthesia (TIVA) is pre-
occur. Hydrocephalus occurs with large tumours. ferred and inhalational agents avoided. This can be
Acoustic neuroma classification, treatment and mor- achieved using a propofol infusion and should be
tality are according to tumour size measured on MRI: supplemented by an opiate. Fentanyl, Alfentanil and
Remifentanil have all been used for this purpose. As
SIZE MORTALITY facial nerve monitoring is used during the procedure,
• Small 0–15 mm 0% further non-depolarising muscle relaxants after intu-
• Medium 16–30 mm < 1% bation should be avoided. Care should therefore be
• Large > 31 mm 4–7% taken to maintain a sufficient depth of anaesthesia to
The main concern in surgery for small tumours is avoid movement intraoperatively. Maintenance of
preservation of CN VII and hearing function. Facial temperature and fluid balance is essential and both of
paralysis is arguably the most disturbing and devastat- these should be carefully monitored. Mild hypother-
ing complication. mia (35°C) is frequently employed.
For large tumours, the aim is to protect the brainstem Positioning of the patient may be lateral, or more fre-
and lower cranial nerves including CN VII. quently the supine position. Care should be taken in
the supine lateral position as obstruction of jugular
vein can occur if the head is excessively rotated.
SURGICAL APPROACHES Surgical manipulation of brainstem structures may
The suboccipital approach can be universally applied cause cardiovascular instability, and this should be
regardless of size and gives excellent exposure. reported to the surgeon. These responses should be
Although there is a possibility of cerebellar retraction, preserved and anticholinergic or long-acting beta-
this approach allows a good probability of hearing blocking drugs should be avoided where possible.
preservation and a low incidence of anterior inferior
cerebellar artery occlusion. Monitoring
With the translabyrinthine approach, exposure of the In addition to the routine monitoring used for a pos-
tumour is accomplished at the expense of bone terior fossa operation, specific monitoring is also
removal rather than cerebellar or brainstem retraction employed. Facial nerve monitoring is routinely used
and allows early identification of CN VII. However, which consists of a stimulator and tremogram to
hearing is necessarily destroyed. detect facial muscle movement via a speaker.
Auditory brainstem response recording can be used in
The middle fossa approach is successful for small patients with serviceable hearing.
tumours especially when hearing preservation is a
goal although is technically difficult due to lack of Emergence
anatomical landmarks.
With large tumour resection, elective postoperative
ventilation with paralysis in an ICU environment may
PREOPERATIVE CONSIDERATIONS be required. This facilitates control of blood pressure
and prevents coughing or straining thereby reducing
Although these tumours generally do not invade tissues the possibility of haematoma formation in the opera-
but tend to displace them, larger tumours cause tive site. Furthermore, difficult dissection of a large
symptoms and signs of brainstem distortion. Hydro- tumour will cause oedema of the brainstem and/or
cephalus may be present and requires treatment before lower cranial nerves. This will obtund the cough or
definitive tumour surgery. The preoperative evalua- swallow reflex, which may delay extubation.
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ACOUSTIC NEUROMA 67

POSTOPERATIVE COMPLICATIONS • Anaesthetic implications are similar to those for


posterior fossa surgery
In addition to the complications that occur for any • Facial nerve monitoring requires the patient to be
posterior fossa operation, additional complications for unparalysed
acoustic neuroma surgery include: • Surgery is often prolonged
• hydrocephalus 1–2% • Cardiovascular instability may occur intraopera-
• CSF leak 6–14% tively
• meningitis 1–5% • Airway reflexes may be obtunded particularly with
• haematoma 0–6% large tumours.
• CN VII paralysis 0–18%.
FURTHER READING
KEY POINTS Sterkers JM, Charachon R, Sterkers O (eds). Acoustic
neuroma and skull base surgery. Kugler Publications,
• Acoustic neuromas arise from CN VIII Amsterdam 1995, pp. 137–163, 439–442
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EPILEPSY SURGERY

M. Smith
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70 NEUROANAESTHESIA

INTRODUCTION high proportion of such patients has hippocampal


sclerosis, and extended temporal lobectomy may offer
Epilepsy occurs in approximately 1 in 200 of the pop- a reduction of seizure frequency and severity.
ulation. It is a chronic illness due to an underlying
disorder of neuronal activity, which is characterised
by recurrent seizure activity. Despite considerable ANTICONVULSANT THERAPY
progress in the medical management of epilepsy and
Choice of anticonvulsant medication is determined
the development of new anti-convulsants, some
by seizure type, seizure history, age of the patient and
patients remain refractory to therapy or develop
side-effects. Monotherapy is sufficient to control
intolerable side-effects. Surgery is an alternative and
seizures in many patients but some require addition of
increasingly favourable option for patients with a dis-
second- or third-line agents (see Chapter 11).
crete seizure focus.

PATHOPHYSIOLOGY PREOPERATIVE ASSESSMENT

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.

POSTOPERATIVE CARE FURTHER READING


The patient should be nursed in a neurosurgical Kofte WA, Templehoff R, Dasheiff RM. Anesthesia for
intensive care/high dependency unit following epileptic patients and for epilepsy surgery. In: Cotteril JE,
Smith DS (eds) Anesthesia for neurosurgery. St Louis:
surgery for epilepsy. Seizures may occur in the Mosby, 1994, p. 495
immediate postoperative period and if untreated may
progress to status epilepticus. Seizures may be precipi- Modica PA, Tempelhoff R, White PF. Pro- and anticon-
tated by metabolic changes, hypercarbia, drugs or by vulsant effects of anaesthetics. (Part 1). Anesth Analg 1990;
the underlying epilepsy (Table 17.2). A CT scan is 70: 303
helpful in excluding a ‘surgical’ cause of postoperative Modica PA, Tempelhoff R, White PF. Pro- and anticon-
seizures. To avoid cerebral damage, seizures should be vulsant effects of anaesthetics. (Part 2). Anesth Analg 1990;
treated aggressively with benzodiazepines, thio- 70: 527
pentone or propofol. Recurrent seizures may require Smith M. Anaesthesia for epilepsy surgery. In: Shorvon SD,
top-up doses of long-acting anticonvulsant drugs or Dreifuss FE, Fish DF, Thomas DGT (eds) The treatment of
the introduction of adjuvant therapy (see Chapter 46). epilepsy. Oxford: Blackwell Scientific, 1996
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18
AWAKE CRANIOTOMY

M. Smith
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74 NEUROANAESTHESIA

INTRODUCTION appropriate for patients to make their own selection


of background music. Routine invasive cardiovascu-
In the UK, most neurosurgical procedures are carried lar monitoring is applied using local anaesthesia and a
out under general anaesthesia. This allows for provi- urinary catheter inserted if the procedure will be pro-
sion of optimal operating conditions with the ability longed.
to control PaCO2 and blood pressure (BP) whilst Some procedures, such as stereotactic brain biopsy,
assuring immobility and lack of awareness. Awake may be carried out entirely under local anaesthesia.
craniotomy is demanding for the neurosurgeon and More complex procedures, particularly those requir-
neuroanaesthetist and requires a high degree of moti- ing craniotomy, are better suited to a combined tech-
vation from the patient. nique of local anaesthesia and sedation.
Some form of airway management may be required
BACKGROUND during the sedation phase of the technique and in
certain circumstances a laryngeal mask airway, which
The technique of awake craniotomy has developed can be removed for the awake phase, may be suitable.
over many years and initially involved local anaesthe- There is a risk that the patient may cough during
sia alone or combinations of local and general anaes- removal of the laryngeal mask and this is unacceptable
thesia together with a variety of intraoperative in patients with an open dura. Furthermore, it can be
wake-up techniques. The advent of neuroleptanaes- difficult to re-insert the laryngeal mask should re-
thesia (e.g. using intravenous droperidol and opioids) sedation be required during surgery.
offer some improvements in technique but the intro-
duction of propofol presented an accurately titratable An alternative option is to insert a soft nasopharyn-
sedative with a rapid wake-up characteristic ideal for geal airway into one nostril after preparation of the
neurosurgical procedures. nasal mucosa with topical vasoconstrictor and local
anaesthesia. This can safely remain in place through-
out the procedure. It also has the advantage of allow-
PROCEDURES SUITABLE FOR ing monitoring of end-tidal CO2 by attachment of a
AWAKE TECHNIQUES side-stream CO2 monitoring device into the end of
• Epilepsy surgery. the nasopharyngeal airway. Oxygen may be adminis-
• Stereotactic surgery. tered via the contralateral nostril.
• Functional surgery, e.g. pallidotomy, thalamotomy. The patient is transferred to the operating table and
• Resection of mass lesions in eloquent areas (partic- settled in a comfortable position prior to sedation.
ularly in the dominant hemisphere). The head is best supported with a three-pin fixator
• Cortical stimulation for recognition of motor, applied using local anaesthesia (bupivacaine 0.5%
sensory and speech areas. with epinephrine). This prevents head movement
• Determination of memory and recognition areas during surgery and maximises airway control during
(when combined with neuropsychological assess- the sedation phase. Surgical drapes are then
ment). positioned to allow continuous access by the anaes-
thetist to the patient and airway.
PREOPERATIVE ASSESSMENT When the patient is comfortable, intravenous seda-
Careful preoperative assessment and explanation are tion is administered as appropriate. A small bolus of
essential for success. It is crucial that the anaesthetist propofol followed by a titrated infusion works well,
develops a good rapport with the patient and gives a although more recently TCI propofol has been rec-
detailed explanation of the procedure. In addition to ommended. Patient-controlled sedation techniques
routine preoperative considerations, the anaesthetist with propofol may also be used. Incremental doses of
must decide whether the patient is sufficiently coop- a short-acting opioid such as fentanyl can be titrated
erative to participate in the procedure and whether against respiratory rate, but vigilance is required to
they can tolerate lying supine and immobile for the prevent apnoea. Low dose remifentanil infusion is
duration of the operation. now a useful alternative. A small dose of droperidol
(0.25–0.5 mg) minimises nausea during craniotomy.
When the patient is settled, local anaesthesia (0.5%
INTRAOPERATIVE MANAGEMENT
bupivacaine with epinephrine) is applied to the skin
All members of the theatre team must be briefed in and tissue layers down to the cranium, ensuring that
advance so that a calm atmosphere prevails. It may be the sensory nerves arising from the branches of the
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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

INTRODUCTION encroachment on the cochlear nucleus and vascular


compromise leading to ischaemia. The incidence of
Surgical decompression of cranial nerves near their complete hearing loss with trigeminal decompression
root entry zones in the brainstem is considered when is 1–4%, and up to 20% have partial hearing loss. Facial
medical treatment has been unsuccessful, and may nerve decompression carries a higher risk due to the
provide symptom relief from trigeminal neuralgia, closer proximity of the nerve with the auditory nerve.
hemifacial spasm and occasionally other conditions Brainstem auditory evoked potentials intraoperatively
including glossopharyngeal neuralgia, tinnitus, reduces the incidence of postoperative deafness.
positional vertigo, spastic torticollis, essential hyper-
tension and intractable hiccups.
PREOPERATIVE MANAGEMENT
Medical treatment for trigeminal neuralgia consists of
CLINICAL FEATURES carbamazepine as a first-line drug or sodium valproate
and phenytoin and all may interact with anaesthetic
Trigeminal neuralgia is characterised by unilateral
agents (see Chapter 11). These drugs must be con-
paroxsyms of stabbing pain in one or more divisions of
tinued and withdrawn gradually postoperatively to
the trigeminal nerve territories. Often specific trigger
avoid rebound convulsions. Baclofen may also be used
zones or stimuli set off the pain many times a day.
for trigeminal neuralgia and may cause bradycardia
Occasionally multiple sclerosis or a benign tumour is
and hypotension with general anaesthetic agents.
the cause, however more commonly it is due to a
small artery causing irritation of the root entry zone of
CN V which can be seen by MR angiography.2 It is INTRAOPERATIVE MANAGEMENT
more commonly seen in old age with atherosclerotic
changes in the arteries. However, juvenile forms are Monitoring
sometimes seen with more severe anomalous vessel
Full monitoring should be used for all cases of poste-
formation involving veins.
rior fossa surgery including direct arterial and venous
Hemifacial spasm is an irregular clonic spasm of the pressure, end-tidal CO2, pulse oximetry, electrocar-
facial muscles usually involving one side of the face. diogram (ECG) and temperature.
Pain is not usually a feature unless fibres from the
nervus intermedius are involved. The cause is usually Positioning
secondary to aberrant blood vessels at the root entry
The patient is placed in the supine position, with the
zone of CN VII. It can be combined with other cra-
ipsilateral shoulder raised with a sandbag. The neck is
nial nerve neuropathies commonly CN V and VIII.
flexed and rotated away from the operative side.
Other causes include acoustic neuroma, Paget’s
Alternatively, the patient may be placed in the lateral
disease and following Bell’s palsy.
or park bench position.
Glossopharyngeal neuralgia is similar in aetiology and
treatment. It manifests with paroxsyms of pain at the Anaesthesia
back of the mouth and throat. Bradycardia and faint-
Anaesthesia is the same as for possa fossa surgery (see
ing may accompany the pain.
Chapter 14). Care must be taken with increased stimu-
lation during laryngoscopy and intubation, pin place-
SURGICAL PROCEDURE ment from the skull pinholder, periosteal dissection,
craniotomy and dural incision together with closure
The surgery, known as the Janetta procedure, consists
and headwrapping. Hypertensive responses can also be
of inserting a muscle pad or Teflon sponge to separate
seen on manipulation of the trigeminal nerve while
the offending vessel and the nerve entry zone. It is
hypotension and bradycardia are seen with vagus nerve
performed via a retromastoid approach into the pos-
stimulation. Confirmation of airway and corneal
terior fossa and usually takes 2–3 hours to complete.
reflexes immediately postoperatively is necessary.
Recurrence of neuralgia after surgery may be due to
slippage of the pad or due to reactive scar tissue
which may also involve other cranial nerves.
ELECTROPHYSIOLOGICAL
The main surgical concern with microvascular
decompression is damage to the auditory nerve
MONITORING
secondary to stretching with the cerebellar retractor. Somatosensory and trigeminal evoked potentials are
Other possible mechanisms of damage include sometimes used to monitor brainstem and trigeminal
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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

Anterior pituitary Release hormone Inhibiting hormone


hormone

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)

* Recommended by IUPAC-IUB Committee on Biochemical Nomenclature 1974


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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

INTRODUCTION Table 21.1 Criteria for general


Image-guided stereotactic surgery allows access to anaesthesia outside the operating
intracranial lesions without the need for craniotomy theatre
enabling safer biopsy of very small lesions and lesions
close to vital centres. Stereotaxis can also be used to 1. Reliable source of oxygen.
choose the craniotomy site for minimal access surgery 2. Portable means of manually and mechanically
such as the removal of secondary tumour deposits on ventilating patient
the surface of the brain or for the delivery of radio- 3. Intubating equipment to place an armoured
therapy via CT-guided radioactive wires. endotracheal tube. (A laryngeal mask airway is
useful for unexpected difficult intubation in the
A mechanical frame is attached to the patient’s head
X-ray department.)
and a CT scan obtained. The scanner’s computer cal-
culates the 3-D coordinates of points in the brain and 4. Portable monitoring including ECG, NIBP and
relates them to the stereotactic space outlined by the pulse oximetry. Capnography is desirable but
frame. Simple calculations convert these radiographic not essential.
coordinates to the coordinate system used by the 5. Immediate access to all drugs that may be
frame. These coordinates are set on the micrometers required.
on the frame through which biopsy instruments can 6. Patient on bed or trolley capable of immediate
be directed with an accuracy of 1–2 mm. head down tilt.
Alternatively, frameless stereotaxy allows surgeons to 7. Working portable suction apparatus.
reassess direction and approach to surgery without
having to repeat imaging of the brain to establish new
3-D coordinates. The initial CT or MR image is stored
on computer in the operating theatre and fixed points The anaesthetic technique is aimed at cardiovascular
on the skull are mapped onto the image using a sen- and respiratory stability to maintain a stable CPP and
sor wand. The tip of the sensor can then define the ICP, minimising oedema and consequent lesion
lesion on all axes of interest on CT, MRI or fused movement with respect to the skull.
images of both. A total intravenous system utilising propofol to
induce and maintain anaesthesia is commonly used.
This avoids the need for an anaesthetic machine dur-
ANAESTHESIA ing transfer and problems of pollution with scaveng-
ing of inhalational agents. Propofol can be used to
External frame systems require the use of metal pins to ease the stimulus of siting the stereotactic frame and
fix the frame to the head. These can be applied under allows fast recovery if the procedure to follow
local anaesthesia supplemented with sedation if requires the patient to be awake, e.g. thalamotomy. A
required. The burrhole for biopsy can also be performed modest dose of short-acting narcotic may also be used
under local anaesthesia. This has the advantage of con- together with monitored muscle relaxation. The
tinuous patient evaluation during transfer between the same anaesthetic technique can be continued in the
radiology suite and operating theatre and during biopsy. operating room.
General anaesthesia, however, is more common All monitors, pumps, O2 cylinders and ventilator
especially for prolonged procedures and for children. should be fixed securely to the transfer trolley and
The patient is anaesthetised prior to application of the arranged for easy observation from outside the CT
frame and CT scan and then transferred anaesthetised scanner. Good venous access should be secured as the
to the operating theatre for burrhole biopsy. biopsy may provoke bleeding which may be fatal.
Patients who are otherwise fit and do not require
invasive monitoring may be induced within the radi-
ology suite. The essential criteria to perform general KEY POINTS
anaesthesia outside the operating theatre are outlined
• Stereotactic surgery usually requires anaesthesia in
in Table 21.1.
a site remote from the operating room.
Patients with multi-system disease requiring invasive • A total intravenous technique based on propofol,
monitoring for safe anaesthesia should be induced in opioid and muscle relaxation provides stability,
the operating theatre, transferred to the radiology adequate depth of anaesthesia for all stages of
suite and returned back to theatre. stereotaxis and a rapid reliable recovery.
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STEREOTACTIC SURGERY 87

FURTHER READING Bone ME, Bristow A. Total intravenous anaesthesia in


stereotactic surgery: one years clinical experience. Eur J
Salcman M. The surgical management of gliomas. In:
Anaesthesiol 1991; 8: 47–54
Tindall GT, Cooper PR, Barrow PL (eds) The practice of
neurosurgery. Baltimore: Williams & Wilkins, 1996, pp. Powell M. Recent advances: neurosurgery. Br Med J 1999;
649–670 318: 35–38
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22
ANAESTHESIA FOR HEAD
INJURY

C. Duffy
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INTRODUCTION 1. Skull fractures depressed greater than skull thick-


ness. Compound fractures with torn dura need
Over one million people present to hospital each year repair to reduce infection risk.
in the UK with head injury (HI) and, of these, over 2. Intracranial mass lesions with > 5 mm midline shift
half are aged under 16 years. HI occurs twice as often or basal cistern compression on CT scan (i.e. a sign
in males and peaks from teenage years up to 40 years of imminent transtentorial herniation).
old. In the UK, 15–20% of all deaths in the 15 to 35- 3. Most acute subdural and epidural haematomas need
year age group are due to head injury. evacuation within 2–4 hours of injury to achieve
The main causes of HI are falls (41%), assaults (20%) optimal chance of recovery.
and road traffic accidents (RTAs) (13%). RTAs are 4. Intracerebral haematoma: The decision to operate is
associated with more severe injuries and account for guided by the patient’s clinical condition and ICP.
58% of all deaths from HI. Urgent surgical management is required for large
temporal lobe lesions (due to risk of transtentorial
The GCS is used as a guide to severity of HI after herniation) and posterior fossa collections (causing
hypovolaemia, hypoxia, drug and alcohol effects have brainstem compression).
been corrected. On the basis of GCS, HI severity can 5. Refractory intracranial hypertension may improve
be divided into mild (GCS 13–15), moderate (GCS with decompressive craniectomy.
9–12) or severe (GCS < 8) injury. 6. Delayed hydrocephalus occurs in 6% of severe HIs,
Although little can be done to repair the neural usually 14 days post-injury.
damage from the primary injury, the secondary injury
which occurs as a result of additional mechanical or
metabolic derangement triggered by the primary PATHOPHYSIOLOGY
event may be amenable to medical intervention.
Secondary injury may be systemic or intracranial in 1. Haemorrhagic contusions are superficial multiple
origin (Table 22.1). Systemic and CNS monitoring bilateral areas of haemorrhage usually affecting
allow for early detection and prompt treatment of grey matter of temporal and frontal lobes. They
factors that may exacerbate secondary injury. account for 3% of severe head injuries. The CT
image is characterised by a ‘salt and pepper’ appear-
Associated injuries occur in half of severe HIs and evi- ance due to interspersed haemorrhage and
dence for these should be sought particularly involv- oedema. Contusions are better delineated with
ing spine (2–5% of severe HIs), chest (e.g. cardiac MRI scans.
tamponade, contusion, pneumothorax), abdomen, 2. Intracerebral haematomas usually affect the white
pelvis and limb fractures. In cases of multi-trauma, matter or basal ganglia and are the cause of delayed
injuries need to be prioritised appropriately. neurological deterioration in 8–19% of patients
admitted with severe HI. Haematoma is differen-
tiated from contusion by demarcation between
INDICATIONS FOR SURGICAL normal and injured brain. The prognosis is usually
MANAGEMENT good unless there is a marked mass effect.
3. Subdural haematomas (SDH) are due to tearing of
The following sequelae need urgent neurosurgical cortical veins between the dura and pia arachnoid
intervention: and appear crescent-shaped on CT scan occurring
most commonly in the inferior frontal and ante-
rior temporal lobes. They can be classified as acute
(< 3–4 days old and appearing hyperdense on CT
Table 22.1 Systemic and intracranial imaging), subacute (4–20 days old, isodense) and
causes of secondary brain injury chronic (> 20 days old, hypodense) and are predis-
posed with increasing age, alcoholism, coagulopa-
Systemic causes Intracranial causes thy, epilepsy and in those with ventricular shunts.
A poor outcome is more likely if SDH is bilateral,
Hypotension, acidosis, Intracranial hypertension, accumulates rapidly, or there is a > 4 hour delay in
hypoxia, hypoglycaemia, oedema, vasospasm,
hyperglycaemia, infection, epilepsy
surgical management of acute SDH. Increased
hyperthermia, patient age and underlying brain contusion also
coagulopathy, sepsis, lead to poor outcome.
anaemia. 4. Extradural haematomas (EDH) are biconvex lentic-
ular lesions between the skull and dura. Most
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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

INTRODUCTION resulted in ischaemic damage to the cord in patients


with normal spines. In spinal cord disease, auto-
Cervical spinal cord disease due to extrinsic causes regulation is unreliable so that even moderate falls
such as compression results from both a combination in pressure may reduce perfusion. Maintenance of
of cord deformation and the duration of deformation. MAP at levels that should ensure an adequate SCPP
Improvements in axonal survival by limiting cord (about 70 mmHg) is a sensible precaution. This
deformation and duration of deformation may have should be continued in the postoperative period and
clinical benefit (e.g. after experimental trauma in may require the use of inotropes. Perfusion may also
animals, those with preserved function had greater be compromised if the CSF pressure is high. CSF
numbers of surviving neurones). The damage to the pressure can vary with position and alignment of the
cord results from hypoperfusion, which suggests that spine. The measurement and adjustment by drainage
patients with severe cervical disease undergoing long, of CSF pressure through a lumbar intrathecal
complicated surgery are likely to be at greater risk. catheter is logical during major cervical surgery but
The contribution of hypoperfusion to spinal cord in practice, case selection is problematic, since
injury (SCI) during anaesthesia has been under- insertion of the catheter is difficult in such patients
estimated, although there has been an over-emphasis and the procedure has considerable morbidity. The
on mechanical trauma due to direct laryngoscopy. use of induced hypertension to ensure an adequate
SCPP may be beneficial, but carries the risk of
increased oedema and haemorrhage in the damaged
PRACTICAL CONSIDERATIONS spinal cord. Pharmacological spinal cord protection
with NMDA receptor blockers (e.g. Mg++) has
An increased risk of neurological deterioration during shown promise in animal studies.
surgery on the cervical spine exists with:
1. Poor pre-operative neurological function
2. Instrumentation SPINAL CORD MONITORING DURING
3. Upper cervical and clival surgery ANAESTHESIA
4. Multisegmental surgery General anaesthesia abolishes the clinical signs of
5. Prolonged hypotension myelopathy - weakness, sensory and reflex changes.
1. Observation of pulse and blood pressure: SCI produced
DIRECT LARYNGOSCOPY by experimental trauma to the cervical cord of
Clear evidence that direct laryngoscopy has produced animals produces initial hypertension, followed by
SCI is lacking. The procedure is generally of short hypotension and bradycardia. Although these
duration, involves little spinal movement below C2 haemodynamic changes are seen in humans, they
and raises spinal cord perfusion pressure (SCPP). Most are not a constant feature and severe damage may
reports alleging that SCI was due to direct laryn- occur without these signs being apparent.
goscopy have come from non-anaesthetic authors. 2. Avoidance of neuro-muscular blockade during anaes-
thesia: Surgical stimulation of the cord or nerve
root may produce movement in a limb, which is a
POSITIONING useful warning. Immobility during general
anaesthesia is largely due to abolition of spinal
Abnormal positioning (excessive flexion or extension) reflexes; brainstem destruction has little effect on
for prolonged periods (typically > 8 hours) may cause MAC. An opioid infusion (e.g. fentanyl or
SCI in patients with normal cervical spine. However, remifentanil) and ventilation with approximately
there have been reports of SCI with shorter periods of one MAC of a volatile agent provides satisfactory
surgery. Positioning patients for protracted surgery is conditions.
largely guesswork; evoked potential monitoring is 3. Sensory evoked potential monitoring: Sensory evoked
currently the best guide to whether a position is being potentials can be monitored by detecting the
tolerated (see below). cortical response to a peripheral stimulus (see
Chapter 57). The median nerve is used for
monitoring cervical cord function. Sensory
PERFUSION PRESSURE
potentials demonstrate continuity of the sensory
Blood flow through healthy arteries of the brain and not the motor tracts, but serious damage to the
spinal cord is autoregulated to remain constant over motor tracts without alteration of sensory
a range of blood pressures. Very low MAP has responses is unusual.
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COMPLEX CERVICAL SPINE SURGERY 95


