Ebook Neurocritical care A guide to practical management Part 1

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Competency-Based Critical Care

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Series Editors
John Knighton, MBBS, MRCP, FRCA
Consultant
Intensive Care Medicine & Anaesthesia
Portsmouth Hospitals NHS Trust
Portsmouth
UK

Paul Sadler, MBChB, FRCA
Consultant
Critical Care Medicine & Anaesthesia
Queen Alexandra Hospital
Portsmouth
UK

Founding Editor
John S.P. Lumley
Emeritus Professor of Vascular Surgery
University of London
London
UK
and
Honorary Consultant Surgeon

Great Ormond Street Hospital for Children NHS Trust (GOSH)
London
UK
Other titles in this series
Renal Failure and Replacement Therapies
edited by Sara Blakeley

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John P. Adams  •  Dominic Bell  •  Justin McKinlay (eds.)

Neurocritical Care
A Guide to Practical
Management

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Editors
John P. Adams
The General Infirmary at Leeds
Great George Street
Leeds LS1 3EX
United Kingdom


Dominic Bell
The General Infirmary at Leeds
Great George Street

Leeds LS1 3EX
United Kingdom


Justin McKinlay
The General Infirmary at Leeds
Great George Street
Leeds LS1 3EX
United Kingdom


ISSN 1864-9998
e-ISSN 1865-3383
ISBN 978-1-84882-069-2
e-ISBN 978-1-84882-070-8
DOI 10.1007/978-1-84882-070-8
Springer London Dordrecht Heidelberg New York
British Library Cataloguing in Publication Data
A catalogue record for this book is available from the British Library
Library of Congress Control Number: 2009931330
© Springer-Verlag London Limited 2010
Apart from any fair dealing for the purposes of research or private study, or criticism or review,
as permitted under the Copyright, Designs and Patents Act 1988, this publication may only be
reproduced, stored or transmitted, in any form or by any means, with the prior permission in
writing of the publishers, or in the case of reprographic reproduction in accordance with the
terms of licenses issued by the Copyright Licensing Agency. Enquiries concerning reproduction
outside those terms should be sent to the publishers.
The use of registered names, trademarks, etc., in this publication does not imply, even in the
absence of a specific statement, that such names are exempt from the relevant laws and regulations
and therefore free for general use.

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.
Printed on acid-free paper
Springer is part of Springer Science+Business Media (www.springer.com)

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John Adams dedicates this book to his wife Kate to compensate
for neglect of his responsibilities as husband and father. The
families of his fellow editors did not specifically notice or comment
and for this we are grateful.

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Preface

Brain injury is a worldwide leading cause of mortality and morbidity and
requires early and appropriate management to minimize these adverse
sequelae. Despite such needs, access to specialist centers is limited, forcing
both immediate and secondary care of these patients onto generalist staff.
These responsibilities are made more problematical by differences in patient
management between and even within specialist centers, due in part to an
insufficient evidence-base for many interventions directed at brain injury.
This book is borne out of the above observations and is targeted at emergency and acute medicine, anesthetic and general intensive care staff caring
for brain injury of diverse etiology, or surgical teams responsible for the
inpatient care of minor to moderate head trauma.
Although explaining the various facets of specialist care, the book is not

intended to compete with texts directed at neurosciences staff, but aims to
advise on optimal care in general hospitals, including criteria for transfer, by
a combination of narrative on pathophysiology, principles of care, templates
for documentation, and highly specific algorithms for particular problems.
It is intended that the content and structure can form the basis of guidelines
and protocols that reflect the needs of individual units and that can be
constantly refined. Our ultimate goal is to promote informed, consistent,
auditable, multidisciplinary care for this cohort of patients and we hope that
this text contributes to that process.



vii

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Acknowledgments

We are indebted to our fellow authors who have not only made this book
possible, but have approached the task with enthusiasm. All understand and
endorse the importance of clear, comprehensive, evidence-based, and consistent advice in the support of colleagues caring for these patients outside
the regional center.
We are also grateful for the observations of colleagues responsible for the
eventual rehabilitation of these patients, mainly that even minor reductions in
neurological deficit by early and appropriate care, can have a significant impact
on quality of life, with proportional benefit not only for the patient, but family,
health and social care institutions, and society. These observations justify the
book and warrant implementation of the contained principles.
Finally, we thank Melissa Morton in the UK and Robin Lyon in New York

for all their help and support in bringing this book to publication.



ix

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Contents

  Chapter 1 Brain Injury and Dysfunction: The Critical
Role of Primary Management...............................................
M.D. Dominic Bell
  Chapter 2 Monitoring the Injured Brain...............................................
Simon Davies and Andrew Lindley

1
9

  Chapter 3 The Secondary Management of Traumatic
Brain Injury............................................................................
Dominic Bell and John P. Adams

19

  Chapter 4 Critical Care Management of Subarachnoid
Hemorrhage............................................................................
Audrey C. Quinn and Simon P. Holbrook

33

  Chapter 5 Central Nervous System Infections......................................
Abigail Walker and Miles Denton

43

  Chapter 6 Cervical Spine Injuries..........................................................
John P. Adams, Jake Timothy, and Justin McKinlay

51

  Chapter 7 Recent Advances in the Management of Acute
Ischemic Stroke......................................................................
Ahamad Hassan

61

  Chapter 8 Seizures on the Adult Intensive Care Unit...........................
Morgan Feely and Nicola Cooper

69

  Chapter 9 Non-Neurological Complications of Brain Injury..............
John P. Adams

77

Chapter 10 Acute Weakness in Intensive Care........................................
Louise Barnes and Michael Vucevic

89

Chapter 11 Coma, Confusion, and Agitation in Intensive Care.............
Matthew Clark and Justin McKinlay

