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practical management of


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practical management of
Edited by Jeffrey V Rosenfeld

Sydneyâ•… Edinburghâ•… Londonâ•… New Yorkâ•… Philadelphiaâ•… St Louisâ•… Toronto

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Churchill Livingstone
is an imprint of Elsevier

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National Library of Australia Cataloguing-in-Publication Data

Author: Rosenfeld, Jeffrey.

Title: Practical management of head and neck injury / Jeffrey Rosenfeld.

ISBN: 9780729539562 (pbk.)

Subjects: Head–Wounds and injuries–Treatment. Neck–Wounds and injuries–Treatment.

Dewey Number: 617.51044

Publisher: Luisa Cecotti

Developmental Editor: Neli Bryant
Publishing Services Manager: Helena Klijn
Project Coordinator: Geraldine Minto
Edited by Carol Natsis
Proofread by Forsyth Publishing Services
Cover and internal design by Darben Design
Index by Cynthia Swanson
Typeset by Toppan Best-set Premedia Limited
Printed by China Translating & Printing Services Ltd

Foreword  vii 6 Injury to the spine and spinal cord  98

Preface  viii A. Spinal injury  98
Susan M Liew, Arvind Jain
Acknowledgments  x
B. Traumatic spinal cord injury  123
Contributors and reviewers  xi
Jin W Tee, Jeffrey V Rosenfeld, Patrick Chan

1 Epidemiology  1
7 Vascular injury  136
Peter Bragge, Russell L Gruen
A. Blunt carotid and vertebral artery
2 Anatomy of the head and neck  10 injuries  136
Tony Goldschlager, Jeffrey V Rosenfeld Jeffrey V Rosenfeld, Jin W Tee

B. Traumatic caroticocavernous fistula  141

3 Pathophysiology of traumatic brain Peter Hwang, Anoop Madan
injury  40
C. Penetrating injury to the cervical carotid and
Tony Goldschlager, Jeffrey V Rosenfeld
vertebral arteries  148
Jeffrey V Rosenfeld, Jin W Tee
4 Pre-hospital management  57
Stephen Bernard
8 Operative surgery  150
5 Emergency department management  64 A. Neurosurgery  150
A. Initial assessment and treatment  64 Jeffrey V Rosenfeld
Mark Fitzgerald, Alfredo Mori, B. Ear, nose and throat (ENT) surgery  176
Jeffrey V Rosenfeld Vince Cousins
B. Maxillofacial injuries  81 C. Ocular injuries  180
David Morgan, Jeffrey V Rosenfeld Anthony Hall
C. Blunt injury of the neck  85 D. Maxillofacial injuries  181
Vince Cousins, Jeffrey V Rosenfeld David Morgan
D. CSF rhinorrhoea  86 E. Cervical spine injuries  194
Vince Cousins, Jeffrey V Rosenfeld Susan M Liew, Arvind Jain
E. Epistaxis  86
Vince Cousins, Jeffrey V Rosenfeld 9 Intensive care management of  
F. Injuries to the ear  88 head injury  212
Vince Cousins, Jeffrey V Rosenfeld Andrew Davies, D James Cooper,
Jeffrey V Rosenfeld
G. Fractures of the temporal bone  89
Vince Cousins, Jeffrey V Rosenfeld
10 Ward care of the head-injured
H. Eye injuries  93 patient  223
Anthony Hall, Jeffrey V Rosenfeld Peter Hwang, Jin W Tee, Antoinette David


11 Rehabilitation following traumatic   20 Prediction of outcome and the prognosis

brain injury  231 of head injury  327
John Olver, Bianca Fedele Lucia M Li, Mathew R Guilfoyle, Peter Hutchinson

12 Head injury in children  242 21 Prevention of head injury and the role of
Jeffrey V Rosenfeld, Simon Young trauma systems  354
Biswadev Mitra, Russell L Gruen
13 Head injury in the elderly  254
Peter Hwang, Jin W Tee, Jeffrey V Rosenfeld Appendixes  363
A Glasgow Coma Scaleâ•… 364
14 Head injury in sport  263 B Paediatric Glasgow Coma Scaleâ•… 364
Gavin A Davis, Michael Makdissi, C Glasgow Outcome Score (Extended)
Paul McCrory (GOSE)â•… 364
D Marshall CT gradingâ•… 364
15 Penetrating head injury  281
E Injury Severity Scoreâ•… 365
Rocco Armonda, Randy S Bell,
Jeffrey V Rosenfeld F American Spinal Injury Association (ASIA)
Scale for Acute Spinal Cord Injury
Assessmentâ•… 366
16 Bleeding diathesis and
anticoagulants  294 G Westmead Post-traumatic Amnesia (PTA)
Scaleâ•… 368
Peter Hwang, Marc Seifman,
Jeffrey V Rosenfeld H Disability scales: short-form 12 (SF-12) â•… 371
I Alfred Cervical Spine Clearance Protocol for
17 Neurotrauma in pregnancy  303 Trauma Patientsâ•… 373
Jeffrey V Rosenfeld, Jin W Tee J Post-traumatic amnesia screening and referral
processâ•… 374
18 Brain death  311 K Essential surgical instruments for emergency
Alvin Teo, Andrew Davies neurosurgeryâ•… 376
L Guidelines bibliographyâ•… 376
19 Persistent vegetative and minimally 1. Evidence-based guidelinesâ•… 376
responsive states following head
2. Mild traumatic head injury guidelinesâ•… 376
injury  317
Bruce Day Index  377

Caring for people with a head or spinal injury is the writing. On one hand, stories of patients enliven
challenging but rewarding. The challenges come the clinical sections; these sit well within the general
from the large numbers of victims, the many sources didactic approach, making telling messages about
of complicating adverse events, and the multiplicity the application of principles to the care of the indi-
of body systems that can be destabilised, the rapidity vidual. On the other hand, the dominant origin of
with which outcome can be worsened and the the authorship—although enhanced from other
urgency of providing often complex treatment. The sources—expresses a clear and appropriate picture
reward for effective care is survival, recovery and of a trauma care system, evolved and owned locally.
restitution of the injured person. Crucial in achiev- The ‘Melbourne approach’ is based on local data,
ing this is a clear understanding of what needs to be is founded on sound principles and practices, is
done—both by individuals and collectively, within coordinated and multidisciplinary and evidently
and across the teams whose multidisciplinary inputs successful. It has yielded valuable additions to
need to be combined and coordinated. knowledge in the field. Nevertheless, its most valu-
Professor Rosenfeld and his team of authoritative able contribution, embedded in this book, is to con-
contributors provide a vivid, comprehensive account tinue making the care of head injuries important,
of the knowledge needed to meet the challenges of interesting, even controversial. This forcefully moti-
care for head and cervical spine injuries and firm vates and underpins provision of the safe, reliable
guidance about how this can be translated into prac- high quality care that is rewarded in improved out-
tice. A wealth of information has been brought comes for patients.
together from a wide array of sources and presented
with clarity, depth and detail. The account is honed Sir Graham Teasdale
by insights from practical experience. The result Emeritus Professor of Neurosurgery University of
conveys assurance that it provides all that a reader Glasgow
could wish to know—whether about fundamental Past President Royal College of Physicians and
basic principles or current advances. Even in the era Surgeons of Glasgow
of electronic technology, the scholarship involved in Past Chairman of European Brain Injury
pursuing so many lines of enquiry, analysing and Consortium and International Neurotrauma Society
synthesising the findings is ‘Herculean’. Sufficient FRCP London, Edinburgh, FRCS Edinburgh,
and authoritative in itself, Practical management of FRCPS Glasgow
head and neck injury is an invaluable resource and Honorary Fellow RCS England, Ireland,
a powerful illustration of the continuing value of the Honorary International Fellow American College
textbook. of Surgeons
Two contrasting aspects seem to me to character- Fellow of the Academy of Medical Sciences UK,
ise the philosophy and breadth of approach behind Fellow of the Royal Society of Edinburgh


Globally, it has been estimated that at least 10 health professionals. Many chapters will also inform
million people each year suffer a traumatic brain practitioners who work in remote locations where
injury (TBI) that results in death or hospitalisation, there is no neurosurgical service.
and an estimated 57 million people worldwide have Why head and neck? A myriad of textbooks on
been hospitalised with one or more TBIs. Even in head injury have been published in the last two
trauma systems with advanced pre-hospital and in- decades. Many are encyclopaedic, but mainly con-
hospital medical care, 50% of patients with severe fined to the brain and skull. However, injuries to the
TBI either die or survive with severe lifelong dis- brain and skull also frequently involve the face and
ability. Most of the severe disability survivors are sinuses, mouth, teeth and jaws, orbits, eyes, ears and
young males who are never able to live indepen- neck, including the great vessels, spine, spinal cord
dently or return to employment. There are also many and pharynx, larynx and trachea. A more holistic
children and elderly people who suffer TBI. Sport approach is required. The interplay between the
and leisure activities are an important cause of TBI various specialties is highlighted and should encour-
in young people. Penetrating brain injury sustained age the multidisciplinary team approach to caring
in war zones and because of urban crime is also a for these patients.
major problem worldwide. Acute spinal cord injury, Practical management of head and neck injury
facial, ocular, auditory and cervical vascular injury captures the essence of the day-to-day management
further contribute to the overall injury burden. of head and neck injury by following all aspects
The cost of severe TBI in Australia in economic of care through the patient’s journey from the acci-
terms has been independently calculated recently by dent scene all the way through to rehabilitation.
Access Economics to be A$4.8 billion annually. This Separate chapters are devoted to specialised topics
does not describe the human cost. In the USA, the covering children, the elderly, pregnancy, coagula-
economic burden of TBI is estimated to be US$60 tion disorders, brain death, persistent vegetative
billion annually. Imagine the cost to nations and state, head injury in sport and penetrating head
families where trauma systems and medical care are injury. These are all pertinent problems that junior
not well developed or resourced, and consider the staff may encounter and with which they should
incalculable worldwide economic burden of brain have some familiarity. The management of head and
and spinal cord injury, particularly in low- and mid- neck injury also depends on a sound understanding
dle-income countries. These sobering statistics can of the essential anatomy, including CT images, as
be improved through education of health providers, well as the pathophysiology. The general issues of
better trauma systems, high quality hospitals and epidemiology, prognosis of TBI, prediction of
ongoing basic and applied research. outcome, head injury prevention and trauma systems
Helping to save lives and improve the outcome complete the coverage. The recent pertinent scien-
of those affected by head and neck trauma is the aim tific evidence and discussion of many controversies
of this book. Practical management of head and are also included.
neck injury is written for the broad audience of We have assembled a group of authors who are
medical students, junior doctors and doctors in all experts in their respective specialties. While
specialist training in emergency medicine, neuroÂ� many who write about the patient’s journey all
surgery, trauma and general surgery, orthopaedics, work together at the Alfred Hospital and Monash
otorhinolaryngology, ophthalmology, rehabilitation University in Melbourne, Australia, other Australian
medicine, neurology and intensive care, and con- and international authorities are included.
tains sections written by experts in all of these spe- I make no apologies for not structuring the many
cialties. We believe it will also be of interest to varied chapters in the same way. I intentionally gave
paramedics, nurses, physician assistants and allied the authors some latitude in the presentation of their

Preface ix

material and the number of references cited. Despite It is my fervent hope that this textbook will help
this, they have managed to write in a similarly to improve the knowledge base and interdisciplinary
engaging way for each topic with an appropriate team approach to the management of head and neck
weighting of literature review. There is inevitable trauma at all types of healthcare facilities and in the
overlap between some of the chapters. This has been full range of healthcare systems, including low-
accepted to maintain the integrity of each of these income countries, where services are sparse and gen-
chapters and to reinforce important concepts. eralists do the best they can with limited resources.

Jeffrey V Rosenfeld
August 2011

I owe a debt of gratitude to my own neurosurgical the outcomes for victims of bomb blast and penetrat­
teachers and mentors Mr JB Curtis, Mr D Brownbill ing brain injury.
and Professor Andrew Kaye at the Royal Melbourne I particularly wish to thank Associate Professor
Hospital, Mr CBT Adams and staff at the Radcliffe Max Esser, Senior Orthopaedic Surgeon at the
Infirmary in Oxford, Dr John Little MD and staff at Alfred Hospital and Monash University for encour­
the Cleveland Clinic, Ohio, and many others too aging me to produce this book. He has co-authored
numerous to name. I wish to thank Professor Sir Practical Fracture Treatment with Dr Ronald
Graham Teasdale, one of the world’s leading experts McRea, also published by Elsevier, which is argu­
in traumatic brain injury research and management, ably one of the definitive current textbooks on frac­
for writing the Foreword. ture management.
I thank the neurosurgery registrars at the Alfred I am indebted to Elsevier for having confidence
Hospital, Dr Jin Wee Tee, Dr Tony Goldschlager as in the aim and conceptual design of this textbook.
well as my neurosurgical colleagues at the Alfred, The superb staff at Elsevier, Ms Neli Bryant, Ms
Clinical Associate Professor Peter Hwang and Mr Sophie Kaliniecki and Ms Geraldine Minto, and
Patrick Chan, for their support and contribution to editor Ms Carol Natsis have been enthusiastic, gra­
the book. I also thank my many Alfred colleagues cious and always very obliging in nurturing this text
and the other Australian and international contri­ to its final form. I sincerely thank my personal assis­
butors very much for sharing their tremendous tant, Ms Sylvia Oklobdzija, for all her tremendous
knowledge and experience. I admire US military assistance.
neurosurgeons Dr Rocco Armonda MD and Dr Last but by no means least, no words can convey
Randy Bell MD for the devotion they have shown the deep appreciation I have for the tremendous love
and the expertise they have developed in improving and support I receive from my wife Debbie and my

Jeffrey V Rosenfeld

Contributors and reviewers

Rocco Armonda MD, COL, MC Bruce Day MBBS, FRACP
Assistant Professor of Surgery, Uniformed Services Clinical Neurophysiologist, The Alfred Hospital,
University of the Health Sciences Melbourne, Victoria
Director, Cerebrovascular Surgery/Neurocritical Care,
Bethesda, Maryland, USA Bianca Fedele BA(Hons)
Research Assistant, Epworth Monash Rehabilitation
Randy S Bell MD, MC Medicine Unit, Melbourne, Victoria
National Naval Medicine Center, Bethesda, Maryland, USA
Mark Fitzgerald MBBS, FACEM
Stephen Bernard MBBS, MD, FACEM, FCICM Adjunct Clinical Associate Professor, Director of Trauma
Associate Professor, Intensive Care Physician, The Alfred Services, The Alfred Hospital, Melbourne, Victoria
Hospital, Melbourne, Victoria
Director of Intensive Care, Knox Private Hospital, Tony Goldschlager MBBS, DCH(London), PhD, FRACS
Melbourne, Victoria Neurosurgical Registrar, The Alfred Hospital, Melbourne
and Monash Medical Centre, Clayton Victoria
Patrick Chan MBBS(Melb), MD(Melb), FRACS
Neurosurgeon, The Alfred Hospital, Melbourne, Victoria Russell L Gruen MBBS, PhD, FRACS
Director, National Trauma Research Institute,
D James Cooper BMBS, MD, FRACP, FCICM Melbourne, Victoria
Professor of Intensive Care Medicine, Monash University, Surgeon and Head of Trauma Quality Assurance,
Melbourne, Victoria The Alfred Hospital, Melbourne, Victoria
Director of the ANZIC Research Centre, Monash Professor of Surgery and Public Health, Monash
University, Melbourne, Victoria University. Melbourne, Victoria
Deputy Director of ICU, The Alfred Hospital, Melbourne,
Victoria Mathew R Guilfoyle BSc, MBBCh, MRCS
Head of Intensive Care Unit (ICU) Research, The Alfred Academic Clinical Fellow, Addenbrooke’s Hospital,
Hospital, Melbourne, Victoria Cambridge, UK

Vincent Cousins BMedSci(Hons), MBBS(Hons), FRACS Anthony Hall MD, FRANZCO

Adjunct Clinical Associate Professor, Ear Nose and Throat Adjunct Clinical Associate Professor, Head of Unit,
Surgeon, Head of Unit, Otolaryngology 2, The Alfred Department of Ophthalmology, The Alfred Hospital,
Hospital, Melbourne, Victoria Melbourne, Victoria

Antoinette David RN, GradCert(Neurosciences) Peter Hutchinson BSc(Hons), MBBS, PhD,

Clinical Support and Development Nurse, Neurosurgery and FRCS(Surg Neurol)
Neurotrauma, The Alfred Hospital, Melbourne, Victoria Reader and Honorary Consultant Neurosurgeon,
Addenbrooke’s Hospital, Cambridge, UK
Andrew Davies MBBS, FRACP, FCICM
Adjunct Clinical Associate Professor, Intensive Care Unit, Peter Hwang MBBS, FRACS, FRCS(Edin), FRCS(Glasg),
The Alfred Hospital, Melbourne, Victoria FCSS, FAMS
Adjunct Associate Professor, Department of Epidemiology Neurosurgeon, The Alfred Hospital, Melbourne, Victoria
and Preventative Medicine, Monash University, Melbourne, Adjunct Clinical Associate Professor, Central Clinical
Victoria School, Monash University, The Alfred Hospital,
Melbourne, Victoria
Gavin A Davis MBBS, FRACS (Neurosurgery)
Associate Professor, Neurosurgery, Department of Arvind Jain MBBS, MS(Ortho)
Neurosurgery, Cabrini Hospital, Malvern, Victoria and Orthopaedic Principal Fellow, The Alfred Hospital,
Department of Neurosurgery, Austin Hospital, Heidelberg, Melbourne, Victoria

xii Contributors and reviewers

Lucia M Li MA(Cantab), MBBChir John Olver MBBS, MD, FAFRM(RACP)

Academic Foundation Doctor in Neurosurgery, Victor Smorgon Chair of Rehabilitation Medicine, Monash
Addenbrooke’s Hospital, Cambridge, UK University, Melbourne, Victoria
Director Rehabilitation, Epworth Healthcare, Melbourne,
Susan M Liew MBBS(Hons), FRACS(Orth) Victoria
Adjunct Clinical Associate Professor, Orthopaedic & Spine
Surgeon, Director of Orthopaedic Surgery, The Alfred Jeffrey V Rosenfeld AM MBBS(Melb), MD(Monash),
Hospital, Melbourne, Victoria MS(Melb), FRACS, FRCS(Edin), FACS, FRCS(Glasg)
Adjunct Clinical Associate Professor, Monash University, Hon, FCNST Hon, FRCST Hon, FACTM, MRACMA,
The Alfred Hospital, Melbourne, Victoria RAAMC
Professor and Head, Department of Surgery, Monash
Paul McCrory MBBD, PhD, FRACP, FACSP, FFSEM, University Central Clinical School, Melbourne
FACSM, GradDipEpidStats Director, Department of Neurosurgery, The Alfred
Associate Professor, Centre for Health, Exercise and Sports Hospital, Melbourne
Medicine & The Brain Research Institute, University of Director, Monash University Brain Institute, Melbourne
Melbourne, Victoria Major General and Surgeon General, Australian Defence
Interventional Neuroradiologist, Department of Radiology, Marc Seifman MBBS, BMedSc
The Alfred Hospital, Melbourne, Victoria Surgical Registrar, The Alfred Hospital, Melbourne,
Adjunct Lecturer, Monash University, Melbourne, Victoria Victoria

Michael Makdissi BSc(Hon) MBBS, PhD, FACSP Jin W Tee MBBS, BMedSc
Research Fellow, Centre for Health, Exercise and Sports Neurosurgery Registrar, The Alfred Hospital,
Medicine & the Brain Research Institute, University of Melbourne, Victoria
Melbourne, Victoria Neurotrauma Research Fellow, The Alfred Hospital,
Melbourne, Victoria
Biswadev Mitra MBBS(Melb), MHSM, MAAFP, FACEM
Consultant Emergency Physician, The Alfred Hospital, Alvin Teo MBBS, MMed, EDIC, FANZCA, FCICM, DDU
Melbourne, Victoria Specialist in Intensive Care, The Alfred Hospital,
Melbourne, Victoria
David Morgan MBBS, FRACS
Plastic and Reconstruction Surgeon, The Alfred Hospital Simon Young MBBS(Hons), DipCrim, FACEM
and Cabrini Brighton Medical Centre, Melbourne, Victoria Director of Emergency Medicine, Royal Children’s
Hospital, Parkville, Victoria
Alfredo Mori MBBS, Dip EBHC(Oxon), FACEM
Emergency Physician, The Alfred Hospital, Melbourne,

Noel Eatough BSc(Med), MBBS, FACEM Andrew Pearce BSc(Hons), BMBS, FACEM, PGCert
Staff Specialist, Royal North Shore Hospital, Sydney, and Aeromed Ret
CareFlight, New South Wales Senior Staff Specialist, Emergency Medicine, Royal
Adelaide Hospital, South Australia
Michael Facek MBBS(Hons), BSc Associate Professor and Clinical Director, MedSTAR
Orthopaedic Registrar, Mater Miscorderiae Hospital, New Emergency Medical Retrieval Service, South Australia
South Wales Group Captain, RAAF Specialist Reserves; Clinical
Director, Emergency Medicine and Aeromedical
Peter Bragge, Russell L Gruen

Every day, in every country, men, women and chil­ a state or a country, this information is essential for
dren sustain head injuries. Trips and falls, transport the planning and monitoring of injury prevention
accidents, sporting injuries, interpersonal violence efforts, and treatment and disability services.
and military conflict all lead to a spectrum of inju­ Of course every country has its own TBI epide­
ries to the face, scalp, skull vault, sense organs and, miology. Rather than being a comprehensive review
most importantly, to the brain itself. of every country’s experience of TBI, however, this
Globally, at least 10 million people each year chapter focuses on the main global patterns of injury,
suffer a traumatic brain injury (TBI) that results in how these patterns are changing and the implica­
death or hospitalisation, and an estimated 57 million tions for the future.
people worldwide have been hospitalised with one
or more TBI.1 Estimates of the annual incidence lie
between 91 and 372 per 100,000,2,3 and estimates of
mortality range from 9 to 89 per 100,000.4 Almost
60% of TBIs worldwide are due to road traffic acci­ Epidemiology relies on reliable and valid data, and
dents, 20–30% to falls, 10% to violence and 10% to there are important challenges that relate to defini­
work or sports injuries5. tions, classification and data availability.
Epidemiology is the science that describes the TBI is usually defined as an injury to the brain
occurrence of disease, risk factors, causal mecha­ resulting from an external force, leading to transient
nisms and outcomes. Epidemiology provides prac­ or permanent neurological dysfunction.6 The most
titioners and policy makers with valuable information commonly used classification for TBI consists of
about incidence (new cases), disease burden (includ­ ‘mild’, ‘moderate’ or ‘severe’, based on duration of
ing prevalence and outcomes such as death, dis­ loss of consciousness and clinical presentation, the
ability and cost), and the effect of prevention and first Glasgow Coma Score and the duration of post-
treatment initiatives. At the level of a health service, traumatic amnesia, as shown in Table 1.1.