4. Motor evoked potential monitoring: Demonstration of POSITIONING FOR SURGERY
intact motor pathways throughout anaesthesia is
attractive, but more difficult in practice than The head is commonly held by a skull pin device
sensory monitoring. such as the MayfieldTM frame. Insertion of these pins
5. Local anaesthesia: More spinal surgery could be is extremely painful and profound analgesia is
performed under local anaesthesia than at present, required, which can result in a period of hypotension
but special characteristics are probably required of if pin insertion is delayed. Inotropic support may be
patient and surgeon. necessary.
The eyes are at risk, particularly with the prone
position. The eye must be closed and waterproofed
AIRWAY MANAGEMENT to prevent damage due to skin preparation fluids and
blood. Rarer causes of eye damage include ischaemic
The method of airway management is influenced by optic neuropathy and retinal vessel thrombosis.
the patient’s neurological condition, the site of
surgery, and the likelihood of the need for re- Posterior approaches
intubation
A posterior approach requires the prone or sitting
position, both of which are problematic for the
Tracheostomy anaesthetist. From a surgical perspective, the
This is often the most sensible option in patients with posterior approach is relatively uncomplicated, since
anteriorly placed lesions at the cranio-cervical the airway and major blood vessels are not in the way.
junction. Tracheostomy should be considered in However, lesions anterior to the cord are not easily
patients with severe high cervical myelopathy. accessible from the back of the neck and retraction of
the spinal cord is dangerous.
Tracheal intubation
Anterior approaches
Difficult tracheal intubation can be expected with
Anterior lesions around the cranio-cervical junction
cranio-cervical junction disease, fixation devices,
may necessitate extensive surgery, since access is
flexion deformity and temporo-mandibular joint
impeded by the maxilla superiorly and the mandible
disease. Flexible fibreoptic technology provides the
and tongue inferiorly. Localised lesions can be reached
best conditions in difficult cases and the nasal route is
by a trans-oral approach, but lesions extending up or
usually easiest, due to the favourable ‘angle of attack’
down may require a maxillotomy or mandibular and
and lack of gagging in awake patients (see Chapter
tongue split. These operations involve problems with
24). Nasal tubes should not remain for more than a
the management of the airway and nutrition. Anterior
few days, because of the risk of sinusitis.
lesions below C2/3 are relatively easily accessed, but
there is a risk of damage to the trachea, pharynx,
Extubation oesophagus, carotid vessels and the vagus or recurrent
The timing of extubation in patients who are known laryngeal nerves. Postoperative haematoma may cause
to be difficult to intubate, and particularly those who airway obstruction.
may be difficult to mask-ventilate is important. These
patients should be extubated during normal working Lateral approaches
hours, be normothermic, cardiovascularly stable, There is a risk of bleeding from the vertebral artery.
with satisfactory gas exchange and acid/base balance,
and be neurologically stable.
NUTRITION
Anterior cervical haematoma Swallowing is frequently difficult after anterior
cervical surgery.
Typically, a surgical collar hides the haematoma post
operatively. The patient complains of not being able
Surgery below C2
to breathe, and stridor and desaturation are late signs.
The wound should be opened immediately and blood It can prove extremely difficult to insert a naso-
clot expressed. Induction of anaesthesia is dangerous as gastric tube in the intubated patient in whom
swelling of the soft tissues around the glottis may laryngoscopy has been difficult. The tube should
make mask-ventilation and intubation impossible. An be inserted before the patient is anaesthetised if a
inhalational induction is recommended. difficult laryngoscopy is expected. A nasogastric
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96 NEUROANAESTHESIA

tube should also be inserted if extensive surgery is KEY POINTS


contemplated. This can be removed when the
patient can swallow. A tube should also be placed • Spinal cord damage is due to a combination of
if the pharynx or oesophagus is perforated during degree and duration of cord compression.
surgery. • Attention to positioning is essential to prevent
cord injury, particularly during prolonged surgery.
• Careful consideration regarding airway manage-
ment is required preoperatively.
Trans-oral maxillotomy, Mandibulotomy with • Maintenance of cord perfusion pressure is essential.
tongue split • Coughing and vomiting at the end of surgery
should be avoided.
Serious consideration should be given to the insertion
of a percutaneous gastrostomy (PEG) before such
surgery. A PEG should always be inserted when the FURTHER READING
tongue is split, since swallowing takes some weeks to Calder l, Calder J, Crockard HA. Difficult direct laryn-
recover. Nasogastric tubes have proved to be better goscopy in patients with cervical spine disease. Anaesthesia
tolerated than feeding pharyngostomies in our 1995; 50: 756-63
experience, but the risk of infection makes prolonged McLeod ADM, Calder I. Spinal cord injury and direct
nasogastric intubation unwelcome when there is a laryngoscopy – the legend lives on. Br J Anaes 2000; 84:
pharyngeal wound, particularly when the dura has 705–9.
been breached.
Singh U, Silver JR, Welply NC. Hypotensive infarction of
the spinal cord. Paraplegia 1994; 32: 314-22
Vale FL, Burns J, Jackson AB, Hadley MN. Combined
Postoperative care medical and surgical treatment after acute spinal cord
injury: results of a prospective pilot study to assess the
Surgery requiring fusion or instrumentation merits of aggressive medical resuscitation and blood
frequently requires a hard collar to prevent excessive pressure management. J Neurosurg 1997; 87: 239-46
movement initially. Opiate analgesia is usually neces- Slucky AV. Acute spinal cord injuries. The Cervical Spine
sary particularly if a bone graft has been taken. Research Society Editorial Committee. The Cervical
Antiemetic administration is essential to avoid the risk Spine. 3rd ed [52], 521-39. Philadelphia: Lippincott-Raven
of vomiting on emergence. Publishers. 1998
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24
FIBREOPTIC INTUBATION

I. Calder
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98 NEUROANAESTHESIA

INTRODUCTION attempt at direct laryngoscopy that involves more


than minimal force.
Flexible fibreoptic technology allows inspection and
intubation of the trachea under vision, and since the Many ‘unstable’ cervical spines have been rendered
introduction of an endoscope is well tolerated by rigid by the application of fixation devices, such as
patients, a tracheal airway can be placed before the halo-body frames, when presented for anaesthesia. In
induction of general anaesthesia. Easy endoscopy these circumstances, flexible fibreoptic intubation is
requires: the best option.
1. An air space
2. Minimal secretions
3. Good patient preparation CONDUCT OF FIBREOPTIC
4. Experience and familiarity with the anatomy of INTUBATION
the airway
5. Time. Successful fibreoptic intubation depends on:
Endoscopy may be of limited use in some difficult • Orientation
airway situations, particularly during emergencies • Vision
where there is swelling, displacement and deforma- • Ventilation
tion of tissue, bleeding and secretions. It is most • Suppression (of reflexes)
successful as an elective procedure in conditions in • Sedation
which airway access is diminished by poor cranio- • Position
cervical extension or mouth opening. • Rotation (of the tracheal tube).

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.
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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.

Coughing, breath holding and laryngospasm are all


frequent problems during endoscopy in anaesthetised SEDATION
patients with normal neuromuscular transmission.
Few patients should be subjected to a literally awake
Neuromuscular blockade solves these problems, but
intubation, and discussion in such terms is alarming
ability to ventilate the lungs should be ensured before
to nervous patients. Some sedation is helpful in
the agent is given.
nearly all cases and the actual intubation can be
Suppression of the glottic reflexes with local accompanied by a more-or-less induction dose of
anaesthetic agents is easily performed in elective intravenous agent. Small increments of midazolam
cases. Lidocaine works better (and is absorbed or a propofol infusion are suitable to provide ‘con-
better) if the mucosa is dry. A drying agent such as scious sedation’. Sedation should be minimal when
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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
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FIBREOPTIC INTUBATION 101


Ovassapian A. Fiberoptic endoscopy and the difficult air- Silk JM, Hill HM, Calder I. Difficult intubation and the
way, 2nd Edn. Philadelphia: Lippincott-Raven, 1996 laryngeal mask. Eur J Anaesth 1991; 4: 47–51
Shaw IC, Welchew EA, Harrison BJ, Michael S. Complete Smith M, Calder I, Crockard HA, et al. Oxygen saturation
airway obstruction during awake fibreoptic intubation. and cardiovascular changes during fibreoptic intubation
Anaesthesia 1997; 52: 576–585 under general anaesthesia. Anaesthesia 1992; 47: 158–161
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25
THORACO-LUMBAR SURGERY

C. Williams
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104 NEUROANAESTHESIA

INTRODUCTION Marfan’s syndrome, collagen vascular disorders or


trauma) or idiopathic. Surgical correction is usually
Thoraco-lumbar surgery is performed for trauma, performed when the angle of scoliosis or Cobb angle
congenital anomalies and tumours involving the exceeds 50º, and is directed at relieving thoracic cav-
spine but it is the degenerative diseases (e.g. spondy- ity deformity. This deformity can cause restrictive
losis, spondylolisthesis and stenosis) that most com- pulmonary disease leading to cor pulmonale. About
monly lead to spine surgery. 25% of patients with idiopathic scoliosis have mitral
valve prolapse. Neurological deficits may be present if
DEGENERATIVE DISEASE scoliosis is associated with neural tissue defects.
Although spondylosis can occur secondary to trauma, Scoliosis surgery may compromise spinal cord blood
progressive desiccation of the vertebral disc’s nucleus flow and some form of spinal cord monitoring, either
pulposus combines with fracture of the surrounding an intraoperative wake-up test or somatosensory
annulus fibrosis to allow the nucleus to herniate, usu- monitoring (SSEP), or both, are usually performed.
ally at L4/5 or L5/S1 level. Initial pain is due to her- Blood loss can also be high and consideration should
niated disc stretching the posterior longitudinal be given to preoperative autologous blood donation,
ligament and this is exacerbated by nerve root com- careful patient positioning, intraoperative hypo-
pression, inflammation and muscle spasm. Urgent tension, red cell salvage, or haemodilution tech-
surgery is indicated if there are signs of spinal cord niques. If induced hypotension is employed to
compression or a progressively deteriorating neuro- decrease blood loss, spinal cord perfusion must never
logical examination. be compromised.
Spondylolisthesis is usually caused by long-standing
instability between vertebral bodies, and results in the TUMOURS
slipping forward of one vertebral body upon its lower Spinal cord tumours can be classified as axial (within
body. It occurs more frequently at L4/5 level partic- the cord itself) or extra-axial (alongside the cord).
ularly in women and the elderly. Posterior lumbar Extra-axial tumours are either intradural or
fusion with iliac crest bone grafting or instrumenta- extradural. Wherever the location, tumour resection
tion is commonly employed to return stability to the requires a laminectomy first to achieve adequate
joint, which can result in surprising blood loss. access. Spinal cord monitoring, e.g. somatosensory or
Degenerative spinal stenosis reduces spinal canal vol- EMG monitoring, is usually employed in order to
ume causing neurogenic claudication. It occurs typi- preserve neurological function.
cally from facet joint hypertrophy or thickening of
the ligamentum flavum and in most cases can be sur-
gically decompressed without the need for spinal
fusion for stabilisation.
GENERAL ANAESTHETIC
CONSIDERATIONS
TRAUMA POSITION
Trauma can occur anywhere along the spine, partic- Patient position for thoraco-lumbar spine surgery
ularly the cervical region, and seldom occurs in isola- depends upon the chosen surgical approach. Lumbar
tion. However, not all spinal injury requires urgent vertebrectomies are easily performed supine with an
surgery. Only patients with progressive neurological anterior approach, whereas a lateral approach is used
deficits or where traction fails to relieve compression for thoracic vertebral body surgery with the patient in
are operated upon, usually within 24 hours of injury, a severe lateral jackknife position. Most spinal
after full evaluation and resuscitation. The manage- surgery, however, is performed using a posterior
ment of spinal cord injury and autonomic hyper- approach with the patient prone on a frame or
reflexia are outlined in Chapters 35 and 63 padded rolls to support the chest, leaving the
respectively. abdomen free. Excessive abdominal pressure com-
presses the inferior vena cava and distends spinal
epidural veins obscuring the surgical field and
SCOLIOSIS
increasing blood loss. It also limits diaphragmatic
Scoliosis can be due to neuromuscular diseases (e.g. excursion leading to dangerous increases in airway
muscular dystrophy, poliomyelitis, Friedreich’s ataxia pressure. Urine output becomes erratic in prone
or cerebral palsy), mesenchymal conditions (e.g. patients, so central venous and arterial blood pressure
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THORACO-LUMBAR SURGERY 105


monitoring may be required in major cases and scoliosis repair and resecting metastatic lesions to the
should be addressed prior to positioning the patient. spine require particular attention.
Deep venous thrombosis leading to pulmonary Heat loss may be a problem, particularly in scoliosis
embolus is possible, especially in spinal cord injury surgery or other surgery with large incisions and sig-
patients turned prone. nificant blood loss. Intravenous fluids may need to be
warmed, and ambient temperature increased.
Venous air embolism is a risk since exposed bone is
Warming blankets should be used wherever possible.
elevated above the level of the heart when prone.
Appropriate precautions should be taken to diagnose Intravenous opioids are generally required both intra-
and treat its complications. (See Chapter 15) and postoperatively. Patient-controlled, or nurse-
controlled opioid infusion systems, supplemented
Pressure applied to an eye can result in retinal injury
with non-steroidal anti-inflammatory drugs, are nor-
and ischaemia exacerbated by hypotension or
mally prescribed for postoperative analgesia.
anaemia. Whatever the patient position, adequate
padding is needed to protect all pressure points.
KEY POINTS
ANAESTHETIC TECHNIQUE
• Spinal cord disease may be accompanied by signif-
A stable anaesthetic is required with particular atten- icant systemic disease.
tion to maintaining spinal cord perfusion. When • Management in alternative positions may be needed.
SSEP monitoring is required, inhalation agents may • Blood loss can be substantial.
affect the tracing even at low doses (< 0.5 MAC). • Spinal cord monitoring, e.g. wake-up tests or
Propofol and/or opiate infusion techniques have SSEPs, are commonly employed.
been reported as being successful in cases that require
wake-up testing intraoperatively. Firm securing of
the endotracheal tube cannot be overemphasised. FURTHER READING
Induced hypotension should be used only if Hagberg CA, Welch WC, Bowman-Howard ML.
absolutely necessary, and can be achieved with short- Anesthesia and surgery for spine and spinal cord proce-
dures. In: Albin MS (ed.) Textbook of neuroanesthesia:
acting vasodilators (SNP, GTN) or β-blockers
with neurosurgical and neuroscience perspectives. New
(esmolol, labetalol). York: McGraw-Hill, 1997
Fluid balance must be maintained. Blood loss can be Mahla ME, Horlocker TT. Vertebral column and spinal
surprisingly high when performing spinal surgery. cord surgery. In: Cucchiara RF, Black S, Michenfelder JD
Decortication of bone in preparation for fusion, har- (eds) Clinical neuroanesthesia, 2nd Edn. New York:
vesting iliac crest bone for grafting, large incisions for Churchill Livingstone, 1998
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26
CAROTID ENDARTERECTOMY

A.K. Gupta
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108 NEUROANAESTHESIA

INTRODUCTION deficit does occur then the clamps should be released,


the blood pressure elevated and a shunt inserted.
Carotid endarterectomy (CEA) has been shown to Confusion, panic or seizures may be a consequence
provide greater benefit than medical treatment in of ischaemia.
patients presenting with transient ischaemic attacks
(TIA) and reversible ischaemic neurologic deficits General Anaesthesia
(RIND) and severe carotid stenosis (70–90% diame- A smooth induction with minimal haemodynamic
ter reduction). Recent surveys indicate that CEA is fluctuations are desirable. The intravenous induction
associated with a perioperative mortality between 0.5 agents have the advantage of reduction in cerebral
and 2%, and morbidity between 2 and 4%. The pri- metabolism which may be protective if ischaemia
mary causes of this morbidity and mortality are new occurs. Administration of short- or intermediate-
neurologic deficits and myocardial infarction. acting opiates (fentanyl, alfentanil, remifentanil) con-
The three main goals in the perioperative manage- tribute towards haemodynamic stability and allow for
ment of CEA are: reduced doses of anaesthetic agents. Short-acting
non-depolarising muscle relaxants (atracurium,
1. Haemodynamic stability during induction, main- vecuronium) are appropriate for the duration of
tenance and emergence. surgery.
2. Maintenance of adequate cerebral and myocardial
perfusion. Maintenance can proceed with nitrous oxide/oxygen
3. Rapid emergence to enable early neurological supplemented with either 1 MAC inhalation agent
assessment. (isoflurane or sevoflurane) or a propofol infusion.
Hypocapnia should be avoided to prevent cerebral
vasoconstriction and hypercapnia may induce a ‘steal’
PREOPERATIVE MANAGEMENT phenomenon, therefore normocarbia is recom-
Patients are usually hypertensive with some degree of mended.
ischaemic heart disease (IHD) for which they are Heparin 3000–5000 units should be administered
being medically managed. A thorough cardiorespira- intravenously before carotid clamping. During ICA
tory history should be taken with a detailed assess- occlusion blood pressure should be maintained at
ment of the degree of IHD and cerebrovascular normotension or up to 20% higher than preinduction
disease. Optimisation of medical therapy for all con- pressure to ensure adequate cerebral perfusion. This
ditions should occur preoperatively, particularly con- may be achieved by decreasing anaesthetic depth or
trol of hypertension. by the use of an a-agonist either by bolus or infusion.
Full blood count, electrolytes, coagulation profile, Myocardial ischaemia must be avoided.
ECG and chest X-ray are regarded as baseline inves- Two intraoperative complications may commonly
tigations. Echocardiography may be useful in patients occur:
with severe IHD and poor exercise tolerance, or
those presenting with a new cardiac murmur. 1. Bradycardia and hypotension: This may be due to
surgical manipulation of the carotid sinus causing
Benzodiazepine premedication is sufficient if an afferent impulse to the brainstem (CN IX and
required. X) and can be prevented by infiltration of the
sinus with local anaesthetic. Occasionally hyper-
ANAESTHETIC TECHNIQUE tension and tachycardia are observed after clamp
application. The variability of response of this
Regional Anaesthesia reflex may reflect the differing degrees of sinus
sensitivity secondary to the atherosclerotic process.
Regional anaesthesia has been advocated for CEA.
2. Decreased cerebral perfusion: This will manifest as a
Surgery is best performed under a combined deep
decrease (> 50% reduction) in EEG amplitude
cervical (C1–4) and superficial cervical plexus block.
and/or mean MCA flow velocity on TCD if
Minimal or no sedation should be used. The advan-
monitored. This should be treated by increasing
tage of this method is that awake patients can serve
arterial pressure and a bolus of propofol or
as their own monitor for neurological function.
thiopentone for cerebral protection.
Patients need to be preselected for their ability to
cooperate and lie flat and still for the duration of the Emergence and extubation is a crucially important
surgery. Problems arise if surgery is prolonged and if period. The aim is to have a patient who awakens
ischaemia occurs during clamping of the ICA. If rapidly but is haemodynamically stable. As the
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CAROTID ENDARTERECTOMY 109


anaesthetic is reversed, blood pressure begins to rise. 2. EEG: Reduction in EEG (or SSEP) activity are
If this is not controlled, anastamotic leakage or considered indicative of potentially serious
rupture may occur. Detrimental effects of cerebral ischaemia.
hyperaemia may also manifest in the postoperative 3. NIRS: Changes in concentrations of oxygenated
period. Many of these patients are smokers and have and deoxygenated haemoglobin measured by
irritable airways and removal of the stimulus of the NIRS may help in assessing regional cerebral
endotracheal tube after extubation often stabilises ischaemia.
blood pressure during emergence. Instillation of 4. Stump pressure: This is a measure of pressure of
80–100 mg lidocaine into the endotracheal tube or the carotid stump distal to the occluded artery.
intravenously may reduce coughing and blunt the Poor perfusion is generally taken as a stump
hypertensive response. pressure < 50 mmHg. However stump pressures
> 50 mmHg do not ensure adequate regional
Other pharmacological interventions may be
perfusion.
required if hypertension is persistent (> 20% above
preoperative pressure). Labetalol, esmolol and nitro- A more detailed description of these monitors are
prusside are useful drugs at this stage. Nitroglycerine given in their individual chapters.
has an added advantage if there is evidence of
myocardial ischaemia.
KEY POINTS
POSTOPERATIVE CONSIDERATIONS • Patients presenting for CEA are at increased risk of
1. Control of BP: Hypertension and hypotension need perioperative morbidity and mortality.
to be prevented. Any deterioration in neurological • CEA can be performed under regional or general
state needs to be investigated rapidly. anaesthesia.
2. Surgical problems: Haematoma formation may com- • Maintenance of haemodynamic stability and ade-
promise the airway and needs to be evacuated quate cerebral perfusion is required.
early. Other surgical complication include paraly- • Appropriate monitoring is required to prevent
sis of CNs (VII, IX, X or XII) and carotid body cerebral ischaemia.
dysfunction. • Tight blood pressure control is important during
3. Cerebrovascular complications: stroke, emboli, carotid the recovery period.
artery thrombosis, hyperperfusion syndrome.
4. Myocardial infarction.
FURTHER READING
Monitoring North American Symptomatic Carotid Endarterectomy
In addition to routine intraoperative monitoring, Trial Collaborators: Beneficial effect of carotid endarterec-
invasive arterial BP monitoring is regarded as manda- tomy in symptomatic patients with high grade carotid
stenosis. N Engl J Med 1991; 325: 445–453
tory. Central venous lines or pulmonary artery
catheters may be inserted if clinically indicated. European Carotid Surgery Trialists’ Collaborative Group.
MRC European Carotid Surgery Trial. Interim results for
Several methods of monitoring cerebral perfusion symptomatic patients with severe (70–99%) or with mild
intraoperatively may be used: (0–29%) carotid stenosis. Lancet 1991; 337: 1235–1243
1. Middle cerebral artery flow velocity (MCAFvx): This is Kirkpatrick PJ, Lam J, Al-Rawi P, Smielewski P, Czosnyka
measured with transcranial Doppler ultrasonogra- M. Defining thresholds for critical ischaemia by using near-
phy (TCD) by insonating the MCA. Greater than infrared spectroscopy in the adult brain. J Neurosurg 1998;
50% reduction in MCAFvx and EEG has been 89: 389–394
shown to be predictive of ischaemia and a shunt Erwin D, Pick MJ, Taylor GW. Anaesthesia for carotid
should be placed. surgery. Anaesthesia 1980; 35: 246
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27
ANAESTHESIA FOR
INTERVENTIONAL
NEURORADIOLOGY

J. M. Turner
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112 NEUROANAESTHESIA

INTRODUCTION thetic routines. New procedures in neuroradiology


may be high-risk procedures and it is important to
Interventional neuroradiology is growing quickly, as train the technical and nursing staff so that they are
better imaging equipment and new materials become familiar with the risks of anaesthesia and therefore able
available to the radiologist. Anaesthesia must develop to help the anaesthetist.
to accommodate the new techniques and, as radio-
logical procedures are associated with a significant
morbidity, a careful audit of results is particularly nec- ANAESTHETIC DRUGS AND
essary in the period of rapid growth to define the ulti- TECHNIQUES
mate usefulness of interventional radiology. Anaesthetic drugs that have an effect on the cerebral
circulation, whether directly, or indirectly by affect-
ing cerebral metabolism, may alter radiographic
GENERAL PROBLEMS OF appearances. The vasodilation produced by some
anaesthetic agents may mean that the angiographic
ANAESTHESIA IN X-RAY
images are less clear, because the bolus of contrast
cannot fill the vascular lumen. Conversely, vasocon-
HOSTILE ENVIRONMENT
striction, such as that produced by hyperventilation,
Anaesthetists need to know how to protect them- not only improves the quality of the images, but also
selves from ionising radiation. A lead apron with a allows more images to be taken because the cerebral
0.35 mm lead equivalent must be worn and close circulation is slowed.
exposure to the radiation source avoided. The room
must be organised so that the anaesthetist can see the
airway, anaesthetic machine, lung ventilator and vital INTERVENTIONAL
signs monitor from behind a lead glass screen.
NEURORADIOLOGY
Interventional neuroradiology is most commonly
MOVEMENT
used for obliterating an aneurysm, for treating an
The X-ray couch on which the patient lies will be arteriovenous malformation or for reducing the blood
moved by the radiologist during the examination to flow to a vascular tumour before surgery. In most
allow screening of different body areas. In neuro- cases, a large vascular sheath (7.5 F) is placed in the
radiology, the movement may extend from screening femoral artery and a catheter passed through the
of the abdomen as the vascular catheter is passed up sheath to one of the major cerebral vessels. Finer
the aorta to screening of the head. The breathing catheters and guidewires are passed through this
tubes, monitoring cables and infusion lines must be catheter into the cerebral vessels and up to the lesion.
arranged and fixed and long enough to be tolerant of Angiography is performed at all stages of the pro-
such movement. cedure to delineate the anatomy. The X-ray image is
processed to subtract out radio-opaque structures such
as bone, so that the vascular anatomy is clearer. A
EQUIPMENT
‘road map’ image is available, where an angiogram
The gantry carrying the X-ray tube is often big and view is retained on the radiologist’s monitor screen
bulky. Nevertheless it needs to move around the with the current screening view superimposed on top.
patient’s head to image the cerebral circulation in
many projections. The placing of monitoring cables
ANEURYSM
and lines must be arranged so that they are out of the
X-ray field and do not impede the rapid movement The treatment of intracerebral aneurysms has been
of the X-ray tube gantry. Interventional procedures advanced by the development of the Guglielmi
may be quite prolonged and if the radiographer is detachable coils,1 which are platinum coils attached to
able to move the X-ray tube quickly, without it a stainless steel guidewire. The coil is passed through
catching on monitoring cable or lines, then the a fine catheter and in the aneurysmal sac opens to
procedure will not be further prolonged. hold itself in position. Angiography is performed to
check that the position of the coil is satisfactory. The
connection between the guidewire and coil is fused
STAFF
by passing an electrical current through the system.
The X-ray Department is not an operating theatre and The guidewire is then removed, leaving the coil in
staff working there may not be familiar with anaes- place. Several coils may be required for an aneurysm.
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ANAESTHESIA FOR INTERVENTIONAL NEURORADIOLOGY 113

ARTERIOVENOUS MALFORMATIONS radiology are haemorrhage and vascular occlusion.