97



xi

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xii

Contents

Chapter 12 Death and Donation in Critical Care:
The Diagnosis of Brainstem Death....................................... 105
Paul G. Murphy
Chapter 13 Death and Donation in Critical Care:
Management of Deceased Organ Donation......................... 113
Paul G. Murphy
Chapter 14 Imaging the Brain-Injured Patient....................................... 121
Tony Goddard and Kshitij Mankad
Chapter 15 Ethical Dilemmas Within Intensive Care............................. 137
M.D. Dominic Bell
Appendices..................................................................................................... 145

Index............................................................................................................... 173

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Contributors

John P. Adams
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX
UK
Louise Barnes
Hull Royal Infirmary
Hull and East Yorkshire Hospitals NHS Trust
Hull HU3 2JZ
UK
Dominic Bell
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX
UK
Matthew Clark
Department of Anesthetics and Intensive Care
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX

UK
Nicola Cooper
Leeds Teaching Hospitals NHS Trust
Leeds General Infirmary
Leeds
West Yorkshire LS1 3EX
UK



Simon Davies
Department of Anaesthetics
York Hospital NHS Trust
York Hospital
York
North Yorkshire YO31 8HE
UK

Miles Denton
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX
UK

Morgan Feely
Department of Neurology
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds General Infirmary

Leeds
West Yorkshire LS1 3EX
UK

Tony Goddard
Department of Neuroradiology
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX
UK

xiii


xiv

Ahamad Hassan
Department of Neurology
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX
UK
Simon Holbrook
Academic Unit of Anesthesia
St. James’s University Hospital
Leeds
West Yorkshire LS9 7TF
UK

Contributors

Paul G. Murphy
Department of Anaesthesia
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX
UK
Audrey C. Quinn
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX
UK

Andrew Lindley
Leeds Teaching Hospitals NHS Trust
Leeds General Infirmary
Leeds
West Yorkshire LS1 3EX
UK

Jake Timothy
Department of Neurosurgery
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX

UK

Kshitij Mankad
Department of Neuroradiology
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX
UK

Michael Vucevic
Department of Anesthetics
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX
UK

Justin McKinlay
Department of Anaesthetics and Neurocritical Care
Leeds General Infirmary
Leeds Teaching Hospitals NHS Trust
Leeds
West Yorkshire LS1 3EX
UK

Abigail Walker
Department of Anesthesia
Christchurch Hospital
Christchurch

Canterbury
NZ


Glossary of Terms
and Abbreviations

A/B/C
ALI
APTT
BAL
BIS
BP
CMV
CNS
COAG
CPP
CRP
CSF
CT
CVP
CXR
ECG
EEG
ESR
EtCO2
FBC
FiO2
GCS
Gluc

HAS
Hb
HIV
HR
HSE
IABP
ICP
ICU
INR
IV
LFTs
LP
MAP



Airway, breathing, circulation
Acute lung injury
Activated partial thromboplastin time
Bronchoalveolar lavage
Bispectral index
Blood pressure
Cytomegalovirus
Central nervous system
Coagulation screen
Cerebral perfusion pressure (MAP-ICP)
C-reactive protein
Cerebrospinal fluid
Computed tomography
Central venous pressure

Chest X-ray
Electrocardiogram
Electroencephalogram
Erythrocyte sedimentation rate
End-tidal carbondioxide concentration
Full blood count
Fraction of inspired oxygen
Glasgow coma scale
Glucose
Human albumin solution
Hemoglobin
Human immunodeficiency virus
Heart rate
Herpes simplex encephalitis
Invasive arterial blood pressure
Intracranial pressure
Intensive care unit
International normalized ratio
Intravenous
Liver function tests
Lumbar puncture
Mean arterial pressure

xv


xvi

MI
MRI

MRSA
NaCl
NEAD
NGT
NICE
NJT
NPE
NSAID
ODM
OGT
PaCO2
PaO2
PCR
PCWP
PE
PEEP
PbtO2
PPI
PVS
SaO2
Spp
SjvO2
TB
U&Es
UK
Vt
VTE
WCC
WFNS

Glossary of Terms and Abbreviations

Myocardial infarction
Magnetic resonance imaging
Methicillin-resistant Staphylococcus aureus
Sodium chloride
Non-epileptic Attack Disorder
Nasogastric tube
National Institute for health and Clinical Excellence
Nasojejunal tube
Neurogenic Pulmonary Edema
Non-steroidal anti-inflammatory drug
Oesophageal doppler monitor
Orogastric tube
Partial pressure of carbondioxide (arterial blood)
Partial pressure of oxygen (arterial blood)
Polymerase chain reaction
Pulmonary capillary wedge pressure
Pulmonary embolism
Positive end-expiratory pressure
Partial pressure of brain tissue oxygen
Proton pump inhibitor
Persistent vegetative state
Arterial oxygen saturation
Species
Jugular venous oxygen saturation
Tuberculosis
Urea and electrolytes
United Kingdom
Tidal volume

Venous thromboembolism
White cell count
World Federation of Neurosurgical Socities


1

Brain Injury and Dysfunction:
The Critical Role of Primary Management
M.D. Dominic Bell

Key Points
1. In traumatic brain injury, maintain mean arterial (MAP) blood pressure >80 mmHg.
2. Avoid hypoxia at all costs; keep PaO2 >13 kPa,
using PEEP if necessary.
3. Keep PaCO2 4.5–5.0 kPa; hyperventilate only if
there are signs of impending brainstem herniation.
4. Keep the neck in neutral position; always consider the possibility of cervical spine injury.
5. Maintain 15° head up position (as long as MAP
adequate).
6. Do not give mannitol if patient is hypotensive.
Speak to a Regional Neurosurgical Center before giving additional doses.