TABLE 1.1â•… Classification of TBI6,7,8,9

Typical duration Typical first Typical duration

of LOC Clinical presentation GCS score of PTA

Mild TBI 30 mins or less Awake; eyes open. Symptoms can include 14–15 Less than 24 hours
(concussion) confusion, memory and attention difficulties,
headache, and behavioural problems.
Moderate TBI More than 30 mins Lethargic; eyes open to stimulation; sleepy, but 9–13 1–7 days
still arousable.
Severe TBI More than 30 mins Coma; eyes do not open, even with stimulation. 3–8 1–4 weeks
LOC = loss of consciousness; GCS = Glasgow Coma Scale; PTA = post-traumatic amnesia.


The Glasgow Coma Scale (GCS)10 is a clinical of the distribution of pathological types of head
prognostic indicator commonly used for the initial injury among major trauma cases (injury severity
assessment of severity of injury that requires the score, ISS >â•›15) for the state of Victoria, Australia,
assessment of eye-opening, motor and verbal respon­ where motor vehicle crashes, falls and interpersonal
siveness. While intended to be used as a repeated violence are the main causes of severe injury and
measure, it is often used as a single assessment and firearm use is uncommon. Population-wide data is
recorded as such in registry data. captured for all major trauma cases in the Victorian
Post-traumatic amnesia (PTA), a term first used State Trauma Registry. In the 5 years from 2005 to
in 1928, refers to the period between the injury and 2009, there were 11,608 cases of major trauma in
the return of full, continuous memory, including any Victoria, and among these 6963 patients (60%) were
time during which the patient was unconscious.11 coded as having a type of head injury. Of the major
PTA is a condition following a TBI that is charac­ trauma patients with head injury, the most frequently
terised by confusion, disorientation, loss of memory coded ICD codes were concussion, subdural haem­
post-injury and ‘clouded’ consciousness.12,13 Conse­ orrhage, fractured base of skull, subarachnoid 
quently, patients in PTA may be unable to state their haemorrhage, diffuse brain injury and focal brain
name and may be unaware of the time and where injury (Table 1.2). Four per cent of patients who had
they are.12 While a patient is in PTA, the ability to moderate-to-severe head injury also had a cervical
store new events in the memory is lost14; therefore, spine injury.
a hallmark of PTA resolution is the return of con­ Other ways of classifying TBI, including clinical
tinuous memory.15 In approximately one-third of descriptions of the lesion and the presentation, vary
PTA cases, a patient has ‘islands of memory’ and with the nature, intensity, direction and duration of
can recall some, but not all, events.14 ‘Retrograde the external forces to the brain.19 The four main
amnesia’ refers to failure to recall events prior to the patho-anatomical sequelae of TBI are contusion,
injury, and ‘anterograde amnesia’ refers to failure to subarachnoid haemorrhage, haematoma (including
lay down new memories for a period following the extradural, subdural and intraparenchymal lesions)
injury. and diffuse axonal injury (DAI).17 Contusion arises
Differences in classification systems affect com­ from contact impact. Haematoma is present in 
parability of data.3 While the mildâ•›/â•›moderateâ•›/â•›severe 25–35% of patients with severe TBI and 5–10% of
distinction is useful for epidemiological purposes, moderate TBI cases. DAI, which is characterised by
there is ongoing debate about its validity for clas­ multiple small lesions in white matter tracts, causes
sification and prognostication. Difficulties in using profound early coma and is associated with poor
these categories, which can lead to inaccuracies, outcomes.19 These sequelae are often found to co-
include the effects of sedation, intoxication, facial exist in patients with severe and fatal TBI but 
injury and intubation on GCS scores, the effect of can also do so in the setting of mild and moderate
the exact timing of measurement and the potential injuries.17 Also important to the clinician is the
influence of shock and other organ system failure on presence of secondary insults, including ischaemia,
the evaluation of GCS, consciousness and the dura­ hypoxia, cerebral oedema, hypotension, hypergly­
tion of PTA, and missing documentation of severity caemia and hypercapniaâ•›/â•›hypocapnia.17,19,20
data in medical records.16 Furthermore the poor cor­ Irrespective of the classification system used 
relation of GCS with the pathophysiological mecha­ for coding TBI, there are factors limiting the 
nisms underlying the neurological deficits gives availability and comparability of data within and
little direction to further management.17 between systems. These limitations include the
New means of assessment of global severity are following:
emerging, including newer-generation imaging tech­ • Most brain injuries (up to 80%) are mild (mTBI),
niques such as diffusion tensor imaging (DTI), but, but data on mTBI are difficult to capture, as such
for the present, the mildâ•›/â•›moderateâ•›/â•›severe classifica­ injuries may receive no medical treatment, or
tion based on clinical features is likely to remain in may not be treated in hospitals where TBI data­
widespread use.17 bases are kept.21,22
Pathological classification, the most widely used • TBI often occurs with multi-trauma and in mili­
being the 10th edition of the International Classi­ tary settings, and therefore is underreported or
fication of Diseases (ICD-10),18 complements func­ rolled into more general death and injury
tional severity scoring. We provide here an example statistics.21,22
1 • Epidemiology 3

TABLE 1.2â•… Distribution of International Classification of Diseases 10th edition (ICD-10) codes of head injury in
Victoria, Australia, 2005–09

Number of cases % major % cases with

ICD Code Injury (1 Jan 2005 – 31 Dec 2009) trauma cases head injury

S060 Concussive injury 3899 33.6% 56.0%

S065 Traumatic subdural haemorrhage 2929 25.2% 42.1%
S021 Fractured base of skull 2027 17.5% 29.1%
S066 Traumatic subarachnoid haemorrhage 1888 16.3% 27.1%
S062 Diffuse brain injury 1725 14.9% 24.8%
S063 Focal brain injury 1534 13.2% 22.0%
S020 Fractured skull vault 987 8.5% 14.2%
S064 Extradural haemorrhage 798 6.9% 11.5%
S061 Cerebral oedema 432 3.7% 6.2%
S068 Other intracranial injuries 259 2.2% 3.7%
S069 Intracranial injury, unspecified 62 0.5% 0.9%
Data provided with permission from the Victorian State Trauma Outcomes Registry (VSTORM).

• Injury reporting and surveillance systems vary increase in high-income countries. Furthermore, 
across the world.21 Hospital records, death cer­ by 2020 traffic-related injuries will become the
tificates, trauma registries and purpose-designed third-ranked cause of disability-adjusted life years
prospective observational studies provide the (DALYs) lost (second-ranked cause of DALYs lost
most reliable sources of data on occurrence and in low-to-middle income countries), with 71.2
outcomes of TBI, but such data rarely capture all million DALYs lost worldwide, representing 5.1%
dimensions of brain injury. of the global burden of disease.24
There is a need for more accurate monitoring of the Motorcycle riders are at particular risk. For
occurrence, severity and outcomes of TBI using example, in the UK, motorcyclists comprise under
standardised measures and processes of data collec­ 1% of road users but represent 14% of road deaths
tion and reporting. National trauma registries are and serious injuries. They are killed or seriously
well suited to this purpose. injured at twice the rate of pedal cyclists and at more
than 16 times the rate of car occupants.25,26
Alcohol is a major contributing factor to traffic-
INCIDENCE AND MECHANISMS OF TBI related head injury in many countries. For example,
Throughout the world, TBI incidence by age is tri- 64% of deaths and over a third of non-fatal injuries
modal, with peaks in early childhood, late adoles­ in child passengers in the USA have been linked to
cence and the elderly.2 Data from the USA and drink-driving.27 Of course other causes of traffic-
Australia show that, overall, males are twice as related injury include speeding, sleepiness, failure
likely as females to experience TBI.22,23 This is pre­ to use safety harnesses, drugs that impair conscious­
dominantly because of the adolescent male’s ness and driver response time, as well as character­
involvement in violence and traffic-related injuries. istics that make the vehicles or roads usafe.
At the extremes of age, males and females have a Of the remaining causes of TBI, falls produce
similar incidence of TBI.2 20–30% of TBIs worldwide, especially among
Traffic-related injuries account for 1.2 million young children and the elderly. The International
deaths each year worldwide. The World Health Multicenter Study of Head Injury in Children,28 con­
Organization Global Burden of Disease Study fore­ ducted in five countries, revealed the relative pro­
casts that by 2020 traffic-related injuries will become portion of minor, moderate and severe TBI sustained
the sixth-ranked major cause of death worldwide, was 56%, 39% and 5%, respectively, with a case
representing 3.4% of all deaths worldwide. An 80% fatality rate of 1.6. However, the burden of injury 
increase in traffic-related deaths is forecast in low- in children falls disproportionately upon poorer
income to middle-income countries and a 30% regions; the WHO estimates that over 95% of injury

deaths in children occur in low- and middle-income PTA duration is significantly associated with attained
countries.29 educational level, cognitive function, anxiety and
In the elderly, a fall may be the result of a trip or recovery, as measured by the Extended Glasgow
stumble, a cardiac or cerebrovascular event, or other Outcome Scale.33
co-morbidities, including the effects of psychoactive
or cardiovascular drugs such as antihypertensives. Moderate-to-severe TBI
Elucidating the actual cause of falls in the elderly In the state of Victoria, the mortality rates in 2007–8
can be difficult. Falls incidence also varies by in the first year after injury were 22.6% for moderate
country; the incidence of TBI due to falls in India is TBI and 35.1% for severe TBI.23 US-based data
43 per 100,000 compared to a worldwide falls- indicates that mortality from TBI has decreased
related TBI incidence of 13.3 per 100,0001; India from 19.3 to 17.8 per 100,000 in the period 1997–
accounts for 50% of the known worldwide falls- 2007,34 continuing a downward trend established in
related TBI.21 earlier studies.35,36
Assault and violence contribute a further 10% of Most survivors of moderate-to-severe TBI face 
the world’s TBI cases. The incidence is dramatically a range of long-term disabilities. For example, in a
higher in some populations. For example, while the study of civilians in the USA, three years after
worldwide incidence of TBI due to assault is 43 per severe head injury only 3 of 45 survivors did not
100,000,1 in Johannesburg the incidence of fatal TBI suffer persisting and disabling symptoms.37 Survi­
in 2003 was 138 per 100,000 in males and 24 per vors face cognitive problems (for example, difficul­
100,000 in females.2 At a time when the incidence ties with concentration, memory and attention),
of assault-related TBI in the whole Australian popu­ psychological problems (depression and other 
lation was 41 per 100,000, in Australian Indigenous mood disorders) and physical disabilities (spasticity,
communities it was 855 per 100,000, with Indi­ speech problems). Although physical disabilities are
genous females having a nearly 70 times higher rate challenging, the neurobehavioural consequences of
than non-Indigenous females.30 In Europe, the rate TBI have a comparatively greater impact on quality
of assault-related TBI is significantly higher in of life.6 Cognitive and behavioural deficits drive
lower and upper-middle income countries than it is many of the lifestyle consequences of TBI, such as
in high-income countries.31 unemployment, relationship difficulties and loss of
The eventual outcome of TBI is determined by
OUTCOMES AND THE OVERALL the initial pathology, management of the head injury
BURDEN OF TBI and of the associated disability, and the presence of
co-morbidities and concomitant injuries. Identified
Mild TBI predictors of TBI outcome include age, neurological
Mild TBI patients make a full recovery in most status, trauma severity and CT characteristics.31,39
cases. However, 10–15% of mTBI patients experi­ Owing to the costs associated with providing optimal
ence ongoing problems, known as post-concussion TBI care, it has also been demonstrated that the
syndrome (PCS).6 This is characterised by a range economic status of a region is significantly associ­
of problems, including physical symptoms (e.g. ated with the outcome of patients with severe TBI.31
headache, vestibular problems, fatigue and sleep
disturbance), cognitive deficits (problems with Burden of disease
attention, memory, concentration) and behavioural Costs of TBI can be divided into direct costs of
changes (irritability, emotional lability).6,7 These medical and other care, and indirect costs—those
non-specific symptoms may present some time after relating to the loss, or partial loss, to society of the
mTBI, when patients attempt to return to previous productive efforts (both paid and unpaid) of injury
activities,7 making the diagnosis of PCS potentially victims and their caregivers.
challenging. The mechanisms of how mTBI leads to An economic analysis has estimated that each
PCS remain uncertain,32 and a range of factors other incident case of TBI in Australia presents an average
than those relating to injury severity, most notably lifetime cost of A$2.5 million for moderate TBI and
psychological factors, are thought to play a role in A$4.8 million for severe TBI.23 The total cost of
PCS development.32,33 A 10-year follow up study moderate and severe TBI in Australia is estimated
found that, among patients with mild head injury, to be A$8.6 billion per year (A$3.7 billion for
1 • Epidemiology 5

TABLE 1.3â•… Direct and indirect cost estimates for TBI in Australia23

Cost (A$ millions)

Category Definitionâ•›/â•›Examples Moderate TBI Severe TBI

Burden of disease Estimated dollar value of the loss of wellbeing due to TBI, 2206.6 2691.9
using DALYs multiplied by the value given to a year of life
(A$157,795 in Australia in 2008)
Lifetime lost earnings due 452.9 256.3
to reduced employment
Long-term care Attendant care, integration teacher aide, accommodation or 300.0 962.5
respite care, independent living unit, special accommodation and
nursing-home supported community options
Healthcare costs Ambulance, hospital, medical, paramedical and administration 269.1 308.0
Administrative costs The costs of administering welfare pensions and raising 174.6 150.5
additional taxation revenues
Aids and modifications Wheelchairs and gait aids, environmental modifications, hoists, 59.7 158.5
home modifications
Lifetime carer costs Informal care: e.g. family and friends 25.1 28.5

moderate TBI and A$4.8 billion for severe TBI). CHANGES IN TBI PATTERNS AND
The breakdown of these costs is given in Table 1.3.
In 2002, TBI patients in the USA averaged an
estimated US$65,600 in direct medical costs In global terms, patterns of TBI are changing as a
(US$4330 per day), US$1,003,140 in societal costs result of trends in motorisation, prevention and
per deceased person, up to US$74,673 in societal ageing. In high-income countries, road-traffic related
costs for non-fatal injuries and US$1631 per day for TBI has declined (Fig 1.1).35,43 Despite large numbers
rehabilitation services.40 Economic modelling not of motor vehicles, fewer transport-related injuries
only reveals important aspects of the burden of are occurring because of safer roads, safer cars, safer
injury, but has also been used to demonstrate the drivers and more timely and higher-quality emer­
cost savings of care improvements. Faul et╯al esti­ gency health services.44 In Australia, much of the
mated that if every patient received care consistent fall in the fatality rate since the late 1960s has been
with the Brain Trauma Foundation guidelines, 3,607 attributed to the introduction of seat belts, random
lives would be saved in the USA, and the savings in breath testing and speed cameras.45
annual medical costs, annual rehabilitation costs and However, the contribution of transport-related
lifetime societal costs would be US$262 million, TBI mortality continues to rise in low- and middle-
US$43 million and US$3.84 billion, respectively.41 income countries (Fig 1.2). While traffic-related
The burden of TBI in low-income and middle- injuries are projected to be the third-highest cause
income countries, therefore, has four important of DALYs lost worldwide by 2020, they are fifth in
dimensions to it. First, there is a high preponderance their contribution to the burden of disease in devel­
of risk factors for TBI. Second, healthcare systems oped regions and second in developing regions.46
in low-income and middle-income countries are the This disparity parallels the dramatic increase in
least prepared to address TBI when it occurs.21 motorisation without a similar increase of invest­
Third, the increased percentage of poor outcomes ment in injury prevention in low-income and 
from TBI relative to high-income countries further middle-income countries. In many countries, the
strains long-term or community services of these growth in use of motorcycles, often without protec­
often poorly resourced health systems. It is esti­ tive helmets, has led to dramatic increases in the
mated that 80% of the world’s disabled population incidence of TBI. For example, in eastern China,
live in low-income and middle-income countries, traffic-related incidence of TBI rose by 30% in 20
but only 2% can access rehabilitation.42 Fourth, low- years, over 50% of which cases did not involve
income countries are less equipped to implement occupants of cars (20% pedestrians, 13% bicycles,
strategies to abate TBI risk. 20% motorcycles).47

FIG 1.1â•… Road traffic fatality trends in three high-income countries (Australia, UK, USA). (Reproduced from World report
on road traffic injury prevention.24)

Ageing of populations has also had an important of the negative effect on outcomes of age itself 
effect on the incidence of TBI. In many high-income and of age-associated comorbidities and medica­
countries, for the first time ever there are now more tions, such as anticoagulants.
people over the age of 60 than children under the Changes in demography and exposure to risk
age of 15. One-fifth of the population of high- factors are changing the profile of head injury in all
income countries is already over 60 years of age, countries. To properly plan for the future, clinicians,
and it is estimated that by 2050 this age group will policy makers, and injury-prevention programs will
account for one-third of the population. The popula­ need to take these trends into account. Because TBI
tion of low-income and middle-income countries is can profoundly effect patients, their families and
also ageing, albeit more slowly. their communities, as well as the costs borne by
As the older population has increased, the inci­ governments, insurers, individuals and workplaces,
dence of falls-related TBI has increased. In the prevention is the key. Clinicians have an important
USA, the number of road-traffic crash and firearm- role in advocating safety initiatives to reduce the
related TBI deaths has fallen over the period 1990– burden of TBI around the world.
2007, but the number of falls-associated TBI deaths
has risen. TBI death rates for the period 1997–2007
have fallen in persons aged 0–44, but increased in
persons over 75 years of age.34 Similarly, in Austra­ 1. At least 10 million people each year suffer a TBI
lia hospitalised head injury in those aged over 60 that results in death or hospitalisation.
years increased 1.4 times in the 5 years to 2. Almost 60% of TBIs worldwide are due to road
2004–05. traffic accidents, 20–30% to falls, 10% to vio­
In addition to increased incidence of TBI, ageing lence and 10% to work or sports injuries.
of the population also affects the pattern of TBI 3. Several classification systems exist, and mild TBI
through increased mortality and morbidity because is grossly underreported.
1 • Epidemiology 7