Haemorrhage takes place into the intact skull, so
This condition presents a dramatic picture on angiog- cardiovascular disturbance is noticeable. Control of
raphy, with many feeding vessels and large, arteri- any undue hypertension with thiopentone or propo-
alised draining veins produced by the fistulae. Flow fol will help to minimise the extent of the intra-
through the AVM is extremely rapid and not under cranial bleeding. In their study, Young and
autoregulatory control. Embolisation is frequently Pile-Spellman are insistent on the necessity for the
performed in several stages and in some centres con- immediate reversal of the heparinisation.3
scious sedation is preferred.2 The main advantage of
conscious sedation is that when a microcatheter is Vascular occlusion may lead to cerebral infarction if it
placed ready for the embolisation, the safety of the is untreated. It may be due to thrombosis, or the
placement can be checked by injection of sodium malpositioning of catheters, coils, or other embolic
amytal (30 mg) or lignocaine (30 mg) with subse- material. Vascular spasm may also be induced and
quent neurological assessment.3 General anaesthesia may be treated by phentolamine. Thrombolysis may
does not easily allow for such an examination, but be required. Induced hypertension may be indicated
does allow the manipulation of the PaCO2 as well as to maintain cerebral perfusion.
the production of hypo- or hypertension as required.
Many materials have been used for embolisation,
including contact adhesive (N-butyl-cyanoacrylate),
coils and pellets of silastic. More recently the use of an
ethylene vinyl alcohol co-polymer in dimethyl KEY POINTS
sulphoxide (DMSO) solvent has been recommended. • Interventional neuroradiology is growing fast,
The successful placement of the embolic material requiring careful audit
within the AVM, avoiding it passing through to the • Anaesthesia in the X-ray Department has special
venous circulation, may be quite difficult and the problems
ability of the anaesthetist to modify blood flow to • Great care must be taken to maintain safety for the
the AVM is valuable. Many techniques can be used, patient
but we use a combination of hypotension, produced • The anaesthetist can manipulate the cerebral cir-
by labetalol and sodium nitroprusside.4 Once a stable culation to aid the radiologist
level of hypotension has been produced, Positive
End-Expired Pressure (PEEP) is applied to the airway
as the radiologist injects the embolic material, tem- REFERENCES
porarily to reduce venous outflow.
1. Guglielmi G, Vinuela F, Duckwiler G et al.
Endovascular treatment of posterior circulation
aneurysms by electrothrombosis using electrically
MONITORING detachable coils. J Neurosurg 1992; 77: 515–524
Full monitoring, with oximetry, direct intra-arterial 2. Menon DK, Gupta AK. Anaesthesia and sedation for
and central venous pressures and ECG is essential. diagnostic procedures. Curr Opin Anesthiol 1994; 7:
495–499
Cerebral function may be monitored clinically if the
3. Young WL, Pile-Spellman J. Anesthetic considerations
patient is under conscious sedation. Anticoagulation for interventional neuroradiology. Anesthesiology
is required and should be closely monitored with 1994; 80: 427–456
hourly measurements of APTT and PT. 4. O’Mahony BJ, Bolsin SNC. Anaesthesia for closed
embolisation of cerebral arterial malformations. Anaesth
Intensive Care 1988; 16: 318–323
COMPLICATIONS 5. Purdy PD, Batjer HH, Samson D. Management of
hemorrhagic complications from preoperative emboli-
Neuroradiology has a significant morbidity.5 The zation of arteriovenous malformations. J Neurosurg
two most serious complications of interventional 1991; 3: 101–106
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28
ANAESTHESIA AND
SEDATION FOR MAGNETIC
RESONANCE IMAGING

D.K. Menon
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116 NEUROANAESTHESIA

INTRODUCTION series of plain radiographs of the orbits does not


demonstrate a radiopaque foreign body, most centres
Magnetic field strengths in use for MRI are measured would agree that an MR scan can be performed
in units termed Tesla (T). One Tesla equals 10 000 safely.
Gauss (G). The magnetic field strength at the surface
of the earth is of the order of 0.5–1.5 G. Field While product information supplied with aneurysm
strengths used in MRI range from 0.05 to 2.0 T. clips will make statements regarding MR compatibi-
Higher strengths are associated with better spatial res- lity or otherwise, repeated handling and sterilisation
olution and tend to be based on cryogenic magnets could induce ferromagnetism in some previously
with superconducting coils operating in liquid non-magnetic alloys. It has been concluded by some
helium. authorities that only one of two criteria permit com-
pletely safe MR studies in a patient who has an
intracranial aneurysm clip: a previous uneventful MR
MRI SAFETY ISSUES scanning at the same field strength, or the implant hav-
ing been tested with a powerful hand held magnet
PROJECTILE RISKS FROM prior to application by the neurosurgeon. Web sites
FERROMAGNETIC OBJECTS AND on the Internet provide useful information regarding
EFFECTS ON FERROMAGNETIC a large range of other implants and devices. These are
IMPLANTS listed in Table 28.1.

Oxygen cylinders, identification badges, scissors and


paging devices carried in by clinical staff constitute
common risks to patients, and all individuals entering NON-FERROMAGNETIC OBJECTS AND
the MRI suite should be screened for such objects, IMPLANTS
which should be left outside the suite. Ferromagnetic These must also be treated with caution as they can
objects that must be in the vicinity of the MRI suite distort or degrade the quality of the image, and the
(such as oxygen cylinders) should be stationed outside application of oscillating radiofrequency (RF) fields
the 50 G line. can lead to heating and burns from any metallic
While many implanted clinical devices are non-fer- equipment or implant. Burns are the most common
romagnetic, movement of implanted ferromagnetic injury to patients associated with MRI, and result
objects under the influence of the magnet can be when a conductive loop is created between the
catastrophic. While categorised lists of implants exist, patient’s skin and a conductor, such as electrocardio-
manufacturers have been known to change the graphic leads or pulse oximeter probes. The risk of
composition of objects without notification. Some burns may be minimised by ensuring that insulation
implanted ferromagnetic objects are safe, either on wires is intact and separating them from skin with
because they are too small or they are firmly padding, avoiding large loops of wire that lead to the
anchored in place by the surrounding tissue, for induction of currents, and applying sensors as far
example surgical clips that have been in-situ for away from the imaged area as possible.
years. Most units have a comprehensive checklist for When patients have metallic implants it is standard
patients to complete prior to entering the scanning practice to ask them to indicate if the area in question
suite. Metal detectors are too insensitive to play any feels warm or uncomfortable. This is not possible in
role in screening patients prior to MR examinations. the anaesthetised patient. An assessment of risk should
Screening for intraocular foreign objects has caused be obtained from the radiological staff in the MRI
controversy, since movement of a metal foreign unit prior to the scan and the patient warned accord-
body in the eye can cause vitreous haemorrhage and ingly. Such potential sites must also be checked for
loss of the eye. If a patient has no symptoms and a evidence of injury at the end of the procedure.

Table 28.1 Useful Internet sites for information regarding MR safety

Federal Drug Agency, USA http://www.fda.gov/cdrh/ode/primerf6.html


UK Medical Devices Agency http://www.medical-devices.gov.uk/
International MR Safety Central Web Site http://kanal.arad.upmc.edu/mrsafety.html
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ANAESTHESIA AND SEDATION FOR M A G N E T I C R E S O N A N C E I M A G I N G 117

IMPLANTED ELECTRICALLY, which the performance of clinical equipment can be


MAGNETICALLY AND MECHANICALLY assessed in an MR environment. The terms MR safe
ACTIVATED DEVICES and MR compatible are used to define equipment prop-
erties so that their use within an MR environment can
MRI may interfere with the operation of such devices, be ascertained. The term MR safe indicates that when
or result in image distortion or burns. Cardiac pace- a device is used in the MR suite it presents no addi-
makers are the most common electrically activated tional risk to the patient; while the term MR compati-
devices found in patients referred for MRI. The accept- ble indicates that a device is both MR safe and has been
able safe level for exposure to magnetic fringe fields for demonstrated to neither significantly affect the diag-
patients with cardiac pacemakers are currently set at nostic quality of the imaging procedure, nor have its
5 G. At fields above this the pacemaker will go into operations affected by the MR scanning system. In
fixed rate mode, and may trigger ventricular fibrilla- practice, many monitoring and infusion devices func-
tion. In essence, MRI is contraindicated in any person tion normally at fields of 50 G or less, but may be nei-
who has any implanted device, unless it is known for ther MR safe (since they present a projectile risk due
absolute certainty that the device will function safely. to ferromagnetic components) nor MR compatible,
since stray RF interference from the device may make
POTENTIAL BIOLOGICAL EFFECTS imaging impossible. Devices such as colour cathode
ray screens may be distorted in fields exceeding 1–2 G,
Higher strength magnetic fields and rapidly switched while monochrome screens function reasonably well
gradient fields can cause sensations of altered taste, up to 5 G. Liquid crystal display screens are not dis-
dizziness and nausea. Exposure to gradient or radio- torted at all. Magnetic tape and computer discs are cor-
frequency fields experienced by scanned subjects can rupted in fields greater than 30 G.
reach biologically relevant levels and produce local
heating effects as described above. This exposure is The ECG shows significant changes within a static
clearly regulated by bodies such as the Federal Drug magnetic field. Leads I, II, V1 and V2 are the worst
Agency (FDA) in the USA and the National affected, with changes in early T waves and late ST
Radiological Protection Board (NRPB) in the UK. segments mimicking hyperkalaemia or pericarditis.
While available human data generally supports the The radiofrequency currents used during MRI also
safety of exposure to low magnetic fields in clinical produce artefacts of the ECG from current induction
staff, there is currently an impetus to measure occu- in ECG cables. ECG output during MRI can be
pational exposure to static, gradient and radio- improved by filtering or gating, the use of shielded or
frequency fields and define safe limits for exposure. carbon fibre cables, telemetry or fibreoptic systems.
Patients have received burns from conventional pulse
oximeter probes. Pulse oximetry systems based on
OTHER ISSUES fibreoptic technology are now available; these devices
The contrast agent, gadopentate dimeglumine (Gd- operate without interference during MRI and are safe.
DTPA, Magnevist®) can improve image quality and While long sampling lines have been used for respira-
has an excellent safety record in comparison to other tory gas monitoring, very long tubing can increase
contrast agents, with only one reported fatality from resistance and lag times to detect disconnection. The
anaphylaxis. Cryogenic magnets with superconduct- availability of MR compatible gas monitors has made
ing coils operate in liquid helium that boils the use of such long sampling tubes unnecessary.
(quenches) rapidly if the cryostat temperature rises. Invasive blood pressure monitoring can be measured
The released helium dilutes room oxygen and the accurately, as can ICP via a ventriculostomy.
cold vapour causes frostbite and cryogenic burns. Parenchymal ICP sensors present more of a problem,
but there are early reports of the safe use of a Codman
microtransducer, monitored through a fibreoptic
link. Both peripheral and central core temperatures
MONITORING DURING MRI can be measured accurately using probes incorporat-
MRI demands an immobile patient be placed in a ing radiofrequency filters.
noisy, dark, cold and uncomfortable space and isolated
from radiology and anaesthetic staff. Anaesthesia or
sedation may be required in paediatric or unco- INTEGRATED MONITORING UNITS
operative subjects, or in critically ill patients. The FDA
in the USA, http://www.fda.gov/cdrh/ode/ In the past many departments have adapted existing
primerf6.html, has provided useful definitions against equipment to form satisfactory integrated monitoring
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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

Table 28.2 Representative list of manufacturers of MRI compatible equipment

Monitoring MR Equipment Corporation, USA www.mrequipment.com


Bruker Gmbh, Germany www.bruker.de/
Masimo Corporation, USA www.masimo.com
Anaesthetic equipment Datex-Ohmeda www.datex-ohmeda.com
North American Drager, USA www.nad.com
Ventilators Sims Pneupac www.pneupac.com
Infusion pumps Mammendorfer Institut für www.mipm.com
Physik und Medezin, Germany
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ANAESTHESIA AND SEDATION FOR M A G N E T I C R E S O N A N C E I M A G I N G 119


initial construction. It is equally important that a • Safe anaesthesia in an MRI environment depends
realistic assessment be made of needs for anaesthesia on well designed protocols and systems, not just
and supervised sedation during scans, and resources on individual competence and care.
be identified (both in terms of money and people) to
meet these needs.
RECOMMENDED READING
KEY POINTS Menon DK, Gupta AK. 1994 Anaesthesia and sedation for
• Sedation and anaesthesia are likely to be increas- diagnostic procedures. Current Opinion in Anaesthesiology 7,
495–499.
ingly required for MRI examinations in specific
patient groups. Menon DK, Peden CJ, Hall AS, Sargentoni J, Whitwam
• The commercial availability of MRI compatible JG. 1992 Magnetic resonance for the anaesthetist. Part I:
monitoring and anaesthetic equipment allows safe physical principles, applications, safety aspects. Anaesthesia
clinical practice without compromises. 47, 240–255.
• It is important that strategic decisions regarding Peden CJ, Menon DK, Hall AS, Sargentoni J, Whitwam
anaesthetic utilities be addressed when new MRI JG. 1992 Magnetic resonance for the anaesthetist. Part 2:
suites are being built. anaesthesia and monitoring in MR units. Anaesthesia 47,
• Careful attention to detail and preparation to MRI 508–517.
safety issues are important before embarking on Shellock FG, Kanal E. 1994 Magnetic Resonance. Bioeffects,
anaesthesia for individual patients. Safety and Patient Management. New York: Raven Press.
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29
SHUNT SURGERY

A. Summors
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122 PHYSIOLOGY

INTRODUCTION which will further increase ICP. In these circum-


stances an inhalation induction is acceptable.
Hydrocephalus is usually due to obstruction of CSF
flow giving rise to increases in volume and conse- Patients should be paralysed with a short-acting non-
quently intracranial pressure. Surgical insertion of a depolarising muscle relaxant prior to intubation. The
shunt enables drainage of CSF from the ventricular pressor responses and ICP changes to laryngoscopy
system into a distal site. The most common drainage and intubation can be limited by a bolus of lignocaine
site is to the peritoneal cavity but the right atrium, or intravenous agent just prior to intubation. This,
cisterna magna and pleural cavity are also sometimes however, seems less of a problem in children with
used. open sutures than in adults. After intubation the
breathing circuit is secured firmly preventing drag-
ging on the endotracheal tube and the eyes and limbs
are protected from injury.
EQUIPMENT AND SURGICAL
Anaesthesia can be maintained with either a total
PROCEDURE intravenous technique using propofol, or with a
Shunt systems usually involve three components: a volatile agent. Analgesia is required to cover the ini-
ventricular catheter, a one-way valve and a distal tial skin incision and burr hole and the tunnelling of
catheter. Other devices may also be incorporated, the drain to the abdomen. Fentanyl (1–3 µg/kg) is
e.g. on–off valves, siphon control devices and cham- usually sufficient.
bers for flushing the shunt system.
Mild hypocapnia helps reduce ICP and surgical infil-
The ventricular catheter is inserted through a burr tration with 1% lidocaine and epinephrine helps
hole connected to the one-way valve which deter- reduce scalp bleeding and provides analgesia.2
mines the draining pressure from the ventricle, which Profound haemodynamic changes may occur if a
is then connected to the peritoneal catheter. This is large volume of CSF is drained rapidly when the ven-
passed subcutaneously from the scalp incision over tricular catheter is inserted.
the occipitoparietal region, over the chest wall to the
Care must be taken when using the rigid tunnelling
abdominal incision made either in the midline above
device as this theoretically reduces chest wall compli-
the umbilicus or just lateral to and above the umbili-
ance and may cause either underventilation during
cus. The tubing is inserted into the peritoneal cavity
pressure controlled ventilation or dangerous increases
through a small abdominal incision. Intravenous
in airway pressures when volume controlled venti-
antibiotics may be given perioperatively.1
lation is used.
At the conclusion of surgery, patients should be extu-
PATIENT POSITION
bated. Any focal neurological signs postoperatively
For ventriculo-peritoneal (V-P) shunts, the child is should prompt an urgent CT scan to exclude an
placed supine with the head turned to the opposite intracranial haematoma.
side allowing occipital insertion of the ventricular
catheter. A towel is placed under the nape of the neck
in children or ipsilateral shoulder in adults in order to
align the head, neck and abdomen in one plane, KEY POINTS
allowing easier passage of the subcutaneous tun-
nelling device for shunt placement. • V-P shunts are a common neurosurgical proce-
dure frequently performed in children.
• Patients usually have raised ICP.
ANAESTHETIC MANAGEMENT • A smooth induction is required.
The patient presenting for insertion of V-P shunt or • Tunnelling the shunt to the abdomen is highly
shunt revision must be considered to have raised ICP. stimulating.
Patients may be neurologically obtunded pre- • Patients should have improved neurology postop-
operatively and premedication is often not required. eratively.

The anaesthetic technique requires a smooth


induction, preferably with an intravenous induction REFERENCES
agent using thiopentone or propofol. As many of
these patients are children, attempts at intravenous 1. Roth PA, Cohen AR. Management of hydrocephalus
cannulation prior to induction may be distressing in children. In: Tindall GT, Cooper PR, Barrow PL
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SHUNT SURGERY 123


(eds) The practice of neurosurgery. Baltimore: Williams FURTHER READING
& Wilkins, 1996, pp. 2707–2728
2. Abou-Madi MN, Trop D, Barnes J. Aetiology and con- Messick Jr JM, Newberg LA, Nugent M, Faust RJ.
trol of cardiovascular reactions during transsphenoidal Principles of neuroanesthesia for the neurosurgical patient
resection of pituitary microadenomas. Can Anes Soc J with CNS pathophysiology. Anesth Analg 1985; 64:
1980; 27: 491–495 143–174
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30
ANAESTHESIA FOR
PAEDIATRIC NEUROSURGERY

J.M. Turner
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126 NEUROANAESTHESIA

INTRODUCTION fontanelle and noting whether it is tense, or frankly


bulging. Vomiting, caused by the raised ICP may
The child requiring neurosurgery presents all the well produce dehydration and electrolyte imbalance.
general problems of paediatric anaesthesia, but in Induction and maintenance of anaesthesia should
addition there are specific problems related to the therefore take into account the raised ICP. The fact
neurosurgical condition. The spectrum of neurosur- that the fontanelles are open and the sutures unfused
gical disease in childhood is different from that in the does not protect the child against high ICP, and as in
adult. There are major differences in cerebral physiol- neuroanaesthesia in the adult all anaesthetic tech-
ogy. The brain represents 10–15% of the body weight niques and agents causing an increase in ICP should
at term and doubles in weight by 6 months of age. be avoided.
The skull is not completely closed, the anterior The well recognised difficulties surrounding intuba-
fontanelle remaining open until 15-18 months. CBF tion of the trachea in the neonate are further compli-
and cerebral metabolic rate (CMRO2 ) are relatively cated if the large head produced by hydrocephalus
higher than in the adult.1 The major neurosurgical results in flexion of the neck. If so, a support under
problems can be broadly divided by age group: the thorax may be required to produce optimal con-
The premature child and the infant: ditions for intubation. A large head may produce a
misleading weight in a small infant.
1. Ventricular drainage
2. Shunt surgery
3. Third Ventriculostomy MYELOMENINGOCOELE AND
4. Myelomeningocoele ENCEPHALOCOELE
5. Vein of Galen aneurysm. Disorders of development affecting the neuraxis may
The child from 2 to 7 years: produce encephalocoele and myelomeningocoele.
Such a defect needs to be closed quickly after deliv-
1. Diagnostic procedures ery, so that neurological deterioration is limited. All
2. Space-occupying lesions the problems of anaesthesia in the neonatal period
3. Trauma therefore apply. In addition, the neonate will have to
4. AVM. be positioned prone. The myelomeningocoele needs
to be protected from damage so, during induction,
THE PREMATURE CHILD AND the neonate may need to be tilted to one side, or if
supine, supported on pads leaving the mengiomyelo-
THE INFANT coele free. The surgeon may need to use a nerve
The management of CSF obstruction and CSF stimulator, so monitoring the degree of neuromuscu-
drainage systems requires careful surgery and atten- lar block may be helpful (see Chapter 32).
tion to detail. Shunt surgery is still affected by a high
complication rate including infection, shunt blockage
PREMATURE FUSION OF CRANIAL
and over drainage of CSF.
SUTURES
The premature infant is prone to intraventricular
Many syndromes may arise, depending on which
haemorrhage and therefore CSF obstruction. Initially
cranial suture, or sutures are involved. The skull base
this may be managed by an external ventricular drain,
and facial sutures may also be affected. High ICP may
or by the subcutaneous implantation of a reservoir
result, depending on how early the abnormal skull
such as an Ommaya reservoir. The complete shunt
shape is recognised.
system of ventricular catheter, valve and drainage tube
either to the peritoneum or right atrium is inserted Surgery involves cutting the fused suture; the skin
when the high CSF protein resulting from the intra- incision is extensive and blood loss may therefore be
ventricular haemorrhage has fallen to normal levels. significant.
On occasions CSF drainage can be improved by an
anterior third ventriculostomy, where a communica- ANEURYSM OF THE VEIN OF GALEN
tion is produced directly between the third ventricle
Aneurysms of the vein of Galen classically present
and the basal cisterns by an endoscopic approach.
during the neonatal period with cardiac failure. Late
The child presenting for surgery to relieve CSF presentation does occur, when the signs may be those
obstruction must be considered to have raised ICP. of space-occupation or peri-orbital venous conges-
This is easily confirmed by palpation of the anterior tion. Successful treatment is difficult.
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ANAESTHESIA FOR PAEDIATRIC NEUROSURGERY 127

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.

GENERAL COMMENTS ON POSTOPERATIVE CARE


ANAESTHESIA Postoperatively the child should be nursed in a spe-
cialised recovery or intensive care unit. The prema-
The principles of good paediatric anaesthesia and
ture infant and the neonate may benefit from a period
good neuroanaesthesia must be applied. The scalp is
of controlled ventilation as may children with tumours
very vascular and significant blood loss may occur,
in the posterior fossa. Otherwise a full recovery allows
though good surgical technique should reduce this
good monitoring of cerebral function.
loss to a minimum. The head is covered by surgical
drapes and therefore the care of the airway must be
faultless. The flexibility of the neck in children and
the awkward position frequently required for neuro- KEY POINTS
surgery means that an armoured endotracheal tube • There are differences in the cerebral physiology
should be used and carefully fixed. Armoured tra- between adults and children.
cheal tubes are available with a Murphy eye, down to • The major neurosurgical problems can be broadly
the smallest sizes. In the neonate, the tip of the endo- divided by age group.
tracheal tube moves an average of 14.4 mm when the • Anaesthetic management combines the principles
head and neck are moved from full flexion to full of paediatric anaesthesia and neuroanaesthesia.
extension3 so auscultation of the chest must be per- • Estimation of fluid balance may be difficult partic-
formed after positioning. Fixation of the tube must ularly after mannitol therapy or blood loss.
not obstruct cerebral venous drainage. • A short period of postoperative ventilation is often
Intravenous induction using thiopentone or propofol required in the premature infant.
is valuable, especially where raised ICP exists.
Sevoflurane is a valuable alternative as its effects on REFERENCES
ICP are minimal4 and induction is rapid and smooth.
1. Ogawa A, Sakurai Y, Kayama K. 1989 Regional cere-
Muscle relaxation is indicated and pressure ventilation bral blood flow with age: changes in cerebral blood flow
should be adjusted to produce mild hyperventilation. in childhood. Neurological Research 11, 173.
The use of PEEP must be carefully monitored to 2. Millar C, Bissonnette B, Humphreys RP. 1994
ensure that ICP is not adversely affected. If hand ven- Cerebral arteriovenous malformations in children.
tilation is employed it is important that the airway Canadian Journal of Anaesthesia 41, 321–331.
pressure should be measured so as to ensure effective 3. Todres ID, De Bros F, Kramer SS, Moylan FMB,
ventilation without raising ICP. The same agents may Shannon DS. 1976 Endotracheal displacement in the
effectively be used for the maintenance of anaesthesia. newborn infant. Journal of Paediatrics 89, 126.
4. Takahashi H, Murata K, Ikeda K. 1993 Sevoflurane
Maintenance of temperature may be difficult. The does not increase intracranial pressure in hyperventi-
exposure of the head promotes cooling. In shunt lated dogs. British Journal of Anaesthesia 71, 551–555.
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31
CONGENITAL CRANIOFACIAL
PROCEDURES

J. Shapiro
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130 NEUROANAESTHESIA

INTRODUCTION Infants under 6 months of age should not require


preoperative medication. The use of premedication
Craniofacial anomalies are frequently a part of a num- in the older infant or toddler should be considered to
ber of common as well as uncommon syndromes. facilitate smooth induction and decrease agitation
The prevalence is difficult to determine because of which may increase ICP with crying and breath-
the number of syndromes in which they present. holding. However, the over-sedated infant may have
These structural defects may be due to fetal develop- decreased respiratory effort and increases in ICP sec-
mental anomalies or premature fusion of one or more ondary to hypercarbia. Oral midazolam (0.5–0.7
of the cranial sutures following birth (craniosynosto- mg/kg – max. dose 10 mg) can be very effective in
sis). these patients if intravenous access is not available
prior to induction.