Introduction
The human brain, in structure and function, represents the pinnacle of biological evolution. Even
the most rudimentary non-volitional role of
matching ventilation to demand or maintaining
homeostasis is phenomenally complex for an
organism vulnerable to disease or dysfunction of
the component tissues and organs, and more particularly when exposed to mechanical, chemical,

and thermal hazard as every environmental
extreme is challenged. The coordination of physical movement, played out at the highest level in
sport and the performing arts, rightly warrants
recognition as a marker of complex neuronal



activity, but conventionally, as a form of intelligence, bows to the cognitive capacity of the human
brain. Numerical and literary skills, communication, memory, and knowledge are entry-level cognitive skills, with man’s advances through
understanding of both science and nature representing a higher plane. Reasoning and judgment,
coupled with awareness of the needs of others and
social skills arguably constitute the highest form
of human intelligence. Interlinked with this function are those characteristics of personality and
emotional status which generate individual
uniqueness. These may be reflected in our achievements, as in career choice, or functional and artistic creativity, or our behavior relating to those
achievements, as in innovation, ambition, and
leadership. These higher functions also have an
emotional dimension covering conscience, charity
and self-sacrifice, enthusiasm, and the ability to
love, rejoice and grieve.
This refinement and complexity of normal
cerebral function is, however, associated with
certain inherent vulnerabilities carrying significant implications for the management of either
primary or secondary brain pathology or dysfunction. Tissues such as bone are able to regain normal
architecture after injury, complex organs such as the
liver and kidney are able to regenerate with restoration of original levels of function, and heart, lung,
and pancreas are able to withstand devascularization
and subsequent transplantation. The specialization of cellular structure and function within the
central nervous system, however, appears to
exclude a capacity for repair and renewal after

anything other than the most trivial insult. Brain

1


2

tissue has a high requirement for oxygen and
energy substrates to maintain both structure and
function, leaving little reserve in the face of
impaired delivery. Even with normal arterial
oxygen content, circulatory arrest will result in loss
of consciousness within 15 seconds, and given the
high oxygen requirements simply to maintain cellular integrity, more than 5 minutes of circulatory
arrest at normothermia will result in neuronal
death and a significant multifaceted neurological
deficit. These aspects demonstrate the exquisite
vulnerability of the brain to the so-called secon­
dary cerebral insults, with cellular hypoxia being
the commonest final pathway.
There is a gradient of sensitivity of the different
neural tissues to a global insult such as hypoxia,
whereby the loss of higher function precedes loss
of motor activity, with ventilatory effort maintained until immediately prior to death. This
pattern parallels the picture of recovery from such
an insult, the extreme end of the spectrum being
the persistent vegetative state, where the patient is
self-ventilating, but has no awareness of environment or self. This demonstrates that survival alone
cannot be considered a satisfactory outcome from
brain injury, and that all effort must be directed

toward preventing, where possible, even the most
subtle changes to personality and cognitive function at the other end of the spectrum, that would
require the skills of a clinical psychologist to
objectively quantify. Failure to address these
aspects results not only in significant disability for
patient and family, but phenomenal burden and
cost to society.
This edition of the series, devoted to neurocritical care and the prevention or minimization of
such avoidable neurological deficit, examines the
theory and evidence-base behind the various management strategies expected of a regional unit. The
secondary aim is to define and promote principles
of care that can be deployed by any discipline, at
any level of seniority, at any location, at any time,
for any patient, with any pathology, and at any
stage. Such principles, both clinical and procedural,
are essential, given that most neuropathology
arises outside the setting of a specialist center, and
many patients will not access that center, either
because neurosurgical intervention is not required,
other injuries require immediate management, or
because of limited bed availability.
Given the vulnerability of the brain as outlined
earlier, it is unacceptable if the patient accrues
additional avoidable morbidity in these circumstances, or indeed while awaiting or during trans-

M.D.D. Bell

fer to the regional unit, through ignorance. Clinical
experience also highlights how patient care can be
compromised due to a lack of clarity and consistency in the referral process and acceptance by the

regional unit, resulting in a hiatus in care with
neither party taking full responsibility for these
aspects. Such a scenario is arguably more unacceptable than ignorance, and demands explicit
policy from the center and audit of process to
monitor compliance.

Role of the Regional Neurosurgical
Center (RNC)
Fundamental to optimal patient management and
any relationship with the regional center is an
understanding of the specific services provided
there. The greatest demand will be for care of traumatic brain injury, followed by subarachnoid
hemorrhage, but the centers also have an emerging involvement in conventional “strokes.” Thrombolysis or interventional radiology for an ischemic
infarct are being increasingly adopted as appropriate emergency care, mirroring the approach
taken to occlusive coronary events. The implications of managing these patients as medical emergencies cannot be overestimated, but the care and
cost implications of the current conservative evaluative approach to strokes are significant, regardless of the impact on the patient and family.
The role of the regional center for this range of
pathology can be summarized as intervention,
neuro-specific monitoring, and advice for referring
units. Given that vascular pathology is addressed in
subsequent chapters, the role is only outlined in
greater depth, as below, for traumatic brain injury:
1. To expedite removal of a significant intracranial hematoma
2. To monitor for the potential expansion of a less
significant hematoma
3. To provide specialized monitoring (e.g., intracranial pressure, jugular venous oximetry) to
direct the neuro-intensive care of the diffuse
axonal injury
4. To undertake radical surgical maneuvers for
refractory intracranial hypertension, e.g., decompressive craniectomy or lobectomy for extensive contusion

Although it could be argued that a patient
should be transferred to a specialized unit for


1.  Brain Injury and Dysfunction: The Critical Role of Primary Management

imaging and assessment of the patient to make the
above distinctions, CT scanning in the referring
hospital has reduced the necessity for this and
digital image transfer should improve the quality
of discussion and decision-making. Furthermore,
it is clearly not in the interest of the majority of
patients to be transferred for the sole purpose
of diagnosis.