FIG 1.2â•… Road traffic fatalities, adjusted for underreporting, 1990–2020. (Reproduced from
World report on road traffic injury prevention.24)

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Anatomy of the head and neck
Tony Goldschlager, Jeffrey V Rosenfeld

Effective management of traumatic brain injury

requires an understanding of neuroanatomy and the Clinical note
pathophysiological processes resulting from injury. As a result of the rich vascularity and frequent
Severe injuries are frequently not evident on exter- anastomoses of the scalp arteries, scalp lacerations
nal physical examination but the clinician should bleed profusely and severed arteries usually bleed
from both ends. It is necessary to control scalp
rapidly apply anatomical knowledge to the particu- bleeding, both in the setting of trauma or in cranial
lar circumstances of the patient, enabling a rapid operations. Closure of the scalp is described in
diagnosis and initiation of emergent treatment. Chapter 8.
Rapid and accurate communication between treating
clinicians is also imperative. This requires the accu-
rate anatomical description of the injuries and an
interpretation of the radiology before formal reports
become available. This chapter will present the fun- auricular branches. The supratrochlear and supraor-
damentals of relevant clinical anatomy and correla- bital branches of the internal carotid artery make a
tive radiological neuroanatomy, which will provide minor contribution. The vessels run in the connec-
the junior clinician or nurse with the essential facts tive tissue layer and freely anastomose with one
for the care of the patient with head and neck trauma. another.
A more detailed coverage can be found in standard
anatomy textbooks. SKULL
The bone of the skull consists of two layers of solid,
SCALP cortical bone that enclose a layer of highly vascular
The scalp extends from the top of the eyebrows to cancellous bone, called the diploë of the skull.
the nuchal line on the occiput and down to the ears
and zygoma on each side. Its layers can be remem- Upper skull
bered by a mnemonic of its name, Skin, Connective The upper skull (calvaria), or skull vault, is com-
tissue, Aponeurosis (galea), Loose areolar tissue prised of the frontal bone extending back from the
and Pericranium (Fig 2.1). The innermost layer of forehead to meet the parietal bone at the coronal
the scalp, the pericranium, is a periosteal layer. suture (Fig 2.2a). The parietal bone ends at the lamb-
Between the galea and the pericranium, there is an doid sutures, and from this point the occipital 
areolar connective tissue layer, which allows the bone continues postero-inferiorly to the foramen
scalp to be mobile over the skull. magnum. Laterally on each side are the temporal
The scalp has the thickest skin in the body. It has bones, which contain the complex middle and inner
a very rich blood supply, mainly from the terminal ear structures.
branches of the external carotid artery, which include In the infant (Fig 2.2b), the skull bones are not
the superficial temporal, occipital and posterior fused and at the confluence of the sutures are the
2 • Anatomy of the head and neck 11

FIG 2.1â•… Layers of the scalp and skull.

two fontanels, which are membranous. The anterior Facial skeleton and mandible
fontanel is the larger of the two and fuses by 18 The front part of the skull is the facial skeleton (Fig
months of age, while the posterior fontanel fuses by 2.4), consisting of the frontal bone in the forehead
about 6 months of age. The turgor of the anterior region, the zygoma (cheekbone), the nasal bone and
fontanel gives some indication of the intracranial then the maxilla and mandible. Surrounding the
pressure. nose are the paranasal sinuses. These air-filled cavi-
ties within the bones that are lined with respiratory
Base of the skull mucosa. There are frontal, sphenoid, ethmoid and
The inner skull is divided into three cranial fossae— maxillary sinuses. The function of the sinuses is
anterior, middle and posterior (Fig 2.3)—which uncertain.
form the skull base. The posterior cranial fossa The orbit (Fig 2.5) is a cone-shaped cavity con-
contains the cerebellum and brainstem, the latter  taining the eye and surrounding structures and is
of which extends through an opening in the tento- comprised of seven bones. Its outer boundaries are
rium cerebelli, known as the tentorial incisura or formed by the frontal bone superiorly, the maxilla
tentorial hiatus. Cranial nerves 7 to 12 pass through inferiomedially and the zygomatic bone laterally.
foramina in the posterior fossa. The middle cranial Inside the orbit are the lacrimal bone, sphenoid,
fossa comprises the sphenoid and temporal bone palatine and ethmoid bones.
and contains the temporal lobes laterally and the
pituitary gland medially, as well as the foramina for
the exit of the cranial nerves 2 to 6. The anterior
cranial fossa is located above the orbits, nasal Clinical note
cavity and ethmoid sinuses and contains the frontal Trauma to the face or skull may result in bone
lobes and the olfactory tracts, ending in the olfactory fractures. The clinician needs to assess not only the
bulbs. The olfactory epithelium lies at the roof of fracture itself but also the surrounding structures
such as the eye. Open or depressed fractures may
the nose, with nerve rootlets passing through the result in leakage of cerebrospinal fluid (CSF), either
cribiform plate to join the olfactory bulbs. The optic directly or through a sinus, and this may lead to
nerve passes through the optic canal in the sphenoid infection or meningitis. The force required to cause a
bones, just medial to the anterior clinoid process, fracture may cause other injuries, such as spinal
and enters the apex of the orbit with the ophthalmic fractures, which need to be excluded.

Frontal bone

Coronal suture

Sagittal suture
Parietal bone

Parietal foramen

Lambdoid suture

Occipital bone Lambda


Anterior fontanel

Posterior fontanel

FIG 2.2â•… a. Bones of the upper skull (calvaria); b. the fontanels in the infant skull. (From Drake RL et al1: a. Fig 8.21;
b. Fig 8.7c.)
2 • Anatomy of the head and neck 13

Frontal crest
Crista galli Foramen caecum

Orbital part (of Foramina of

frontal bone) cribriform plate

Cribriform plate

Lesser wing (of sphenoid)

Body (of sphenoid)
Anterior clinoid process Middle clinoid process
Chiasmatic sulcus Optic canal
Foramen rotundum
Tuberculum sellae
Superior orbital fissure
Greater wing (of sphenoid)

Opening of
carotid canal
Groove for
Posterior artery
Dorsum sellae
process Foramen lacerum
Foramen ovale
Groove and
hiatus for Trigeminal impression Foramen
lesser petrosal Tegmen tympani spinosum
nerve Groove and hiatus
for greater petrosal nerve
Arcuate eminence

Jugular tubercle

Groove for inferior petrosal sinus Internal acoustic meatus

Superior border of petrous
Jugular foramen
part of temporal bone
Groove for sigmoid sinus Hypoglossal canal

Groove for transverse sinus

Foramen magnum

Internal occipital crest

Internal occipital protuberance

FIG 2.3aâ•… The base of the skull: floor of the cranial cavity showing the cranial fossae and important bony
landmarks. (From Drake RL et al1: Fig 8.25; Fig 8.26; Fig 8.27.)

Posterior nasal spine Incisive fossa

Hard palate (maxilla)

Alveolar arch Hard palate (palatine bone)

Posterior nasal aperture (choana)

Greater palatine foramen
Hamulus Lesser palatine foramen
Pyramidal process of Body of sphenoid
palatine bone
Medial plate of pterygoid
Pterygoid fossa process
Lateral plate of pterygoid
Vomer process
Greater wing
Scaphoid fossa
(of sphenoid bone)
Opening of
pterygoid canal Foramen lacerum

Foramen ovale
Articular tubercle
Mandibular fossa Foramen spinosum
Groove for auditory tube

Carotid canal
Styloid process
Jugular foramen
Stylomastoid foramen

Mastoid process

Mastoid notch

Basilar part of
occipital bone
Hypoglossal canal
Pharyngeal tubercle
Occipital condyle

Foramen magnum

External occipital crest Inferior nuchal line

Superior nuchal line

External occipital protuberance

FIG 2.3bâ•… External surface of the base of the adult skull. (From Drake RL et al1: Fig 8.23.)
Superciliary arch

Frontal bone

Supra-orbital notch


Zygomatic process
Nasion (of frontal bone)
Nasal bone

Piriform aperture Frontal process (of maxilla)

Zygomatic bone
Inferior nasal concha Infra-orbital foramen
Nasal crest

Anterior nasal spine

Zygomatic process (of maxilla) Alveolar process

Oblique line
Ramus of mandible

Maxilla Alveolar part of mandible

Angle of mandible
Body of mandible
Mental foramen
Mental protuberance Mental tubercle

FIG 2.4â•… Bones of the facial skeleton. (From Drake RL et al1, Fig 8.18.)

Lesser wing of sphenoid

Frontal bone
Superior orbital fissure
Optic canal
Greater wing Ethmoidal foramina
of sphenoid
Ethmoid bone

Zygomatic bone Lacrimal bone

Inferior orbital fissure Palatine bone

FIG 2.5â•… Bones of the right orbit. (From Drake RL et al1, Fig 8.70.)

Superior sagittal
Emissary vein
Diploic vein
Trochlear nerve

Falx cerebri
Trigeminal nerve
Inferior sagittal sinus
Oculomotor nerve Abducens nerve
Optic nerve Great cerebral vein
Sigmoid sinus

Straight sinus
Olfactory bulb
Facial and
Diaphragma sellae nerves
Confluence of sinuses
Internal carotid artery Tentorium cerebelli

Inferior petrosal sinus vagus and
accessory nerves
Superior petrosal sinus Hypoglossal nerve

Optic nerve Internal carotid artery

Cavernous sinus
Oculomotor nerve

Inferior petrosal sinus

Basilar plexus
Superior petrosal sinus
Foramen magnum

Tentorium cerebelli, free border

Attached periphery of
Left transverse sinus tentorium cerebelli

Straight sinus Tentorium cerebelli

Confluence of sinuses Right transverse sinus

FIG 2.6â•… Cerebral dura mater, showing the falx cerebri, the tentorium cerebelli and the associated major sinuses:
a. sagittal view; b. view of the skull base from above showing the major venous sinuses. (From Standring S2: a. Fig 15.1;
b. Fig 15.3.)
2 • Anatomy of the head and neck 17

Skull bone

of the left
lateral ventricle)

Left extradural

Right haematoma

FIG 2.7â•… Axial CT scan showing a left extradural

haematoma with the associated mass effect
demonstrated by compression of the left lateral ventricle.
The haematoma has stripped the dura off the skull.

Present on all bones, the periosteum also surrounds
the inner surface of the skull and is called endos-
teum. The endosteal layer is the outer layer of the
dura mater and is mostly attached to the inner dural
layer, known as the true dura, which completely
encloses the brain (Fig 2.6). The spinal dura that
encloses the spinal cord comprises only one dural Clinical notes
layer. A vertical dural sheet, called the falx cerebri, • Severe brain swelling may obliterate the basal
separates the two hemispheres and a horizontal dural cisterns. This is called ‘effacement’ of the cisterns
on CT imaging. The subarachnoid space over the
sheet, called the tentorium cerebelli, separates the convexity also narrows as the brain swells. This is
cerebrum from the cerebellum. called sulcal effacement on CT imaging.
The inner dural layer supports a very thin trans- • Because the dura is attached to the bone, an
parent membrane known as the arachnoid mater. extradural haematoma will not usually cross a
The blood vessels of the brain run beneath the arach- suture line (the point at which two bones fuse,
such as the coronal suture between the frontal
noid in the subarachnoid space, which also contains and parietal bones).
the cerebrospinal fluid (CSF). The gyri of the brain • The presence of intracranial air (pneumocephalus)
are closely covered by the pia mater. Together  following trauma is indicative of a dural breach
the dura, arachnoid and pia form the meninges. (Fig 2.8).
Extradural haematoma (Fig 2.7) occurs between • The bridging veins may be torn during trauma
and cause subdural haematomas. In the elderly,
bone and dura, subdural haematoma between dura in whom the brain is atrophic and the subdural
and arachnoid and subarachnoid haemorrhage space is therefore larger, these bridging veins are
between arachnoid and pia. even more susceptible and can be torn by trivial
The subarachnoid space expands to form cisterns trauma. Elderly patients often present later with
at the base of the brain. These thin CSF cisterns chronic subdural haematomas (see Chapter 5).
include the cisterna ambiens, which is between 

Bridging Outer table Inner table Sagittal

vein of skull of skull suture
Dura mater

Pia mater
white Superior Sub- Falx Arachnoid
matter sagittal arachnoid cerebri villus
sinus space
FIG 2.8â•… Axial CT scan showing pneumocephalus in
the left frontal region (the arrow indicates areas of
pneumocephalus, which are black on the CT scan); the Meningeal layer Foramen Periosteal layer
white line in the middle indicates haemorrhage along of dura mater magnum of dura mater
the falx.

Periosteum Skull
the tentorium and the midbrain, and the cisterna Spinal
magna, which surrounds the lower brainstem and space
cerebellum. Spinal
The separation of the two dural layers forms the dura mater
large venous sinuses, the largest of which is the
superior sagittal sinus (Fig 2.9). (Care is required
when referring to the term sinus, because it also
describes the air-filled cavities within the skull.)
Surrounding the superior sagittal sinus are arach- b
noid granulations, through which CSF is reabsorbed.
Veins from the cerebral cortex, which are called FIG 2.9â•… Cranial meninges: a. superior coronal view
showing the splitting of the dura to form the sagittal
bridging veins, drain into the superior sagittal sinus. sinus—note the three layers of the arachnoid beneath
the skull; b. coronal view of the craniocervical junction
THE BRAIN and upper cervical spine showing the continuity of the
cranial dura with the spinal dura. (Based on Drake RL et al1,
Lobes Fig 8.30a & b.)

The cerebral hemispheres are divided into lobes (Fig

2.10). The frontal lobe is separated from the parietal
lobe by the central sulcus (Rolandic fissure) and
from the temporal lobe by the lateral sulcus (Sylvian each region of the body is represented on a particu-
fissure). The insula lobe is hidden in the depths of lar section of the motor strip. This arrangement is
the sylvian fissure, between the frontal, temporal called the motor homunculus and is shown in 
and parietal lobes. Figure 2.11.
The posterior frontal lobe contains the precentral The primary sensory strip (Fig 2.12) is located
gyrus, which is the primary motor strip. The preÂ� in the postcentral gyrus in the anterior parietal 
central gyrus is arranged somatotopically: that is, lobe. The dominant hemisphere, usually the left
2 • Anatomy of the head and neck 19

FIG 2.12â•… Lateral view of hemisphere showing sensori-

FIG 2.10â•… Lobes of the cerebral hemispheres. (Based on motor cortex and the speech areas. (Based on Standring S2,
Stern TA et al3, Fig 40.3b.) Fig 22.16.)

a b




Kne Hip





Litt g



Rin dle

Lit ing s


R dle
Th dex

Mi ndex b ali
Ey umb
I m No e nit
Th eck s Ge
N ow Fac e
Br all e
d eye Upper
a n e
lid Fac
Eye Lips

Lower lip
Teeth, gums and jaw
Ton Tongue

Sw gue




TI C Intra

FIG 2.11â•… Schematic coronal section through the cerebral hemisphere, illustrating the approximate somatotopic
representation of the contralateral body half in the motor and sensory cortices: a. motor; b. sensory. (From Standring S2,
Fig 22.13.)

Corpus callosum
Anterior horn of left ventricle Head of caudate nucleus
Anterior limb of internal capsule
Globus pallidus
Posterior limb of internal capsule

FIG 2.13aâ•… Basal ganglia and internal capsule in the axial plane.
(From Standring S2, Fig 23.1.)

side, contains the speech areas, of which Broca’s diencephalon. The basal ganglia are large nuclei
area, the expressive centre, is located in the inferior consisting of nerve cells and are situated deep 
frontal gyrus and Wernicke’s area, the receptive in each hemisphere. They comprise the putamen,
centre, is located in the posterior end of the superior globus pallidus and caudate nucleus, which are
temporal gyrus. The gyrus surrounding the posterior structures involved in gross movement control and
upward extension of the superior temporal sulcus  posture. The internal capsule lies between the
is the angular gyrus. The gyrus surrounding the  caudate and putamen laterally and the thalamus
posterior upward extension of the lateral sulcus medially and contains the main motor fibre tracts
(Sylvian fissure) is the supramarginal gyrus. Both from the motor cortex, called the corticospinal 
these gyri are also involved in receptive language tracts or pyramidal fibres (Fig 2.13a & b). Traumatic
function. haemorrhage in this deep location may result in a
The medial occipital lobe contains the primary contralateral hemiparesis. Figure 2.14 shows a hori-
visual cortex above and below the calcarine fissure. zontal section through the cerebrum.
The corpus callosum is the large, white-matter
structure joining the two hemispheres and com� Brainstem and cerebellum
prises nerve fibres that allow cross-communication The cerebral peduncles connect the two hemispheres
between the hemispheres (Fig 2.13a & b). The thal- to the brainstem. The brainstem comprises three seg-
amus, which is a relay station for sensory informa- ments: the midbrain, pons and medulla oblongata.
tion, is situated in the deepest part of each hemisphere The brainstem joins the spinal cord at the foramen
adjacent to the third ventricle in the midline. The magnum. The demarcation between the spinal cord
hypothalamus extends inferiorly and anteriorly from and medulla of the brainstem is at the point where
the thalamus. These two structures comprise the the C1 nerve root emerges. The reticular formation
2 • Anatomy of the head and neck 21

Corpus callosum

Anterior horn of Head of caudate nucleus

lateral ventricle

Internal capsule Thalamus

Globus pallidus
lateral segment

Globus pallidus
medial segment Subthalamic nucleus

Red nucleus
Substantia nigra
Crus cerebri


Medulla oblongata

FIG 2.13bâ•… Basal ganglia and internal capsule in the coronal plane. (From Standring S2, Fig 23.2.)

is a heterogeneous collection of nuclei spread

throughout the brainstem, which is important for
consciousness. The vital cardiovascular and respira-
tory control systems of the reticular formation are
located in the medulla.
The three parts of the brainstem contain cavities
filled with CSF and are part of the ventricular system
(Fig 2.15a–c):
1. The cavity of the midbrain is the cerebral aqueduct
(aqueduct of Sylvius). Anterior to the aqueduct is
the tegmentum of the midbrain and posterior to it
is the tectum. The tectum contains the quadrigemi-
nal plate, so called because there are two pairs of
colliculi. The superior colliculi control eye move-
ments (upward gaze) while the inferior colliculi
are involved in the auditory pathways.
FIG 2.14â•… Diagram of the basal ganglia: lateral view.
(Based on Crossman AR et al11, Fig 16.2.)

a Mammillary body

Crus cerebri


Middle cerebellar peduncle



Decussation of pyramids

Pineal body
Superior colliculus

Inferior colliculus
Corona radiata
Inferior quadrigeminal
brachium Pulvinar

Medial Superior
geniculate body quadrigeminal brachium
medullary velum Lateral
geniculate body
Lateral lemniscus
Superior cerebellar complex
peduncle Trochlear nerve

Middle cerebellar Optic tract

Base of
cerebral peduncle
Oculomotor nerve
Dorsolateral Pons
Trigeminal nerve
(sensory and motor roots)
Roots of spinal
accessory nerve
Olive Pyramid Roots of vagus and
glossopharyngeal nerves

FIG 2.15â•… The brainstem: a. ventral aspect; b. lateral aspect. (a. From Crossman AR & Neary D9, Fig 9.3; b. From
Standring S2, Fig 19.4.)
2 • Anatomy of the head and neck 23


Trochlear notch
Trigeminal nerve
sulcus of
fourth Transverse dural
ventricle venous sinus
Facial and
Hypoglossal nerves
nerve Glossopharyngeal,
Posterior vagus and
spinal artery accessory nerves
Accessory nerve,
Digastric, spinal root
posterior belly
Atlas, Vertebral artery
process First cervical
(suboccipital) nerve
Spinal accessory
nerve Atlas, posterior arch

Second cervical
spinal ganglion Dura mater
Vagus nerve
Internal Third cervical nerve
jugular vein dorsal ramus
mastoid Denticulate ligament
Superior cervical

Spinal accessory

Vagus nerve (displaced medially)

Common carotid artery Vertebral artery

FIG 2.15câ•… The brainstem: dorsal aspect, showing the floor of the 4th ventricle, the cerebellar peduncles, the lower
cranial nerves, the spinal cord and spinal nerves. (From Standring S2, Fig 19.2.)