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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CONGENITAL CRANIOFACIAL PROCEDURES 131


transfusion totalling 20–25 ml/kg over the remaining day should be about 10 g/dl. Analgesia is often satis-
course of the procedure will usually increase the factory using non-opiate medication.
haemoglobin to 12–14 g/dl by the end of the proce-
dure.
KEY POINTS
At the conclusion of the surgical procedure, the
patient can usually be safely extubated, placed in a • There may be other congenital abnormalities asso-
head up position, and transported on oxygen to the ciated with craniofacial abnormalities.
high dependency or intensive care unit. • Elevated ICP may be present.
• The airway may be difficult.
• Blood loss may be significant.
POSTOPERATIVE CONSIDERATIONS • Non-opioid analgesia is usually adequate postop-
eratively.
Careful assessment of the airway must be made dur-
ing the early postoperative period. Most of the facial
swelling, however, will be in the upper face and will FURTHER READING
not effect the airway. Postoperative blood loss can be Ward CF. Pediatric head and neck syndromes. In: Katz J,
substantial, but if adequate transfusion occurs intraop- Steward DJ (eds) Anesthesia and uncommon pediatric diseases,
eratively, the haemoglobin on the first postoperative 2nd Edn. Philadelphia: WB Saunders, 1993, pp. 322–329
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32
CONGENITAL SPINE
LESIONS

J. Shapiro
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134 NEUROANAESTHESIA

INTRODUCTION infection or meningitis which may result in early


mortality.
Congenital spinal defects result from the failure of the 2. Thermal loss: In addition to the inability to
neural tube to close during the third or fourth week adequately control their thermal environment,
of gestation. The spectrum of defects ranges from spina neonates are prone to evaporative thermal losses
bifida occulta, to myelomeningocoele, to anencephaly from the cyst.
(failure of closure of the cephalad end of the neuro- 3. Airway management: Patients are often intubated
tube). The most common lesions requiring surgical while in a lateral position to avoid pressure or
repair are the various forms of myelomeningocoele traumatic injury to the defect. Postoperatively, the
(MMC). The cause of MMC defects is multifactorial patient is supported in a prone or lateral position.
including both environmental (drug use, malnutrition,
radiation) as well as a probable genetic predisposition.
The incidence is thought to be about 1/1000 live ASSESSMENT AND PREMEDICATION
births. However, in families with one affected child, Because neural tube defects do not appear to be asso-
the risk of recurrence is 3–4% and after two abnormal ciated with other congenital anomalies or syndromes,
pregnancies, the risk approaches 10%. MMCs may an in-depth assessment for cardiac, renal, or other sys-
occur anywhere along the neuroaxis, though the most temic problems, which are not apparent at birth is
common site is in the lumbosacral spine region. probably not warranted. A thorough neurological
assessment is, however, an essential component of the
preoperative evaluation. It is important to remember
CLINICAL FEATURES that a prolonged delay in operative repair increases
the risk of meningitis which carries a high mortality.
Common manifestations include bowel and bladder Nevertheless, the usual assessment of cardiopul-
dysfunction and varying degrees of motor and sensory monary systems and airway anatomy must be under-
loss below the spinal level of the lesion. Orthopaedic taken to assure that other issues do not result in
abnormalities are also common, including club foot and perioperative complications. Prior to surgery, the
hip subluxation. Almost all patients with MMC develop neonate should be kept in a warm environment.
hydrocephalus within the first month of life due to asso- Intravenous access should be obtained, and adequate
ciated Arnold–Chiari malformations (displacement of i.v. hydration begun. In anticipation of surgery, the
the cerebellar vermis through the foramen magnum, patient should remain nil by mouth. Positioning of
elongation of the brainstem and fourth ventricle, and the patient is of utmost importance. The neonate
non-communicating hydrocephalus) and require CSF should be kept either prone or in a lateral position
shunting procedures. Clinical examination usually unless he can be supported in such a way as to avoid
reveals a midline cystic structure filled with CSF and any contact or pressure on the cystic structure. Some
neural elements. Often, the cyst is covered with a thin sort of impervious dressing should be applied over the
layer of epithelial cells and the terminus of the spinal area of the defect to decrease the risk of infection. A
cord (placoid). Despite the fact that this is a midline bowel bag, similar to that used for omphalocoeles
abnormality, there does not seem to be any relationship may be useful in this regard.
between MMCs and other congenital defects.
Two to three decades ago, attempts were made to CONDUCT OF ANAESTHESIA
determine which of these newborns should receive
surgical treatment and which should be provided Following stabilisation after birth, the patient is
‘comfort care’ in anticipation of imminent death. brought to the operating theatre in a heated isolette
Several recent studies have confirmed that long-term to prevent hypothermia. Appropriate monitors
survival of these patients is excellent, and their ability including ECG, pulse oximetry, precordial stetho-
to function in society can be greatly enhanced with scope and non-invasive BP cuff are applied.
early repair and appropriate physiotherapy. Following induction, core temperature monitoring
should also be added. If there are no obvious airway
abnormalities, induction may proceed by either an
inhalation technique with halothane or sevoflurane,
ANAESTHETIC MANAGEMENT
or by i.v. agents such as thiopentone or propofol.
Intubation is either accomplished with the patient in
KEY PROBLEMS
the lateral position, or, if supine, while being sup-
1. Risk of rupture of the cystic structure: Loss of ported by foam pillows or towel rolls which ensure
integrity of the MMC increases the risk of system that the back is suspended above the operating table.
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CONGENITAL SPINAL LESIONS 135


Short-acting muscle relaxants may be utilised to facil- horizontal position, either prone or lateral for several
itate intubation if the practitioner prefers, but their days until the dural closure has had an opportunity to
use is not needed for the surgical procedure, and may begin healing. This decreases the risk of CSF leak or
interfere with the surgeon’s ability to test for nerve flap pressure ischaemia. If a CSF shunt is not placed at
root function during dissection and subsequent clo- the time of initial surgery, these patients are usually
sure of the defect. Local anaesthetics are often used by returned to the operating theatre within the first
the surgeon on the field. It is important to keep in postoperative week for placement of a V-P or
mind acceptable doses so as to avoid overdose. ventriculo-atrial shunt to manage hydrocephalus.
Because the area of the lesion is usually relatively
insensate, the use of narcotic analgesics is unnecessary
and unwarranted unless closure requires a large KEY POINTS
musculocutaneous flap from above the lesion for
coverage. Fluid requirements are the same as any • Early repair improves outcome in these children.
other paediatric case, based on weight of the baby. • Positioning is a common problem, and may com-
Heat loss from the neonate should be minimised. plicate intubation.
• Narcotic analgesia is usually not required.
• Hydrocephalus may co-exist.
POSTOPERATIVE CONSIDERATIONS • Other major congenital abnormalities are not
As with all neonates (and particularly premature associated.
infants), the risk for apnoea and bradycardic spells fol- • Close postoperative observation is required for the
lowing general anaesthesia exists. These patients first 2–3 days.
should be monitored closely in an intensive care unit
equipped and staffed to handle airway problems.
Continued care to maintain a neutral thermal envi- FURTHER READING
ronment is essential. The patient is also observed for Krane EJ, Domino KB. Anesthesia for neurosurgery. In:
signs of irritability, nausea or vomiting, or decreased Motoyama EK, Davis PJ (eds) Smith’s anesthesia for infants
neurological function which might be indicative of and children. St Louis: CV Mosby, 1990
hydrocephalus and increased ICP. Postoperative McLone DG. Congenital spinal cord anomalies. In:
bleeding is seldom an issue if haemostasis is controlled Menezes AH, Sonntag VKH (eds) Principles of spine
at the time of closure. The patient is maintained in a surgery. New York: McGraw Hill, 1996
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33
PAEDIATRIC CRANIOSPINAL
TRAUMA

C. Duffy
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138 NEUROANAESTHESIA

PAEDIATRIC HEAD INJURIES PREOPERATIVE MANAGEMENT


Head injuries account for over half of trauma-related Neurological assessment is performed after adequate
deaths in children. The mechanism of injury is related resuscitation. Persistent hypotension should alert to
to age, with infants suffering mainly falls and assaults the possibility of associated injury (e.g. high cervical,
while motor vehicle and bicycle accidents account abdominal or thoracic injury) or cervicomedullary
for injuries in older children. Outcome after injury injury with vasomotor centre damage.
depends on: Patients with a GCS ≤ 8 require urgent intubation
• Admission GCS (or modified score for children; with manual in-line stabilisation since up to 10% of
Chapter 36). paediatric head injuries are associated with cervical
• Presence of epidural or subdural haematoma. spine injuries. After intubation, the lungs are venti-
• Duration of coma. lated aiming for a PaCO2 of 4–4.7 kPa, maintaining
• Multisystem trauma (with doubled mortality). neutral head and neck position with head elevation of
15–20o. Diuretics are given with caution (e.g. manni-
The paediatric brain responds differently to the adult tol 0.25–0.5 g/kg or furosemide 1 mg/kg) as diuresis
brain when injured: can result in hypotension and electrolyte abnor-
1. The relatively large head size and weak neck mus- malities. Mannitol can cause congestive heart failure
cles render the child’s brain more susceptible to in neonates. Therapeutic aims are for a CPP
acceleration–deceleration injuries. > 50 mmHg in infants and > 60 mmHg in older
2. Swelling is accommodated by skull expansion children. A CPP of < 40 mmHg is associated with a
before the age of 2 and examination of the reduced survival rate (the normal ICP is 5 mmHg in
fontanelles and head circumference are important infants and 10 mmHg in 5-year-olds). A CT scan can
in the assessment of head injuries in this group. give an indication of prognosis. Subdural haematoma
After this age, the skull sutures close and the (evidence of severe trauma), ablated basal cisterns,
cranial vault thickens. midline shift and reversal of grey/white matter differ-
3. Surgically treatable lesions are less common in entiation are all associated with a poor prognosis.
children than in adults. Intracranial haematomas
occur in 20–30% of paediatric head injuries, com- INTRAOPERATIVE MANAGEMENT
pared with 50% in adults. Due to the combination
of a relatively small blood volume and large head The aims of intraoperative management have been
size, scalp lacerations and intracranial haematomas outlined in Chapter 12, i.e. maintaining adequate
may result in hypovolaemia and hypotension. anaesthesia, analgesia, sedation, muscle paralysis and
4. Children are less likely to have open skull fractures cerebral perfusion together with ventilation to a
than adults because the calvarium is flexible and PaCO2 of 4–4.7 kPa, mild hypothermia (34–36ºC),
allow closed depressed skull fractures to occur. normovolaemia, an appropriate haematocrit for the
5. Cerebral blood flow is thought to be higher in patient’s age and underlying medical condition and a
children than adults and tolerance to ischaemia normal blood sugar. An ICP monitor can be inserted
may decrease as age increases. Overall, the func- intraoperatively and used as a guide to ensure CPP is
tional outcome is better for children than for adequate. Destruction of brain tissue can cause release
adults with a similar GCS on admission. of thromboplastin and lead to DIC. Coagulopathy
should be treated with appropriate haemostatic factors.

PATHOPHYSIOLOGY POSTOPERATIVE MANAGEMENT


Infants and children respond to head trauma initially Due to the risk of early cerebral vasodilatation, patients
with diffuse swelling lasting 1–2 days due to cerebral who have required surgical intervention are ventilated
vasodilatation. Deterioration in a child after this time with ICP monitoring in the immediate postoperative
is more likely to be due to increased swelling or period. Further neuroprotective strategies are con-
seizure activity than to a surgically treatable lesion. sidered in severe head injury (Chapter 40).
Post-traumatic seizures, even with minor head
injuries, are more common in children aged < 2 years
than in older patients. Prophylactic phenytoin (20
mg/kg) should be considered in a paralysed child
PAEDIATRIC SPINAL INJURIES
when EEG monitoring is not available, especially in Spinal injuries are usually due to motor vehicle acci-
the younger child. dents in younger children, either as a pedestrian or
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PAEDIATRIC CRANIOSPINAL TRAUMA 139


passenger. In older children, they tend to result from the head and torso to a board with sandbags on
falls or diving accidents. More than one spinal level is either side of the neck helps reduce mobility.
affected in up to 20% of paediatric spinal injuries. Adequate sedation and muscle relaxant are given to
aid intubation. Suxamethonium can be given safely
Like the paediatric brain, the paediatric spine
within 48 hours of spinal injury. After 48 hours, the
responds differently to the adult spine when injured.
risk of hyperkalaemia precludes the use of suxam-
Ligamentous laxity and incomplete bony ossification
ethonium. Once the airway is secured, aim for ade-
protect the child against spinal injury but increase the
quate anaesthesia, analgesia, sedation, muscle
likelihood of subluxation without fractures and
paralysis and cord perfusion together with ventila-
SCIWORA (spinal cord injury without obvious
tion to a PaCO2 of 4–4.7 kPa, normovolaemia, mild
radiological abnormality). SCIWORA occurs in
hypothermia, a normal haematocrit and a normal
20–60% of spinal injuries. Clinical suspicion or
blood sugar.
equivocal radiology should be treated as spinal injury
until definitive tests (e.g. CT, MRI) have been per- Both the surgeon and anaesthetist should position the
formed. patient. Neutral head and neck position should be
maintained during transfer to the operating table.
Neck movement has greater momentum than in
Patients are positioned so that there is free diaphrag-
adults due to the relatively large head and poor neck
matic excursion and minimal venous congestion at
muscle support. The fulcrum of mobility is at C2–3
the surgical site. Bony prominences, eyes and nose
in children and C4–5 in adults. Injuries between the
should be protected. Traction on peripheral nerves
occiput and C2 account for 40% of paediatric spinal
should be minimised. Blood pressure should be main-
injuries, compared with 20% in adults.
tained at preoperative levels using CVP and urine
output as a guide to volume status. Any bradycardia
PATHOPHYSIOLOGY should be treated with anticholinergic agents.
Spinal cord injury can be suspected in the uncon-
scious patient with unexplained hypotension and POSTOPERATIVE MANAGEMENT
bradycardia, priapism, flaccidity, immobility and
arreflexia below level of lesion, apnoea for lesions at Ventilation should be continued postoperatively
or above C3, impaired ventilation for lesions at or when respiration has been impaired preoperatively.
above C5 and paradoxical respiration from paralysed In the early postoperative period, sedation can be
intercostal muscles for lesions below C6. Spinal shock lightened in order to assess adequacy of cough, venti-
occurs for the first 3–5 days following injury followed lation and neurological function.
by autonomic hyperreflexia. Other systemic effects
include paralytic ileus, urinary retention and poikilo- KEY POINTS
thermia below the level of the lesion.
• Mechanisms of head and spinal injuries in children
differ from adult injury.
PREOPERATIVE MANAGEMENT • Target CPP is lower in infants compared to older
Urgent neurosurgical intervention is required to children and adults.
reduce and stabilise the spine where conservative • Adequate fluid resuscitation is of paramount
measures are unlikely to succeed; to decompress ± importance.
fuse the spine in a neurologically deteriorating • Cervical spine injuries are more likely to be at a
patient; and for non-spinal surgery for associated higher level in children.
injuries. Early administration of methylprednisolone
has been shown to improve clinical outcome at 6
FURTHER READING
weeks and 6 months post-injury. A dose of 30 mg/kg
should be given within 8 hours of injury followed by Simpson D, Reilly P. Paediatric coma scale (letter). Lancet
5.4 mg/kg/h for the next 23 hours. 1982; 2: 450
Muizelaar JP, Marmarou AM, DeSalles AA, et al. Cerebral
blood flow in severely head injured children. Part 1:
INTRAOPERATIVE MANAGEMENT Relationship with GCS score, outcome, ICP and PVI. J
Manual in-line stabilisation performed with an assis- Neurosurg 1989; 71: 63–71
tant applying gentle traction to the mastoid processes Muizelaar JP, Ward JD, Marmarou AM, et al. Cerebral
should be used to secure the airway. Padding under blood flow in severely head injured children. Part II:
the torso keeps the head position neutral. Splinting Autoregulation. J Neurosurg 1989; 71: 72–76
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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

INTRODUCTION performed to determine any focal lesion and if a


patient’s GCS does not improve after the post-ictal
There is perhaps no other branch of surgery where a period an EEG should be performed and anticonvul-
postoperative complication has such a devastating sants commenced.
effect. The post-anaesthesia care of the neurosurgical
patient requires careful monitoring, exquisite atten-
tion to maintenance of cardiorespiratory stability and CARDIOVASCULAR SYSTEM
frequent neurological assessment. Appropriate staff,
equipment and monitoring is mandatory for proper Uncontrolled hypertension during emergence and
care of patients. recovery has been implicated as a causative factor of
postoperative intracranial haemorrhage after
aneurysm clipping.1 Patients with atherosclerosis are
AIRWAY AND VENTILATION likely to be hypertensive preoperatively, and may be
more susceptible to postoperative hypertension.
Hypoxia or hypercapnia may result from hypo- If there is no apparent primary cause of hypertension,
ventilation due to residual neuromuscular blockade, aggressive efforts at control are warranted because of
perioperative use of opioids, electrolyte imbalance or the risk that hypertension will precipitate haemor-
brainstem compression due to oedema or rhage or worsen cerebral oedema. Treatment consists
haematoma. Hypoventilation will increase ICP and of administering titrated doses of either labetalol
impair brain oxygenation. (5–10 mg increments i.v.), small doses of esmolol or
Patients with good GCS scores who are haemo- sublingual nifedipine (10–20 mg).
dynamically stable with adequate oxygenation pre- Patients with cerebrovascular or cardiovascular
operatively may be extubated following neurosurgery disease are also susceptible to large variations in BP,
if the intraoperative course has been uneventful. both hypertension and hypotension. This will
Normothermia and adequate neuromuscular reversal increase the likelihood of cerebral or myocardial
are prerequisites to extubation. ischaemia or infarction.
Protective airway reflexes may be compromised for a
variety of reasons, in particular cranial nerve injury or
depressed level of consciousness. NAUSEA AND VOMITING

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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RECOVERY: GENERAL CONSIDERATIONS 143


of inappropriate secretion of ADH is associated with PERSONNEL AND MONITORING
CNS trauma or tumour. Diagnosis and treatment of
electrolyte and fluid balance abnormalities are Recovery personnel experienced in assessing the
described in Chapters 42 and 43. CNS are central to an adequate recovery facility.
Invasive arterial monitoring and pulse oximetry
should be continuous from the operating room to the
POSTOPERATIVE PAIN recovery room and during the patient’s stay in recov-
ery. Full monitoring should also continue when
Postoperative pain is controlled by regular doses of transferred to ICU. An experienced anaesthetist
paracetamol and NSAID (if no contraindications should also be immediately available while a patient
exist) supplemented either by carefully titrated doses remains in the recovery area.
of codeine phosphate or morphine sulphate ensuring
against excessive sedation. Nausea and vomiting due
to opioids should be treated promptly. KEY POINTS
• Recovery personnel should be experienced in
neurological assessment.
DISCHARGE
• Any deterioration in neurology should be rapidly
Patients should not be discharged to the surgical assessed and investigated.
wards until an adequate conscious level has returned • Correction of fluid and electrolyte balance can
fully, a patent airway can be maintained, ventilation is continue in recovery.
adequate and the cardiovascular system is stable. • Adequate analgesia should be established prior to
discharge.
Patients whose GCS is compromised and/or whose
• A detailed handover between recovery and ward
ability to maintain an airway is in doubt should not be
staff is essential.
extubated immediately postoperatively and should be
transferred to an intensive care environment. Patients
who have had intracranial vascular surgery, pro- REFERENCE
longed posterior fossa surgery or carotid artery 1. Kalfas IH, Little JR. Postoperative haemorrhage: a
surgery should be nursed in a high dependency area survey of 4992 intracranial procedures. Neurosurgery
with invasive monitoring for at least 24 hours. 1988; 23: 343
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35
MANAGEMENT OF SPINAL
CORD INJURY

I. Ng, R. J. C. Laing
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146 NEUROINTENSIVE CARE

INTRODUCTION The release of glutamate activates NMDA receptors


resulting in an influx of calcium. This causes activa-
The management of patients with spinal cord injury tion of calcium-dependent proteases and lipases that
requires a multi-disciplinary approach to achieve break down the cytoskeleton. The excess production
maximal neurological recovery and to prevent, of arachidonic acid and its metabolites and conse-
recognise and treat any complications. quent lipid peroxidation and free radical production
Mortality is at its highest in the early stages of treat- leads to further injury.
ment and most patients with spinal cord injury have Current research into the mechanisms of injury has
other associated injuries. led to the use of methylprednisolone to lessen the
An understanding of the pathophysiological processes effects of lipid peroxidation (see below). Further
has led to a more rational approach to spinal cord research is being conducted to establish the effective-
injury, with the main thrust aimed at prevention of ness of other agents in modifying the pathophysiolog-
cord ischaemia and worsening secondary injury and ical processes which contribute to spinal cord injury
more recently, the use of steroids to reduce the harm- at the molecular level. The aims are to promote neu-
ful effects of lipid peroxidation. ronal salvage and ultimately improve clinical out-
come.

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
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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.

ASSOCIATED INJURIES AND DECUBITUS ULCERS


MANAGEMENT ISSUES Direct pressure on weight-bearing areas, sensory loss,
Sixty per cent of patients with spinal cord injuries reduced mobility and reduced tissue perfusion expose
have associated injuries: head, thoracic, abdominal or the patient to a high risk of skin breakdown. This can
vascular injuries. This underlies the importance of be prevented by careful nursing with frequent turn-
meticulous initial assessment and subsequent regular ing of patients. Padding of pressure areas with soft
review of the patient. foam or nursing on oscillating or air flotation beds
can help prevent this problem.
CARDIOVASCULAR
The presence of hypotension may indicate neuro- SURGICAL TREATMENT
genic shock with loss of sympathetic innervation to Intuitively, it would be expected that the surgical
the heart and peripheral vasculature. Hypovolaemic decompression of bony fragments encroaching on
hypotension secondary to concealed or overt blood neural elements would result in improved neurologi-
loss may be concurrent and useful indicators are un- cal outcome. Many reports have been published that
explained tachycardia with narrowed pulse pressure. show that emergency attempts at surgical decompres-
Aggressive fluid resuscitation is necessary to prevent sion have led to a worse outcome than patients treated
further injury. Invasive haemodynamic monitoring conservatively. This may be due to problems of inad-
may be indicated to guide fluid and inotrope therapy. equate resuscitation pre and per-operatively and com-
plications secondary to poorly planned or executed
PULMONARY FUNCTION surgery. Operative treatment can restore normal spinal
alignment, allow early mobilisation and prevent
Respiratory dysfunction following spinal cord injuries delayed deformity. Emergency decompression may be
occurs from loss of neural control of ventilatory muscles indicated for cord compression without laceration due
(high cervical injuries) or is secondary to parenchymal to disc fragments in the canal. Most spinal surgeons
injury, e.g. pulmonary contusion, pneumothorax, therefore adopt a more conservative approach with
haemothorax, atelectasis, neurogenic pulmonary delayed surgical decompression and spinal stabilisation
oedema, adult respiratory distress syndrome, fat when indicated. The stabilisation procedure with bone
embolism, pulmonary embolism or aspiration. grafting and instrumentation facilitates nursing.
Patients requiring mechanical ventilation need active
chest physiotherapy including suction, humidifica-
tion and bronchodilators to prevent retention of METHLYPREDNISOLONE
secretions and optimise gas exchange. THERAPY
Early tracheostomy for patients with multiple injuries The results of the NASCIS III trial1 have shown that
and pulmonary dysfunction is strongly advocated. patients arriving within 3 hours and given a bolus
dose of 30 mg/kg methylprednisolone followed by
5.4 mg/kg/h for 24 hours, as well as patients who
NUTRITION arrive between 3 and 8 hours after injury and having
Patients with spinal cord injury are often in a cata- had the same loading dose followed by 48 hours of
bolic state and therefore feeding should be started as methylprenisolone, have improved motor scores and
soon as possible. Enteral feeding via an indwelling better functional independence scores at 1 year post-
nasogastric tube is the method of choice. Patients injury compared to patients receiving no methyl-
with associated abdominal injuries or those with ileus prednisolone. Patients who arrive later than 8 hours
secondary to cord injury (thoraco-lumbar injuries), do not derive any benefit from methylprednisolone
may require parenteral nutrition. treatment.