Indications for Patient Transfer
·· Group 1: Transfer delayed only for correction of
secondary cerebral insults or for life-saving
surgery (e.g., expanding extradural hematoma
with localizing signs).
·· Group 2: Requires urgent transfer following
optimization and life and limb saving surgery
(e.g., subdural hematoma with no mass
effect).
·· Group 3(a): Patients should only be transferred
after absolute stabilization given that the overall
principles of care are to avoid secondary cerebral insults, rather than to offer neuro-specific
therapies (e.g., contusional injury with no mass
effect).
·· Group 3(b): Some non-neurosurgical intensive

care units (ICU) monitor ICP in cases of diffuse
axonal injury; transfer may become necessary
if the ICP subsequently becomes difficult to
control.

Organizing the Response
Groups 1-3(a) above demonstrate the importance
of the primary decision-making which involves
diagnostic skills, confident liaison with the
regional center, and an appropriate level of care in
the event of retention of the patient. This responsibility usually falls to the attending anesthetist or
intensive care specialist following initial stabilization in the emergency department. This individual
has a pivotal role in coordinating this process and
therefore assumes both clinical and logistical
responsibilities (see Table 1.1).

3

Table  1.1.  Roles of the attending specialist during the primary
management of patients with traumatic brain injury
  1. Primary resuscitation
  2. Neurological assessment
  3. Deciding on the need for intubation, sedation and ventilatory
support
  4. Management of problems such as convulsions
  5. Interpretation of CT scans adequate for prioritization of
treatment options
  6. Prioritizing and expediting essential general surgical and
orthopedic interventions
  7. Deciding on transfer or retention after such interventions

  8. Maintaining neurological observations
  9. Avoiding secondary cerebral insults or expansion of any
intracranial pathology
10. Organizing further CT scans in the event of retaining a patient
11. Maintaining dialog with the neurosurgeons and the
neurosurgical intensive care
12. Deciding, in the face of massive injury, that no overall benefit
from transfer exists

be done to avoid preventable secondary neuronal
death and subsequent deficit. These secondary
insults share a final common pathway that takes
areas of the brain compromised by the primary
injury, or indeed the whole brain, toward irreversible ischemia (see Fig. 1.1).
Secondary cerebral insults can be triggered by
intracranial or systemic factors, which either
reduce cerebral oxygen delivery or increase cerebral oxygen consumption (Table 1.2). In addition,
an increase in the volume of brain, blood, or CSF,
or an expanding space occupying lesion (e.g.,
hematoma) may increase the pressure within the
rigid skull and trigger global ischemia. Focal
damage may be caused by local compression or
shearing forces.

Cerebral Oxygen Delivery
Cerebral oxygen delivery depends upon:
(a) An adequate circulating volume at a perfusion
pressure above the lower level of cerebral
autoregulation.
(b) An adequate amount of oxygenated hemoglobin that dissociates appropriately at tissue

level.

Avoidance of Secondary Cerebral Insults Cerebral Oxygen Consumption
No treatment strategy can reverse neuronal death
caused by the primary brain injury, but much can

To avoid excessive cerebral oxygen consumption
in the context of compromised cerebral oxygen


4

M.D.D. Bell
MECHANISM OF ISCHEMIA
SECONDARY INSULT S
CLOSED
BOX

OXYGEN
REQUIREMENTS

ISCHAEMIA

PRESSURE
ANAEROBIC
METABOLISM
OEDEMA
OSMOTIC
PRESSURE

ACID
PRODUCTION

SUPEROXIDES
HYDROPEROXY RADICALS
CALCIUM MEDIATED CELL DEATH
APOPTOSIS

EXCITATORY
NEURO-TRANSMITTERS

MEMBRANE
DYSFUNCTION

CALCIUM
INFLUX

Figure 1.1.  Mechanism of ischemia in brain injury.

Table  1.2.  Intracranial and systemic causes of secondary brain
injury
Intracranial

Systemic

Expanding contusion/hematoma
Cerebral edema
Vascular injury/carotid dissection
Seizures
Hydrocephalus

Vasospasm

Hypotension
Hypoxia
Hypo or Hypercapnia
Pyrexia
Coagulopathy
Hypo or
hyperglycemia
Anemia
Sepsis

Pneumocephalus
Intracranial infection

delivery, it is essential to recognize and actively
treat any seizure activity and to provide adequate
analgesia and sedation, once a patient is intubated
and ventilated. Pyrexia should be treated with
active cooling measures once the patient is stabilized on the ICU. Hyperglycemia, which is believed
to increase cerebral oxygen consumption, should
be targeted during all epochs of care.

Expansion of Intracranial Contents
(a) Space-Occupying Lesions, for example, hematomata or contusions

The key priority is to determine whether urgent
neurosurgery is required. General supportive
care includes avoidance of aspects that allow a
hematoma to expand through loss or dilution of

platelets or coagulation factors. Hypothermia,
hypocalcemia, and administration of large
volumes of colloid solutions should be avoided.