2. The cavity of the pons is the rostral (upper) part nuclei, except for the fourth nerve, which emerges
of the fourth ventricle. dorsally.
3. The medulla oblongata, located between the pons The cerebellum is connected to the brainstem by
and spinal cord, has the caudal (lower) part of the peduncles: the superior cerebellar peduncles connect
fourth ventricle as its cavity. to the midbrain, the middle to the pons and the
Behind the posterior aspect, or roof, of the fourth inferior to the medulla. The cerebellum functions to
ventricle lies the cerebellum (Fig 2.16). The cranial
nerve nuclei are spread throughout the brainstem:
cranial nerves 3 and 4 are in the midbrain; 5 to 8 are
in the pons and 8 to 12 are in the medulla. The first
two cranial nerves, olfactory and optic, do not have
Clinical note
Trauma to the cerebellum or haemorrhage within it
brainstem nuclei. Motor nuclei of the cranial nerves can be life threatening as a result of brainstem
are organised medially and sensory nuclei more lat- compression or obstructive hydrocephalus because of
erally. The cranial nerves emerge either from the the proximity of the cerebellum to the fourth
ventral (3, 6, 12) or lateral (5, 7, 8, 9, 10, 11) aspects ventricle and the brainstem.
of the brainstem roughly at the same levels as their

a Superior b
vermis Superior cerebellar Anterior lobe
Horizontal Middle cerebellar
fissure Hemisphere Posterolateral
fissure peduncle

Inferior cerebellar
Inferior Nodule Flocculus
Medulla peduncle
Posterior lobe Flocculonodular lobe

FIG 2.16â•… Cerebellum: a. posterior aspect; b. anteroinferior aspect. (From Crossman AR & Neary D9: a. Fig 11.3; b. Fig 11.4.)

maintain equilibrium and coordinate complex move- CRANIAL NERVES

ments. Phylogenetically and functionally the cere-
bellum is divided into three parts: the archicerebellum The cranial nerves are summarised individually in
(vestibulocerebellum), which is concerned with Table 2.1.
balance, the paleocerebellum (spinocerebellum),
which is concerned with control of limb movements
and the neocerebellum (ponto-cerebellum) which is
concerned with the fine coordination of complex Clinical note
movement. Trauma may affect the cranial nerves directly or
indirectly. A base-of-skull fracture in the frontal bone
may result in anosmia due to damage to the
olfactory nerves. A fracture in the temporal bone
may cause facial weakness due to damage to the
seventh nerve. Swelling or pressure within the brain
could result in compression or stretching of cranial
nerves, as they run through the subarachnoid space.
A sixth-nerve palsy in this setting is referred to as a
CT brain anatomy made simple false localising sign. The medial and anterior part of
the temporal lobe is called the uncus and rests near
The clinician should be familiar with the relevant CT the tentorial edge. As the brain swells or is deformed
and MR anatomy, which is in tomographic (or slice) from above by a haematoma, the uncus herniates
format. This is presented in Figures 2.17 and 2.18. over the edge of the tentorium and compresses the
Note that intra-axial refers to structures inside the midbrain and the third cranial nerve. This is called
brain, whereas extra-axial refers to structures external transtentorial coning. (See also Brain shift and
to the brain but within the skull. herniation in Chapter 3.)
2 • Anatomy of the head and neck 25

TABLE 2.1â•… Cranial nerves9

Cranial nerve Cranial nerve Component

number name fibres Structures innervated Functions

I Olfactory Sensory Olfactory epithelium via Olfaction

olfactory bulb
II Optic Sensory Retina Vision
III Oculomotor Motor Superior, inferior and medial Movement of the eyeball;
recti; inferior oblique; elevated upper eyelid
levator palpebrae superioris
Parasympathetic Sphincter papillae and ciliary Pupillary constriction and
muscle of the eyeball, via accommodation
ciliary ganglion
IV Trochlear Motor Superior oblique muscle Movement of the eyeball
V Trigeminal Sensory Face, scalp, cornea, nasal General sensation
and oral cavities, cranial
dura mater
Motor Muscles of mastication Opening and closing the
Tensor tympani muscle Tension on tympanic
VI Abducens Motor Lateral rectus muscle Movement of the eyeball
VII Facial Sensory Anterior two-thirds of tongue Taste
Motor Muscles of facial expression Facial movement
Stapedius muscle Tension on the bones of the
middle ear
Parasympathetic Salivary and lacrimal glands Salivation and lacrimation
via submandibular and
pterygopalatine ganglia
VIII Vestibulocochlear Sensory Vestibular apparatus Vestibular sensation (position
and movement of head)
Cochlea Hearing
IX Glossopharyngeal Sensory Pharynx, posterior third of General sensation and taste
Eustachian tube, middle ear General sensation
Carotid body and carotid Chemo- and baroreception
Motor Stylopharyngeus muscle Swallowing
Parasympathetic Parotid salivary gland via otic Salivation
X Vagus Sensory Pharynx, larynx, oesophagus, General sensation
external ear
Aortic bodies, aortic arch Chemo- and baroreception
Thoracic and abdominal Visceral sensation
Motor Soft palate, pharynx, larynx, Speech, swallowing
upper oesophagus
Parasympathetic Thoracic and abdominal Control of cardiovascular
viscera system, respiratory and
XI Accessory Motor Sternomastoid and trapezius Movement of head and
muscles shoulders
XII Hypoglossal Motor Intrinsic and extrinsic Movement of the tongue
muscles of the tongue

a Scalp (white/grey)
b Bone (bright white)
c Cerebellum (in posterior
cranial fossa)
d Mastoid air cells (black) h
e Brainstem g
f Pituitary fossa
g Frontal lobe (in anterior
cranial fossa)
h Orbit
i Frontal sinus j
j Temporal lobe (in middle
cranial fossa)
d e

FIG 2.17 (i)â•… Normal CT anatomy of the brain: basal slice showing skull posterior fossa
contents and temporal lobes in the middle fossa.

a Cerebellum
b Fourth ventricle
c Brainstem
d Petrous temporal bone
e Temporal lobe and temporal g
horn of lateral ventricle
f Basal cisterns (suprasellar
cistern) f
g Frontal lobe

FIG 2.17 (ii)â•… Normal CT anatomy of the brain: basal slice through the base of the cerebral
hemispheres and the midbrain and cerebellum.
2 • Anatomy of the head and neck 27

a Cerebellum
b Temporal lobe
c Basal cisterns (quadrigeminal
cistern) h
d Brainstem (midbrain)
e Third ventricle f
f Frontal horn of lateral
g Sylvia fissure
h Frontal lobe

FIG 2.17 (iii)â•… Normal CT anatomy of the brain: slice through the lower part of cerebral
hemispheres showing the lateral and third ventricles.

a Occipital lobe
b Atrium of lateral ventricle
c Insular cortex
d Frontal horn of lateral f
e Internal capsule
f Frontal lobe

FIG 2.17 (iv)â•… Normal CT anatomy of the brain: slice through the lower middle part of the
cerebral hemispheres showing the lateral ventricles.

a Occipital lobe
b Parietal lobe
c Occipital horn of lateral
ventricle f
d Frontal horn of lateral
e Temporal lobe
f Frontal lobe
e d

FIG 2.17 (v)â•… Normal CT anatomy of the brain: slice through the upper middle part of the
cerebral hemispheres showing the lateral ventricles.

a Grey matter
b White matter of centrum
c Interhemispheric fissure

FIG 2.17 (vi)â•… Normal CT anatomy of the brain: slice through the upper part of the cerebral
hemispheres above the lateral ventricles showing the centrum semiovale.
2 • Anatomy of the head and neck 29

FIG 2.18â•… Sagittal magnetic resonance image (MRI) of

the head: 1 cerebral hemisphere; 2 corpus callosum;
3 cerebellum; 4 spinal cord; 5 medulla; 6 pons;
7 midbrain; 8 thalamus.

VASCULAR ANATOMY IN THE NECK (ICA). The ECA supplies the structures in the neck,
AND CRANIUM face and scalp. The ICA ascends to the base of the
skull, enters the petrous temporal bone and runs
Carotid and vertebral arteries horizontally within the carotid canal before it makes
The arterial supply to the brain occurs via the anas- an ‘S’ bend within the cavernous sinus, which is
tomosis of four vessels: the paired internal carotid called the carotid siphon. After emerging from the
arteries anteriorly and the paired vertebral arteries cavernous sinus it enters the subarachnoid space at
posteriorly (Fig 2.19). the base of the brain, just lateral to the optic nerve.
The vertebral arteries arise from the subclavian It then supplies the eye via the ophthalmic artery 
arteries at the root of the neck and then enter the and gives off a branch called the posterior commu-
bony cervical spine through the intervertebral nicating artery (PCOM), which joins the posterior
foramina. They pierce the dura between the occiput cerebral artery (PCA). The PCA is the terminal
and C1 and then enter the foramen magnum, where branch of the basilar artery. The ICA terminates by
they converge in front of the pons into the single bifurcating into the anterior cerebral artery (ACA)
basilar artery. Before this convergence, they give off and middle cerebral artery (MCA). The anterior
important branches that supply the spinal cord, cerebral arteries pass medially and anastamose with
brainstem and cerebellum. The basilar artery also each other via the anterior communicating artery
supplies the brainstem (Fig 2.20). (ACOM). The anterior (carotid) circulation thus
The common carotid artery (CCA) bifurcates in meets the posterior (vertebral circulation) and forms
the neck at the level of C3 or C4 into the external the circle of Willis. The MCA passes laterally over
carotid artery (ECA) and the internal carotid artery the insular cortex and supplies the lateral aspect 

FIG 2.19â•… Extracranial and intracranial

Basilar artery Posterior cerebral artery
arterial supply to the brain: ACA = anterior
cerebral artery; MCA = middle cerebral artery;
PCA = posterior cerebral artery; ICA = internal
carotid artery; ECA = external carotid artery;
CCA = common carotid artery; ACOM =
anterior communicating artery; PCOM =
posterior communicating artery; SCA =
superior cerebellar artery; AICA = anterior
inferior cerebellar artery; PICA = posterior
inferior cerebellar artery. (Based on Goldman L &
Schafer A4, pp 430–2.)

FIG 2.20aâ•… Vertebrobasilar arteriogram:

lateral projection. (From Standring S2, Fig 17.9. By
kind permission from Professor PD Griffiths, Academic
Vertebral artery Posterior inferior cerebellar artery Unit of Radiology, the University of Sheffield.)
2 • Anatomy of the head and neck 31

of the hemisphere. The ACA supplies the medial Galen, which then joins the straight sinus along with
aspect of the hemisphere and a strip on the upper the inferior sagittal sinus. The straight sinus meets
lateral side of the hemisphere, and the PCA supplies the superior sagittal sinus at the confluence of
the occipital and posterior temporal lobes. The  sinuses or torcula and then drains via the transverse
deep hemisphere structures are supplied by per� sinuses into the sigmoid sinus, which exits the skull
forator arteries from the circle of Willis (Fig 2.21). through the jugular foramen becoming the internal
The posterior inferior cerebellar artery (PICA) is  jugular vein. The jugular foramen is just posterior
a branch of the vertebral artery and supplies the
adjacent medulla and cerebellum. The anterior infer�
ior cerebellar artery (AICA) and the superior cere-
bellar artery (SCA) are important branches of the
basilar artery and supply the brainstem and the 
cerebellum. (See Figs 2.19, 2.20 and 2.24.)
Clinical note
Internal jugular veins Trauma to the neck may cause dissection of the
carotid or vertebral artery. The dissection may lead
The venous drainage of the brain is by superficial to stroke. It is important to consider this in patients
and deep systems (Fig 2.22). The superficial veins who have signs of neck trauma or cervical spine
drain into dural venous sinuses, mentioned above, fractures , particularly if the fracture extends near to
and the deep structures including the thalamus, basal the vertebral artery in the transverse foramen (see
ganglia and ventricles drain into deep veins. The Chapter 7).
deep veins converge into the great cerebral vein of

Right posterior cerebral artery Superior cerebellar artery

FIG 2.20bâ•… Vertebrobasilar arteriogram:

Towne’s projection. (From Standring S2, Fig 17.10.
By kind permission from Professor PD Griffiths, Academic
Anterior inferior cerebellar artery Basilar artery Left vertebral artery Unit of Radiology, the University of Sheffield.)

to the carotid canal, and the internal jugular vein THE VENTRICLES AND CEREBRO-
passes down the neck just posterior and lateral to the
carotid artery; both are surrounded by the carotid
sheath. The vagus nerve passes between these two The brain is bathed in cerebrospinal fluid (CSF),
vessels. which provides a protective buffer and reduces the
weight of the brain from approximately 1500╯g to
Cavernous sinus effectively 50╯g. The CSF is largely produced by the
The cavernous sinus (Fig 2.23) is a unique dural choroid plexus, which can be found within all the
sinus, as it is not an open venous chamber but con- ventricles (Fig 2.25).
tains multiple fibrous septae within it. It receives Within the cerebral hemispheres are the lateral
blood from nearby veins and mainly drains into the ventricles, which communicate with the third ven-
internal jugular vein via the petrosal sinuses; tricle via the interventricular foramen of Munro. The
however, it does communicate with the face via the third ventricle is located between the thalami. The
ophthalmic and facial veins. The internal carotid horns are extensions of the lateral ventricle in each
artery (ICA) (Fig 2.24) passes through the cavern- of the lobes of the hemisphere. The frontal horns 
ous sinus. Below and lateral to the ICA is the abdu- are separated by the septum pellucidum, which is a
cens nerve. In the lateral wall of the cavernous sinus thin membrane. The third ventricle communicates
run the oculomotor, trochlear, ophthalmic and max- via the aqueduct of Sylvius to the fourth ventricle,
illary nerves. It has been proposed that the cavern- which is located posterior to the pons and medulla.
ous sinus functions as a shock absorber, reducing The fourth ventricle has two lateral apertures, the
the pulsations of the internal carotid artery as it foramina of Luschka, and one median aperture, 
emerges into the subarachnoid space. the foramen of Magendie. CSF flows from these

Anterior cerebral artery

Anterior communicating artery

Medial striate artery

Anteromedial group Internal carotid artery

Middle cerebral artery

Posterior communicating artery

Lateral striate group
Anterior choroidal artery

Posteromedial group

Oculomotor nerve Posterolateral group

Posterior cerebral artery

Superior cerebellar artery

Trochlear nerve

Pontine rami

Basilar artery

FIG 2.21â•… Cerebral arterial circle of Willis. (From Standring S2, Fig 17.6.)
2 • Anatomy of the head and neck 33

FIG 2.22â•… Venous drainage of the brain: CS = cavernous sinus; ISS = inferior sagittal sinus; LS = lateral sinus;
PS = petrosal sinus; SS = sigmoid sinus; SSS = superior sagittal sinus; StS = straight sinus; TS = transverse sinus;
CV = cortical vein; GV = great vein (of Galen); ICV = internal cerebral vein; IJ = internal jugular vein; TH = torcula
herophili. (Based on Gates P et al10.)

FIG 2.23â•… Optic chiasm and cavernous sinuses (coronal section). (From Yanoff M & Duker JS5,
Fig 9-11-3.)

FIG 2.24â•… Internal carotid arteriogram: a. lateral projection; b. Towne’s
2 • Anatomy of the head and neck 35

Cerebral aqueduct Body of lateral ventricle

Fourth ventricle Inferior horn of
lateral ventricle

Anterior horn of Body of lateral Posterior horn of

lateral ventricle ventricle lateral ventricle

Interventricular Third ventricle Inferior horn of Cerebral Fourth ventricle
foramen lateral ventricle aqueduct

FIG 2.25â•… Resin cast of the ventricular system: a. posterior

view; b. lateral view. (From Standring S2, Fig 16.1a & b. Prepared by DH
Tompsett of the Royal College of Surgeons of England.)

Clinical notes
1. The ventricles are frequently accessed in patients
with severe traumatic brain injury by inserting an
external ventricular drain, which is typically placed
within the right frontal horn of the lateral ventricle.
This allows for direct monitoring of the ICP and for
drainage of CSF, which is one method of reducing
ICP. The ventricular CSF can also be sampled to
exclude infection.
2. Midline shift of brain structures is a displacement
measured on CT by lateral movement and distortion
of the third ventricle and septum pellucidum in
relation to the midline of the scan. This is
caused by brain swelling or a lateral expanding
haematoma. The degree of shift correlates with the
prognosis (see Chapters 5 and 20).

FIG 2.26â•… CSF fluid circulation and the cisterns. (Based on Brain Research Reviews6, pp 241–2,
Fig 1.)

foramina around the spinal cord and up over the

surface of the brain, where it is reabsorbed by the
arachnoid granulations (Fig 2.26). CSF is constantly
produced and reabsorbed at a rate of about 500╯mL
per day.


The cervical spine can be divided into the suboc-
cipital region and the subaxial region (Figs 2.27a, b
& c).
The suboccipital region is comprised of the atypi-
cal vertebrae of the atlas and the axis, which func-
tion to support the head and allow for the majority
of its rotational movement (Fig 2.28). The atlas, C1,
is shaped like a ring and articulates with the axis,
C2, via facet joints and anteriorly via a unique pro-
jection called the dens, or odontoid process. It is at
this joint that rotation occurs. The stability of the
joint is maintained by multiple ligaments projecting
mainly from C2 to the base of the skull. FIG 2.27aâ•… Normal sagittal MRI of the cervical spine.
2 • Anatomy of the head and neck 37




ventral lip

Raised lateral
lip of body
Uncinate process
3rd to 7th
vertebrae Carotid



FIG 2.27bâ•… Anterior view of the cervical spine. (From Standring S2, Fig 45.15.)


4 11


1. Anterior tubercle of the atlas

2. Soft palate
8 3. Characteristic cervical body
4. Pharyngeal part of the tongue
5. Intervertebral disc
6. Body of the hyoid bone
7. Epiglottis
8. Thyroid cartilage which is undergoing calcification
9. Air in trachea
9 10. Spinous process of the axis
11. Zygapophyseal joint

FIG 2.27câ•… Lateral radiograph of the cervical spine. (Provided by Shawn Gallagher, GKT School of Medicine,
London; photo by Sarah-Jane Smith.)

FIG 2.28â•… Views of C1 and C2: a. atlas in a lateral view; b. atlas in a frontal view; c. atlas in an above view;
d. axis in a lateral view; e. axis in a frontal view; f. axis in an above view; g. & i. open-mouth view; h. & j. closed-
mouth view. (Based on Marx J et al8, Fig 40.24.)
2 • Anatomy of the head and neck 39

FIG 2.29â•… Typical cervical vertebra. (Based on Mercier L7, p 27.)