BLADDER KEY POINTS


During the acute period of spinal cord injury, the • Spinal cord injury should be suspected after major
bladder is atonic. An indwelling urinary catheter will trauma.
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148 NEUROINTENSIVE CARE

• 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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150 NEUROINTENSIVE CARE

INTRODUCTION Scores range from 3 to 15. Scores less than 9 usually


indicate a requirement for airway and ventilatory
The Glasgow coma scale (GCS) in adults (Table 36.1) support and ICP monitoring.
is a method of continuous rapid neurological assess- In children, a modified GCS can be obtained using the
ment and is commonly used in the acutely brain- same scores for eye opening and best motor response
injured patient and perioperatively in neurosurgical and a modified best verbal response (Table 36.2).
patients. It may also help as a prognostic indicator.
A Glasgow coma outcome scale (GCOS) (Table
36.3) of function is commonly performed 6 months
Table 36.1 Glasgow coma scale following traumatic brain injury. This allows individ-
ual centres to compare results and to compare new
Eye opening: Spontaneous 4 therapies.
To speech 3
To pain 2
None 1 FURTHER READING
Best motor response: Obeys commands 6 Teasdale C, Jennet B. Assessment and prognosis of coma
Localises to pain 5 after head injury. Acta Neurochir (Wien) 1976; 34: 45–55
Withdraws to pain 4
Abnormal flexion 3
Extension 2
None 1 Table 36.3 Glasgow Coma Outcome
Scale
Best verbal response: Orientated 5
Confused 4 Good recovery 4
Inappropriate words 3 Moderately disabled (disabled but independent) 3
Incomprehensible sounds 2 Severely disabled (disabled and dependent) 2
None 1 Died 1

Table 36.2 Modified paediatric GCS

Eye opening: Spontaneous 4


To speech 3
To pain 2
None 1
Best motor response: Obeys commands 6
Localises to pain 5
Withdraws to pain 4
Abnormal flexion 3
Extension 2
None 1
Best verbal response Smiles, follows objects, interacts 5
Crying: Interaction:
Consolable Inappropriate 4
Inconsistently Moaning 3
Consolable
Inconsolable Irritable 2
None None 1
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37
SEVERE HEAD INJURY: INITIAL
RESUSCITATION AND
TRANSFER

B. Matta
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152 NEUROINTENSIVE CARE

INTRODUCTION than 4 kPa) and an adequate PaO2. Oxygenation and


ventilation is optimised and should be regularly veri-
Although better pre-hospital care and the ready avail- fied by arterial blood gas analysis. The patient is best
ability of multi-disciplinary teams have improved the sedated and paralysed. Patients should not cough or
very poor outlook that was previously associated with strain on the endotracheal tube. Clearly, not all
head trauma, outcome continues to be affected by patients with head trauma require tracheal intubation,
abnormal physiology in the immediate post-injury and the protocol used in our unit is outlined in Table
period. 37.1.
The primary injury, which is not treatable and can only Except for young children, in whom blood loss from
be prevented, describes the damage that occurs at the a scalp wound is sufficient to cause a reduced MAP,
time of initial impact. Severe HI renders the patient hypotension should prompt an investigation for sites
comatose from impact; those able to talk at any stage of blood loss with immediate laparotomy or thoraco-
following the injury are unlikely to have sustained a tomy if necessary. The combination of an increased
substantial primary injury. ICP and systemic hypotension leads to cerebral
Secondary injury is the additional insult imposed on the ischaemia. Hypovolaemia may be masked by systemic
neural tissue following the primary impact. The two hypertension secondary to intense sympathetic stim-
most important contributors to secondary ischaemia ulation of the reflex response to intracranial hyper-
in the head-injured patient are hypoxaemia and sys- tension. Therefore, moderate levels of hypertension
temic hypotension. should not be treated but a BP above the upper limit
of autoregulation (MAP > 130 mmHg) must be
actively treated, as it will increase CBV and ICP.
The choice of fluid used for resuscitation is less
INITIAL RESUSCITATION
important than the amount given. The use of glu-
The importance of securing the airway, maintaining cose-containing solutions is discouraged unless hypo-
adequate oxygenation and BP in the head-injured glycaemia is suspected, as hyperglycaemia worsens
patient cannot be over-emphasised. Secondary brain
damage begins and continues to occur from the
moment of impact and for every second that the
patient is hypoxaemic or hypotensive. Severely head- Table 37.1 Indications for intubation and
injured patients (GCS < 9) are unlikely to be able to ventilation after head injury
protect their airway and often have impaired gas
exchange. Early use of endotracheal intubation is Immediately
often necessary to maintain adequate oxygenation. It ● Coma (not obeying commands, not speaking,
not eye opening i.e. GCS < 9)
is important to remember that a significant propor-
● Loss of protective laryngeal reflexes
tion of severe HIs are associated with injuries to the ● Ventilatory insufficiency as judged by blood
cervical spine and therefore, manual in-line stabilisa- gases:
tion of the neck during induction and tracheal intu- Hypoxaemia (PaO2 < 13 kPa)
bation is essential. Nasal intubation is best avoided in Spontaneous hyperventilation causing PaCO2
the patient with basal skull fracture because of the risk < 3.5 kPa
of passing the endotracheal tube into the brain ● Respiratory arrhythmia
through the skull defect, and of the added risk of ● Uncontrolled seizures
infection. Before start of journey to the neurointensive care
Severely head-injured patients have a full stomach. unit
● Deteriorating level of consciousness (decrease in
Therefore, a rapid sequence induction with a small GCS by > 2 points since admission, and not
dose of induction agent followed by suxamethonium due to drugs), even if not in coma
1 mg/kg is mandatory. Apart from ketamine, which ● Bilaterally fractured mandible
is contraindicated because of concerns about its ● Copious bleeding into mouth (e.g. from a basal
effects on ICP, the choice of induction agent is not skull fracture)
important as long as it is administered with care and ● Seizures
large variations in BP or significant hypotension is
avoided. An intubated patient must also be ventilated,
aiming for a PaO2 > 13 kPa and PaCO2 of 4.0–4.5
Once the airway is secured, the lungs are mechani- kPa.
cally ventilated to maintain mild hypocapnia (not less
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SEVERE HEAD INJURY: INITIAL RESUSCITATION AND TRANSFER 153


outcome after HI. Hyperglycaemia should be actively
treated and blood glucose levels controlled with an Table 37.2 What the neurosurgical centre
infusion of insulin. Because the majority of head- needs to know at time of referral
injured patients receive mannitol, an adequate urine
Patient’s age and past medical history (if known)
output is often a poor indicator of volume status in History of injury
these patients. CVP monitoring is often very useful as ● Time of Injury
an aid to assessing intravascular fluid volume and ● Cause and mechanism (height of fall,
effectiveness of resuscitation, and should be com- approximate impact velocity)
bined with the use of a pulmonary artery flotation Neurological state
catheter in the elderly, patients with heart disease and ● Talked or not after injury
in those patients requiring the use of inotropic sup- ● Consciousness level on arrival at A&E dept
port. ● Trends in consciousness level after arrival
(sequential GCS)
● Pupil and limb responses
Cardiorespiratory state
● Blood pressure and pulse rate
TRANSFER OF THE ● Arterial blood gases, respiratory rate and
HEAD-INJURED PATIENT pattern
Adequate resuscitation and a thorough re- Injuries
● Skull fracture
examination of the patient must be completed ● Extracranial injuries
before making decisions about further treatment pri- Imaging findings
orities. Blind burrhole exploration is rarely effective, ● Haematoma, swelling, other
can be harmful to the patient, and delays the transfer Management
of the patient and the initiation of definitive therapy. ● Airway protection, ventilatory status
There is no longer any indication for this procedure ● Circulatory status and fluid therapy
in the modern Accident and Emergency Depart- (Mannitol)
ment. Once the patient has been stabilised, a deci- ● Treatment of associated injuries
sion can be made regarding transfer to a regional (? emergency surgery)
neurosurgical unit for further treatment. Inter- ● Monitoring
● Drug doses and times of administration
hospital transfer of the head-injured patient is a
potentially hazardous procedure and often poorly
managed (Table 37.2). The key to a successful and
safe transfer involves:
• Adequate resuscitation and stabilisation of the
sufficient supply of drugs and portable gases, and that
patient prior to transfer.
there is enough power in battery-operated monitor-
• Adequate monitoring during transfer with appro-
ing equipment for the duration of the journey.
priate resuscitative equipment and drugs.
• The presence of an accompanying doctor with Monitoring during transfer should be of a standard
suitable training, skills and experience of HI appropriate to a patient in intensive care, and should
transfer. include invasive arterial BP monitoring, CVP moni-
• Good communication between referring and toring where indicated, and the use of capnography.
receiving centres, and an adequate, efficient and The transferring doctor must have appropriate expe-
stable hand-over to the receiving team care. rience in the transfer of patients with HIs, should be
familiar with the pathophysiology and management
The fundamental requirement during transfer is to
of such a patient, and with the drugs and equipment
ensure adequate tissue oxygen delivery and to main-
they will use. It is also of paramount importance to
tain stable perfusion. The head-injured patient is at
discuss the patient with the neurosurgical centre at
risk of respiratory compromise, and this risk is
an early stage, so that treatment priorities can be
increased during transfer. Patients with a signifi-
decided upon, and that the receiving team is pre-
cantly altered conscious level should be sedated,
pared for the arrival of the patient. The care of the
intubated and ventilated during transfer. There is no
transferring doctor does not end at the door of the
place for transferring unstable patients to neurosurgical
receiving hospital, but continues until he ensures
units.
that the stability of the patient is maintained and a
The transferring team must ensure that all lines and full and accurate hand-over to the receiving team is
tubes are secured before transfer, that they have a made.
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154 NEUROINTENSIVE CARE

KEY POINTS FURTHER READING


• Hypotension and hypoxia are two major contrib- Matta BF, Menon DK. Management of acute head injury:
pathophysiology and initial resuscitation. Anaes Rev 1995;
utors to secondary brain injury and should be
13: 163–178
avoided.
• The cervical spine should be assumed to be Matta BF, Menon DK. Severe head injury in the United
unstable until cleared by radiological examina- Kingdom and Ireland: a survey of practice and implications
tion. for management. Crit Care Med 1996; 24: 1743–1748
• Rapid resuscitation and adequate stabilisation is Gentleman D, Dearden M, Midgley S, Maclean D.
essential prior to transfer. Guidelines for the resuscitation and transfer of patients with
• Good communication between the referring serious head injury. Br Med J 1993; 307: 547–552
centre and the neurosurgical centre is required. The Association of Anaesthetists of Great Britain and
• Appropriate personnel, equipment and monitor- Ireland. Recommendations on transfer of the severely head
ing should accompany the patient. injured patient
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38
INTENSIVE CARE
MANAGEMENT OF ACUTE
HEAD INJURY

D.K. Menon
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156 NEUROINTENSIVE CARE

DETERMINANTS OF OUTCOME therapies is futile if stable cardiorespiratory and cere-


IN ACUTE HEAD INJURY: brovascular physiology cannot be achieved.
PRIMARY VS SECONDARY INSULTS
Little can be done about the extent of primary injury MONITORING IN ACUTE HEAD
following head trauma, but secondary neuronal
injury, much of which is triggered by physiological
INJURY
insults to the injured brain, can be a major determi-
None of the interventions that are widely used by
nant of outcome. The most important physiological
specialist centres in severe head injury have ever been
insults that affect outcome (Table 38.1) can be graded
subjected to prospective randomised control trials,
for severity with respect to their effect on secondary
but a large body of clinical experience provides a rel-
neuronal injury. Physiological insults are additive in
atively strong basis for their recommendation as treat-
their effect on outcome, both when multiple insults
ment guidelines.
(e.g. hypoxia and hypotension) occur at the same
time point, or when the same insult occurs repeatedly
(e.g. hypotension in the prehospital and ICU phases DEFINING THERAPEUTIC TARGETS: A
of the illness). The intensive care of head injury cen- RATIONAL APPROACH TO SELECTING
tres on avoiding, detecting and treating such physio- MONITORING MODALITIES
logical derangements.
Basic physiology suggests the benefit of maintaining
Targets for basic intensive care practice in this area
CBF and oxygenation. Hypotension (systolic blood
have been widely debated and systematically
pressure < 90 mmHg) and hypoxia (PaO2 levels
reviewed. These involve the monitoring, preven-
< 60 mmHg (8 kPa)) in the early and later phases of
tion and treatment of secondary physiological
head injury worsen outcome. Several studies in
insults. Novel neuroprotective agents may hold
patients with head injury have suggested preserved
considerable promise in the future, but their general
cerebrovascular autoregulation with maintenance of
failure in clinical phase III suggests that these drugs
CBF at CPP above 60–70 mmHg. Further, ischaemia
are unlikely to materially alter outcome in the short
is a consistent post-mortem finding in fatal head
term.
injury, and retrospective studies from several groups
However, there appears to be much room for have suggested that outcome is improved in patients
improvement in conventional clinical practice. A who have fewer episodes of CPP or MAP reduction
series of surveys suggest that basic recommendations or aggressive CPP management. There is, however,
for severe head injury management have not been some emerging concern that relatively high perfusion
consistently followed in many neurosurgical centres pressures may contribute to oedema formation, and at
in the USA and UK. As an example, ICP was moni- least one group have targeted relatively low CPP in
tored in only half the centres surveyed. While prelim- order to minimise oedema formation (the Lund
inary results suggest that this situation may now be protocol). Other small studies show worse outcomes
improving, the application of novel neuroprotective in patients who suffer episodes of jugular venous

Table 38.1 Physiological insults following head injury and their relation to outcome

Insult Significant relation to


Mortality Grades within
Glasgow outcome score

Duration of hypotension (SBP < 90 mmHg) Yes Yes


Duration of hypoxia (SpO2 < 90%) Yes No
Duration of pyrexia (Tcore > 38oC) Yes No
Intracranial hypertension (ICP > 30 mmHg) Yes No
Cerebral perfusion pressure (CPP < 50 mmHg) Yes No
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INTENSIVE CARE MANAGEMENT OF ACUTE HEAD INJURY 157


desaturation below 50%, or blood glucose elevation. vasodilatation in response to a fall in CPP. ‘A waves’
Elevations in body temperature may worsen outcome tend to occur on a high baseline pressure and elevate
in acute brain injury. ICP to 50–100 mmHg for several minutes, usually
terminated by a marked increase in mean arterial
These findings emphasise the importance of mainte-
pressure. Shorter lived fluctuations lasting about a
nance of CPP, rather than isolated attention to ICP as
minute are referred to as B waves. The frequency of
a therapeutic target. There are, however, data that
both A and B waves may be decreased by increasing
show that ICP is an independent, albeit weaker,
MAP, thus preventing the reflex cerebral vasodilatory
determinant of outcome in severe head injury, with
cascade that initiates CBV increases and ICP eleva-
levels greater than 15–25 mmHg constituting an
tion (see Chapter 52 for further information).
appropriate threshold for initiation of therapy.

MONITORING SYSTEMIC TCD ULTRASONOGRAPHY


PHYSIOLOGY Reductions in middle cerebral artery flow velocity
Monitoring of direct arterial blood pressure along with (MCA FV) provide a useful marker of reduced cere-
measurement of ICP is essential for computing and bral perfusion in the setting of intracranial hyperten-
manipulating CPP. The need to rationally manipulate sion, but episodic rises in ICP may also be caused by
mean arterial pressure will also require the placement hyperaemia, which may be diagnosed by increases in
of a right atrial or pulmonary artery catheter as appro- TCD FV. Transcranial Doppler ultrasonography can
priate. Continuous pulse oximetry, regular arterial also be used as a non-invasive monitor of CPP.
blood gas analysis, core temperature monitoring and Tests of autoregulation involve recording TCD
regular measurement of blood sugar are also required responses to induced changes in mean arterial pres-
in order to optimise physiology in these patients. sure or carotid compression (the transient hyperaemic
response test; THRT). More recent algorithms con-
GLOBAL CNS MONITORING stantly assess autoregulation by on-line calculation of
MODALITIES changes in MCA FV in response to small spontaneous
alterations in MAP.
While the monitoring described above may help to
ensure the maintenance of optimal systemic physiol-
ogy, detection of local changes in CNS physiology JUGULAR VENOUS OXIMETRY
will require other tools. These include transcranial Classically, right jugular venous oximetry has been
Doppler ultrasound for non-invasive estimation of used to assess the adequacy of CBF in head injury, but
CBF, jugular venous saturation (SjvO2) monitoring, a case can be made for targeting the side of injury or
and monitoring of brain electrical activity. These for using bilateral catheterisation. Reductions in SjvO2
techniques seek to estimate CBF in the presence of an or increases in arteriojugular differences in oxygen
adequate CPP, estimate the adequacy of oxygen content (AJDO2) to greater than 9 ml/dl provide use-
delivery to the brain, and document the conse- ful markers of inadequate CBF, and SjvO2 values
quences of possible oxygen deficit or drug therapy on below 50% have been shown to be associated with a
brain function respectively. worse outcome in head injury. Conversely, marked
elevations in SjvO2 may provide evidence of cerebral
ICP MONITORING hyperaemia. The major deficiencies of jugular venous
oximetry are its invasiveness and the poor reliability
ICP monitoring is needed because clinical signs of of signal obtained. Other techniques that have been
intracranial hypertension are late, inconsistent and employed investigationally in acute head injury
non-specific. Further, it has been shown that episodic include near infra-red spectroscopy (NIRS), direct tis-
rises in ICP may occur even in patients with a normal sue oximetry and cerebral microdialysis.
X-ray CT scan. While intraparenchymal micro-
manometers (Codman, USA) or fibreoptic probes
(Camino, USA) are increasingly used due to ease of MULTIMODALITY MONITORING
use and a lower infection risk, they are more expen-
The correlation of data from several modalities has
sive than ventriculostomies and do not permit CSF
several advantages in head injury management.
drainage for the reduction of elevated ICP.
Integration of monitored variables allows cross vali-
Patients with head injury may also develop phasic dation and artifact rejection, better understanding of
increases in ICP, often triggered by cerebral pathophysiology and the potential to target therapy.
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158 NEUROINTENSIVE CARE

THERAPY animal data. Fluid flux across the normal BBB is


governed by osmolarity rather than oncotic pressure.
ACHIEVING TARGET CPP VALUES Consequently, hypotonic fluids are avoided and
serum osmolality is maintained at high normal levels
Most centres agree on the need to maintain cerebral (290–300 mosm/l in our practice). Dextrose contain-
perfusion by keeping CPP above 60–70 mmHg, ing solutions are avoided since the residual free water
either by decreasing ICP or by increasing MAP. after dextrose metabolism can worsen cerebral
While MAP is usually maintained with volume oedema, and because the associated elevations in
expansion, inotropes and vasopressors, the relative blood sugar may worsen outcome.
efficiency of each of these interventions in maintain-
ing CPP have not been investigated. Drainage of CSF Head-injured patients have high nutritional require-
(where possible), mannitol administration, hyperven- ments and feeding should be instituted early (within
tilation and the use of CNS depressants (typically bar- 24 hours), aiming to replace 140% of resting meta-
biturates) have all been used to reduce ICP. bolic expenditure (with 15% of calories supplied as
protein) by the seventh day post trauma. Enteral feed-
ing is associated with a lower incidence of hypergly-
VENTILATORY SUPPORT AND THE USE caemia and may have a protective effect against gastric
OF HYPOCAPNIA FOR ICP ulceration. Impaired gastric emptying can be treated
REDUCTION with prokinetic agents such as metoclopramide. In
those who cannot be fed enterally, parenteral nutri-
It is generally agreed that patients with a GCS of < 8 tion should be considered together with rigorous
require intubation for airway protection, and that blood sugar control and some form of prophylaxis
such patients should receive mechanical ventilatory against gastric ulceration (H2 antagonists or sucralfate).
support to optimise blood gases. Airway control and
ventilation are also required for patients with ventila-
tory failure, central neurogenic hyperventilation or HYPEROSMOLAR THERAPY
recurrent fits. Mannitol (0.25–1 g/kg, usually as a 20% solution) has
Hyperventilation, once the mainstay of ICP reduc- traditionally been used to elevate plasma osmolarity
tion in severe head injury, is now the subject of much and reduce brain oedema in the setting of intracranial
debate. The aim of hyperventilation is to reduce hypertension. Side effects can be minimised if its use
cerebral blood volume and hence ICP, but can cause is discontinued when it no longer produces signifi-
accompanying reductions in global CBF, sometimes cant ICP reduction, volume status is monitored
below ischaemic thresholds. Such ischaemia can be and plasma osmolality is not allowed to rise above
documented using jugular bulb oximetry, which may 320 mosm/l. Recent reports also highlight the
worsen outcome, specially when hyperventilation is successful use of 23.4% saline for treatment of
prolonged or profound. The diffusible hydrogen ion intracranial hypertension refractory to mannitol.
acceptor, tetra-hydro-aminomethane (THAM), may
restore ECF base levels and restore cerebrovascular SEDATION AND NEUROMUSCULAR
CO2 reactivity. While such an approach has been BLOCKADE
shown to reduce ICP and the need for intensification
of ICP therapy after head injury, it does not alter out- Intravenous anaesthetic agents preserve pressure
come. autoregulation and the cerebrovascular response to
CO2 (even at doses sufficient to abolish cortical activ-
ity) and decrease CBF, cerebral metabolism and ICP.
FLUID THERAPY AND FEEDING
While the reduction in flow and CBV are secondary
Accurate fluid management may be complicated by to a reduction in metabolism, flow-metabolism cou-
continuing or concealed haemorrhage from associ- pling is not perfect, and the decrease in CBF may
ated extracranial trauma, but every effort must be exceed the corresponding decrease in CMRO2, with
made to restore normovolaemia and prevent a widening of the cerebral arteriovenous oxygen con-
hypotension. Fluid replacement should be guided by tent difference. Barbiturates have been largely
clinical and laboratory assessment of volume status replaced by other agents such as propofol, which
and by invasive haemodynamic monitoring, but gen- possesses similar cerebrovascular effects but better
erally involves the administration of 30–40 ml/kg of pharmacokinetic profiles. However, propofol can
maintenance fluid per day. The choice of hydration induce hypotension and decrease CPP. Problems with
fluid is largely based on inconclusive results from lipid loading have been substantially ameliorated by
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INTENSIVE CARE MANAGEMENT OF ACUTE HEAD INJURY 159


the introduction of a 2% formulation of propofol. of the drugs that have been tested thus far in phase III
Midazolam is often used as an alternative in combina- trials have proved beneficial on an intention to treat
tion with fentanyl for sedating the patient with head basis.
injury. Opioids generally have negligible effects on
CBF and CMRO2. However, the newer synthetic
opioids fentanyl, sufentanil and alfentanil, can increase HYPOTHERMIA
ICP in patients with tumours and head trauma due to
Mild to moderate hypothermia (33–36oC) has been
changes in PaCO2 (in spontaneously breathing sub-
shown to be neuroprotective in animal studies which
jects) and reflex cerebral vasodilatation secondary to
demonstrated improved outcome from cerebral
systemic hypotension. These changes can be avoided
ischaemia with small (1–3oC) reductions in tempera-
if blood pressure and ventilation are controlled.
ture. Three early clinical studies demonstrated benefit
Neuromuscular blockade in the head-injured patient from moderate hypothermia in head injury, and
receiving intensive care is currently the subject of much interim results from a large ongoing outcome trial
debate. Neuromuscular blockers can prevent rises in were encouraging, suggesting benefit in a subgroup
ICP produced by coughing and ‘bucking on the tube’. of patients with GCS of 5–7. However, the study was
However, overall outcome is not improved, perhaps terminated early on grounds of futility, with no clear
because of increased respiratory complications and benefit established. Initial post-hoc analysis suggests
neuromyopathy remains a concern after long-term use that younger patients with higher ICPs may benefit
(especially with the steroid-based agents). Atracurium from hypothermia.
is non-cumulative and has not been associated with
myopathy, and theoretical concerns about the accu-
mulation of laudanosine are not clinically relevant.
SEQUENTIAL ESCALATION VS
ANTIEPILEPTIC THERAPY TARGETED THERAPY FOR THE
INTENSIVE CARE OF HEAD
Post-traumatic seizures are commonest in patients
INJURY
with a GCS < 10, an intracranial haematoma, contu-
sion, penetrating injury or depressed skull fractures. It is clear that a diverse range of pathophysiological
Such patients may form the most appropriate sub- processes operate in acute head injury, and that there
group for acute (days to weeks) seizure prophylaxis exist a wide range of therapeutic options, few of
following head injury. which have proven efficacy. One of two approaches
may be used in the choice of therapy in such a setting.
The first of these is to use a standard protocol in all
CEREBRAL METABOLIC SUPPRESSANTS
patients, and introduce more intensive therapies in a
Intravenous barbiturates have been used for ICP reduc- sequence that is based either on intensity of interven-
tion for over 20 years. While they clearly result in car- tion or on local experience and availability.
diovascular depression, increased ICU stay and Alternatively, individual therapies can be targeted at
increases in pulmonary infections, it appears that they individual pathophysiological processes. Examples are
may benefit patients with intractable intracranial hyper- the use of hyperventilation in the presence of hyper-
tension that responds to intravenous anaesthetics. They aemia, mannitol for vasogenic cerebral oedema or the
are administered as an intravenous infusion and titrated use of blood pressure elevation in the presence of B
to produce burst suppression on EEG. The prolonged waves.
recovery associated with barbiturates suggests a role for
In practice, many established head injury protocols
other intravenous anaesthetics (etomidate and propo-
represent a hybrid approach. Initial baseline monitor-
fol) with more desirable pharmacokinetic profiles.
ing and therapy are applied to all patients, and refrac-
However, the efficacy of these agents remains
tory problems are dealt with by therapy escalation,
unproven, and they have their own drawbacks.
with the choice of intervention determined by clini-
cal presentation and physiological monitoring. Often,
interventions that are more difficult to implement or
NOVEL NEUROPROTECTIVE present significant risks (e.g. barbiturate coma) are
used as a last resort. Figure 38.1 represents the
INTERVENTIONS
ICP/CPP management protocol used in the
While a variety of novel pharmacological neuropro- Neurosciences Critical Care Unit at Addenbrooke’s
tective agents are currently under investigation, none Hospital.
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160 NEUROINTENSIVE CARE

Addenbrooke’s NCCU: ICP/CPP management algorithm

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

• 20% mannitol 2 ml/kg ⴒ 3 or till plasma 320 mosm/l


• PAC, volume, vasoactives to increase MAP (CPP 90–100)
• Reduce PaCO2 to 3.5–4.0 kPa providing SjO2 stays ≥ 55%,
• Temp ⯝ 35°C, Daily lipid screen if still on propofol
• EEG/CFM: ? fits –> Phenytoin 15 mg/kg iv > 300 mg/day no

CPP < 70; ICP > 25 (Check probe, ? re-CT)


no CT
III
Temp 33°C (discontinue propofol)
Surgical lesion?
CSF drainage?
CPP < 70; ICP > 25 (Check probe, ? re-CT) Role for surgical
decompression?