These aspects assume greatest significance
in the context of a subdural or intracranial
hematoma, where such attention may avoid
the need for surgical intervention.
(b) Brain Edema – Four Mechanisms:
1. Hydrostatic edema: occurs when arterial
pressure exceeds the upper limit of auto­
regulation or when there is venous congestion
(head-down position, pressure on the jugular
veins, high intrathoracic pressure).
2. Osmotic edema: non-ionic crystalloid
solutions such as dextrose become, in effect,
free water once the sugar component is
metabolized.
3.Oncotic edema: due to low plasma proteins;
can become important when the blood–
brain barrier (BBB) is damaged.
4. Inflammatory edema: the inflammatory
response to insults such as trauma or hypoxia can lead to increased capillary permeability and disruption of the BBB. It is
critically important to avoid preventable
insults such as osmotic edema when this
has arisen.
The management of cerebral edema and raised
intracranial pressure traditionally involves administration of mannitol. This can only be effective if
the BBB is intact, there is mass rapid movement of
water from the tissues into the circulating compartment, and finally rapid excretion via the

kidneys of both mannitol and water. The main
role of mannitol is to temporarily reduce the
amount of brain water and thereby reduce overall
intracranial pressures and relieve pressure on vital
structures such as the brainstem. This buys time
before definitive neurosurgical intervention. By
reducing the size of normal brain, abnormal areas
including hematomata can expand, generating a
greater shearing effect. If mannitol is used indiscriminately with a deranged BBB, the molecule
can diffuse across and ultimately contribute to the
development of osmotic edema. This is more likely
to occur with hypotension and poor renal perfusion such that the mannitol is not excreted.

Increase in Cerebral Blood Volume
1. Arterial: ↑PaCO2 is the commonest avoidable
cause of cerebral arterial vasodilatation.
2. Venous: discussed earlier, for example, neck positioning, endotracheal tube ties.


1.  Brain Injury and Dysfunction: The Critical Role of Primary Management

Cerebrospinal Fluid
The ventricular system and contained CSF are
usually capable of reducing in size to accommodate
brain edema without causing a rise in intracranial
pressure. Pathologies such as subarachnoid
hemorrhage and bacterial meningitis can cause
obstructive hydrocephalus. This requires insertion
of a ventricular drain.

Overall Management Strategy
Optimal patient care derives from an understanding
of the common pathologies that compromise brain
structure or function, and of the principles underpinning appropriate treatment options. The key
goal of this edition is to demystify this area of activity and thereby empower clinicians caring for these
patients, particularly within the primary receiving
hospital, since it is in this setting that there is the
greatest opportunity for patient harm through act,
omission, or delay in accessing the regional center.
The clinical aspects of care, both neuro-specific and
general, need to be formalized through protocols to
ensure consistency, regardless of grade or discipline
of attendant staff. It is vital that the logistical aspects
of care be similarly formalized, namely documentation, particularly observation charts, investigations,
involvement of other disciplines, communication,
and any referral process to the regional neurosurgical center. Only with such a structure will the right
things be done on the right patient, in the right order,
and at the right time. The challenge for clinicians
working within a regional unit is to recognize the
fundamental importance of achieving these goals in
the referring hospital, and to actively promote and
support such a system. The challenge for those
working in the referring hospital is to ensure that this
responsibility of the regional unit is discharged.
Such goals and the system directed at these are
defined as “care bundles”: strategies to not only
optimize care based on the strongest available evidence, but also to facilitate audit of process.
Readers are referred to the appendices for examples of how the principles are translated into explicit
recommendations for care within the author’s region,
with responsibility for dissemination and implementation resting with the local critical care network1

There is, however, still much to be done to eradicate
inconsistencies of care through ignorance and
limited formalization of process, as much as limited
availability in the regional centers. It is hoped that
those readers who recognize the magnitude of the
problem will be stimulated by this edition to confi-

5

dently address those issues, which are so critical for
patient care and professional satisfaction.

Principles of Management
of Brain Injury
The primary clinical management of any patient with
a brain injury, regardless of the diagnosis or severity,
consists of routine resuscitation maneuvers and diagnosing the nature and severity of both CNS and
non-CNS pathology. Consideration should always be
given to the possibility of a lesion for which there is
a specific surgical or medical intervention, or interim
supportive measures that can prevent that lesion generating morbidity or mortality. In the event of there
being more than one pathology, clinical judgment
has to determine the priorities of treatment.
Running parallel to that clinical process is a
logistical process, which incorporates aspects such
as teamwork, leadership, communication, prioritization, documentation, and timekeeping.

The Clinical Process
1. Resuscitation: as per ALS/ATLS guidelines.
2. Diagnosis: CNS pathology/non-CNS injury/

co-morbidity.
Indications for a CT brain scan after head
injury are outlined in Table  1.3 (see NICE
Guideline 2007).
(a) CNS pathology: diagnosis, CT findings, severity
(GCS, pupils, focal neurology, seizures),
trends, confounding variables (e.g., drugs,
alcohol, hypotension, hypothermia).
(b) Non-CNS pathology: remember the possibility of spinal injury.
3. Consideration of need for neurosurgical referral:
Use standardized form for transfer of information
(see example, Appendix).
4. Neuro-specific observations/monitoring: Use a
standardized chart.
5. Neuro-specific treatment: for example, mannitol
(see Table  1.4), hypertonic saline (HSL),
anticonvulsants.
6. Define priorities for treatment:
(a)  Urgent transfer
(b)  Life or limb-saving surgery
1  (c)  General support and stabilization
/>

M.D.D. Bell

6
Table 1.3.  Indications for a CT brain scan after head injury
•
•
•

•
•

Depressed conscious level
Focal neurological deficit
Suspected open or basal skull fracture
Age >65, with loss of consciousness or amnesia
GCS 15 with no fracture, but other concerning features (severe
persistent headache, vomiting, seizure, altered behavior)
• Unable to assess properly (e.g., alcohol, drugs)
• Prior to anesthesia for treatment of other injuries

Table 1.4.  Indications for Mannitol
Unilateral pupillary dilatation, or unilateral progressing to bilateral
dilatation (primary bilateral dilatation may represent fitting, drug
intoxication or overdose, or overwhelming brain injury).
Dose: 0.5 g/kg (approximately 200 mL of 20% solution) over
10–15 min. Can be repeated at 1–2 hourly intervals to maximum
serum osmolarity of 320 mosmol/L or Na+ of 160 mmol/L. Speak to
the Regional Neurosurgical Center prior to giving additional doses.
Alternative: Hypertonic saline (HSL) is being increasingly used for the
same purpose with good effect. We use 30 mL of 20% HSL over
20 min via a CVC, with a similar serum [Na+] cut-off of 160 mmol/L.
Precautions: Mannitol should not be given to patients who are
hypotensive or have evidence of inadequate renal perfusion. All
patients require bladder catheterization.