The typical vertebrae (Fig. 2.29) of C3 to C7 2. Standring S. Gray’s anatomy: the anatomical basis of
inclusively form the subaxial cervical spine. As in clinical practice. 40th ed. Philadelphia: Churchill
the thoracic and lumbar spine, an intervertebral disc Livingstone; 2009.
3. Stern TA, Rosenbaum JF, Fava M, eds. Massachusetts
separates each vertebral body. The vertebral bodies General Hospital comprehensive clinical psychiatry.
and discs are anterior to the spinal cord, which 1st ed. Philadelphia: Mosby; 2008.
descends in the spinal canal surrounded by bone. 4. Goldman L, Schafer A. Goldman’s Cecil medicine.
Laterally, the cord is enclosed by the pedicles, which 23rd ed. Philadelphia: Saunders; 2008.
join the vertebral bodies to the laminae posteriorly, 5. Yanoff M, Duker JS. Ophthalmology. 3rd ed. St Louis:
completing the spinal canal. The laminae connect Mosby; 2008.
the spinous processes, which project posteriorly, and 6. Brain Research Reviews 2010;64(2):241-262.
7. Mercier L, ed. Practical orthopedics. 5th ed. St Louis:
the transverse processes, which project laterally. The Mosby; 2000.
cervical nerve roots emerge from the spinal foram- 8. Marx J, Hockberger R, Walls R. Rosen’s emergency
ina above the numbered vertebra below; for example medicine. 7th ed. St Louis: Mosby; 2009.
the C7 nerve root emerges above C7, and the C8 9. Crossman AR, Neary D. Neuroanatomy: an illustrated
nerve emerges above T1. colour text. 4th ed. Edinburgh: Churchill Livingstone;
10. Gates P, Barnett HJ, Mohr JP, et al, eds. Stroke:
REFERENCES Pathophysiology, Diagnosis and Management. New
Your: Churchill Livingstone; 1986.
1. Drake RL, Vogl W, Mitchell AWM. Gray’s anatomy 11. Crossman AR, Neary D. Neuroanatomy: an illustrated
for students. 39th ed. Philadelphia: Churchill colour text. 2nd ed. Edinburgh: Churchill Livingstone;
Livingstone; 2005. 2000.
Pathophysiology of traumatic brain injury
Tony Goldschlager, Jeffrey V Rosenfeld

Trauma to the brain initiates a cascade of events that with egress of CSF into the venous system and into
may cause severe aberrations to normal physiology. the spinal canal, but eventually this compensation is
This occurs at molecular, subcellular, cellular and exhausted and the pressure rises exponentially.
whole organ levels. Secondary systemic factors Swelling of the brain may kink and block the drain­
further complicate the mix. These events may  ing veins near the sagittal sinus and further compro­
exacerbate brain injury, which leads to a further mise any compensation. Moreover, extracranial
increase in morbidity and mortality. Management of venous obstruction, such as can occur with tight
brain injury necessitates an understanding of normal cervical collars or endotracheal tube ties, can also
physiology and the pathophysiology following increase ICP. Removal of only a few millilitres of
impact. This chapter presents the key pathophys­ CSF may drop the pressure significantly if the
iology in all of these domains. The specific path­ patient is on the steep part of the exponential curve
ological patterns of injury resulting from these (Fig 3.1).
perturbations are also described and the pertinent As an intracranial mass lesion grows and expands,
aspects of the normal physiology are presented. a patient moves along the curve from point A to
point B. During this time, compensatory changes
occur, including displacement of CSF and blood, as
INTRACRANIAL PRESSURE well as compression of normal brain, to maintain
ICP in the normal range. At point B, the ability of
Monro-Kellie doctrine the brain to further compensate is limited. Thus, a
The cranial cavity is of a fixed volume, containing small additional increase in volume results in a large
the brain, blood and cerebrospinal fluid (CSF). A increase in pressure. It is important to recognise
change in one of these three principal components patients who are approaching point B on the volume–
must be accompanied by a compensatory change in pressure curve, because they are at risk of a rapid
another. This principle was described by two Scot­ increase in ICP with small additional increases in
tish anatomists, Alexander Monro in 1783 and volume. This rapid increase in ICP can lead to rapid
Gordon Kellie some years later, and has become neurological decline.
known as the Monro-Kellie doctrine. In the event of
a traumatic intracranial bleed, expansion of the
haemorrhage within the skull will cause secondary Blood–brain barrier and cerebral oedema
compression of the brain, which may be rapidly fatal The blood-vessel endothelium within the brain con­
if not removed. Alternatively, brain swelling follow­ tains tight junctions, unlike the endothelium in
ing trauma can reduce cerebral blood flow (CBF). extracranial vessels. The endothelial tight junctions
This is sometimes treated with CSF drainage, which are adjacent to the astrocytic foot processes, which
results in a compensatory reduction in intracranial form a functional unit called the blood–brain barrier.
pressure (ICP) and allows CBF to increase. The This barrier prevents free passage of molecules 
pressure–volume curve has a gentle slope over the from the blood into the brain parenchyma. If the
initial segment because there is some compensation blood–brain barrier is disrupted, cerebral oedema
3 • Pathophysiology of traumatic brain injury 41

FIG 3.1â•… Volume–pressure curve, depicting the change

in intracranial pressure (ICP) that occurs with changes FIG 3.2â•… In cytotoxic oedema, the Na+â•›/â•›K+â•›/â•›ATPase
in the volume of an intracranial mass. (Based on Winn HR1, pump system fails secondary to a depletion of cellular
Fig 48.1.) energy. Sodium accumulates intracellularly, leading to
the creation of an osmotic gradient, along which water
moves from the extracellular to the intracellular space.
results. There are three main forms of cerebral (Based on Winn HR1, Fig 39.1.)
1. Cytotoxic oedema is the most common form of
oedema following traumatic brain injury (TBI) 3. loss of grey–white matter differentiation
(Fig 3.2). It occurs as a result of dysfunction of 4. small ventricle(s)
the Na+â•›/â•›K+â•›/â•›ATPase (adenosine triphosphotase) 5. loss or effacement of the basal cisterns, especially
pump on the cell membrane, which leads to fluid around the upper brainstem
accumulation within the cell. Mitochondrial 6. brain shift of midline structures
failure following TBI may also be a key factor in 7. signs of cerebral coning with subfalcine, uncal or
producing this metabolic failure in the cell. cerebellar herniation (see below). Falcine hernia­
2. Vasogenic oedema results from the breakdown tion can be seen at the front end of the falx, with
of tight junctions within the endothelium, which the frontal lobe displaced across to the other side
allows passage of plasma proteins which accu­ and loss of the adjacent interhemispheric fissure.
mulate around cells within the brain. This may When the uncus is herniated, the subarachnoid
occur early following trauma. space (ambient cistern) at the level of the tento­
3. Interstitial oedema typically results from hydro­ rial hiatus is filled with medial temporal lobe
cephalus, which causes CSF to flow through the brain tissue (the uncus), and there may be some
ependymal wall of the ventricles, leading to tran­ midbrain distortion and compression. When the
sependymal oedema. cerebellar tonsils are prolapsed, the brain fills the
It is not possible to distinguish between these foramen magnum and there is a loss of the CSF
types of oedema on a CT scan. All oedema is space at this level.
hypodense on the scan, that is, it is a lighter grey Cerebral oedema frequently develops around
density than normal brain. Furthermore, swelling of areas of cerebral contusion, creating a so-called
the brain due to dilatation of blood vessels cannot ischaemic penumbra.
be distinguished from oedema on a standard CT but Aquaporins are a family of molecules that provide
is distinguishable on a blood flow study. The degree a mechanism for movement of water across cell
of swelling of the brain can be identified and assessed membranes. They have been studied in animal
on a CT scan and will show variable features of: models of TBI, in which a reduction in the develop­
1. reduction in the subarachnoid space ment of post-traumatic cerebral oedema was dem­
2. loss of surface sulcal markings onstrated in those animals in which aquaporin-1 was

FIG 3.3â•… Intracranial herniation syndromes evoked by supratentorial masses. The mass
lesion and its surrounding oedema (red arrows) have produced the following (blue
arrows): cingulate gyrus herniation under the falx cerebri; diencephalic herniation across
the midline, compressing the ipsilateral ventricle and producing the hydrocephalus in
the contralateral ventricle; hippocampal gyrus herniation through the tentorial notch,
compressing the posterior cerebral artery and brainstem; and herniation of the
cerebellar tonsils through the foramen magnum. (Based on Abeloff MD21, Fig 70.2, adapted from
Plum F & Posner JB3.)

blocked. The aquaporin system is very complex, and nerve against the brainstem, causing a dilated pupil.
blocking aquaporins has not yet produced any thera­ This is termed uncal or transtentorial herniation.
peutic benefit in humans.2 Global raised ICP or mass lesions in the posterior
fossa may cause herniation of the cerebellar tonsils
Brain shift and herniation downward through the foramen magnum. This is
Mass lesions, such as a haematoma, may cause the called tonsillar herniation.
brain to herniate away from the mass (Figs 3.3 &
3.4). Lesions in the frontal lobe may cause subfalcine Cerebral blood flow
herniation, in which the cingulate gyrus of frontal The brain receives about 15% of cardiac output 
lobe is pushed toward the other side beneath the falx. and this is tightly regulated to meet the brain’s 
This may lead to compression of the anterior cerebral metabolic demands. The brain requires an average
arteries and is detected on CT by midline shift and of 55╯mL of blood per 100╯g of brain tissue per
compression of the lateral ventricles. A temporal minute. This requirement is higher in areas of grey
contusion can cause the medial part of the temporal matter (approx. 75╯mL╛/╛100╯g╛/╛min) compared to
lobe, the uncus, to herniate and compress the third white matter (approx. 35╯mL╛/╛100╯g╛/╛min).
3 • Pathophysiology of traumatic brain injury 43

FIG 3.4â•… CT scans showing large right subdural haematoma, causing subfalcine and uncal herniation: a. coronal
view; b. axial view. The temporal horn of the lateral ventricle can be seen herniated under the tentorial notch to the

Cerebral blood flow (CBF) is determined by the The diameter of the arterial vessels is mainly
net pressure of the flow of blood into the brain, regulated by the partial pressure of carbon dioxide
called the cerebral perfusion pressure (CPP), divided (PaCO2), a potent vasodilator (Fig 3.5). The auto­
by the cerebral resistance (CVR). Therefore: nomic nervous system, hypoxia, anaemia, nitric
oxide and other vasoactive substances also have an
CPP affect on the diameter of blood vessels. In trauma, if
CVR there is haemorrhage within the subarachnoid space
(the space within which the intracranial vessels are
This is based on Ohm’s law. The main driving force located), the blood will break down over time and
of CPP is the arterial blood pressure, and the mean release vasoactive substances that can be an irritant
arterial blood pressure (MAP) is used. The main to the vessels and cause vasospasm. Vasospasm
resistance to flow (assuming normal venous outflow reduces the vessel diameter and can result in isch­
from the brain) is the ICP. Therefore: aemia and infarction. The flow within the vessels can
be measured by transcranial Doppler ultrasound, and
CPP = MAP − ICP in cases with subarachnoid haemorrhage an increase
in the blood velocity measured by Doppler may
The major determinant of CBF is the difference indicate that vasospasm is occurring. Vasospasm
between CPP and ICP. However, the diameter of the worsens the prognosis of severe TBI and should be
intracranial vessels and the viscosity of the blood diagnosed early and treated (see Chapter 5).
also influence CBF. Poiseuille’s law states that flow Blood viscosity can be influenced by a number
(Q) is proportional to the pressure gradient ΔP (or of factors in trauma, such as haemoglobin concentra­
CPP) and vessel radius (r) and inversely propor­ tion, blood loss, dehydration and systemic response
tional to the vessel length (l) and blood viscosity (η). to injury, which may alter protein concentration in
Therefore: the plasma. The osmotic diuretic mannitol improves
the blood rheology, thus reducing viscosity and ICP.
∆Pπr 4 This is apart from its diuretic effect. Indications for
CBF(Q) =
8lη its use are discussed in Chapter 5.

FIG 3.5â•… Effect of arterial partial pressure of carbon dioxide (PaCO2) on CBF. Note that
there is a linear relationship between CBF and PaCO2 across the physiological range of
PaCO2, as marked by the vertical broken lines. (Based on Winn1, Fig 86.4.)

As the PaCO2 level drops below 30╯mmHg, there that the blood flow drops at a higher MAP than
is significant vasoconstriction and a drop in CBF, normal and rises at a lower MAP than normal (Fig
which may be sufficient to cause ischaemia, par­ 3.7). This renders the affected parts of the brain
ticularly in zones of brain injury that are already susceptible to critical ischaemia with milder drops
borderline for cerebral perfusion. Levels below in the blood pressure, and to engorgement of vessels,
30╯mmHg due to hyperventilation should be avoided brain swelling and rises in ICP with increasing blood
in TBI management. It is safest to aim for a normal pressure. It is clearly a challenge to reach an optimal
PaCO2 level (35–40╯mmHg), except in the early CPP for the individual patient. This will be dis­
stages to correct hypercapnia, when a short period cussed below in relation to the clinical assessment
of hyperventilation will be helpful to bring the of autoregulation.
PaCO2 level back to the normal range. End-tidal
CO2 is easily measured constantly from the expired Cerebral ischaemia
air in the endotracheal tube. This provides a close Cerebral autoregulation is a major protective mech­
correlation with the PaCO2 measurement. End-tidal anism against ischaemia; however, outside its limits,
CO2 monitoring is very helpful for ensuring the arte­ which may be exceeded by trauma, ischaemic brain
rial CO2 levels are kept in the required range. damage can occur. The three stages of ischaemic
brain injury (Fig 3.8) can be visualised on the per­
Autoregulation fusion CT scan in Figure 3.9. Positron emission
Under normal circumstances, CBF is maintained at tomography (PET) scans, or in some institutions
a constant rate, despite fluctuations in blood pres­ xenon inhalation blood-flow studies, give a more
sure andâ•›/â•›or intracranial pressure, by a process called accurate picture of the CBF patterns in focal regions
cerebral autoregulation (Fig 3.6). of the brain.
In the injured brain, cerebral autoregulation is • Oligaemia (CBFâ•›=â•›20–50╯mLâ•›/â•›100╯gâ•›/â•›min): usu­
frequently impaired or lost in individual regions of ally a reversible area of ischaemic brain.
the brain or in the entire brain, depending on the • Penumbra (CBFâ•›=â•›10–20╯mLâ•›/â•›100╯gâ•›/â•›min): an
patterns of injury. Loss of autoregulation produces area of electrically inactive but potentially viable
vessels in which flow is more directly pressure- brain cells that often surrounds infarction. This is
dependent; that is, a more linear curve results such a potentially reversible injury.
3 • Pathophysiology of traumatic brain injury 45

FIG 3.6â•… Classical cerebral autoregulation curve. Cerebral autoregulation maintains a

relatively constant rate of CBF across a wide range of CPPs, as shown by the plateau.
The normal pressure limits of autoregulation (vertical broken lines) may be shifted to the
left or right (arrows) in certain conditions, and impaired or abolished in others (see text
for details). Note the relatively steep rise and fall in CBF as CPP changes above and
below, respectively, the normal limits of autoregulation. (Based on Winn HR1, Fig 86.3.)

FIG 3.7â•… Cerebral autoregulatory curves. Normal autoregulation maintains CBF across
a range of MAPs. Disturbed autoregulation causes a shift of the curve to the right
and introduces a more linear component (i.e. CBF is less stable with rising MAP).
If autoregulation is completely abolished, CBF rises linearly with MAP. (Based on Winn HR1,
Fig 7.7.)

FIG 3.8â•… Cerebral blood flow and neuronal dysfunction. (Based on Winn HR1, Fig 324.4.)

FIG 3.9â•… Computed tomography brain perfusion scan with sequencing maps:
a. Cerebral blood volume (CBV) showing no clear evidence of core infarct;
b. Cerebral blood flow (CBF) showing a decrease in the right middle cerebral
artery (MCA) territory; c. Mean transit time (MTT) showing delayed perfusion
in the right MCA territory. These sequences together indicate a large ischemic
penumbra in the right MCA territory. (From Vincent et al4, Fig 34.2A)

• Infarction (CBFâ•›<â•›10╯mLâ•›/â•›100╯gâ•›/â•›min): an irre­ MAP increases. The PRx may predict changes in ICP
versible area of brain injury or stroke. and patient outcome. An example of its utility is
An index of autoregulation is called the pressure shown in Figure 3.10. A value of more than +0.2
reactivity index (PRx). This index is calculated by a reflects a poor state of cerebrovascular pressure-
computer program, which performs waveform anal­ reactivity, whereas a value less than −0.2 demon­
ysis on the continuous recordings of ICP and MAP strates excellent reactivity.5 It is possible to alter the
captured from an ICU monitor at the bedside. If MAP progressively using pressor agents and to
autoregulation is impaired, ICP will increase as measure the PRx to obtain an optimal level of PRx
3 • Pathophysiology of traumatic brain injury 47

FIG 3.10â•… Examples of the use of the pressure reactivity index (PRx) to assess autoregulatory reserve and predict
patient outcome: a. Mean arterial blood pressure (MAP), intracranial pressure (ICP), middle cerebral artery flow
velocity (FV) and PRx in a patient with a fatal increase in ICP. PRx rises with ICP increase and remains high.
b. Comparable data from a patient experiencing a plateau wave in ICP with subsequent recovery. It is notable
how PRx falls with recovery and reduction in ICP. (Courtesy M Czosnyka. Based on Winn HR1, Fig 7.6a & b.)

at a particular MAP. This can guide targeted or indi­ is discussed below. Therefore, with a normal increase
vidualised ICU therapy. Whether this alters outcome in focal cortical activity, CBF increases 30% while
or prognosis has not yet been proved. CMRO2 increases by 5%. The amount of oxygen
extracted from the blood is called the oxygen 
CEREBRAL OXYGEN AND CEREBRAL extraction fraction (or ratio: O2EF or O2ER), which
is normally 50%. Oxygen consumption is increased
METABOLISM by seizures and fever, and decreased by hypother-
Concepts of cerebral oxygen consumption and mia and barbiturate coma. Oxygen consumption 
delivery and cerebral metabolism are important is increased by hypoxia, anaemia and low CBF
aspects of cerebral pathophysiology and are pre­ owing to high ICP, hypotension, hypocapnia and
sented below (Table 3.1). However, it should be vasospasm.
emphasised that these parameters are currently mea­ The oxygen extraction fraction (O2EF) describes
sured only in research centres. These measurements the relative balance between oxygen consumption
require jugular bulb venous blood gas monitoring, and delivery and is described by the formula:
xenon inhalation, or PET scans.
The uptake of oxygen from the blood circulation O2 consumption
O2 EF =
by a region of brain is influenced by its metabolic O2 delivery
rate. There is a lower metabolic rate in white matter
than in grey matter, and a lower rate during sleep or This formula can be simplified to:
sedation than when awake. Brain function also
affects metabolic rate: for example, during speech AVDO 2 × CBF AVDO 2
there will be a higher metabolic rate in Broca’s area, O2 EF = =
CaO2 × CBF CaO2
while a seizure significantly increases metabolic
rate. The cerebral metabolic rate of oxygen con­ where CaO2 = arterial oxygen content; AVDO2 =
sumption (CMRO2) is defined as the amount of arteriovenous difference of oxygen; CBF = cerebral
oxygen consumed by 100╯g of brain in a minute and blood flow.
on average is 3.5╯mL╛/╛100╯g╛/╛min in the normal state. The AVDO2 is calculated as follows:
The ratio between CBF and CMRO2 is 14–18 in the
normal state; this is known as the coupling ratio and AVDO 2 = (SaO 2 − SjvO2 ) × 1.34 × Hb
+ (PaO2 − PjvO2 ) × 0.0031
TABLE 3.1â•… Changes in cerebral oxygen delivery
and oxygen consumption parameters after head where SaO2 = saturation of arterial oxygen; SjvO2 =
injury6 saturation of jugular venous oxygen; Hb = haemo­
globin; PaO2 = partial pressure of arterial oxygen;
of cerebral Changes in head
PjvO2 = partial pressure of jugular venous oxygen.)
oxygenation Normal values injury O2EF can be simplified as follows:
Oxygen 1.5 µmolâ•›/â•›gâ•›/â•›min 50% decrease but
SaO2 − SjvO2
consumption can be increased O2 EF =
with fevers, seizures SaO2
Oxygen delivery
CBF 0.54╯ml╛/╛g╛/╛min Can be increased, CMRO2 is coupled to CBF in the normal brain.
decreased or normal
Many metabolic products are responsible for the
SaO2 98% Usually maintained
at normal with
coupling in order to maintain the brain with a con­
supplemental oxygen stant oxygen supply. These are PaO2, PaCO2, extra­
Haemoglobin 14–15╯gâ•›/â•›dL Usually maintained cellular pH, adenosine, potassium ions and nitric
at slightly less than oxide. CBF and CMRO2 become uncoupled after
normal, 10╯g╛/╛dL head injury, so that CBF may be independent of
Derived parameters to monitor oxygenation AVDO2 in the injured brain. The mechanism is not
SjvO2 62 ±â•›4% 68 ±â•›10% well understood, but acidosis may play a role in
AVDO2 6.7 ±â•›0.8╯mLâ•›/â•›dL 4.5 ±â•›1.6╯mLâ•›/â•›dL cerebral vessel dilation, and cerebral vasoconstric­
O2EF 35% 31 ±â•›10% tion has many causes. The normal AVDO2 is 1.8–3.9
3 • Pathophysiology of traumatic brain injury 49

micromolâ•›/â•›mL.6 A normal AVDO2 suggests CBF is constant, SjvO2 is reflective of CBF. A SjvO2 of
normally coupled to CBF, a reduced AVDO2 sug­ <â•›50% is associated with a worse outcome. SjvO2
gests CBF is excessive for cerebral requirements should be maintained above 50%. The O2ER and
(i.e. hyperaemia) and an elevated AVDO2 suggests CMRO2 can also be calculated from a PET scan or
that CBF is reduced (i.e. ischaemia). xenon inhalation blood flow study.
The relationship between AVDO2, CBF, OEF and If CBF is reduced in TBI patients with raised ICP
SjvO2 is complex, but certain patterns emerge and or impaired autoregulation, an increasing O2EF and
indicate the degree of ischaemia: maintenance of CMRO2 compensate for this.
• Hypoperfusion with a compensating (coupled) However, as CBF falls below the brain’s ability to
brain. As CBF decreases, the AVDO2 increases, compensate, hypoperfusion results in a decrease in
the OER increases and the CMRO2 is held stable; CMRO2. Persistent CBF reductions lead to isch­
lactate does not rise. SjvO2 falls. aemia and, ultimately, infarction.
• Ischaemic brain. As CBF decreases below an
ischaemic threshold, the CBF can no longer be Brain oxygen monitoring
compensated by any more oxygen extraction The local partial pressure of brain tissue oxygen
(OEF Max), the CMRO2 falls, and lactate (PbrO2) can be measure by the insertion of a micro­
increases. SjvO2 falls further. These initial catheter into the brain. This was measured in a study
changes of ischaemia may be reversible. of 100 patients with severe head injury. It was found
• Infarcted brain. The ischaemic changes become that brain tissue hypoxia was associated with poor
irreversible. CMRO2 further falls, lactate remains outcome (Fig 3.11).
high, CBF may increase and AVDo2 decreases. The level of critical ischaemia for the brain 
SjvO2 increases. (This is so-called luxury is uncertain but is generally accepted to be PbrO2
perfusion.) <â•›20╯mmHg. Infarction will occur at PbrO2 <â•›10–
Jugular venous saturation can be measured by 15╯mmHg. The methods of treating a low PbrO2 are
sampling blood from the jugular bulb in the skull discussed in Chapter 9. Brain oxygen monitoring is
base with a catheter, and arterial oxygen saturation a practical technology that involves placing a fine
is measured by arterial blood sampling from an arte­ sensing electrode in the parenchyma at the same
rial line. When arterial oxygen saturation and Hb are time as the placement of the ICP monitor. It is a