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

Figure 38.1 Addenbrooke’s NCCU: ICP/CPP management algorithm


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INTENSIVE CARE MANAGEMENT OF ACUTE HEAD INJURY 161

KEY POINTS RECOMMENDED READING


• The primary aim in the management of head- Brain Trauma Foundation. 1996. Guidelines for the
injured patients is the prevention of secondary management of severe head injury. Journal of Neuro-
brain injury. trauma. 1996 13(11), 639–734
• Hypoxia and hypotension must be avoided. Jones PA, Andrews PJD, Midgley S et al. 1994 Measuring
• There is regional heterogeneity in cerebral blood the burden of secondary insults in head injured patients
flow and metabolism after injury. during intensive care. Journal of Neurosurgical
• Multimodal monitoring facilitates the early identi- Anesthesiology 6, 4–14
fication of secondary insults. Menon DK. 1999 Cerebral protection in severe brain
• Many centres target therapy to maintain CPP injury: physiological determinants of outcome and their
above 60–70 mmHg optimisation. British Medical Bulletin 55, 226–258
• ICP should be kept below 25 mmHg. Menon DK, Summors AC. 1998 Neuroprotection (includ-
ing hypothermia). Current Opinion in Anaesthesiology 11,
485–496
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39
MANAGEMENT OF
SUBARACHNOID
HAEMORRHAGE

J. Ulatowski
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164 NEUROINTENSIVE CARE

INTRODUCTION arrhythmia. Patients successfully arriving at emergency


departments complain of severe headache (‘worst
Although subarachnoid haemorrhage (SAH) is a rela- headache of their life’) with nausea, vomiting,
tively uncommon cause of stroke, it remains the most photophobia and stiff neck (meningismus). Diagnosis
targeted stroke condition for diagnosis and treatment begins with CT scan and, if negative, lumbar punc-
because of the possibility of a reasonable outcome ture performed meticulously to avoid traumatic
with timely intervention. Urgency in diagnosis and puncture. Conventional angiography, CT angio-
treatment cannot be overstated as estimates for 30- graphy and MR angiography will confirm the pres-
day mortality reach 40%. This high-risk period also ence of an aneurysm in most spontaneous SAH cases.
offers a window for successful therapies and critical Patients with normal angiograms have a repeat study
care intervention (Table 27.1). prior to diagnosing non-aneurysmal SAH.
The critical care management of patients with SAH Initial treatment involves stabilisation of vital signs (air-
begins prior to hospitalisation. SAH presents suddenly, way, breathing, circulation) and preventing sequelae
and a large number of patients succumb prior to of SAH such as rebleeding, hydrocephalus, seizures
hospital admission due to raised intracranial pressure and vasospasm in the period before and after surgical
causing syncope, respiratory depression and cardiac or angiographic-guided ablation of the aneurysm.

Table 27.1 Critical care intervention after SAH

Condition Diagnosis Treatment

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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166 NEUROINTENSIVE CARE

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

A. Summors, P. Doyle, A.K. Gupta


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170 NEUROINTENSIVE CARE

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

Table 40.1 Mechanisms of brain injury. Initial event: trauma, ischaemia

Primary Secondary Systemic insult

• Tissue destruction • Pressure effects • Hypoxaemia


• Haemorrhage • Hydrocephalus • Hypotension
• Pressure effects • Herniation • Hypercarbia
• Diffuse axonal injury • Vasospasm • Excessive hypocarbia
• Reduced metabolic rate • Hyperthermia
• Impaired autoregulation • Anaemia
• Secondary hyperaemia • Electrolyte disturbance
• Oedema • Hyperglycaemia
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NEUROPROTECTION IN ICU 171


decrease in CMRO2 and reduction in the energy used Calcium channel blockade
for synaptic transmission. Other mechanisms are
Intracellular calcium accumulation is thought to be a
given in Table 40.2.
major cause of cellular injury during ischaemia due to
Barbiturates have been found to be particularly useful a disruption of certain subtypes of voltage gated Ca++
in focal ischaemia, although there is little evidence of channels (i.e. N, Q and P) regulating Ca++ influx into
neuroprotective effects in global ischaemia (e.g. post cells and mitochondria. Whilst the exact protective
cardiac arrest). Thiopentone has proven useful in sta- mechanism of calcium channel blockers is still not
tus epilepticus and during periods of ischaemia in fully understood, it is probable that they reduce the
refractory intracranial hypertension. It may also allow influx of Ca++ across plasma and mitochondrial mem-
prolonged temporary clipping during aneurysm branes.
surgery, although there is no evidence of improve-
Calcium channel antagonists (e.g. nimodipine) pro-
ment in overall outcome. Thiopentone should be
vide protection following SAH. The mechanism of
titrated to EEG burst suppression (250 mg bolus up to
protection is not by prevention of vasospasm as ini-
3–5 g, followed by infusions of 4–8 mg/kg/h) in
tially thought, but probably by direct cytoprotective
refractory intracranial hypertension, and care should
effects. There is no good evidence of benefit of these
be taken to maintain CPP.
agents in traumatic brain injury.
There is currently no good evidence demonstrating
the clinical benefit of other intravenous anaesthetic
Sodium channel blockade
agents such as propofol, etomidate, ketamine, opioids
or benzodiazepines as neuroprotective agents. Anticonvulsants such as phenytoin (and its prodrug
fosphenytoin), lamotrigine, lubeluzole and riluzole
Although the volatile anaesthetic agents reduce
act by Na+ channel blockade, decreasing neuronal
CMRO2, it appears that this only extends to cortical
transmission and energy requirements for neuronal
activity and not membrane/organelle function. This
transmission. Attenuation of release of the excitatory
provides cerebral protection for only a short time and
amino acid glutamate also occurs. All have been
is of no proven clinical benefit.
proven effective experimentally in providing neuro-
protection, but have been disappointing in the clini-
Steroids
cal setting.
Although there is evidence of benefit in the early
Other sodium channel blockers that have shown
administration of high dose methylprednisolone in
promise in vitro are the local anaesthetic agents,
spinal cord injury (see Chapter 35), there is no such
QX314 and QX222 and a new opioid with Na+
evidence of benefit from corticosteroids in the inten-
blocking properties, called Enadoline. These are still
sive care management of head injury.
under investigation.

Excitatory amino acid (EAA) antagonists


Table 40.2 Neuroprotection mechanisms Glutamate and aspartate are the major EAAs present
of anaesthetic agents
during ischaemia and concentrations of these EAAs
are vastly increased in the extracellular space. This
• Reduction in synaptic transmission causes a surge of neuronal activity mediated by four
• Reduction in Calcium influx different types of glutamate receptor – NMDA,
• Na+ channel blockade AMPA (a-amino-3-hydroxy-5-methyl-4-isoxazole
• Membrane stabilisation propionic acid), Kainate, metabotropic receptors.
• Improvement in distribution of regional blood flow
• Suppression of cortical EEG activity
The NMDA receptor is the major route allowing
• Reduction in cerebral oedema Ca2+ into the cytosol (a process normally blocked by
• Free radical scavenging Mg2+). Excessive activation of these receptors can
• Potentiate γ-aminobutyrate activity trigger a huge influx of Ca2+ intracellularly with
• Alteration of free fatty acid metabolism concomitant increases in permeability for other ions.
• Suppression of catecholamine-induced
hyperactivity The neuroprotective effects of EAA antagonists have
• Reduction in CSF secretion been demonstrated in animal models of head injury.
• Deafferentation and immobilisation Selfotel was a recent compound, which like others
• Uptake of glutamate in synapses showed promise in animal models but did not
progress into clinical use.
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172 NEUROINTENSIVE CARE

NSAIDS Intraoperative hypothermia during aneurysm surgery


is currently being investigated in a large multicentred
Prostoglandin inhibitors such as indomethacin cause
randomised trial which has recently commenced.
cerebral vasoconstriction by reducing prostacyclin
synthesis, thus reducing ICP, but a rebound phenom- The success of hypothermic neuroprotection in
ena may be seen if stopped suddenly. models of head injury may simply be the avoidance of
hyperthermia in the injured brain, which is detrimental
Other novel therapies to outcome. Ischaemic brain is warmer than systemic
temperature, and maintenance of normothermia is
No efficacy has been demonstrated in multicentred
important – the best means of achieving this is forced
trials with antioxidants; (tirilazad mesylate, pegor-
convective cooling. Pharmacological methods for
gotein) or Deltibant (a bradykinin antagonist).
temperature reduction have unsustained effects.
A number of different successful experimental thera-
pies (Table 40.3) are awaiting clinical trials.
HHH THERAPY (HYPERTENSION,
HYPERVOLAEMIA, HAEMODILUTION)
NON-PHARMACOLOGICAL METHODS HHH therapy gives short-term improvement in neu-
rological function for vasopasm following SAH.
Hypothermia Evidence of long-term benefit is scarce and there is
Moderate hypothermia (32–33°C) improves out- the potential for many complications (Table 40.4).
come in animal models by reducing: MAP is increased to a level consistent with clinical
improvement or to a systolic maximum of 140–150
1. CMRO2 mmHg for unclipped aneurysms, or 180–200 mmHg
2. Neurotransmitter synthesis, release and reuptake for secured aneurysms. This can be achieved with
3. Frequency of energy depleting ischaemic depolar- hypervolaemia with intravenous crystalloid or colloid
isations solutions to a PAWP of 16–18 mmHg, followed by
4. Free radical production the addition of inotropes or vasoconstrictors.
5. Intracranial hypertension. Haemodilution to a haematocrit of approximately
In addition there is better preservation of the blood– 30% ensures maximal O2 delivery to cerebral tissue.
brain barrier, cytoskeleton integrity and modulation
of apoptotic gene expression.
In the clinical setting, the debate over efficacy con-
KEY POINTS
tinues. The Multicentre National Hypothermia Trial • Neuroprotection aims to prevent secondary brain
has been stopped prematurely although no results injury
have been published as yet. However, Marion et al, • Individual therapy can be targeted with modern
in a large single-centred study of head injured patients imaging techniques and cerebral monitoring
demonstrated an improvement in outcome after • Guiding principles are optimal physiology aug-
hypothermia (33°C) at 3 and 6 months in a subgroup mented with pharmacological and non-pharma-
of patients with GCS 5–7.2 cological methods

Table 40.3 Novel neuroprotective mechanisms and targets

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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NEUROPROTECTION IN ICU 173


injury in the Traumatic Coma Data Bank. Acta
TABLE 40.4 Potential complications Neurochirurgica 1993; 59(suppl): 121–125
following HHH therapy 2. Marion DW, Penrod LE, Kelsey SF et al. Treatment of
traumatic brain injury with moderate hypothermia. N
Cerebral Vasogenic oedema Engl J Med 1997; 336: 540–546
Haemorrhage
Aneurysmal rupture FURTHER READING
Increased ICP
Pulmonary Oedema Menon DK, Summors AC. Neuroprotection (including
Cardiac Ischaemia/infarction hypothermia). Cur Opin Anethesiol 1998; 11: 485–496
Doyle PW, Gupta AK. Mechanisms of injury and cerebral
protection. In: Matta B, Menon DK, Turner JM (eds)
Textbook of neuroanaesthesia and critical care. Greenwich
• Success of pharmacological therapies in animal Medical Media, London 2000, pp. 35–51
models has not translated into drugs which Bracken MB, Shepard MJ, Collins WF et al. A randomized
improve outcome in clinical practice controlled trial of methyl-prednisolone or naloxone in the
• The beneficial effects of moderate hypothermia in treatment of acute spinal cord injury. N Engl J Med 1990;
acute brain injury is still under debate 322: 1405
• Methylprednisolone administered soon after spinal Eker C, Asgeirsson B, Grande PO, Schalen W, Nordstrom
cord injury is of proven benefit. CH. Improved outcome after severe head injury with a
new therapy based on principles for brain volume regula-
tion and preserved microcirculation. Crit Care Med 1998;
REFERENCES 26: 1881–1886
1. Chesnut RM, Marshall SB, Piek J et al. Early and late Doppenberg EMR, Bullock R. Clinical neuroprotection
systemic hypotension as a frequent and fundamental trials in severe traumatic brain injury: Lessons from previ-
source of cerebral ischaemia following severe brain ous studies. J Neurotrauma 1997; 14(2): 71–80
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41
INOTROPES IN
NEURO-CRITICAL CARE

R. Shankar
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176 NEUROINTENSIVE CARE

INTRODUCTION Table 41.1 Physiological effects of


Prevention of secondary brain damage is the primary dopamine infusion
aim of the intensive care management of the head
Predominant
injured patient. Many studies have demonstrated that
Dose Receptors Clinical effects
increasing CPP improves the outcome in acute brain (µg/kg/min) stimulated
injury.
Cerebral perfusion may be increased by: Up to 5 Dopamine Renal and mesenteric
vasodilatation causing
• reducing ICP hypotension
• increasing MAP Increased urine output
• increasing CBF by injection of papaverine (for
5–15 β1 Positive cardiac inotropy
vasospasm after sub-arachnoid haemorrhage) or and chronotropy
balloon angioplasty of spastic vessels
>15 α1 Peripheral
vasoconstriction
THEORIES OF HEAD INJURY
MANAGEMENT
There are two approaches to CPP management in
head injury. The first preserves a CPP of >70 mmHg Epinephrine
(controlled hypertension concept), and the other sug- Epinephrine stimulates b receptors at low doses leading
gests reducing the CPP in an attempt to prevent to tachycardia and increased cardiac index. a receptors
oedema (Lund concept). are stimulated at higher doses leading to systolic hyper-
tension, but the diastolic pressures may remain low
with the MAP remaining the same or decreasing
INDICATIONS FOR INOTROPE slightly. It is for this reason that epinephrine is not the
SUPPORT favoured inotrope to drive the MAP in the neuro-
intensive care setting. The initial infusion rate is
• Maintain CPP in the presence of a raised ICP 0.05 mg/kg/min.
• To enhance blood flow across spastic blood vessels
associated with subarachnoid haemorrhage Norepinephrine
• Manipulation of autoregulation
• Maintain cardiac output and haemodynamic Norepinephrine stimulates a receptors predomi-
support. nantly although there are some b effects. The haemo-
dynamic effects are systolic and diastolic hypertension
with an increase in MAP and possibly reflex brady-
PHARMACOLOGY cardia. The initial infusion rate is 0.05 mg/kg/min.
Although CPP is increased, the effect on CBF is still
Catecholamines undetermined as cerebral vasoconstriction may also
Dopamine, norepinephrine, epinephrine and phenyl- occur.
ephrine are the agents frequently used in the intensive
care unit. The physiological effects are due to dose- Side-effects of inotropes
dependent stimulation of DA, a and b receptors. Side- Tachyarrhythmias, hypoperfusion of organs, myo-
effects are an extension of these physiological effects. cardial ischaemic hyperglycaemia, hypophosphat-
Receptors undergo down-regulation when exposed aemia and hypocalcaemia may all be seen.
to a continuous infusion of large doses of catechol-
amines and frequent adjustments in infusion rate are
required to maintain the haemodynamic targets. CLINICAL APPLICATIONS
Dopamine Continuous monitoring of MAP, ICP, and CPP helps
to optimise CBF and improve the outcome of patients
Dopamine is a naturally occurring catecholamine,
with acute brain injury.
and a precursor of epinephrine and norepinephrine.
The haemodynamic effects and side-effects vary The arterial transducer should be zeroed to the level
according to the type of receptor stimulated, which of the foramen of Monroe. The external landmark is
in turn depends on the rate of infusion (Table 41.1). the junction between the middle and posterior thirds
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INOTROPES IN NEURO-CRITICAL CARE 177


of a line joining the lateral angle of the eye to the dilatation in an attempt to improve CBF and in turn
tragus. The difference between the MAP measured at this leads to an increased CBV and increased ICP in a
the level of the heart and the foramen of Monroe is brain with poor intracranial compliance. This cycle of
directly proportional to the height of the patient and events is represented in Figure 41.1. In such a
the degree of elevation of the head. In a critical state situation, vasopressors may be used to increase the
of reduced intracranial compliance, even a small MAP to break the cycle and reduce the ICP.
differences become clinically significant.

Maintainance of cerebral blood flow


Inotropes should be titrated to maintain a CPP of
approximately 70 mmHg. Driving the CPP over
105 mmHg increases the formation of oedema in
areas of contusion and increases the risk of myocardial
ischaemia. It is imperative to optimise intravascular
volume prior to commencement of inotropes.
In our institution, the first choice inotrope is often
dopamine with infusion rates of 2–10 mg/kg/min,
where b effects predominate. In this situation Figure 41.1 Cycle of events associated with a fall in MAP.
Reproduced with permission from Rosner et al.
dopamine is considered to have a more specific effect
on the force of contraction than on the heart rate,
although tachycardia and arrhythmias may be a prob- KEY POINTS
lem especially if the intravascular compartment is
contracted. • Inotropes are used to enhance CPP and CBF
If dopamine fails to improve the CPP, or if side- • Optimisation of intra-vascular volume prior to use
effects are problematic, an infusion of norepinephrine of inotropes is mandatory
should be commenced in an effort to maintain an • The ideal agent to improve CPP is still undeter-
adequate CPP. Floating a pulmonary artery catheter mined.
at this juncture will guide fluid management and help
assess the haemodynamic effects of norepinepherine.
FURTHER READING
Enhancement of blood flow across spastic
Rosner MJ et al. 1995 Cerebral perfusion pressure: man-
blood vessels
agement protocol and clinical results. J Neurosurgery,
Inotropes are used to increase the MAP as part of 83(6): 949–962.
HHH therapy. The aim is to increase the MAP Chestnut RM. 1998 Hyperventilation versus cerebral per-
sufficiently to reverse the neurological deficit, fusion pressure management, time to change the question.
usually with MAP ranging between 100 and [editorial; comment]. Crit Care Med 26(2): 210–212.
110 mmHg. Grande PO. 1997 Aspects on the cerebral perfusion pres-
sure during therapy of a traumatic head injury. Acta
Manipulation of autoregulation Anaesthesiol Scand Suppl 110: 36–40.
A fall in the MAP will reduce the CPP, if the ICP is Nates JL. 1997 Cerebral perfusion pressure monitoring
stable. This fall in CPP results in cerebral vaso- alert! Crit Care Med 25(5): 895–896.
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42
ELECTROLYTE DISORDERS
IN THE NEUROINTENSIVE
CARE UNIT

J. Ulatowski
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180 NEUROINTENSIVE CARE

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
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ELECTROLYTE DISORDERS IN THE NEUROINTENSIVE CARE UNIT 181


hypotonic intravenous fluids are required to maintain Hypokalaemia
sodium and vascular volume near normal. Hyper-
natraemia due to the administration of hypertonic Hypokalaemia may be due to excessive hyperventila-
fluids usually is not associated with intravascular tion, stress-induced sympathetic stimulation, or
volume depletion. Correction will usually occur diuretic therapy, and is included in the differential
slowly by administration of isotonic fluids. diagnosis of muscle weakness. Hypokalaemia may
also be associated with cardiac conduction and
Hyponatraemia rhythm abnormalities which may be potentiated by
the administration of digoxin. Treatment requires an
Hyponatraemia can be caused by a relative increased
evaluation of the chronicity of hypokalaemia.
retention of water, or as a result of relative loss of
Chronic hypokalemia should be reversed slowly
sodium. Long-term anticonvulsant intake (e.g. carba-
using the enteral route if possible. Intravenous
mazepine) should also be considered. Cerebral salt
therapy is frequently required for patients at risk of
wasting is a syndrome commonly associated with
cardiovascular complications.
neurological disease where natriuretic compounds
secreted from the atria of the heart, and possibly the
periventricular organs in the brain, are responsible for Calcium
inducing sodium loss in the kidney. Hyponatraemia Calcium is essential for nerve and muscle excitability
seen in these conditions may be potentiated by an and contractility, and derangements in calcium con-
appropriate ADH secretion in an attempt to com- centrations are rare in the neurologic intensive care
pensate for hypovolaemia. Treatment of hypo- unit. A more common finding of hypocalcemia in
natraemia in the face of hypovolaemia is by repletion the intensive care patient occurs with extensive blood
with isotonic or hypertonic solutions depending on transfusions.
severity (≤ 125 mmol/L). Rapid correction of hypo-
natraemia (> 3 mmol/h) may result in a demyelinat-
ing state called central pontine myelinolysis. Magnesium

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
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182 NEUROINTENSIVE CARE

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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184 NEUROINTENSIVE CARE

INTRODUCTION ISOTONIC FLUIDS


The goal of initial fluid therapy in a patient with neu- Normal saline is isotonic with an osmolarity of 308
rologic injury is to restore intravascular volume, opti- mosm/l and is a useful crystalloid for volume expan-
mise haemodynamic parameters and maintain tissue sion. The overall efficacy of normal saline as a resus-
perfusion, integrity and function. The selection of citative fluid is well established but it requires four
fluids for resuscitation in patients who have decreased times the volume of blood lost to restore haemody-
intracranial compliance requires an understanding of namic parameters. Since it is isotonic it has a negligi-
the relationship between intravenous fluids, brain ble effect on brain water and in large quantities it may
water and ICP. cause a brief rise in brain volume secondary to the
increase in intravascular volume.
PATHOPHYSIOLOGY Gelatins are modified collagen derivatives with a mol-
ecular weight of approximately 35,000 Da. Modified
Cerebral autoregulation and the BBB are two protective fluid gelatin (Gelofusine®) is a 4% solution in normal
mechanisms that may be affected in a patient with saline whereas urea-bridged gelatin is a 3.5% solution
neurologic injury. in normal saline (Haemaccel®). Both are effective
The influence of Cerebral autoregulation on cerebral plasma volume expanders with an intravascular half-
blood flow and oxygen delivery is discussed in life of 2–3 hours. The low molecular weight leads to
Chapter 5. rapid renal elimination. The most significant toxicity
is anaphylactoid reactions. Depression of fibri-
The BBB is composed of brain endothelial cells with nonectin levels and dilutional coagulopathy is possi-
tight junctions creating an effective pore size of ble with the administration of large volumes but no
0.7–0.9 nm.These tight junctions are permeable only independent defect in haemostasis is noted.
to water, hence an osmotic gradient is produced by
small molecules and ions. Thus even small increases Hydroxyethyl starch solutions contain particles of vari-
in the concentrations of plasma electrolytes can exert ous molecular weights and degrees of hydroxyethyl
a large osmotic pressure gradient across the BBB and substitution, resulting in extremely heterogenous
redistribute water to the intravascular space. mixtures. Clinically it is available as a 6% solution in
Normally changes in oncotic pressure do not normal saline. It has an average molecular weight of
significantly influence the osmotic pressures in the 69,000 Da. The oncotic pressure of the solution is
brain. However, if the BBB is damaged it becomes 30 mmHg and it has an osmolarity of 310 mosm/l.
permeable to a variety of molecules and hydrostatic The kinetics of the entire infusion are complex, with
pressure then becomes important in determining 90% of the infusion eliminated in 42 days although
brain water content. the effective plasma volume expander effects last for
3–24 hours. Tissues such as the liver, spleen and the
reticuloendothelial system retain molecules which do
PHARMACOLOGY not appear to be detrimental to organ function. The
The osmotic properties of intravenous fluids are product insert recommends a dose limit of 1500 ml or
important in determining their efficacy and safety for 20 ml/kg/day. However, in cerebrovascular disease
use in the presence of neurologic injury. (Table 43.1). the dose should be restricted to 500 ml because of the
risk of intracranial bleeding.