7. Avoidance of secondary insults: see targets
outlined here.
8. Regular re-evaluation of all the aforementioned

components.

The Logistical Process
1.
2.
3.
4.

Involve all relevant specialties
Determine team leadership
Establish documentation of observations
Ensure explicit communication:

(a) Internally within the team
(b) With key support specialties; radiology,
transfusion, pharmacy, etc.
(c) With the regional neurosurgical center
5. Determine satisfactory timescale for:





(a) Diagnostic procedures
(b) Care/interventions
(c) Communication with neurosurgical center
(d) Transfer

(e) Re-evaluation of all aspects of care
6. Ensure documentation (using standardized

templates where available) of:





(a) Observations
(b) All above clinical undertakings
(c) Criteria for transfer
(d) Results of discussion with regional center

7. Ensuring all appropriate support for any transfer is available (functioning equipment, trained
personnel, means of communication).
8. Define criteria for stabilization prior to transfer.

Avoidance of Secondary Cerebral
Insults
1. Maintaining cerebral oxygen delivery
(a) Adequate circulating volume: Aim for capillary refill time <2 s and CVP>PEEP+5 with
crystalloids (0.9%NaCl) up to 2 L followed
by a colloid (e.g., voluven, gelofusine). Give
blood and clotting factors to maintain Hb
~10  g/dL or hematocrit 30, INR <1.2 and
platelet count >100,000.
(b) Adequate oxygenation: Maintain PaO2
>13  kPa with supplemental oxygen and
PEEP if necessary. Intubate and ventilate
for GCS <8, primary ventilatory disturbance or airway management problems.
Keep PaCO2 4.5–5.0  kPa. Insert orogastric
tube after intubation to decompress the

stomach and prevent gastric dilatation.
(c) Adequate perfusion pressure: Maintain MAP
>80 mmHg or within 15% of normal values
if normally hypertensive. After volume
resuscitation, vasopressors or inotropes
may be required to maintain an adequate
blood pressure, the choice depending upon
the cardiovascular profile (see Appendix).
Advanced monitoring (e.g., esophageal
doppler, pulmonary artery catheter) may
be required to guide this process, especially if there is uncertainty about volume
status.
2. Controlling cerebral oxygen consumption

/>Guideline.pdf

(a) Control seizure activity: Seizure activity is
usually treated with a benzodiazepine (e.g.,

www.ebook3000.com


1.  Brain Injury and Dysfunction: The Critical Role of Primary Management

lorazepam 2–4  mg IV bolus) in the first
instance, followed by a longer-acting agent
(e.g., phenytoin 15  mg/kg over 20  min).
See Chap. 8 for detailed description, and
the Appendix for the status epilepticus
algorithm.

(b) Ensure adequate analgesia and sedation
if intubated: Use fentanyl or alfentanil by
infusion with propofol (midazolam can be
used if there is cardiovascular instability).
Maintain paralysis with infusion of muscle
relaxant (e.g., cisatracurium or vecuronium)
and monitor with a nerve stimulator.
All head-injured patients require bladder
catheterization.
3. Avoiding increases in intracranial pressure
(a) Avoid expansion of intracranial hematoma/
contusion: Maintain normal clotting and
platelet counts. Monitor calcium in face of
massive transfusion. Consider Factor VIIa
if intracranial hematoma or contusion in
the face of nonsurgical major hemorrhage
despite administration of platelets and
clotting factors (see Chap. 3 for detailed
description).

7

(b) Avoid brain edema: Use 0.9% NaCl, avoid
dextrose.
(c) Avoid hyperemia: Maintain PaCO2 4.5–5.0 kPa.
(d) Avoid venous congestion: 15° head up tilt.
Avoid external compression and high
intrathoracic pressures.
For full details of the current NASGBI guidelines for transfer of brain injured patients, visit
www.nasgbi.org.uk.

Further Reading
Clayton TJ, Nelson RJ, Manara AR (2004) Reduction in
mortality from severe head injury following introduction of a protocol for intensive care management.
Br J Anaesth 93(6):761–762
Modernisation Agency/Department of Health (2004)
The Neurosciences Critical Care Report. London
www.dh.gov.uk/publications
NICE (2007) Head Injury: Triage, assessment, investigations and early management of head injury in infants,
children and adults. London />nicemedia/pdf/CG56NICEGuideline.pdf
The Neuro Anaesthesia Society of Great Britain and
Ireland and The Association of Anaesthetists of
Great Britain and Ireland (2006) Recommendations
for the Safe Transfer of Patients with Brain Injury.
London www.nasgbi.org.uk


2

Monitoring the Injured Brain
Simon Davies and Andrew Lindley

Key Points

Clinical Assessment

1. Repeated clinical assessment through the Glasgow Coma Scale (GCS) is the cornerstone of
neurological evaluation.
2. Ventilated head-injured patients with intracranial pathology on CT require ICP monitoring.
3. Invasive or noninvasive neuro-specific monitoring requires careful interpretation when assisting goal-directed therapies.