FIG 3.11â•… Brain tissue hypoxia in relation to severe head injury. (Based on van den Brink WA
et al7, Fig 4.)

readily available and increasingly used technology damage. This is called secondary injury (Fig 3.13).
in the intensive care unit. Secondary-injury prevention and treatment is the
aim of traumatic brain injury management and, with
advances in this area, mortality following severe
PATTERNS OF TBI brain injury has steadily declined since secondary
Brain injury is divided into primary and secondary injury was first described by Miller in 1978.8
injury (Fig 3.12). Primary injury is that which occurs The causes of secondary injury are listed in 
at the moment of impact. At the present time, despite Box 3.1.
tremendous research, it is not possible to reverse the Even a single episode of hypotension, hypoxia or
primary injury. Apoptosis is a consequence of the anaemia following the primary injury can cause sec­
primary injury and evolves during the hours follow­ ondary injury. These factors have been shown to
ing the injury. It may be possible in the future to use independently increase morbidity and mortality fol­
anti-apoptotic agents to reduce neuronal loss result­ lowing severe head injury.9 Patients with severe head
ing from the primary injury. injury frequently have multiple injuries, which makes
Following the impact, a cascade of events is  them extremely vulnerable to blood loss, hypoten­
initiated that may exacerbate or extend the initial sion, anaemia and hypoxia. Early management of the

FIG 3.12â•… With severe traumatic brain injury, the primary injury results in some
permanent neural damage. This primary injury may be diffuse or focal, but it is often a
combination of injury types. Cascades of different mechanisms of secondary injury begin
immediately after the primary injury and may continue for days. This secondary injury
may occur adjacent to the primary injury or at remote sites. (Based on Winn HR1, Fig 326.1.)

FIG 3.13â•… Events leading to secondary brain injury.

3 • Pathophysiology of traumatic brain injury 51

BOX 3.1â•… Causes of secondary brain injury

• Hypoxia
• Hypercapnia
• Hypocapnia
• Epilepsy
• Brain shift
• Cerebral vasospasm
• Haematomasâ•›/â•›contusion
• Hydrocephalus
• Venous obstruction in the neck
• Hypotension
• Critical anaemia
• Hypoglycaemia
• Hyperglycaemia
• Infection

multi-trauma patient, both pre-hospital and in hospi­

tal, needs to be rapid and targeted to minimise sec­
FIG 3.14â•… CT scan of a skull fracture.
ondary brain injury.
Seizures cause secondary brain injury because
they increase metabolic demand in the already com­ patient and in the same patient where multiple pro­
promised brain. CMRO2 increases and glutamate is cesses may be occurring simultaneously. Despite the
released, causing further excitotoxic damage to the complexities, there are certain patterns of injury that
injured brain. In patients with severe TBI in ICU, need to be appreciated. A haemorrhage may be
continuous electroencephalographic (EEG) moni­ extra-axial, such as a subdural or extradural haema­
toring reveals that 17–20% have non-convulsive toma. It can occur within the brain, causing an intra­
seizures.10 cerebral haemorrhage or contusion. Shearing and
Spreading depression (SD) of Leao has been deceleration forces may result in traumatic sub­
observed to occur commonly after severe traumatic arachnoid haemorrhage or injury to the axons,
brain injury and is a further source of secondary termed diffuse axonal injury or traumatic axonal
brain injury. It is a large spreading wave of cell injury. In many cases many of these processes may
membrane depolarisation in the brain, which also be present at the same time in one patient. Although
occurs after stroke and subarachnoid haemorrhage principles exist for treating the various patterns of
and is associated with migraine. Slow potential brain injury, therapies need to be individualised to
changes are demonstrated on EEG. Fever increases each patient.
the risk of SD. It has a bimodal distribution with
peaks at day 1 and day 7 post-injury. The depolarisa­ A.╇ Extra-axial injury
tion is associated with failure of the brain ion Skull fractures
homeostasis, efflux of excitatory amino acids from Skull fracture (Fig 3.14) occurs when the tensile
neurons, increased energy metabolism and changes strength of the skull is exceeded. They are an indica­
in CBF. SD is thought to aggravate ischaemic injury tion of the degree of force and therefore have an
to the brain.11,12 The waves can be abolished by association with underlying brain injury. Brain
N-methyl-D-aspartate (NMDA) receptor antago­ injury, however, commonly occurs in the absence 
nists such as ketamine13 and by cooling the brain. It of a skull fracture. Skull fractures may be linear 
is likely that, in the future, SD will gain in impor­ and these commonly occur near suture lines on the
tance in the clinical management of the severe TBI skull. Comminuted fractures are multiple fractures
patient in ICU. in the same area of the skull. The fractures can be
The manifestations of traumatic brain injury are depressed into the brain and therefore associated
complex and highly variable, both from patient to with extra- or intra-axial haematomas, which may

require evacuation, and with dural tears, cortical TABLE 3.2â•… Fisher grading system
laceration, cortical contusion, intracerebral bleeding
and subdural bleeding. If a skull fracture occurs Grade Appearance of haemorrhage
beneath a lacerated scalp, it is termed a compound
1 None evident
fracture, and this requires surgical elevation and
2 Less than 1╯mm thick
repair to prevent infection.
3 More than 1╯mm thick
Extradural haematoma 4 Any thickness with intraventricular haemorrhage
Extradural haematomas are also called epidural hae­ parenchymal extension
matomas. These occur between the skull and dura
and therefore classically do not cross a suture line
where the dura is most adherent; they characteristi­ subdural greater than 10╯mm thick or midline shift
cally form a biconvex or lens shape appearance on greater than 5╯mm necessitate surgical evacuation,
scans. A bleeding meningeal artery, such as the regardless of the patient’s conscious state.16
middle meningeal, typically causes the haematoma. Traumatic subarachnoid haemorrhage
Patient presentation may vary widely from deep Tearing of vessels on the surface of the brain fol­
coma to minimal symptoms. A patient may have a lowing trauma causes bleeding into the subarach­
lucid interval and then rapidly deteriorate as the noid space. The larger the volume of subarachnoid
haematoma increases in size, leading to death. Reilly blood the greater the chance of secondary vaso­
et al described this phenomenon in a patient who spasm. The degree of haemorrhage is classified on
‘talks and dies’ in 1975;14 fortunately, it has become CT with the Fisher grading system (Table 3.2).17
less common. According to the Brain Trauma Foun­ Less commonly a patient will appear to have a
dation guidelines, any extradural haematoma with a primary TBI when they are found on the floor after
volume greater than 30╯cm3 should be evacuated, a head strike, but in fact they have a ruptured intra­
regardless of the patient’s neurological state.15 Rapid cranial aneurysm or other vascular intracerebral
diagnosis, transfer and management are key in treat­ lesion with subarachnoid haemorrhage (SAH).
ing this neurosurgical emergency. These patients who have SAH with minimal trauma
Subdural haematoma will need angiography to detect an aneurysm.
An acute subdural haematoma (SDH) is associated SAH may cause communicating hydrocephalus
with a greater magnitude of impact than an extradu­ because the drainage of CSF has been affected.
ral haematoma. Typically it results from a high-speed
deceleration injury following a motor vehicle acci­ B.╇ Intracerebral injury
dent in a younger individual. The elderly may develop Intracerebral haematoma and cerebral contusion
an acute SDH with more minor degrees of trauma. A haematoma within the brain parenchyma accounts
SDH is frequently associated with underlying for about 20% of traumatic intracranial haemor­
brain injury. It is caused either by a laceration of rhages. Intracerebral haematomas (ICHs) are caused
parenchyma and surrounding accumulation of blood by rupture of small cortical arteries or associated
from the bleeding cortical vessels or by the tearing with depressed skull fractures. A laceration into the
of surface or bridging vessels that may occur during parenchyma or extravasation of blood into a damaged
rapid deceleration. The laceration of the brain often area results in a contusion. A contusion may be indis­
occurs to the frontal and temporal lobes at the Sylvian tinguishable from an intracerebral haemorrhage, and
fissure as the brain impacts the sharp lesser sphenoid often both processes have occurred within the same
wing of the skull base. Called a ‘bursting’ injury of lesion. Contusions frequently occur in the frontal
the brain, this involves a combination of laceration, poles or temporal lobes, where the brain is in close
intracerebral haematoma and SDH. The SDH is proximity to the skull. Contrecoup contusions are
usually crescentic in shape on a CT scan and white also common. These occur on the side opposite to
in colour in the acute phase. There is usually no lucid that of the impact, because rapid movement of the
interval because of the severe underlying brain brain inside the skull causes it to strike the inner side
injury. Secondary injury results from the mass effect of the skull on the opposite side. Close monitoring
on the brain, causing midline shift, and from raised of patients with contusions is required, as contusions
ICP and cerebral ischaemia underlying the SDH. The may ‘blossom’ and increase in size during the first
Brain Trauma Foundation guidelines suggest that a 24–48 hours after injury and become confluent,
3 • Pathophysiology of traumatic brain injury 53

FIG 3.15â•… Categorisation of primary brain injury. (From Marshall LF19.)

forming an ICH. Patients are also at risk of seizures lesions may not be present initially, and secondary
and electrolyte disturbance. Evacuation of lesions axotomy may occur as a result of altered axonal
causing mass effect may be required. transport, leading to cytoskeletal collapse. Histo­
Diffuse axonal injury logically, with axonal swelling there are punctate
Diffuse axonal injury (DAI), also called traumatic areas within the brain. A classic histological finding
axonal injury (TAI),18 results from shearing due to is that of ‘axonal retraction balls’, which are a result
rapid acceleration or deceleration forces. Patients of the swollen ends of severed axons. The degree of
typically do not have gross contusions or cerebral associated swelling of the brain, identified by
lacerations; rather, punctate haemorrhages may be midline shift or basal cistern effacement on CT scan,
seen in the deep white matter around the lateral determines the grade of diffuse injury, known as the
ventricles, in the dorsal midbrain or near or in the Marshall grade19 (Fig 3.15).
corpus callosum. A larger haemorrhage in the brain­ DAI is a major contributor to poor outcome and
stem is called a Duret haemorrhage and carries a death following severe TBI.
poor prognosis, as it is indicative of severe forces Intraventricular haemorrhage
torting the brainstem. Tearing of delicate vessels in the wall of the ven­
Gradient echo MRI sequences are the most sensi­ tricle or adjacent parenchyma causes intraventricu­
tive modality to demonstrate these small haemor­ lar haemorrhage. This is very common in severe TBI
rhages and white matter lesions. Some of these and is another index of the severity of the injury.

FIG 3.16â•… Contributing events in the pathophysiology of secondary brain injury. (Based
on Marx J et al20, Fig 38.3.)

With a supine patient, the blood is often seen in one cellular depolarisation. In addition, intracellular
or both occipital horns. The blood will eventually calcium leads to mitochondrial membrane disorgani­
dissipate but may result in hydrocephalus in the sation and the subsequent release of oxygen free
acute phase or as a delayed phenomenon. radicals, which contribute to further internal neuro­
nal injury. Intracellular calcium precipitates degra­
Pathophysiology of TBI at the cellular and dation of the cellular membrane, which leads to lipid
molecular level peroxidation. This further causes breakdown of the
The two mechanisms of neuronal cell death that blood–brain barrier, leading to cerebral oedema and
occur following trauma are necrosis and apoptosis. the release of prostaglandins and thromboxanes,
Necrosis is unregulated and occurs acutely. It results which affect cerebral blood flow. (See Fig 3.16.)
from direct cellular damage or from cellular energy Trauma-induced alterations to the cell’s mem­
loss secondary to ischaemia. Apoptosis is usually a brane potential cause release of excitatory neu­
later manifestation that evolves through a highly rotransmitters such as glutamate. This leads to cell
regulated process mediated by proteins such as cas­ death through an increase in intracellular sodium,
pases, calpain and cytokines. which causes cell swelling, and an increase in intra­
TBI disrupts cell membrane pumps and thus cellular calcium, leading to the sequence of events
sodium and calcium homeostasis. Sodium and mentioned above. It is as though a chain reaction is
calcium may enter traumatised cells, leading to set in motion.
3 • Pathophysiology of traumatic brain injury 55

TBI induces neurons and astrocytes to release microdialysis catheters. Glycerol, which is a measure
inflammatory peptides of the interleukin and tumour of cell membrane destruction, can also be measured.
necrosis factor subtypes. These mediate an inflam­ Microdialysis can also be used to measure cyto­
matory response, contributing to breakdown of the kines. This technology is currently used only in
blood–brain barrier and cellular infiltration of  intensive care research centres, but is the ultimate
macrophages, lymphocytes and neutrophils into  clinical measure of brain metabolism at the bedside.
the brain parenchyma. This inflammatory process
potentiates cerebral oedema and reduces cerebral
blood flow. The circulating cytokines and inflamma­
tory peptides lead to altered gene expression in sur­ The resultant clinical state of the brain following
rounding cells, which leads to gliosis, demylination TBI is due to a complex interplay of mechanical
and apoptosis. (See Fig 3.17.) forces and chemical factors at both the systemic and
Brain metabolites including glucose, pyruvate intracranial levels that extend from the molecular 
and lactate are measured in the human brain using to the whole organ level. Although we cannot alter

FIG 3.17â•… Neurometabolic cascade after traumatic injury. (J Athl Train 2001;36(3):228-235,
Fig 2.)

the primary injury at this time, we can alleviate the continuous electroencephalographic monitoring.  
secondary factors. Prevention and treatment of the J Neurosurg. 1999;91(5):750-760.
secondary factors are the basis of most of the therapy 11. Lauritzen M, Dreier JP, Fabricius M, et al. Clinical
relevance of cortical spreading depression in
for TBI, saving many lives and improving the quality neurological disorders: migraine, malignant stroke,
of outcome of those who survive TBI. subarachnoid and intracranial hemorrhage, and
traumatic brain injury. J Cereb Blood Flow Metab.
REFERENCES 12. Hartings JA, Strong AJ, Fabricius M, et al. Spreading
1. Winn HR, ed. Youman’s neurological surgery. 5th ed. depolarizations and late secondary insults after
Philadelphia: Saunders; 2004. traumatic brain injury. J Neurotrauma. 2009;26(11):
2. Tran ND, Kim S, Vincent HK, et al. Aquaporin-1- 1857-1866.
mediated cerebral edema following traumatic brain 13. Sakowitz OW, Kiening KL, Krajewski KL, et al.
injury: effects of acidosis and corticosteroid Preliminary evidence that ketamine inhibits spreading
administration. J Neurosurg May. 2000;112(5): depolarizations in acute human brain injury. Stroke.
1095-1104. 2009;40(8):e519-e522.
3. Plum F, Posner JB. The diagnosis of stupor and coma. 14. Reilly PL, Graham DI, Adams JH, et al. Patients with
3rd ed. Philadelphia: FA Davis; 1980. head injury who talk and die. Lancet. 1975;2(7931):
4. Vincent J-L, Abraham E, Moore FA, Kochanek P,   375-377.
Fink MP. Textbook of critical care. 6th ed. 15. Bullock MR, Chesnut R, Ghajar J, et al. Surgical
Philadelphia: Saunders; 2011. management of acute epidural hematomas.
5. Czosnyka M, Smielewski P, Kirkpatrick P, et al. Neurosurgery. 2006;58(3 Suppl):S7-S15
Continuous assessment of the cerebral vasomotor (discussion Si-iv).
reactivity in head injury. Neurosurgery. 1997;41(1): 16. Bullock MR, Chesnut R, Ghajar J, et al. Surgical
11-17 (discussion 7-9). management of acute subdural hematomas.
6. Woodman TW, Robertson CS. Jugular venous oxygen Neurosurgery. 2006;58(3 Suppl):S16-S24
saturation monitoring. In: Narayan RK, Wilberger JE, (discussion Si-iv).
Povlishok JT, eds. Neurotrauma. New York: McGraw 17. Fisher CM, Kistler JP, Davis JM. Relation of cerebral
Hill; 1996:521. Ch 36. vasospasm to subarachnoid hemorrhage visualized by
7. van den Brink WA, van Santbrink H, Steyerberg EW, computerized tomographic scanning. Neurosurgery.
et al. Brain oxygen tension in severe head injury. 1980;6(1):1-9.
Neurosurgery. 2000;46(4):868-878. 18. Wang HC, Ma YB. Experimental models of traumatic
8. Miller JD, Sweet RC, Narayan R. Early insults to the axonal injury. J Clin Neurosci. 2010;17(2):157-162.
injured brain. JAMA. 1978;240(5):439-442. 19. Marshall LF, Marshall SB, Klauber MR. A new
9. Fearnside MR, Cook RJ, McDougall P, et al. The classification of head injury based on computerized
Westmead Head Injury Project outcome in severe head tomography. J Neurosurg. 1991;75(1):S14-S20.
injury. A comparative analysis of pre-hospital, clinical 20. Marx J, Hockberger R, Walls R. Rosen’s emergency
and CT variables. Br J Neurosurg. 1993;7(3):267-279. medicine. 7th ed. Philadelphia: Mosby; 2009.
10. Vespa PM, Nuwer MR, Nenov V, et al. Increased 21. Abeloff MD, Armitage JO, Niederhuber JE, et al.
incidence and impact of nonconvulsive and convulsive Abeloff’s Clinical Oncology. 4th ed. Philadelphia:
seizures after traumatic brain injury as detected by Churchill Livingstone; 2008.
Pre-hospital management
Stephen Bernard