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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FLUID MANAGEMENT 185


dehydration and central pontine myelinosis due to ANF increases renal sodium excretion thereby caus-
rapid changes in serum sodium levels are possible. ing a decrease in plasma volume. Cerebral salt wast-
Recommendations for the use of hypertonic saline are ing syndrome is characterised by hyponatremia,
close monitoring of serum sodium levels (less than 160 hypovolemia, and a urine sodium > 50 mmol/l. The
meq/l) and serum osmolarity (less than 350 mosm/l). management involves rapid restoration of the blood
volume and the recommended fluid for resuscitation
is 0.9% saline.
HYPOTONIC FLUIDS
Dextrose (5%) was traditionally given perioperatively in
SIADH
an effort to prevent hypoglycaemia and to limit protein
catabolism. However, surgical and traumatic stress The syndrome of inappropriate antidiuretic hor-
normally stimulates gluconeogenesis. Only infants and mone secretion (SIADH) often is associated with
patients receiving insulin or drugs that interfere with ectopic neoplastic ADH secretion or excessive
glucose synthesis are at a significant risk of hypogly- hypothalamic-pituitary release of ADH secondary to
caemia. Glucose infusions are known to produce hyper- neurologic pathologic states, pain, surgery or neu-
glycaemia in neurosurgical patients even in moderate roendocrine abnormalities. It is characterised by a
doses. In humans, hyperglycaemia is associated with urinary sodium of > 20 mmol/l, hyponatremia,
worse outcomes in both ischaemic and traumatic brain hypervolemia and hyposmolarity. It is managed by
injury. The dextrose in water is quickly metabolised, free water restriction sufficient to reduce total body
leaving free water. These hypotonic solutions thus water by 0.5–1.0 l/day. The resultant reduction in
increase brain water due to the osmotic gradient. glomerular filtration rate enhances proximal tubular
reabsorption of salt and water and stimulates aldos-
terone secretion. Demeclocycline (a tetracycline) or
lithium antagonise the renal actions of ADH in
FLUID MANAGEMENT
refractory cases of SIADH. Neurological symptoms
with profound hyponatremia (serum Na+ < 115–120
FLUID RESUSCITATION
meq/l) requires aggressive therapy. Three per cent
Neurosurgical procedures and isolated HI are associ- saline is indicated in patients who have seizures or
ated with minimal losses of extracellular fluid, although who develop signs of water intoxication. Three per
associated injuries may necessitate aggressive fluid cent saline at a rate of 1–2 ml/kg/h to increase
replacement. Surgical and traumatic losses in patients serum Na+ by 1–2 meq/l/h can be used and should
at risk for intracranial hypertension can be replaced be monitored every 1–2 hours to avoid over-correc-
with 0.9% saline or colloid. Substantial or chronic loss tion.
of gastrointestinal fluids requires replacement of other
electrolytes (i.e. potassium, magnesium, phosphate).
Diabetes Insipidus
Replacement of fluid losses also must compensate for
sequestration of interstitial fluid that accompanies This is common following pituitary and hypothala-
trauma, haemorrhage and tissue manipulation. Based mic lesions and can also occur with other cerebral
on estimates of fluid sequestration associated with pathology such as head trauma and intracranial
extensive tissue manipulation, simple guidelines have surgery. It is characterised by polyuria, dehydration,
been developed for replacement of third space losses. hypernatremia, a low urinary sodium and a low
The simplest formula provides, in addition to mainte- urine specific gravity. It is managed according to
nance fluids and replacement of estimated blood loss, whether its aetiology is central or nephrogenic.
4 ml/kg/h for procedures involving minimal trauma, Central diabetes insipidus requires exogenous
6 ml/kg/h for those involving moderate trauma and replacement of ADH with either desmopressin
8–15 ml/kg/h for those involving severe trauma. (DDAVP) or aqueous vasopressin. DDAVP may be
given subcutaneously in a dose of 1–4 µg every
12–24 hours or intra-nasally in a dose five times
COMMONLY ENCOUNTERED FLUID
larger. Incomplete ADH deficits (partial diabetes
ABNORMALITIES IN NEUROINTENSIVE
insipidus) are effectively managed with chlor-
CARE
propamide 250–750 mg/day, clofibrate, 250–500
mg/6–8 hours or carbamazepine, 400–1000 mg/day.
Cerebral Salt Wasting Syndrome
Nephrogenic diabetes insipidus is managed by
This is caused by the release of atrial natriuretic factor restricting sodium and water intake and hydro-
(ANF) in response to SAH or areas of cerebral injury. chlorothiazide, 50–100 mg/day.
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186 NEUROINTENSIVE CARE

KEY POINTS FURTHER READING


• Early detection and correction of fluid abnormali- Sutin KM, Ruskin KJ, Kaufman BS. Intravenous fluid ther-
ties helps in minimising cerebral oedema. apy in neurologic injury. Crit Care Clin 1992; 8 (2): 367–408
• Osmotic gradients occur across the BBB. Tommassino C, Moore S, Todd MM. Cerebral effects of
• Isotonic solutions (crystalloid and colloids) are isovolemic hemodilution with crystalloid or colloid solu-
good resuscitation fluids. A greater volume of tions. Crit Care Med 1988; 16: 862
crystalloid is required due to redistribution. Damon L, Adams M, Sticker RB. Intracranial bleeding
• Hypertonic saline is useful in reducing cerebral during treatment with hyroxyethyl starch. N England J
oedema and ICP after brain injury. Med 1987; 317: 964
• Avoid glucose containing fluids except in hypo- Longstreth WT, Inui TS. High blood glucose level on hos-
glycaemia. pital admission and poor neurological recovery after cardiac
• Do not fluid restrict unless the patient is fluid arrest. Ann Neurol 1984; 15: 59–63
overloaded or has SIADH. Campbell IT, Baxter JN, et al. IV fluids during surgery. Br
J Anaes 1990; 65: 726
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44
SEDATION

J. Monteiro
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188 NEUROINTENSIVE CARE

INTRODUCTION SEDATIVES AND ANXIOLYTICS


Sedation in neurointensive care is used to minimise Midazolam is a water-soluble, non-analgesic benzo-
cerebral metabolic demands following injury to diazepine giving peak sedation within 5–10 minutes.
balance the effects of large amounts of circulating cat- The duration of sedative effect ranges from 3 to 120
echolamines, and to help control intracranial hyper- minutes and the elimination half-life is 2–4 hours.
tension. The actual level of sedation required varies The active metabolite 1-hydroxymidazolam is
enormously. Patients recovering from uneventful 60–80% as potent as the parent drug and undergoes
craniotomy require less sedation and analgesia than renal elimination with a half-life of 1 hour. Reports
those with multiple trauma and refractory intracranial of prolonged sedation with midazolam are related to
hypertension. Indications for sedation are shown in the pharmacokinetics, which are markedly altered in
Table 44.1. critically ill patients.
Propofol shows a linear relationship between infusion
PHARMACOLOGY rate and steady-state blood concentration allowing
easy titration in the intensive care setting. It can be
The pharmacodynamic effects of sedative medica- safely used in patients with altered intracranial compli-
tions are influenced by the complexity of critical ill- ance. Infusion at a rate of 2–4 mg/kg/h in severe HI
ness. Combinations of analgesic, sedating and provides satisfactory sedation without changes in
tranquillising agents help to individualise patient-spe- CPP. Serum lipid levels may increase following pro-
cific therapy. Short-acting drugs are commonly used longed infusion due to the formulation in oil emulsion
either intermittently or more usually, as a continuous and altered lipid clearance in critical illness. Serum
infusion (Table 44.2). triglyceride levels should be monitored and parenteral
nutrition supplements adjusted accordingly. Care
A N A L G E S I C S (see Chapter 10) must be taken with induced hypothermia, which
further reduces lipase activity and hepatic clearance.
Morphine is sometimes used as the sole agent or in
combination with neuromuscular blocking drugs, Propofol is usually preferred to midazolam if a short
particularly in the USA. Its analgesic properties last period of sedation is anticipated or fast reversal of
for 2–4 hours as a bolus and there is an associated sedation is planned (e.g. neurological reassessment,
sedative effect. It is metabolised to morphine-6- weaning from ventilation, performance of brainstem
glucuronide, an active compound, which accumu- death criteria).
lates in renal failure. Shorter-acting agents (e.g.
fentanyl, alfentanil) should be used in renal dys-
function. Fentanyl has no active metabolites but Table 44.2 Drug dosages for intravenous
sedation
significant amounts may accumulate with prolonged
administration as elimination half-life depends on Bolus Infusion
the duration of continuous infusion. The residual
sedative and respiratory depressant effects of long- Morphine 0.1–0.2 mg/kg 0.05–0.07 mg/kg/h
term fentanyl infusions may also last well beyond Fentanyl 2–5 µg/kg 1–10 µg/kg/h
any analgesic effects. Remifentanil may be useful Alfentanil 10–25 µg/kg 10–50 µg/kg/h
but is expensive and unlicensed for intensive care Midazolam 0.2–1 mg/kg 20–200 µg/kg/h
use. Propofol 1–2 mg/kg 2–10 mg/kg/h

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

MONITORING LEVEL OF SEDATION • Combinations of sedatives and analgesics are com-


monly used.
Sedation scales have been described that are easy to • Neuromuscular paralysis is frequently used if ICP
use but they cannot discriminate between subtle is elevated.
changes in the level of sedation or distinguish differ- • Causes of agitation need to be identified and
ent levels from abnormal mental states. No satisfac- treated prior to sedation.
tory objective clinical measure of sedation exists and • No satisfactory objective clinical measure of seda-
therapy is usually guided by intermittent clinical tion exists.
assessment. Use of sedation scales is precluded when
neuromuscular blocking agents are administered.
Non-pharmacological methods should also be consid- FURTHER READING
ered to provide relief from the stressful intensive care
environment. Efforts to reduce noise and lighting, Butterworth JB, DeWitt DS. Severe head trauma: patho-
good communication and education, restoration of physiology and management. Crit Care Clin 1989; 5: 807
privacy, a flexible visiting policy, and reinstitution of Aitkenhead AR, Pepperman ML, Willatts SM, et al.
patient control may provide relief from anxiety. Comparison of propofol and midazolam for sedation in
Treatable causes of agitation and confusion such as critically ill patients. Lancet 1989; 2: 704
hypoxia, hypercarbia, hypoglycaemia, electrolyte dis- Farling PA, Johnston JR, Coppel DL. Propofol infusion for
orders, drug or alcohol withdrawal, pain, sleep depri- sedation of patients with head injury in intensive care: a
vation, organic psychosis, meningitis or other systemic preliminary report. Anaesthesiology 1989; 44: 222
infections, and ischaemic or thrombotic cerebrovascu- Hansen-Flaschen J, Cowan J, Polomano R. Beyond the
lar events should be investigated before sedation is ini- Ramsay scale: need for a validated measure of sedating drug
tiated or increased to treat anxiety or combativeness. efficiency in the intensive care unit. Crit Care Med 1994;
22: 732
Park GR, Sladen RN (eds). Sedation and analgesia in the
KEY POINTS critically ill. Oxford: Blackwell Science, 1995
• Sedation aims to optimise cerebral perfusion and Wheeler A. Sedation, analgesia and paralysis in the inten-
oxygenation. sive care unit. Chest 1993; 104: 566–577
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45
COAGULATION DISORDERS

P. Doyle
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192 NEUROINTENSIVE CARE

INTRODUCTION factors rather than microthrombosis the primary


pathologic event.
Haemostasis is a continual dynamic equilibrium
between the clotting cascade and the fibrinolytic
system, the vascular endothelium and adequately MANAGEMENT
functioning platelets. It is imperative to correct any
coagulation abnormalities early to minimise mass Prothrombin time, activated partial thromboplastin
effects of intracranial bleeding and haematoma forma- time, platelet count, fibrinogen and D-dimer levels
tion. test routine coagulation disorders. If time allows, a
number of further tests may be employed to specifi-
cally look for abnormal bleeding profiles including
specific clotting assays (e.g. clotting factor levels,
PATHOPHYSIOLOGY antithrombin, plasminogen, protein C and complexes
A number of transient but normal physiological of thrombin-antithrombin and plasmin-antiplasmin).
responses may occur during elective neurosurgery Pre-existing coagulation defects, haemorrhage from
(Table 45.1). other injuries and hypothermia need urgent atten-
tion. There is a significant prolongation in clotting
Table 45.1 Normal haemostatic response time for every degree decrease in temperature.
to brain injury Clinical bleeding may be observed in the hypother-
mic patient in the presence of normal laboratory val-
Haemostatic Response Mechanisms ues performed at 37°C – an important point to
(via increased levels of:) remember when induced hypothermia is used as a
neuroprotective strategy.
Activation of Thrombin; antithrombin
coagulation More extensive brain injury is associated with greater
disruption of the coagulation/fibrinolytic system.
Activation of Plasmin-antiplasmin; Checks on clotting status should be performed early
fibrinolysis d-Dimers
and regularly. Abnormalities should be corrected with
Activation of platelets β-thromboglobulin; transfusions of fresh frozen plasma, cryoprecipitate and
platelet-factor-4 platelets as indicated. If a screen for DIC has elevated
Acute phase response Fibrinogen; α2-antiplasmin D-dimer levels and minimal other abnormalities, the
activity tests should be repeated within two hours to ascertain
progress and the advice of a haematologist sought.
The following events may accompany and influence
the above processes including thrombocytopaenia, KEY POINTS
platelet dysfunction, haemodilution, ongoing haem-
• Brain tissue levels of thromboplastin are high and
orrhage, hypocalcaemia, acidosis and hypothermia.
are potent stimulants of the coagulation cascade,
Following brain injury, the magnitude of intravascu- fibrinolytic system and platelet activation.
lar coagulation is proportional to the amount of • Severe brain injury and intracranial haemorrhage
intracranial blood and injured brain tissue. The fol- activates these pathways more than lesser injuries.
lowing hypotheses may play a role: • Coagulopathy is a risk factor for adverse outcome
in brain injured patients.
1. Damaged brain tissue contains large amounts of
• Perform early assessment and correction of clot-
tissue thromboplastin, which enters the circula-
ting abnormalities.
tion and activates the coagulation pathway.
2. Dissolving clot in the subarachnoid space also
enters the circulation with CSF and activates the RECOMMENDED READING
coagulation system. Fujii Y, Takeuchi S et al. 1995 Hemostasis in spontaneous
3. Rapid rises in intracranial pressure or severe subarachnoid hemorrhage. Neurosurgery 37(2), 226–234.
meningeal stimulation may induce systemic acti- Hulke F, Mullins RJ, Frank EH. 1996 Blunt brain injury acti-
vation of haemostatic systems through unknown vates the coagulation process. Archives of Surgery 131: 923–928.
neurogenic and/or humoral mechanisms.
Levine SR, Tietjen GE, Dafer R, Feldman E. 1999 Hemato-
Fibrinolytic activity matches fibrin generation and clot logic abnormalities and stroke. In: Ginsberg MD,
is rapidly cleared, making consumption of clotting Bogousalavsky J, eds. Cerebrovascular Disease. Pathophysiology,
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COAGULATION DISORDERS 193


diagnosis and management. Mass. USA: Blackwell Science, pp. Rohrer MJ, Natale AM. 1992 Effect of hypothermia on the
1698–1726. coagulation cascade. Critical Care Medicine 20, 1402-1405.
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46
STATUS EPILEPTICUS

N. Hirsch
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196 NEUROINTENSIVE CARE

DEFINITION AND INCIDENCE Phase 2 is characterised by a failure of cerebral


autoregulation, a rise in ICP and hypotension result-
Generalised convulsive status epilepticus (GCSE), the ing in decreased cerebral perfusion. Hypoxaemia
most common form of status epilepticus, may be occurs due to decreased central respiratory drive, pul-
defined as a condition in which continuous or rapidly monary hypertension and oedema, cardiac failure and
repeating tonic-clonic seizures persist for 30 minutes the increased oxygen demand. At this stage, oxygen
or more. Its incidence is approximately 25 per delivery cannot keep pace with demand, and electro-
100,000 of the population and it is estimated that mechanical dissociation may occur, in which
9–14,000 cases occur annually in the UK. In about although electrical cerebral seizure activity continues,
one-third of cases, GCSE is the first presentation of its clinical manifestations may be restricted to minor
epilepsy. twitching. The longer the attack lasts the less respon-
Overall mortality of adult GCSE is approximately sive it becomes to therapy and the greater the chance
20%. of permanent brain damage, especially to limbic
structures such as the hippocampus. This damage is
further compounded by the systemic complications
AETIOLOGY described above.
The aetiology of adult GCSE may be conveniently Other complications include acute tubular necrosis,
divided into acute and chronic processes (see Table rhabdomyolysis, hypoglycaemia, lactic acidosis, multi-
46.1). organ failure and disseminated intravascular coagu-
lation.
CLINICAL FEATURES
During the initial stages of GCSE, the diagnosis is MANAGEMENT
apparent, with tonic and clonic movements of the Morbidity and mortality of GCSE is directly related
limbs in an unresponsive, often incontinent patient. to the duration of the seizures and therefore manage-
However, in the later stages the movements often ment should be rapid and effective. It is conveniently
become subtle with only minor twitching of the face, divided into general management and drug therapy.
eyelids, hands or feet. It is vital to recognise this stage
as treatment must be rapid to avoid permanent cere-
bral damage (see below).
GENERAL MANAGEMENT
PATHOPHYSIOLOGY Assessment of cardiopulmonary function should be carried
out immediately and oxygen administered. Tracheal
The physiological derangement that occurs in GCSE
intubation is necessary if the airway is compromised
is often divided into two phases, the second occurring
or hypoxaemia continues despite administration of
after approximately 30 minutes of seizure activity.
oxygen by mask. If intubation is necessary, a short-
During Phase I, the increased cerebral metabolic acting neuromuscular blocking agent (e.g.
demand is satisfied by an increase in CBF and an atracurium) should be used so that the ability to
increase in autonomic activity resulting in increased detect clinical seizures is rapidly regained.
arterial blood pressure, increased blood glucose levels, Intravenous access should be established and a blood
sweating, hyperpyrexia and salivation. glucose assay performed. 50 ml of 50% glucose should

Table 46.1 Aetiology of generalised convulsive status epilepticus in adults

Acute processes Chronic processes

• Electrolyte imbalance (e.g. Na+, Ca++ etc.) • Pre-existing epilepsy


• Renal failure • Poor compliance – low anticonvulsant drug levels
• Sepsis syndrome • Chronic alcoholism
• Head injury • Cerebral tumours or other space occupying lesions
• Cerebrovascular accident
• Drug toxicity (e.g. cocaine, alcohol abuse)
• CNS infection – encephalitis, meningitis
• Hypoxic brain injury
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STATUS EPILEPTICUS 197


be given if this is low. Any suggestion of malnutrition diazepam result in a decreased volume of distribution
or chronic alcoholism should be treated with thiamine and clearance leading to accumulation and cardiores-
(100 mg) to avoid precipitating Wernicke’s piratory depression. Only two doses should be used
encephalopathy. before lorazepam is given.
Following resuscitation, regular monitoring of car- If seizures continue despite this therapy, the stage of
diorespiratory function, neurological observations established status has been reached. Phenytoin and/or
and temperature should be instituted. Anticonvulsant phenobarbitone are the drugs of choice at this stage.
therapy (see below) should be commenced. They must be given in appropriate doses, underdos-
ing being a major factor in failure to control status.
Acidosis is often profound in patients with GCSE but
More recently fosphenytoin, a water-soluble prodrug
usually corrects itself following resuscitation. However,
of phenytoin has been introduced and appears to have
intravenous bicarbonate may be necessary. Hyperthermia
a lower incidence of hypotension than its parent
reflects increased muscle activity and may worsen neu-
drug.
ronal damage; passive cooling and rectal paracetamol
may be used if the increased temperature persists. If seizures persist despite therapeutic levels of pheny-
toin and phenobarbitone, the stage of refractory status
Once emergency treatment has been carried out, a
has been reached. At this stage, patients require trans-
detailed history (usually from relatives) and examination
fer to a specialist neurointensive care unit where con-
is performed and this often gives a clue to the aetiol-
tinuous EEG can be provided. Refractory status
ogy (e.g. previous epilepsy, co-existing medical con-
requires anaesthesia; traditionally this has been pro-
dition, drug abuse etc.). Haematological and biochemical
vided by thiopentone or pentobarbitone but the saturable
studies should be performed as well as anticonvulsant
kinetics of the barbiturates make regular clinical
drug levels and a toxicology screen if indicated.
assessment difficult. Propofol is emerging as the drug of
Other systemic complications of GCSE described choice in these patients.
above should be treated in the standard manner.

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.

Table 46.2 Suggested drug treatment of status epilepticus

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
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198 NEUROINTENSIVE CARE

• 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
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200 NEUROINTENSIVE CARE

INTRODUCTION CLINICAL FEATURES AND DIAGNOSIS


Guillain–Barré syndrome (GBS), is an acute inflam- GBS is an acute neuropathic weakness of more than
matory neuropathy characterised by a progressive one limb, areflexia and a duration of progression of
neuropathic weakness and areflexia and is the com- fewer than 4 weeks. By convention, disease progress-
monest cause of neuromuscular paralysis seen in the ing for longer periods is termed chronic inflammatory
Western world. Approximately one-third of patients demyelinating polyneuropathy.
with GBS will develop respiratory failure which may Criteria necessary for diagnosis may be divided into
be protracted, and therefore patients may occupy essential and supportive criteria (Table 47.1). Differ-
intensive care beds for considerable periods. ential diagnosis is found in Table 47.2.
The incidence of GBS lies between 1–2 per 100,000
of the population. A history of a preceding infection, Neurological features
usually of the upper respiratory or gastrointestinal GBS usually presents with pain (especially of the back
tract, is found in at least 75% of cases. Bacterial and and sides), mild sensory symptoms (e.g. glove and
viral triggering agents that have been implicated stocking parathesiae) and relatively symmetrical
include Campylobacter jejuni, Mycoplasma pneumoniae, weakness. The latter often starts in the legs before
Epstein–Barr virus, human immunodeficiency virus and affecting the arms (hence ‘ascending polyneuropa-
cytomegalovirus. The use of specific vaccinations (e.g. thy’) and is more pronounced proximally. Cranial
swine flu vaccine and older preparations of rabies nerves (especially the facial nerve and bulbar nerves)
vaccine) has also been associated with outbreaks of are frequently affected.
GBS.
The Miller–Fisher syndrome has been classified as a
variant of GBS and is characterised by ataxia, oph-
PATHOPHYSIOLOGY thalmoplegia and areflexia. It is usually associated
The association of GBS with preceding infection sug- with anti GQ1b antibodies and often has little in the
gests an immune basis for the inflammatory demyeli- way of limb weakness.
nation of peripheral nerves. Animal models of the
condition suggest a cell-mediated process, but the Respiratory features
presence of a large variety of complement-fixing Respiratory muscle weakness requiring positive pres-
antibodies found in patients with GBS correlates with sure ventilation occurs in 25–30% of patients. Bulbar
the degree of demyelination seen; furthermore, weakness predisposing to pulmonary aspiration
recovery is associated with a fall in antibody levels. occurs in a similar proportion and may require tra-
More recently, an association between an anti- cheal intubation for airway protection.
ganglioside antibody (GM1) and C. jejuni infection
suggests that antibodies raised to this infecting agent Autonomic dysfunction
may cross-react with the ganglioside of host neural Sinus tachycardia is the most common manifestation
tissue. of autonomic dysfunction and occurs in 75% of

Table 47.1 Diagnostic criteria for Guillain–Barré syndrome

Essential criteria Supportive criteria

● Progressive weakness of more than one Clinical features


● limb due to neuropathy ● Weakness usually progressive
● Areflexia ● Sensory signs mild
● Duration of progression less than four weeks ● Cranial nerve involvement common
● Autonomic dysfunction common
Laboratory features
● CSF – total protein increased after first week
(in 80%)
● White cell count normal (in 90%)
● EMG – nerve conduction slowed suggesting
demyelination
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GUILLAIN–BARRÉ SYNDROME 201


patients should be treated with graduated elastic
Table 47.2 Differential diagnosis of stockings and prophylactic subcutaneous heparin.
Guillain–Barré syndrome
Pain occurs in up to 70% of patients with GBS and is
● Acute myasthenia gravis often very distressing, especially at night. Although
● Botulism simple analgesics such as aspirin or paracetamol may
● Acute intermittent porphyria be effective, patients intermittently require stronger
● Lead and organophosphate poisoning analgesia. Meptazinol is a useful agent, providing
● Poliomyelitis good analgesia without the troublesome constipating
● Polymyositis
effects of other opioids. In addition, neurogenic pain
● Transverse myelitis
● Shellfish poisoning is often helped by carbamazepine or amitriptyline.

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
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202 NEUROINTENSIVE CARE

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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204 NEUROINTENSIVE CARE

INTRODUCTION • Tracheal/laryngeal damage.