4. Multimodal monitoring using a combination
of techniques can overcome some of the limitations of individual methods.

The Glasgow Coma Scale

Neuro-Specific Monitoring
Accurate neurological assessment is fundamental
for the management of patients with intracranial
pathology. This consists of repeated clinical examination (particularly GCS and pupillary response)
and the use of specific monitoring techniques,
including serial CT scans of the brain. This chapter
provides an overview of the more common monitoring modalities found within the neuro-critical
care environment.
In general terms, a combination of assessments
is more likely to detect change than one specific
modality. Real-time continuous monitoring (e.g.
ICP) will provide more timely warning about
adverse events (e.g., an expanding hematoma) as
compared to static assessments such as sedation
holds or serial CT brain scans.



The Glasgow Coma Scale (GCS) provides a standardized and internationally recognized method
for evaluating a patient’s CNS function by recording their best response to verbal and physical
stimuli. A drop of two or more GCS points (or one
or more motor points) should prompt urgent
re-evaluation and a repeat CT scan. The GCS is
described in detail in Chap. 10.
NB. Eye opening is not synonymous with

awareness, and can be seen in both coma and Persistent vegetative state(PVS). The important detail
is that the patients either open their eyes to
command or fixes or follows a visual stimulus.

Pupillary Response
Changes in pupil size and reaction may provide
useful additional information:
·· Sudden unilateral fixed pupil: Compression of
the third nerve, e.g., ipsilateral uncal her­niation
or posterior communicating artery aneurysm
·· Unilateral miosis: Horner’s syndrome (consider
vascular injury)
·· Bilateral miosis: Narcotics, pontine hemor­
rhage
·· Bilateral fixed, dilated pupils: Brainstem death,
massive overdose (e.g. tricyclic antidepressants).

9


10

S. Davies and A. Lindley

In the non-specialist center, neurological assessment of the ventilated patient consists of serial CT
brain scans, pupillary response, and assessment of
GCS during sedation holds. A reduction in sedation level will usually be at the suggestion of the
Regional Neurosurgical Center (RNC) and its
timing will depend upon a number of factors.
Responses such as unilateral pupillary dilatation,

extensor posturing, seizures, or severe hyper­
tension should prompt rapid re-sedation, repeat CT
scan, and contact with the RNC. In the patient
with multiple injuries, consideration must be
given to their analgesic requirements prior to any
decrease in sedation levels.

treating ICP values above 20 mmHg and to target
CPP in the range of 50–70  mmHg. Patients with
intact pressure autoregulation will tolerate higher
CPP values. Aggressive attempts to maintain CPP
>70 mmHg should be avoided because of the risk
of ARDS.
ICP values
Normal ICP <15 mmHg.
Focal ischemia occurs at ICP >20 mmHg
Global ischemia occurs at ICP >50 mmHg
Usual treatment threshold is 20 mmHg

Measuring ICP
Invasive Monitoring
Intracranial Pressure Monitoring
Cerebral perfusion pressure (CPP) reflects the
pressure gradient that drives cerebral blood flow
(CBF), and hence cerebral oxygen delivery. Measurement of intracranial pressure (ICP) allows
estimation of CPP.
CPP = Mean Arterial Pressure − ICP
Sufficient CPP is needed to allow CBF to meet the
metabolic requirements of the brain. An inadequate CPP may result in the failure of autore­
gulation of flow to meet metabolic needs whilst

an artificially induced high CPP may result in
hyperemia and vasogenic edema, thereby worsening ICP. The CPP needs to be assessed for each
individual and other monito­ring modalities (e.g.,
jugular venous oximetry, brain tissue oxygenation) may be required to assess its adequacy.
Despite its almost universal acceptance, there
are no properly controlled trials demonstrating
improved outcome from either ICP- or CPP-targeted
therapy. However, in the early 1990s Marmarou
et al. showed that patients with ICP values consi­
stently greater than 20  mmHg suffered worse
outcomes than matched controls, and poorer
outcomes have been described in patients whose
CPP dropped below 60 mmHg (Juul 2000; Young
et al. 2003). As such, ICP- and CPP-targeted therapy
have now become an accepted standard of care in
head injury management.
The 2007 Brain Trauma Foundation Guidelines
(Brain Trauma Foundation 2007) recommend

·· Intraventricular devices consist of a drain
inserted into the lateral ventricle via a burr
hole, and connected to a pressure transducer,
manometer, or fiber optic catheter. This remains
the gold standard but is associated with a higher
incidence of infection and greater potential
for brain injury during placement. It has
the added benefit of allowing CSF drainage.
Historically, saline could be injected to assess
brain compliance.
·· Extraventricular systems are placed in parenchymal tissue, the subarachnoid space, or in

the epidural space via a burr hole. This can be
inserted at the bedside in the ICU. These systems
are tipped with a transducer requiring calibration, and are subject to drift (particularly after
long-term placement). Examples of extraventicular systems are the Codman and Camino
devices. These devices have a tendency to
underestimate ICP.
In general, both types of device are left in situ for
as short a time as possible to minimize the risk of
introducing infection. Prophylactic antibiotics are
not generally used.

Indications for ICP monitoring
Head injury + ventilator + abnormal CT brain scan = ICP monitor

More specific indications:
·· Traumatic brain injury, in particular:
·· Severe head injury (GCS <8)


2.  Monitoring the Injured Brain

··
··

Coagulopathy is the primary contraindication to
insertion. The ICP device will generally be removed
as soon as the patient is awake with satisfactory neurology (GCS motor score M5 or M6) or when physiological challenges (removal of sedation, normalizing
PaCO2) no longer produce a sustained rise in ICP.