Severe traumatic brain injury (TBI) is a devastating continuously monitor the respirations. If these
injury that carries a high rate of morbidity and mor- should cease, the patient should be immediately
tality.1 Immediately following the initial (primary) placed supine, the airway cleared and expired air
traumatic injury, there are a number of possible resuscitation commenced.5 Since a pulse check per-
additional (secondary) neurological insults that have formed by a bystander is regarded as unreliable,
the potential to worsen outcome. Common causes of cardiac arrest should be presumed if respirations
secondary injury in the pre-hospital setting include cease and chest compressions should then be
hypoxia andâ•›/â•›or hypotension.2,3 In addition, altera- commenced.
tions in ventilation leading to an increase or decrease The unconscious patient may be trapped in a
in the carbon dioxide level may occur, and this is motor vehicle. In such cases, the EMS call-
also associated with adverse outcomes.4 The goals takingâ•›/â•›dispatch centre may recommend that a
of the pre-hospital emergency medical service bystander enter the vehicle and support the head in
(EMS) treatment are to: a neutral position. If the patient is a motorcyclist
• provide rapid assessment with a full-face helmet, the helmet should be
• institute treatment at the scene that may prevent removed to facilitate airway management. Consid-
or correct any secondary insults erable care needs to be taken during this procedure,
• transport the patient expeditiously to an approÂ� since removal of the helmet may lead to movement
priate hospital emergency department (ED) for of an unstable cervical spine and subsequent spinal
definitive trauma care. cord injury.
Concurrent with the delivery of bystander instruc-
tions for first aid, the call takingâ•›/â•›dispatch centre
BYSTANDER ACTIONS should dispatch an ambulance on a Code 1 (lights,
In the majority of cases of severe TBI, a bystander sirens) response. If the patient is in a motor vehicle
will be present. The bystander should immediately and possibly trapped, the fire service will also be
call the EMS to request the urgent attendance of an dispatched for possible assistance with extrication
ambulance. When the EMS is called, the call- from the vehicle and to provide fire suppression in
takingâ•›/â•›dispatch centre should provide the bystander the case of ignition of spilt fuel. Police are also
with first-aid instructions. dispatched whenever an injury has been caused by
Patients who are unconscious after TBI are at risk a motor vehicle.
of aspiration of blood from upper airway injury
andâ•›/â•›or acid aspiration from vomiting. Therefore,
patients who are comatose but who have adequate
respirations should be placed gently in the left As soon as the first paramedics arrive at the scene,
lateral, or ‘coma’, position to prevent aspiration of their initial assessment of the unconscious trauma
blood or vomit. Once the patient has been placed in patient is DRABC (Fig 4.1):
a coma position or the head is maintained in neutral D danger
alignment, the bystander should be instructed to R responsiveness

A airway
B breathing
C circulation
There are a number of dangers to be considered
by paramedics when a patient has suffered a severe
TBI after a motor vehicle accident. In particular, it
is common for passing traffic to be distracted by the
activity at the scene of the crash. The EMS should
take immediate action to make the scene safe. This
will generally involve appropriate diversion of
traffic away from the scene to prevent passing traffic
from crashing into parked emergency vehicles or
personnel. If police are not immediately available,
the patient may need to be promptly moved into a FIG 4.1â•… Initial evaluation and management may need
to be undertaken prior to extrication of the patient from
safe area (i.e. the rear of the ambulance) prior to the vehicle. (From www.ambulance.vic.gov.au, with permission.)
initial assessment and management. Other dangers
at the scene of a motor vehicle accident include the
risk of electrocution from fallen power lines and the an oropharyngeal airway may lead to a gag response
risk of fire from leaking fuel. and cause vomiting. If an oropharyngeal airway is
The first clinical assessment of any patient who not tolerated, consideration may be given to the
appears to have altered conscious state after trau- gentle insertion of a nasopharyngeal airway and 
matic injury is the ‘response’ of the patient. This  suctioning of the upper airway with a suction cath-
is a simple four-point evaluation of the response of eter.6 The insertion of a nasopharyngeal airway is
the patient to voice commands or painful stimulus. contraindicated, however, in patients with signifi-
The conscious state of the patient can then be clas- cant injuries to the mid-face, since this may lead to
sified as Awakeâ•›/â•›Verbal responseâ•›/â•›Pain responseâ•›/â•› epistaxis.
Unresponsive (AVPU). Once the airway is clear and spontaneous ven�
The next action of the paramedic is to carry out tilation is assessed and considered adequate, sup�
the ‘primary survey’. This is the rapid assessment plemental oxygen by mask is recommended. If
and correction of any immediate life threats due to respirations are considered inadequate, assisted ven-
airway, breathing or circulatory disturbances. The tilation using a bagâ•›/â•›valveâ•›/â•›mask technique should
primary survey also involves immobilisation of the be undertaken.
spinal column using the application of a cervical If there is respiratory distress, hypoxia andâ•›/â•›or
collar and laying the patient supine. Concurrent  profound hypotension, tension pneumothorax should
with the initial assessment and primary survey, always be considered. If the clinical signs are sug-
bystanders should be questioned about the mecha- gestive, testing for pneumothorax and drainage is
nism of the injury. This may be valuable in predict- indicated. While many EMS teams use decompres-
ing the pattern and severity of injury. If a bystander sion by inserting an intravenous cannula through the
is a friend or relative of the patient, relevant past second rib interspace in the midclavicular line,7 this
medical history and current medications may be may be inadequate, and some recommend that blunt
known. dissection and digital decompression through the
pleura with insertion of an intercostal tube be per-
Airwayâ•›/â•›breathing formed.8 Concurrent with airway assessment, a cer-
The initial paramedic assessment of the upper airway vical collar is placed to minimise movement of the
involves an inspection inside the mouth to deter- cervical spine.
mine whether there is any material such as vomit  Definitive airway management in the uncon-
or blood that may lead to obstruction of the airway. scious TBI patient is rapid sequence intubation
If possible, an oropharyngeal airway should be (RSI) for airway protection, oxygen administration,
inserted. However, the unconscious patient may tracheal suction, the control of ventilation and the
have the teeth firmly clenched and this restricts safe performance of computerised tomography
access to the upper airway, making placement of an scanning. However, there is debate whether RSI
oropharyngeal airway difficult. Also, the insertion of should be undertaken at the scene by paramedics or
4 • Pre-hospital management 59

FIG 4.2â•… Endotracheal intubation may be undertaken prior to transport.

(From www.ambulance.vic.gov.au, with permission.)

deferred until arrival at the hospital where this pro- latter transported without intubation in the period
cedure can then be performed by an experienced prior to the study. Mortality was significantly
physician (Fig 4.2).9 increased in the RSI patients versus control patients
Paramedic RSI has a number of potential advan- (33.0% versus 24.2%). The overall success rate of
tages. There is early correction of hypoxia, control intubation was 86%. Subsequent analysis of the data
of ventilation and the intubated patient can be trans- suggested that the cause of increased mortality was
ported safely in the supine position. In addition, most likely inadvertent hyperventilation after suc-
definitive control of the airway and ventilation cessful intubation, rather than complications of
allows bypass of nearby emergency departments  failed intubation.4
that do not provide neurosurgical care. Instead, the In a prospective randomised trial conducted in
patient can be more safely transported relatively long Victoria, Australia, 312 patients were allocated to
distances for definitive neurosurgical management. paramedic RSI or transport without intubation.11
In addition, the performance of RSI in the field The success rate for paramedic RSI was 97%. The
increases scene time and this may be associated with proportion of patients with favourable outcome as
an adverse outcome if the patient has massive bleed- measured by the Extended Glasgow Outcome Scale
ing. In that situation, immediate transport and defin- at 6 months post-injury was 51% of patients in the
itive surgical care is required. paramedic RSI group compared with 39% of patients
There have been two major studies of paramedic in the hospital intubation group. This data suggests
RSI in patients with TBI.10,11 In a beforeâ•›/â•›after study that paramedic RSI is associated with improved
conducted in San Diego, USA, the impact of the outcomes.
introduction of paramedic RSI into a road-based However, there are significant barriers to the wide-
EMS was assessed.10 Over two years adult major spread implementation of paramedic RSI. This skill
trauma victims who had a Glasgow Coma Scale requires considerable training and skills-maintenance
(GCS) score of 3–8 following trauma and suspected programs to maintain a high success rate.
head injury with a transport time >10 minutes and In order to avoid the risks of administration of
inability to intubate without RSI were prospectively sedation or muscle relaxants, some EMS teams
enrolled. The drugs used for RSI were midazolam permit intubation without the use of supplemental
and succinylcholine administered before laryngos- drugs.9 However, given that many patients with
copy and rocuronium given after endotracheal tube severe TBI retain upper airway reflexes, this
placement was confirmed using capnometry. There approach has a relatively low success rate. In 
were 209 RSI patients matched to 627 controls, the addition, the stimulation of the upper airway with

laryngoscopy without sedation may lead to vomit- A number of different fluid types have been used
ing. Finally, manipulation of the airway without in the setting of blood loss and severe TBI, including
appropriate anaesthesia would be expected to isotonic crystalloids, hypertonic saline andâ•›/â•›or col-
increase intracranial pressure. loidal solutions. These three fluid types have recently
Although there have been no randomised con- been compared in two separate but concurrent clini-
trolled trials in adults comparing intubation without cal trials.19,20 In a multicentre, randomised clinical
supplemental drugs with other approaches, there is trial, 853 adult patients with hypotension due to
compelling evidence from trauma registries that suspected blood loss received 250╯mL of either
paramedic intubation without drugs is associated 7.5% saline with 6% dextran 70, 7.5% saline (hyper-
with worse outcomes compared with basic airway tonic saline) or 0.9% saline as part of intravenous
management.9,12 fluid resuscitation.19 There was no difference in
In summary, while there is now evidence that 28-day survival, but there was a higher mortality in
paramedic RSI in patients with severe TBI improves the subset of patients who received hypertonic fluids
outcome, this approach will be applicable only for but who did not receive a blood transfusion in the
EMS teams with a high level of skills training. For first 24 hours. The trial was stopped early because
most EMS teams, basic airway management and of this safety concern with hypertonic solutions. In
immediate transport to hospital for RSI by a physi- a concurrent trial, 1331 adult patients with a pre-
cian is appropriate. Attempts by paramedics to intu- hospital GCS score of less than 9, but without hypo-
bate without sedation should be undertaken only in tension, received a 250╯mL bolus of one of the three
patients with absent airway reflexes. Such patients solutions above.20 Survival at 28 days was 74.3%
are very deeply comatose and unlikely to survive.13 with hypertonic salineâ•›/â•›dextran, 75.7% with hyper-
tonic saline and 75.1% with normal saline (pâ•›=â•›0.88).
Circulation These two studies suggest that colloidal andâ•›/â•›or
Hypotension in the pre-hospital phase of care is hypertonic solutions are not beneficial in the pre-
common after severe TBI and is associated with hospital resuscitation of the patient with severe TBI.
worse outcomes compared to those patients without At present, the optimal resuscitation fluid for patients
hypotension.3,14 Hypotension has previously been with severe TBI plus shock appears to be isotonic
defined as a systolic blood pressure <╛90╯mmHg, but crystalloid solutions such as 0.9% saline or lactated
more recent evidence suggests that a systolic blood Ringer’s solution.
pressure <╛110╯mmHg is associated with increased
mortality after trauma.15 Additional initial procedures
Common causes of hypotension include blood After the primary survey, application of the cervical
loss, spinal cord injury, tension pneumothorax andâ•›/â•›or collar and decompression of tension pneumothorax
the administration of sedative drugs during intuba- (as above), there are several additional procedures
tion. Therefore, once the airway has been cleared  that should be undertaken prior to the secondary
and ventilation with supplemental oxygen has been survey. First, continuous monitoring of the electro-
administered, measurement of blood pressure and cardiogram and pulse oximeter are routine in most
pulse rate is undertaken to assess the circulation. EMS. In addition, regular non-invasive monitoring
The treatment of hypotension due to blood loss of the blood pressure is undertaken. Also, intra�
initially involves direct compression at the point of venous access is required to administer fluid for
obvious external bleeding, plus application of a cir- hypovolaemic shock and to administer sedation and
cumferential pelvic binder if open-book pelvic frac- muscle relaxants if RSI is to be undertaken.
tures are suspected. An arterial tourniquet may be
required for limb bleeding that is not able to be
controlled using pressure alone.16
Once external bleeding is controlled, hypotension After the primary survey and initial interventions 
in the setting of severe TBI should be promptly as above, paramedics should then undertake a 
treated with the rapid administration of intravenous secondary survey. This is the head-to-toe examina-
fluid.17 If intravenous access is unable to be estab- tion to determine the extent of the injuries. At this
lished, then intraosseous access should be consid- time, any limb fractures identified should be splinted.
ered. This has a high success rate in both adults and As part of the secondary assessment, the formal
children using proprietary devices.18 neurological examination consists of assessment of
4 • Pre-hospital management 61

pupil size and reactivity and an assessment of the outcome was poor (severe disability, vegetative state
GCS score, noting whether left and right responses or death) in 31 of 52 patients in the hypothermia
to a painful stimulus are equal. group and in 25 of 56 in the normothermia group
(pâ•›=â•›0.67). This trial was stopped early due to futility.
OTHER TREATMENTS Therefore, at this time, pre-hospital therapeutic
hypothermia cannot be recommended in patients
Temperature control with severe TBI outside the setting of a clinical trial.
The trauma patient is at risk of accidental hypo�
thermia (<35°C) if the ambient temperature is cold Blood sugar
andâ•›/â•›or if the patient receives large volumes of cold In patients with coma from any cause, it is wise to
intravenous fluid in the pre-hospital setting. While exclude hypoglycaemia as a cause or contribution to
hypothermia may lead to coagulopathy and increased the altered conscious state.23
bleeding, there is also some evidence that hypother-
mia protects the injured brain.21
A number of clinical trials have been undertaken
examining the possible role of therapeutic hypother- After initial assessment and management, safe trans-
mia in the pre-hospital setting. In a recent study, port of the patient from the scene of the injury to the
patients with severe TBI were allocated to pre- appropriate centre as soon as possible is a key role
hospital therapeutic hypothermia (using a rapid of the EMS.
infusion of ice-saline) or normothermia.22 Patients In many cities, there are designated trauma
randomly assigned to hypothermia were cooled to centres that provide definitive neurosurgical care for
35°C until their trauma assessment was completed, patients with severe TBI. If possible, patients with
then further cooled to 33°C for 48 hours. The control severe TBI should bypass smaller hospitals and be
patients were maintained at normothermia. Initially transported directly to such centres.24 For patients
119 patients were allocated to hypothermia and 113 who are more than approximately 50╯km away from
to normothermia. In the ED, patients were evaluated a trauma service, consideration should be given to
for bleeding. Those without exclusion criteria were transport by an appropriately staffed EMS helicop-
either cooled to 33°C for 48 hours and then gradu- ter (Fig 4.3).
ally rewarmed or treated at normothermia, depend- The exact role of air transport compared with
ing upon their initial treatment assignment. The road transport remains uncertain. In general, the

FIG 4.3â•… Helicopter transport may decrease the total pre-hospital time that
elapses before definitive care. (From www.ambulance.vic.gov.au, with permission.)

helicopter emergency medical service is staffed with paramedic rapid sequence intubation of severely
a senior doctor andâ•›/â•›or paramedic and this staffing head-injured patients. J Trauma. 2004;57:1-8.
skill set may allow definitive airway and other man- 5. Ashour A, Cameron P, Bernard S, et al. Could
bystander first-aid prevent trauma deaths at the scene
agement at the scene. On the other hand, this of injury? Emerg Med Australas. 2007;19:163-168.
resource is extremely expensive and there may be 6. Roberts K, Whalley H, Bleetman A. The
limited availability due to weather. Overall, there is nasopharyngeal airway: dispelling myths and
evidence that transport by helicopter decreases mor- establishing the facts. Emerg Med J. 2005;22:394-396.
tality after trauma.25 7. Mistry N, Bleetman A, Roberts KJ. Chest
decompression during the resuscitation of patients in
prehospital traumatic cardiac arrest. Emerg Med J.
8. Fitzgerald M, Mackenzie CF, Marasco S, et al. Pleural
1. The optimal management of the airway at the decompression and drainage during trauma reception
scene is uncertain. One recent study has sug- and resuscitation. Injury. 2008;39:9-20.
gested benefit with paramedic RSI, but additional 9. Bernard SA. Paramedic intubation of patients with
studies are required. severe head injury. Review of current Australian
2. Decompression of tension pneumothorax using practice and recommendations for change. Emerg Med
needle thoracocentesis may be unreliable. Australas. 2006;18:221-228.
10. Davis DP, Hoyt DB, Ochs M, et al. The effect of
However, the role of digital tube decompression
paramedic rapid sequence intubation on outcome in
and intercostal catheter insertion in the field is patients with severe traumatic brain injury. J Trauma.
uncertain. 2003;54:444-453.
3. The exact role of helicopter transport versus road 11. Bernard SA, Nguyen V, Cameron P, et al. Prehospital
transport is uncertain. rapid sequence intubation improves functional outcome
for patients with severe traumatic brain injury:  
a randomized controlled trial. Ann Surg. 2010;
SUMMARY 252:959-965.
12. von Elm E, Schoettker P, Henzi I, et al. Pre-hospital
In cases of severe head trauma, well-trained para-
tracheal intubation in patients with traumatic brain
medics save lives and improve the outcomes by: injury: systematic review of current evidence. Br J
1. prompt ambulance despatch and arrival at the Anaesth. 2009;103:371-386.
scene 13. Lockey D, Davies G, Coats T. Survival of trauma
2. rapid assessment of injuries patients who have prehospital tracheal intubation
3. securing the airway and respiration without anaesthesia or muscle relaxants: observational
4. treatment of bleeding and shock study. BMJ. 2001;323:141.
14. Shafi S, Gentilello L. Hypotension does not increase
5. protection of the spine
mortality in brain-injured patients more than it does  
6. minimising scene time in non-brain-injured patients. J Trauma. 2005;59:
7. rapid transport to the appropriate hospital. 830-834.
15. Hasler RM, Nuesch E, Jüni P. Systolic blood pressure
below 110╯mmHg is associated with increased
REFERENCES mortality in blunt major trauma patients: multicentre
1. Gross CP, Anderson GF, Powe NR. The relation between cohort study. Resuscitation. 2011;82:1202-1207.
funding by the National Institutes of Health and the 16. Sambasivan CN, Schreiber MA. Emerging therapies in
burden of disease. N Engl J Med. 1999;340:1881-1887. traumatic hemorrhage control. Curr Opin Crit Care.
2. Chi JH, Knudson MM, Vassar MJ. Prehospital hypoxia 2009;15:560-568.
affects outcome in patients with traumatic brain injury: 17. Brain Trauma Foundation Guidelines for the
a prospective multicenter study. J Trauma. 2006;61: management of severe traumatic brain injury. I. Blood
1134-1141. pressure and oxygenation. J Neurotrauma. 2007;24:
3. Franschman G, Peerdeman SM, Andriessen TM, et al. S7-13.
For the Amsterdam Lifeliner: analysis of results and 18. Hartholt KA, van Lieshout EM, Thies WC, et al.
methods–traumatic brain injury (ALARM-TBI) Intraosseous devices: a randomized controlled trial
investigators. Effect of secondary prehospital risk comparing three intraosseous devices. Prehosp Emerg
factors on outcome in severe traumatic brain injury in Care. 2010;14:6-13.
the context of fast access to trauma care. J Trauma. 19. Bulger EM, May S, Kerby JD, et al. Out-of-hospital
2011;71:826-832. hypertonic resuscitation after traumatic hypovolemic
4. Davis DP, Dunford JV, Poste JC, et al. The impact of shock: a randomized, placebo controlled trial. Ann
hypoxia and hyperventilation on outcome after Surg. 2011;253:431-441.
4 • Pre-hospital management 63

20. Bulger EM, May S, Brasel KJ, et al. Out-of-hospital Hypothermia II): a randomised trial. Lancet Neurol.
hypertonic resuscitation following severe traumatic 2011;10:131-139.
brain injury: a randomized controlled trial. JAMA. 23. Brady WJ, Butler K, Fines R, et al. Hypoglycemia in
2010;304:1455-1464. multiple trauma victims. Am J Emerg Med.
21. Nichol AD, Cooper DJ. POLAR Study Investigators, 1999;17:4-5.
EPO Study Investigators. Can we improve neurological 24. Cameron PA, Gabbe BJ, Cooper DJ, et al. A statewide
outcomes in severe traumatic brain injury? Something system of trauma care in Victoria: effect on patient
old (early prophylactic hypothermia) and something survival. Med J Aust. 2008;189:546-550.
new (erythropoietin). Injury. 2009;40:471-478. 25. Butler DP, Anwar I, Willett K. Is it the H or the EMS
22. Clifton GL, Valadka A, Zygun D, et al. Very early in HEMS that has an impact on trauma patient
hypothermia induction in patients with severe brain mortality? A systematic review of the evidence.  
injury (the National Acute Brain Injury Study: Emerg Med J. 2010;27:692-701.
Emergency department management
Jeffrey V Rosenfeld, Mark Fitzgerald, Alfredo Mori,
David Morgan, Vince Cousins, Anthony Hall