• Surgical emphysema.
Tracheostomy is one of the oldest recorded surgical • Ventilator disconnection.
procedures and was practised by the ancient • Hypoxia.
Egyptians. Although the indications for tracheostomy
have not changed (see below), the introduction of Delayed complications
dilatational percutaneous tracheostomies in the 1980s
has seen a rapid expansion in their use. Some 12–15% • Tracheostomy tube obstruction.
of ICU patients now undergo tracheostomy. This has • Infection.
an effect on ward care after ICU discharge where • Erosion into tracheal cartilages, oesophagus or
fewer than 50% of nurses in a study were found to blood vessels.
have confidence in detecting and managing a blocked
tracheostomy tube and even fewer had received any Late complications
formal training in managing patients with a tra- • Post-extubation tracheal stenosis.
cheostomy. • Persistent fistula.
• Tracheomalacia.
INDICATIONS FOR TRACHEOSTOMY
PERCUTANEOUS TRACHEOSTOMY
• Prolonged ICU ventilation.
• Prolonged tracheo-bronchial toilet. Little interest was shown in percutaneous tra-
• Protection of airway and lungs with depressed cheostomy when described by Sheldon in 1957.
consciousness and laryngeal reflexes. However, since the description of a Seldinger wire
• Acute airway obstruction. technique for percutaneous dilatational tracheostomy
• Integral part of a surgical procedure such as laryn- by Pascale Ciaglia in 1985, it has rapidly gained
gectomy. acceptance and may be considered the technique of
choice for many ICU patients.
ADVANTAGES OF TRACHEOSTOMY The nature and incidence of perioperative complica-
tions and infection has been found to be similar to or
Tracheostomy has been established as the airway of better than those associated with surgical tra-
choice where either prolonged mechanical ventila- cheostomy. A number of authors believe that direct
tion or airway protection is required in the ICU. visualisation of the procedure by an assistant with a
Sedation and analgesia are rarely needed once a tra- fibreoptic bronchoscope may reduce complications
cheostomy is in place allowing more rapid and con- still further. More recently, ultrasound-guided inser-
trolled weaning, easier access to airway secretions and tion has been described which is useful in patients
a potentially shorter ICU stay. with landmarks that are difficult to palpate or visual-
The ideal timing of tracheostomy in patients with ise. Particular care should be taken during trache-
neurological deficit has yet to be established. Patients ostomy to avoid hypoventilation with hypercarbia as
requiring continued ventilation and/or airway pro- well as hypoxia in the patient with neurological
tection after 7–10 days of translaryngeal intubation injury and non-compliant ICP. The incidence of late
should be considered for tracheostomy unless suc- tracheal stenosis is difficult to quantify since patients
cessful extubation is considered imminent. Important may be asymptomatic with greater than 50% narrow-
influences on this decision are the degree of continu- ing of the trachea and stridor may not occur until tra-
ing neurological deficit (GCS < 8), the presence of cheal diameter is less than 5 mm.
respiratory infection and the nature and amount of Percutaneous dilatational tracheostomy is a bedside
secretions. procedure that can be carried out on any ICU with-
out the need to transfer patients to the operating the-
atre. This removes the risks of transferring critically ill
COMPLICATIONS OF TRACHEOSTOMY
patients, frees theatre time and staff and allows tra-
cheostomy to occur more rapidly once the decision
Immediate procedural complications
has been made. Timpson et al1 have found a doubling
• Haemorrhage. of the incidence of tracheostomy since the introduc-
• Pneumothorax. tion of percutaneous techniques in one ICU, coupled
• Malposition of tracheostomy tube in peritracheal with a very large decrease in the number of surgical
tissues. tracheostomies performed.
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TRACHEOSTOMY 205

DECANNULATION OF FURTHER READING


TRACHEOSTOMY Hatfield A, Bodenham A. Portable ultrasonic scanning of
The initial cuffed tracheostomy tube should be replaced the anterior neck before percutaneous dilatational tra-
with an uncuffed and subsequently fenestrated (speak- cheostomy. Anaesthesia 1999; 54: 660–663
ing) tracheostomy tube as a part of weaning prior to Holdgaard HO, Pederson J, Jensen RH, et al. Percutaneous
decannulation of the tracheostomy. The tracheostomy dilational tracheostomy versus conventional surgical
site rarely needs more than an occlusive dressing. tracheostomy. Acta Anaethes Scand 1998; 42: 545–550
Plummer AL, Gracey DR. Consensus conference on artifi-
cial airways in patients receiving mechanical ventilation.
KEY POINTS Chest 1989; 96: 712–713
• Tracheostomy is useful for prolonged ICU venti-
lation and tracheo-bronchial toilet.
• It may hasten the weaning process. REFERENCE
• Tracheostomy can be performed surgically or per- 1. Timpson TP, Day CJE, Jewkes CF, Manara AR. The
cutaneously by the bedside. impact of percutaneous tracheostomy on intensive care
• Tracheostomy should be considered after 7–10 unit practice and training. Anaesthesia 1999; 54:
days of ventilation. 186–189
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49
BRAINSTEM DEATH

Q. Milner
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208 NEUROINTENSIVE CARE

INTRODUCTION after an interval of at least 30 minutes. The time of


death is noted at completion of the first set of tests:
The development of artificial ventilation in the 1950s
has enabled cardiopulmonary function to be main- Pupillary Reflexes
tained in apnoeic patients with severe intracranial
pathology who would otherwise have died. This has Pupillary response to bright light should be absent in
changed our understanding of the nature of death and both eyes. This tests afferent pathways of the optic
we now define it as ‘the irreversible loss of the capac- nerve (CN II) and efferent pathways of the oculomo-
ity for consciousness, combined with the irreversible tor nerve (CN III). Pupil size is irrelevant and normal
loss of the capacity to breathe’. doses of atropine have no effect on this reflex.
As the brainstem maintains consciousness, the Corneal reflex
sleep–wake cycle and ventilation, death of the brain-
stem is equivalent to death of the entire brain. Asystole Corneal reflexes should be tested with cotton wool in
follows brainstem death without exception and may the lateral part of the cornea. (CN V and VII).
occur within minutes or rarely up to a few weeks after.
Facial sensation and motor responses
The diagnosis of brainstem death allows humanitar-
ian, ethical and economic management of critical care Firm pressure on the supra-orbital ridge should elicit
resources and may allow the optimisation of organs no facial responses (CN V and VII). Spinal cord
for transplantation. reflexes may persist in brainstem death.

Oculocephalic reflex (Doll’s eye movement)


KEY FEATURES This test should not be carried out in the presence of
Brainstem death may only be diagnosed in patients cervical spine fracture. Rapid lateral movement of the
with apnoeic coma resulting from known irreversible head normally results in eye deviation to the contra-
intracranial pathology. This is most frequently seen lateral side, testing brainstem gaze mechanisms. In
in: brainstem death the eyes remain in a fixed position
within the orbit.
• Severe head injury.
• Intracranial haemorrhage. Caloric testing
• Cerebral oedema with brainstem herniation.
• Hypoxic-ischaemic encephalopathy. This tests vestibular reflexes in CN VIII. Both ears
are irrigated with 20–30 ml ice cold water after
A number of exclusions must be satisfied before the inspection of the intact drum. Nystagmus to the stim-
diagnosis of brainstem death may be made including ulated side is absent in brainstem death.
the absence of:
• Depressant drugs which may cause unconscious- Gag and cough reflexes
ness. The gag and cough reflexes are absent in response to
• Hypothermia (< 35ºC). a pharyngeal and tracheal stimulus (CN IX and X).
• Severe hypotension.
• Gross endocrine, biochemical and metabolic Apnoea testing
abnormality.
• Abnormal PaCO2. Normocapnoea should be achieved and the patient
ventilated with 100% oxygen for 3 minutes prior to
disconnection from the ventilator. Apnoeic oxygena-
DIAGNOSTIC TESTS TO CONFIRM tion is achieved by placing a catheter with oxygen
BRAINSTEM DEATH flowing at 4 l/min in the trachea. The patient is
inspected for signs of respiration for 10 minutes or
In the UK, two doctors carry out the brainstem
until arterial blood gases confirm that the PaCO2
death tests according to a strict protocol. One doctor
exceeds 6.5 kPa. Significant hypotension and hypox-
must be a consultant and the other must be qualified for
aemia (SaO2 < 90%) should be avoided.
at least 5 years. If organs are to be transplanted, neither
doctor may be a member of the transplant team. The
Further tests
tests should be carried out more than 6 hours after the
events leading to brainstem death. UK law requires The above tests are sufficient for the diagnosis of
only one set of tests but it is common to repeat the tests brainstem death in the UK and USA. Some other
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BRAINSTEM DEATH 209


countries require confirmatory tests such as EEG, donation is planned, the focus of patient care should
transcranial Doppler ultrasonography and angio- be redirected to optimising organ function prior to
graphy, but there is no evidence that these tests con- transplantation (see Chapter 64).
tribute to the diagnosis.

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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212 NEUROINTENSIVE CARE

INTRODUCTION nutrients. Neither bowel sounds nor flatus are


required for successful enteral feeding.
The provision of adequate nutritional support is an
essential component of caring for the critically ill Enteral feeding should be started if gastric aspirates
patient. During starvation, homeostatic mechanisms are less than 400 ml/day and there are no obvious
are designed to burn fat rather than protein as an contraindications. Commence with standard enteral
energy source until the fat stores are significantly feed at 25 ml/h, increasing the rate every 12 hours
depleted. The catabolic state that occurs in critical ill- until 100 ml/h is achieved. Aspirate residual volume
ness, however, ensures significant protein loss from and rest for 1 hour in every 6 hours of feeding, and
early in the illness. rest continuously for 8 hours overnight.

Moderate to severe head injury is characterised by the


development of an hypermetabolic and hypercata- COMPLICATIONS OF ENTERAL
bolic state. Plasma and urine levels of catecholamines FEEDING
and cortisol are elevated. Hyperglycaemia occurs fre- 1. Large residual gastric volumes.
quently and is a major cause of ketone production, 2. Regurgitation and aspiration.
increasing lactic acid production by the brain and 3. Diarrhoea.
cellular acidosis. The severity and duration of hyper- 4. Ulceration of nares.
glycaemia following head injury has been shown to 5. Contamination of feed (rare).
correlate with longer term outcome. Efforts to avoid
hyperglycaemia are important. Gastric atony and delayed emptying occur commonly
in HI and may make establishing early enteral feeding
Immune suppression occurs in head-injured patients difficult. Pro-kinetic agents such as metoclopramide
with a decrease in the T cell lymphocyte CD4/CD8 or erythromycin are used to promote gastric motility.
ratio. The early instigation of effective nutritional A nasojejunal tube may be inserted to bypass the
support may decrease secondary neurological injury pylorus. The passage of nasal feeding tubes should be
and improve outcome. avoided in patients with facial injuries and basal skull
fracture.
Diarrhoea is also common with enteral feeding and
ENTERAL NUTRITION may resolve with a different formula of feed.
Persistent diarrhoea may represent infection with
Enteral nutrition is preferred in the critically ill. Clostridium difficile, particularly in patients receiving
This can be achieved by either nasal tube feeding or multiple antibiotics. A specimen should always be
via a percutaneous gastrostomy (PEG) if prolonged sent for microbiological culture. Loperamide (2 mg)
feeding is envisaged. Standard enteral feeding in each 500 ml feed and after each loose stool is an
regimes aim to provide 1500–2500 kcal in 24 hours effective treatment for simple diarrhoea.
with 70 g protein in a volume of 1.5–2 L. More
concentrated feeds and low electrolyte feeds are
available for patients in renal failure.
TOTAL PARENTERAL
Advantages associated with enteral rather than par- NUTRITION (TPN)
enteral nutrition include:
Although protein calorie requirements are more
1. Maintenance of mucosal integrity and prevention
easily met by parenteral nutrition, it is a poor substi-
of villous atrophy.
tute for enteral nutrition. Energy requirements are
2. Reduced infection rate.
1500–2500 kcal/day depending on the patient’s
3. Absence of requirement for central venous line.
catabolic state. Excessive calorie intake, particularly
4. Better maintenance of fluid balance.
as carbohydrate, serves no purpose, increasing
5. Reduced cost.
oxygen consumption, carbon dioxide production,
Contraindications to enteral feeding are few, particu- the respiratory quotient (RQ) and lipogenesis. The
larly in the patient with isolated intracranial pathol- calorie:nitrogen ratio for TPN is 150:1.
ogy, but include abdominal sepsis, obstruction, acute
TPN should provide:
malabsorption and inflammatory syndromes and
enteric fistulae. Only a short segment of small 1. Lipid.
intestine (30 cm) is required for adequate absorption 2. Carbohydrates.
since hypertrophy will occur in response to lumenal 3. Amino acids.
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NUTRITION IN THE NEUROCRITICAL CARE UNIT 213


4. Electrolytes. calcium, phosphate, magnesium and chloride should
5. Trace elements. be met by TPN.
6. Vitamins.
Trace elements
Lipids
Trace elements essential for homeostasis include zinc,
Lipids are essential for cell wall integrity, prostaglandin copper, manganese, iron, cobalt, chromium, selenium,
synthesis and the action of fat-soluble vitamins, but molybdenum and iodine.
should provide no more than 33% of the energy
requirements. Intralipid, the only current source of Vitamins
lipid available, is an isotonic emulsion of soyabean oil
Commercially prepared vitamin supplements contain
with egg phosphatides and lecithin. The particle size of
most water-soluble and fat-soluble vitamins (A, D
the emulsion is similar to a chylomicron, and the lipid
and E) with the exception of folic acid, vitamin B12
is handled in a similar manner. The energy yield from
and vitamin K (fat-soluble).
fat is 9 cal/g, but the presence of the egg phosphatides
increase the calorific value of intralipid to 11 cal/g. Increasingly, hospital pharmacies are supplying pre-
mixed ‘big bag’ TPN containing the complete 24-
The lipid load should be decreased in the presence
hour nutritional requirements.
of:
• Sedation with propofol.
• Severe jaundice.
• Severe hypoxaemia. KEY POINTS
• Thrombocytopaenia.
• Hypothermia. • HI is associated with the development of an
hypermetabolic and hypercatabolic state with
Carbohydrates immunosuppression.
• Hyperglycaemia worsens brain acidosis and sec-
Two-thirds of the energy requirement is provided by ondary injury and should be avoided.
carbohydrate in the form of glucose (energy yield = • Early and effective nutritional support improves
4 cal/g). An insulin sliding scale will frequently be longer term outcome after HI.
required to tightly control plasma glucose levels. • Gastric atony and paresis is common following HI.
Proteins
Protein is usually omitted from calorific calculations. FURTHER READING
A wide range of amino acids are supplied as the Dark DS, Pingleton SK. Nutrition and nutritional support
L-isomer in commercial preparations. Protein require- in critically ill patients. J Intens Care 1993; 8: 16–33
ments increase in sepsis and burns and are 12–17 g Povlishock J, Bullock MR. Nutritional support of brain-
nitrogen/day (1 g nitrogen = 6.25 g protein). injured patients. J Neurotrauma 1996; 13: 721–729

Electrolytes Robertson CS, Goodman JC, Narayan R, et al. The effects


of glucose administration on carbohydrate metabolism after
Daily electrolyte requirements of sodium, potassium, head injury. J Neurosurg 1991; 74: 43–50
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51
NURSING ISSUES

S. Rees-Pedlar, S. Walters
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216 NEUROINTENSIVE CARE

INTRODUCTION different challenges to the nurse. As well as patient


safety and comfort during ventilation, maintenance of
The nursing role within a neurointensive care unit arterial CO2 tension is reliant on skilled nursing care.
requires an in-depth knowledge of factors that con-
tribute to secondary brain damage. This is augmented
using a range of skills enabling the nurse to effectively CARDIOVASCULAR MANAGEMENT
assess and monitor the patient and so meet their phys- Haemodynamic management and manipulation is
ical and psychological needs. important to ensure an adequate CPP. CPP should be
continually monitored to determine the parameter
NEUROLOGICAL MANAGEMENT causing adverse change (i.e. a fall in MAP or a rise in
ICP). It is frequently the nurse who will identify the
Assessment of neurological status is based primarily on initiating factor and take appropriate measures to
GCS and pupil reaction. Continuous individual man- rectify the problem.
agement detects early, subtle changes in patient
response which may not be reflected in GCS but may Hypertension is often the result of deranged vasomo-
reflect deteriorating function (e.g. a higher level of tor control but assessment of other causative factors is
stimulus required to achieve the same response). This essential for correct treatment. Inappropriate sedation
one-to-one patient care also facilitates detection of limb levels may cause hypertension in a paralysed, non-
and CN deficits, receptive/expressive disorders and sedated patient. Pain and discomfort may also precip-
impaired muscle tone. The assessment of GCS is limited itate hypertensive episodes. Simple but important
in sedated patients but small pupil changes (e.g. to ovoid measures such as communicating by speech or touch
shape) can be significant. and comforting may be all that is needed. Particular
attention is required with patients who have an
Continuous monitoring of ICP levels and ICP wave- unclipped cerebral aneurysm. Untreated hyperten-
form gives information about both early changes in sion may result in re-bleeding.
intracranial hypertension and monitor accuracy.
Nursing staff are responsible for accurate calibration of Fever has an adverse effect on cerebral metabolism and
monitors after insertion and should ensure the ICP bolt should be actively managed. Temperature is generally
site is kept clean and protected. In the event of uncon- monitored centrally if ICP control is required. Anti-
trolled rises in ICP, the nurse may be able to promptly pyretics and early multiple-site bacterial cultures are
identify the cause and take appropriate measures to employed. Measures to prevent cross-infection should
reduce the pressure (e.g. repositioning). be maintained by all staff. Active cooling may be
required to maintain normothermia or induce hypo-
Accuracy of jugular bulb monitoring relies on regular thermia as a means of controlling ICP. Cooling blan-
calibration through jugular venous blood sampling. kets are used to gradually reduce body temperature to
Recognition of artefact and maintenance of a contin- desired levels (e.g. 34–35.5ºC). This has implications
uous jugular bulb sensor can be time-consuming. for tissue perfusion, tissue viability and pressure care.
The monitoring catheter is cared for in the same Absorption of enteral feed may slow or stop completely.
manor as a central line.

PAIN AND SEDATION MANAGEMENT


RESPIRATORY MANAGEMENT
Accurate assessment and appropriate treatment of pain
The degree of respiratory support required varies
and sedation is ongoing. The use of scoring systems for
according to condition. This may range from an
medical and nursing staff helps give consistent care and
assessment of breathing pattern (which may change
analysis of the response to treatment is an important
with rises in ICP) to management of oxygen therapy
part of the nursing role if treatment is to be successful.
or the need for positive pressure ventilation.
As most patients are unable to verbally communicate
Suctioning is probably the most invasive procedure
pain or discomfort, nursing staff will use non-verbal
regularly carried out by nurses in intensive care and so
clues such as restlessness or increases in MAP, heart rate
should only be undertaken when indicated by
and ICP as indications for intervention.
changes in breath sound or blood gas tension.
Titration of the effects of chest care on ICP is a major
component of nursing care. NUTRITION MANAGEMENT
Modern ventilator technology allows the critical care Nutritional requirements in neurointensive care
practitioner to achieve a desired blood gas tension with depend on the neurological condition, associated
a variety of ventilatory modes all of which present injuries and level of sedation. As with any critically ill
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NURSING ISSUES 217


patient, it is a primary nursing responsibility to com- out in a chair, using lifting aids as appropriate, assists
mence and establish enteral nutrition early and with physical and psychological care.
research-based feeding guidelines are recommended.
Staff should always ascertain correct position of the
tube in the stomach before starting feed avoiding the HYGIENE MANAGEMENT
nasal route if base of skull fracture is suspected. Patients are frequently completely dependent on
Problems with absorption are common due to heavy nursing care for hygiene needs. These needs should
sedation requirements and gut pro-kinetic agents are be balanced against the normal physiological response
frequently required. After feeding is established, a to fever as frequent washing can affect this response.
safer and more comfortable long-term feeding tube There is also a need to keep the normal flora of the
should be placed. Nursing staff must be extra vigilant skin intact. However, the psychological impact of
to monitor for normoglycaemia and normona- feeling clean and cool together with the therapeutic
traemia. With continued improvement, eating and use of touch and the stimulating smell of familiar
drinking should be commenced as appropriate. products should not be underestimated.
Problems with swallow or gag reflexes should be
referred to a speech therapist for assessment.
PSYCHOSOCIAL NEEDS

ELIMINATION MANAGEMENT The psychological impact of critical care is well doc-


umented but is compounded when the patient also
Nursing staff must also be vigilant to monitor hourly has neurological impairment. Nurses should aim to
and cumulative fluid balances. Salt and water imbal- create an environment that maintains sensory and
ances are common and staff should look for symptoms sleep balance, and involve families in keeping
of common syndromes. Changes in urine volume and patients in touch with reality. Allowing the patient
concentration can aid in diagnosis and identify the need to reserve some control (when appropriate) and the
for laboratory analysis of serum and urine osmolality. linking of touch to verbal communication helps to
prevent feelings of helplessness and altered body
Urinary tract infections are a significant risk to image. Nursing skills are also central to supporting
patients who are immobile for many days or weeks, families, partners and friends particularly in the fol-
have indwelling catheters and altered immune lowing areas:
systems. A major aim of nursing care is to reduce this
risk and identify problems early, i.e. good catheter • Reducing knowledge deficit.
hygiene and regular bacteriological screening. • Decreasing anxiety and feelings of powerlessness.
• Allowing grief.
Gut motility is also impaired through immobility and • Preventing isolation.
critical illness. Problems with constipation can con-
tinue after the acute phase of illness and can detract The need for information and hope has always been
from speed of recovery as well as cause distress to the high in both the critically ill patient and their rela-
patient. Early bowel assessment and the use of aperi- tive. All members of the multi-disciplinary team
ents can assist in the management of these problems. have a role in providing this, but it is the nursing
Antibiotic use and an impaired immune system lead- staff who are in contact with the patient and family
ing to diarrhoea are a common problem exacerbated for the longest time periods. They often best gauge
by incontinence. This has implications for skin patient needs, the family situation and any specific
integrity and patient comfort and dignity and concerns and worries. Good communication
demands skill and attention from the nursing staff. between medical and nursing staff is vital if infor-
mation is to be consistent and family support is to
be optimal.
MOBILITY MANAGEMENT
Nursing skill is required to balance the needs of the
patient with clinical condition. Regular assessment is KEY POINTS
required for the presence of risk factors associated with
The nursing role is multi-faceted and includes:
compromised skin integrity. Frequent position changes
are also needed to protect pressure areas as well as aid • Baseline assessment and ongoing patient monitor-
physiotherapy. Patients should be nursed ‘head-up’ to ing.
prevent decreased venous drainage. Physiotherapy aids • Meeting patient needs including sensitive care of
early mobilisation of the patient. Mobilising patients psychological, spiritual and social issues.
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218 NEUROINTENSIVE CARE

• Continued support of family and significant FURTHER READING


others, including education and preparation for
Gelling L, Prevost AT. A comparison of the perceptions of
future life changes.
relatives, nurses and doctors. Care of the Critically Ill. 1999;
• Collaborating with other members of the multi- 15(2): 53–58
disciplinary team
Heath DL, Vink R. Secondary mechanisms in traumatic
brain injury: a nurse’s perspective. Journal of Neuroscience
Nursing 1999; 31(2): 97–105
Shah S. Neurological assessment. Nursing Standard 1999.
13(22): 49–54
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52
INTRACRANIAL PRESSURE

M. Czosnyka
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220 MONITORING

INTRODUCTION from a burrhole either at the bedside or post


craniotomy (Codman® system). With the most
The continuous measurement of ICP is an essential common intraparenchymal arrangement however,
modality in most brain monitoring systems and measured pressure may be localised and not
currently requires an invasive sensor. Attempts to necessarily representative of true ICP (i.e. ventric-
monitor ICP non-invasively (most promisingly with ular CSF pressure). Microtransducers cannot
TCD) are still in a phase of technical evaluation. generally be recalibrated after insertion and con-
Measurement of ICP allows us to estimate cerebral siderable zero drift may occur during long-term
perfusion pressure where CPP = mean arterial monitoring.
blood pressure (ABP) - mean ICP. 3. Others. The least invasive systems available use
epidural probes but there is still uncertainty
This provides information regarding autoregulation regarding the precise relation between ICP and
of CBF, compliance of the cerebrospinal system and extradural pressure. Contemporary epidural sen-
waveform analysis. sors are now much more reliable than 10 years
ago. Lumbar CSF pressure is seldom measured in
neurointensive care.
METHODS OF MEASUREMENT
1. Intraventricular drains: An external pressure trans-
ducer connected to a catheter placed in the ven- TYPICAL EVENTS AND TRENDS
tricular system allowing direct pressure SEEN IN ICP MONITORING
measurement is still considered the ‘gold standard’
for ICP measurement. Additional advantages Specific patterns of the ICP waveform can be identi-
include ability for periodic external calibration and fied when mean ICP is monitored continuously.
CSF drainage. However, insertion of the ventric- Patients with a low and stable ICP (below 20 mmHg)
ular catheter may be difficult or impossible in cases characteristically have no ICP vasogenic waves (Fig.
of advanced brain swelling and the risk of infec- 52.1) with the exception of a phasic response of ICP
tion is increased significantly after 3 days of moni- to rapid variations in arterial blood pressure (ABP).
toring. This pattern typically occurs during the initial hours
2. Transducer tipped systems: Modern ventricular, sub- following HJ, before ICP begins to rise.
dural or intraparenchymal microtransducers
The most common picture of high but stable ICP
reduce infection rates and have excellent metro-
(above 20 mmHg) following HI produces vasogenic
logical properties revealed during bench tests. The
waves of limited amplitude (Fig. 52.2).
intraparenchymal systems may be inserted through
an airtight support bolt (e.g. Codman® or Other examples of ICP waves are shown in Figs
Camino® systems) or tunnelled subcutaneously 52.3–52.5.

Figure 52.1 Example of ICP and ABP monitoring in


patients with low and stable ICP. Characteristically, there are
no ICP vasogenic waves (line is very smooth), with exception Figure 52.2 Example of a stable but elevated ICP.
of a phasic response of ICP to rapid variations in ABP. X-axis Vasogenic waves of a limited amplitude are clearly visible
is time in minutes along with the response to a rapid (2 min) fall in ABP
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INTRACRANIAL PRESSURE 221

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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INTRACRANIAL PRESSURE 223


Czosnyka M, Guazzo E, Whitehouse H, et al. Significance Czosnyka M, Smielewski P, Kirkpatrick P, Laing RJ,
of intracranial pressure waveform analysis after head injury. Menon D, Pickard JD. Continuous assessment of the cere-
Acta Neurochir (Wien) 1996; 138: 531–542 bral vasomotor reactivity in head injury. Neurosurgery
1997; 41: 11–19
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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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JUGULAR VENOUS OXIMETRY 227

SjvO2 There are also benefits in measuring SjvO2 to assess


cerebral hypoperfusion during the perioperative
management of patients with SAH.
CMRO2 can be calculated using the equation:
CMRO2 = CBF ¥ (SaO2 – SjO2).
Assuming haemoglobin concentration is the same in
arterial and venous blood and the amount of dis-
Oxygen delivery Oxygen consumption
solved oxygen is minimal, arteriojugular oxygen con-
tent difference can be substituted for arteriojugular
oxygen saturation difference. Hence:
ICP CPP Increased metabolism (e.g. seizures)

Excessive hypocapnia Hyperthermia


CMRO2 = CBF ¥ (SaO2 – SjvO2).

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