Intracranial Pressure Waveforms

and Analysis
The normal ICP waveform is a modified arterial
trace and consists of three characteristic peaks.
The “percussive” P1 wave results from arterial
pressure being transmitted from the choroid
plexi, the “tidal” P2 wave varies with brain compliance (fig. 2.1), whilst P3 represents the dicrotic
notch and closure of the aortic valve. It is important to establish the accuracy of the ICP trace and

Intracranial Pressure

P1

P2

P3
Compliant Brain

P2
P1

P3
Non-compliant Brain

Intracranial Pressure (mmHg)

··
··

value before initiating therapy based upon the
numbers generated. Transient sequential occlusion of the internal jugular veins or removing the

head-up tilt should produce an increase in ICP.
In addition to simple pressure measurement, if
ICP is recorded against time, a number of characteristic wave forms (Lundberg waves) can be seen.
A-waves: Pathological sustained plateau waves of
50–80 mmHg lasting between 5 and 10 min, possibly
representing cerebral vasodilatation and an increase
in CBF in response to a low CPP (Fig. 2.2).
B-waves: Small, transient waves of limited
amplitude every 1–2 min representing fluctuations
in cerebral blood volume. These may be seen in
normal subjects, but are indicative of intracranial
pathology when the amplitude increases above
10 mmHg (Fig. 2.3).

40
30
20
10
0
10

Figure  2.1.  ICP traces showing the three distinct peaks. In the
non-compliant brain, the amplitude of P2 increases. Reproduced
with kind permission from Anaesthesia UK (www.frca.co.uk).

30
40
50
Time (minutes)

60

40
30
20
10
0

Time

20

Figure 2.2.  Lundberg A waves. Reproduced with kind permission
from Anaesthesia UK (www.frca.co.uk).

Intracranial Pressure (mmHg)

··

·· Focal pathology on CT brain scan
·· Head injury and age >40
·· Normal CT brain scan but systolic blood
pressure persistently <90 mmHg
·· Where other injuries and their treatment
necessitate the use of sedation or anesthesia
Subarachnoid hemorrhage with associated
hydrocephalus.
Hydrocephalus
Hypoxic brain injury for example, after near
drowning

Postoperative in patients at risk of severe cerebral edema
Encephalopathy (e.g., in liver failure)

11

1

2

3
4
5
Time (minutes)

6

Figure 2.3.  Lundberg B waves. Reproduced with kind permission
from Anaesthesia UK (www.frca.co.uk).


12

S. Davies and A. Lindley

C-waves: Small oscillations in ICP that reflect
changes in systemic arterial pressure.
With cerebral autoregulation intact, a rise in
MAP produces vasoconstriction and a fall in ICP.
However, when autoregulation fails, the circulation becomes pressure passive and changes in
MAP are reflected in changes in the ICP. Continuous analysis of MAP and ICP allows a correlation

coefficient called the pressure reactivity index to
be derived (PRx). Positive values indicate disturbed cerebral vascular reactivity, whilst negative
values indicate that reactivity remains intact
(Gupta 2002).
Despite the fact that trial results have not always
been compelling, most clinicians regard the ICP
monitor as an essential tool that allows estimation
of CPP (Czosnyka and Pickard 2004; Czosnyka
et  al. 1996), gives early warning of developing
pathology, allows the response to therapy to be
objectively measured, and also has value as a
prognostic indicator (Joseph 2005).

Jugular Venous Oximetry (SjvO2)
SjvO2 is an indicator of global oxygen extraction
of the brain. Jugular venous desaturation suggests an increase in cerebral oxygen extraction
which indirectly implies that there has been a
decrease in cerebral oxygen delivery, and hence
perfusion.
The internal jugular vein drains the majority of
blood from the brain, and in most patients the
right lateral sinus is larger. Despite the fact that
flow is different on the two sides, oxygen saturations are normally very similar. This also appears
to be the case in diffuse brain injury, whilst in
focal injuries there tends to be a greater difference
in the saturations of the two veins.
Jugular venous saturations can be measured
using the principle of infrared refractometry via
a specially designed catheter (Gopinath et  al.
1994).

SjvO2 values
··
··
··
··

55–75% – normal
>75% – luxury perfusion
<54% hypoperfusion
<40% suggests global ischemia and is associated
with increased cerebral lactate production.

Insertion of Jugular Venous Saturation
Catheter
Insertion involves retrograde cannulation of the
internal jugular vein. A pediatric pulmonary
artery catheter introducer can be used through
which the fiber optic SjvO2 catheter is advanced
beyond the outlet of the common facial vein to the
level of the jugular bulb at the base of the skull.
Ultrasound is often used for accurate identification of vein position to avoid arterial puncture,
and to minimize the risk of hematoma formation
which can in turn impede venous drainage. Correct
positioning is confirmed on a lateral neck X-ray
with the catheter tip lying at the level of the
mastoid air cells.

Indications for SjvO2 Monitoring
·· Acute brain injury. An association between

SjvO2 desaturation and poor neurological out­come
has been observed. Fandino showed that in
traumatic head injury SjvO2 was the only factor
associated with outcome, whilst Gopinath
showed that multiple SjvO2 desaturations were
associated with an increased incidence of poor
neurological outcome compared to those who
showed no desaturations (Moppett and Mahajan
2004).
Optimal CPP would appear to be at the point when further increases
in MAP do not lead to a rise in SjvO2.

·· Monitoring of therapy response. If ICP and SjvO2
are both raised, hyperemia is implied and hyperventilation is appropriate. SjvO2 should be monitored and kept above 55% in these circumstances,
as excessive hyperventilation may cause profound cerebral vasoconstriction and cerebral
ischemia. More recent work using PET scanning,
however, has cast some doubt on the value of
SjvO2, with hyperventilation appearing to increase
ischemic brain volume without necessarily producing a fall in jugular venous saturation.
·· To guide optimal blood pressure and PaCO2 management during operative treatment of aneurysms following SAH. During the operative
treatment of an aneurysm, hypertension must be
avoided because of the risk of rupture and
bleeding. However, excessive reductions in