Neurotrauma contributes to 60% of all deaths from Effective trauma triage identifies the severely injured
injury. The establishment of regional trauma systems patient with life-threatening problems and allocates
and associated advances in care have reduced neu- the patient to the most appropriate treatment area.
rotrauma mortality by 50%. However, despite The report from the paramedics or bystanders is
guidelines, protocols and continuous performance important to understand the mechanism of injury
improvement, management errors in the basics of and the pace of deterioration. It is also important, if
trauma care continue, even in established trauma possible, to establish whether patients have any
centres.1 It is estimated that over 50% of preventable known medical conditions, such as epilepsy, diabe-
errors that contribute to death occur during the tes and cardiac or respiratory disease, and what
initial reception and resuscitation of the injured medication they are taking.
patient in the emergency department.2 Unconscious patients are considered to have
Neurotrauma evolves over time. Changing clini- immediately life-threatening problems and require
cal signs indicate changing pathology that may immediate and simultaneous assessment and treat-
require urgent action. An expanding intracranial ment (Table 5.1). Emergency staff need to rapidly
haematoma or a hypoxic injury developing due to a guarantee airway patency, ensure ventilation is ade-
period of inadequate cerebral perfusion are exam- quate and that a circulation is present. Patients with
ples of this evolution. In response to this, regular decreased responsiveness or with a lateralising neu-
neurological observation over time has developed as rological deficit are considered to have an immi-
an essential component of trauma care. The role of nently life-threatening problem. Even patients who
emergency staff is to identify patients with neu- present following a brief loss of consciousness
rotrauma, anticipate the evolution of neural injury (LOC) may have a potentially life-threatening head
and prevent subsequent secondary neurological injury.
injury. Even a minor head injury requires a period
of observation. TRAUMA RECEPTION
A. INITIAL ASSESSMENT Unresponsive patients or those with compromised
AND TREATMENT airway or breathing are at immediate risk of death
and require immediate intervention. Severely injured
TRIAGE patients commonly arrive in emergency departments
Triage is a process undertaken on arrival at the with undiagnosed and undifferentiated injuries. An
emergency department (ED), or prior to arrival if algorithmic approach to trauma reception and resus-
adequate information is received. Triage sorts those citation has been demonstrated to improve outcomes
patients most at risk of death or disability from less and reduce the likelihood of missed injury.
time-critical patients. ED triage aims to ensure that Multidisciplinary trauma teams allow resuscita-
patents are treated in order of their clinical urgency tion and diagnoses to occur simultaneously. The role
and their need for time-critical interventions. of the trauma team is to produce organisation out of
5 • Emergency department management • A. Initial assessment and treatment 65

TABLE 5.1â•… Guidelines for triage of neurotrauma, adapted from The Australasian Triage Scale (ATS)3

ATS category and description Response Clinical descriptors (indicative only)

Category 1: Immediate simultaneous Cardiac/respiratory arrest

Immediately life-threatening assessment and treatment Airway obstruction—impending arrest
for conditions that are a Respiratory rate <â•›10â•›/â•›min
threat to life Extreme respiratory distress
Unresponsive or responds to pain only (GCS <â•›9)
Ongoingâ•›/â•›prolonged seizure
Category 2: Assessment and treatment Major multiple trauma requiring a rapid, organised team
Imminently life-threatening (often simultaneous) within response (not covered by Category 1)
10 minutes Airway risk—severe stridor
Drowsy, decreased responsiveness (Glasgow Coma Scale <â•›13)
Acute hemiparesisâ•›/â•›dysphasia
Category 3: Assessment and treatment Seizure (now alert)
Potentially life-threatening within 30 minutes of arrival Persistent vomiting
Head injury with short LOC—now alert
Category 4: Assessment and treatment Minor head injury—no LOC
Potentially serious within 60 minutes of arrival
Reprinted with permission of the Australasian College for Emergency Medicine.

chaos. Providing severely injured patients with 4. Imaging/disposition

organised trauma team reception ensures that life- • Imaging, including CT head scans, provides
threatening problems are identified and corrected by detailed diagnostic information about the inju-
following an ordered and algorithmic approach. ries. Imaging of the cervical spine is discussed
Trauma callout criteria are agreed conditions that in Chapter 6. The trauma patient may also
identify those injured patients most at risk and will require CT imaging of the other regions,
trigger an immediate, multidisciplinary response for including the thoracolumbar spine but discus-
seriously injured patients (Fig 5.1). With adequate sion of the indications for imaging of other
pre-hospital notification, the trauma team can gather regions is beyond the scope of this book.
and assign roles before the arrival of the patient • Procedural and surgical interventions are
(Box 5.1). undertaken where indicated.
Upon arrival of the patient in the ED, manage- • The patient is admitted to an appropriately
ment should progress in a rapid and systematic staffed and equipped facility for ongoing mon-
manner, following well-established trauma guide- itoring and interventions.
lines, either Early Management of Severe Trauma 5. Tertiary survey
(EMST) or Advanced Trauma Life Support • A detailed head-to-toe examination, with
(ATLS®)4 (Fig 5.2). This algorithmic approach review of the pathology and diagnostic results,
focuses on treating the greatest threat to life first. determines the response to interventions and
The EMST and ATLS® programs emphasise that any missed injuries.
the lack of a definitive diagnosis and detailed history Careful attention to the ABCs of resuscitation
should not hamper indicated treatment for life- must not be neglected in the head-injured patient
threatening injury. The most time-critical interven- (Table 5.2).
tions take precedence. Primary brain injury is the brain injury that
Management follows an established approach: occurs at the time of the initial insult. Secondary
1. Primary survey brain injury may occur as a result of hypoxia,
• Life threats are identified and corrected  hypercarbia, hypotension, hypoglycaemia, brain
(Table 5.2). swelling or expanding intracranial haematoma, dis-
2. Resuscitation phase placement of brain structures and associated raised
• Physiological monitoring tracks restoration of intracranial pressure, coagulopathy, seizures, acido-
an adequate ventilation and circulation. sis and infection. The aim of emergency treatment
3. Secondary survey is to prevent secondary brain injury.
• A detailed head-to-toe examination identifies The immediate priority is to establish a secure
observable injuries. airway by intubation, provide adequate ventilation

FIG 5.1â•… Lanyards with trauma callout criteria. TBSA = total body surface area; MCI = multiple casualty incident.
(From the Alfred Hospital.)

BOX 5.1â•… Typical trauma team composition

• Emergency physician/registrar
• Trauma registrar ± trauma surgeon
• Anaesthetist
• Trauma nurse leader
• Airway nurse
• Circulation nurse
• Radiographer
• Trauma centre orderly

and correct or prevent hypoxia and hypotension. FIG 5.2â•… Coordinated trauma team reception.
During the primary survey, initial resuscitation 
and secondary survey, the diagnosis of head injury to normal levels (PaCO2 35–45╯mmHg, but preÂ�
is established and the priority of treatment is  ferably in the lower normal range with PaCO2
determined. Throughout this time it is essential to 35–40╯mmHg). Hypercarbia (PaCO2 >â•›45╯mmHg)
maintain adequate oxygenation, systemic blood causes cerebral vasodilation and may further increase
pressure and ventilation with control of the PaCO2 intracranial pressure (ICP). Hypocarbia is caused by
5 • Emergency department management • A. Initial assessment and treatment 67

TABLE 5.2â•… Major trauma primary survey and resuscitation interventions4

ABCs of resuscitation Primary survey problem Intervention

A Airway management • Clear airway and ensure an unobstructed airway.

Airway • Consider adjunctive airway devices including intubation.
Cervical spine control Splint cervical spine
B Ventilation • Apply high flow O2.
Breathing • Assist ventilation with bag–mask ventilation if respiratory rate <â•›10â•›/â•›min.
• Seal sucking chest wounds with three-sided dressings.
• Decompress pleural space on affected side(s) if evidence of tension
• Perform supine chest X-ray.
C Haemorrhage control Control bleeding wounds with direct pressure.
Circulation Splint bleeding fractures Apply pelvic binder and long bone splints for suspected fractures.
Vascular access Insert two ≥â•›18╯G intravenous lines.
Pathology Send blood for full blood examination, group and hold, coagulation profile,
glucose, electrolytes and urea, LFTs, β-HCG and troponin-I when indicated.
Restoring circulating • Administer IV crystalloid and packed red blood cells (PRBCs).
volume • Exclude spinal injury as a cause for hypotension.
Physiological monitoring Perform ECG, blood pressure, SpO2, EtCO2.
Ultrasound Perform focused ultrasound (FAST) to exclude massive haemothorax,
pericardial tamponade and haemoperitoneum.
D GCS Determine GCS.
Disability Pupils Assess direct and consensual pupil response, check for ocular palsy. Remove
contact lenses.
Lateralising deficit Check for facial movements and the sensation and movement of all limbs as
part of the GCS.
Spinal level • Exclude spinal injury when possible. Document spinal function using
American Spinal Injury Association chart.5 (See Chapter 6.)
E Temperature control Measure temperature and maintain normothermia.
Expose Communication • Communicate all suspected and confirmed diagnoses to trauma team.
Environment • Update next of kin.
Seek neurosurgical Indications for referral:
opinion • GCS <â•›14
• Lateralising neurological deficit
• Penetrating head or neck injury
• Acute spinal cord injury

hyperventilation to levels of PaCO2 <â•›30╯mmHg and from coughing or from movement of the patient 
carries a significant risk of causing cerebral isch- or over a sustained period from intracranial bleed-
aemia.6 Hypotension is tolerated poorly by the head- ing and cerebral oedema. Attention should be
injured patient because autoregulation is often directed to reducing or controlling ICP in the
impaired and the threshold for ischaemia occurs at severely head-inured patient. Simple ways to achieve
relatively higher levels of blood pressure than in the this include raising the trauma bed by 15 degrees
normal brain. The blood glucose should be checked head-up, loosening cervical collars and ensuring
on arrival. endotracheal tube ties are tied above one ear 
Hypoxia (PaO2 <â•›65╯mmHg) and hyperoxia (PaO2 to avoid a venous tourniquet, and aiming for high–
>â•›200╯mmHg) have been associated with secondary normal PaO2 (~â•›100╯mmHg), and low–normal
brain injury. Regular monitoring of blood gases PaCO2 (35–40╯mmHg).
requires the placement of an arterial line in intubated Patients with severe TBI (GCS <â•›9) are comatose
trauma patients with traumatic brain injury (TBI), and require intubation for airway protection and
but this should not delay their transport to the CT adequate ventilation. Intubation of patients with TBI
scanner or to the operating theatre should they need is often difficult because of:
to be moved urgently. 1. the urgency of the situation
Focal brain acidosis and hypoxia may develop 2. the possibility of facial and laryngeal  
secondary to raised ICP, whether raised temporarily injuries

1. Oxygen and ventilation

• Regular arterial blood gases are required in
addition to oximetry
• PaO2 >â•›80╯mmHg
• SaO2 >â•›95%
• PaCO2 35–40╯mmHg (no routine hyperventi-
Once successful intubation has occurred (confirmed 
using capnography in addition to auscultation), the
initial aim should be for a PaCO2 level of 35–
40╯mmHg. An arterial blood gas immediately post-
intubation is essential
2. Blood pressure
In the resuscitation phase, a systolic blood pressure
FIG 5.3╅ Rapid sequence intubation using cricoid (SBP) >╛90╯mmHg is the aim in non-penetrating
pressure and in-line stabilisation. trauma. Ideally the mean arterial pressure (MAP)
should be determined and kept >╛80╯mmHg. This
assumes an ICP of 20╯mmHg when not measured,
3. the requirement for neck immobilisation due to thereby maintaining a cerebral perfusion pressure
the presence or risk of cervical spine injuries. (CPP) of approximately 60╯mmHg.
A clinician with high-level airway experience should Sedation titrated to effect may be continued post-
perform the procedure and have several experienced intubation. A usual combination would be morphine
assistants. 50╯mg and midalozam 50╯mg in a 50╯mL syringe
The technique used in most situations is rapid driver at 5╯mL per hour, following a 5╯mg bolus.
sequence intubation (RSI). Patients should initially Alternatively, propofol at 5–10╯mgâ•›/â•›min through a
be sedated deeply and paralysed, ensuring that no syringe driver may be used for brief periods of intu-
coughing or skeletal muscle movement occurs. RSI bation and sedation (such as transfer to and from the
includes pre-oxygenation, application of cricoid CT scanner only). These agents are negatively
pressure aimed at reducing the risk of aspiration, inotropic—that is, they may all cause hypotension
manual in-line neck stabilisation and a rapid and must be used with care by expert staff. Paralysis
sequence of drugs (Fig 5.3). may be maintained with drugs such as atracurium
An accepted combination of drugs for RSI is (0.5╯mgâ•›/â•›kg boluses every 20–40 minutes), or cisa-
thiopentone (1–6╯mgâ•›/â•›kg), usually 125–325╯mg tracurium (0.1╯mgâ•›/â•›kg boluses every 20–40 minutes).
bolus IV, and suxamethonium 1–1.5╯mgâ•›/â•›kg IV, Vecuronium is generally avoided.
usually as a 100╯mg bolus. Thiopentone and suxa- Fentanyl is commonly used in elective neurosur-
methonium are the most reliable intubating agents, gical anaesthetic induction to blunt the rise in ICP
but both have significant side effects, such as hypo- associated with intubation. Its use in emergency
tension. They must be administered only by staff intubation should be considered. However, there is
expert in their use. no evidence for the pre-induction use of lignocaine
The causes of hypotension during the resuscita- in humans in RSI.
tion phase require rapid diagnosis but should not Sedated patients may still feel pain, which also
delay the resuscitation. Causes such as hypovolae- raises ICP, so intravenous analgesia should be judi-
mia, cardiac tamponade, tension pneumothorax, ciously administered. Simple agents such as mor-
vasodilation from drugs, anaphylaxis and myocar- phine, either in infusion as above, or alone in boluses
dial depression should be considered and ruled out. of 2.5–5╯mg, are acceptable. We do not use prophy-
Hypotension during intubation should be corrected lactic antiemetics because they are not effective.
rapidly using intravenous fluid. Sometimes meta- They are used if vomiting occurs. Although ket-
raminol or pressor agents are used to correct hypo- amine is used as an agent for RSI in some pre-
tension, but these drugs are not substitutes for hospital and hospital settings, we do not favour its
correction of hypovolaemia. use in patients with TBI. It should be used with
In the resuscitation phase, the following goals are caution, because it may cause a rise in blood pres-
recommended: sure and pulse rate and possible rises in ICP.
5 • Emergency department management • A. Initial assessment and treatment 69

Seizures, which may not be noticeable in intu- TABLE 5.3â•… Glasgow Coma Scale
bated, sedated, paralysed patients, may result in
hypoxic brain injury from an increase in local cere- Feature Response Score
bral metabolism and tissue hypoxia. Seizures fol-
Eye-opening Spontaneous 4
lowing brain injury may be prevented by intravenous
To speech 3
phenytoin 1╯g (15╯mg╛/╛kg IV) over 30 minutes.
To pain 2
Hypotension, whether brief or sustained, is also
No response 1
associated with a higher mortality and worse out-
Best verbal Oriented to time, place and 5
comes in TBI. The multiple-injured, haemodynamic, response person
unstable patient (SBP <╛100╯mmHg) with TBI, or Confused 4
one requiring more than 3 litres of fluid or in whom Inappropriate words 3
a blood transfusion has been commenced, may be Incomprehensible sounds 2
subject to massive shifts in fluid through loss and No response 1
administration. Central and arterial line placement Best motor Obeys commands 6
with invasive monitoring is indicated for these response Moves to localised pain 5
patients. Hidden causes of blood loss should be Flexion withdrawal from pain 4
sought and bleeding stopped. These areas include Abnormal flexion (decorticate) 3
the posterior scalp (so patients must be logrolled Abnormal extension 2
early), the peritoneum (excluded by the FAST ultra- (decerebrate)
sound scan) and retroperitoneum (excluded by chest No response 1
and abdominal CT scan). Closed long-bone frac- Total score Best response 15
tures may result in significant cumulative blood loss, Coma 8 or less
causing shock. For example, a fractured femur may Unresponsive 3
bleed by up to 2 litres, a fractured tibia 1 litre and a
fractured humerus 500╯mL.7
Multiple-injured patients may suffer from acute
traumatic coagulopathy; TBI may itself cause a TABLE 5.4â•… The classification of TBI according to
bleeding disorder; therefore multiple-trauma patients the Glasgow Coma Scale
with head injuries are at particular risk of develop-
Mild TBI GCS 13–15*
ing a coagulopathy. Bloods for pathology should be
Moderate TBI GCS 9–12
taken early and repeated frequently (hourly at first)
Severe TBI GCS 3–8
to identify abnormal bleeding parameters. Consulta-
*GCS 14–15 is an alternative (see text).
tion with hospital haematologists, anaesthetists,
intensivists and trauma staff is needed to plan for
the control of coagulopathy.
Care should be taken to prevent or correct hypo- become the primary triage tool for the initial assess-
thermia by covering the patient and using warm ment, investigation and management of the head-
resuscitation fluids. injured patient.9 The GCS also allows observational
tracking of the patient’s conscious state.
Lateralising neurological deficits may indicate
focal brain injury. During the primary survey, pupil-
INITIAL ASSESSMENT OF DISABILITY lary response should be assessed (Fig 5.4a & b)
The Glasgow Coma Scale (GCS) (Table 5.3) remains as well as gross motor and sensory pathways (see
the most widely used assessment for measuring the Table 5.2). The pupillary reflex is a significant pre-
level of consciousness.8 Calculating the GCS is dictor of outcome in head-injured patients. Absence
simple and expedient with good interobserver reli- of pupillary reflexes is associated with a poor 
ability. Determination of the GCS is the key to head prognosis in patients with a GCS <â•›9.10,11 Patients
injury classification and forms the basis for interven- with focal neurological deficits require rapid access
tions (Table 5.4). to CT scanning to exclude evolving intracranial
Although the initial validation of the GCS as a haematomas.
prognostic tool occurred in haemodynamically Current consensus delineates a GCS <â•›9 as severe
stable patients 6 hours post-trauma, the GCS has impairment of conscious state. At this GCS most

patients show unresponsiveness to the point to be

described as comatose.
Most patients show a blunting of airway reflexes
at GCS <â•›9.12 With a GCS <â•›9 airway integrity, ade-
quate oxygenation and ventilation are at risk.12,13
FIG 5.4aâ•… Unconscious patient with right third nerve Maintenance of optimal oxygenation and minimisa-
palsy—non-reactive dilated right pupil with abduction of tion of secondary cerebral damage mandates airway
the eye. and ventilation control in these patients.13 Most
studies of neurotrauma patients have used GCS <â•›9
as a criterion for airway intervention with support
of ventilation. The need for intubation may have
been determined at an earlier stage in the primary
survey for airway protection and ventilation. Pre-
hospital and hospital protocols use this threshold to
trigger airway intervention.
Five per cent of head-injured patients have spinal
injuries. Sedation and intubation with in-line stabi-
lisation of the cervical spine have been shown to be
safe and effective methods of securing a definite
airway while immobilising the patient. It is impor-
tant not to apply a venous tourniquet around the
neck when securing the endotracheal tube. An oro-
gastric tube should be placed once the endotracheal
tube is secured.
FIG 5.4bâ•… Bilateral fixed dilated pupils in a patient Finally, where oxygenation, ventilation and
with severe TBI and GCS3. airway protection are all intact, the patient with a


A 28-year-old male was transferred from a regional The decision to transfer this patient to a trauma
hospital one hour away from the Level 1 Trauma centre with a neurosurgical service was appropriate,
Centre. The diagnosis was extradural haematoma. because such a patient can deteriorate rapidly and
He initially had a GCS of 9 and was intubated at the require urgent craniotomy due to progressive
regional hospital before transfer. He was transferred enlargement of the extradural haematoma (EDH).
with a junior medical officer in attendance. Upon However, the lessons to be learnt from this case are
arrival in the emergency department of the trauma as follows:
centre, he was coughing strenuously, sitting up with • Patients with severe TBI should be transferred
each cough, fighting the ventilator, and requiring with an experienced paramedic or medical
re-sedation and paralysis. support.
Coughing and straining in a patient with an • Adequate equipment and drugs to maintain
injured and compromised brain could result in adequate oxygenation should be available.
hypercapnia, sustained rises in ICP, and coning. • The patient should arrive sedated,
The patient’s bed tilt was not in a head-up position, relaxed and without any straining at
which would have helped with ICP management. the transfer destination, able to be suctioned
The medical officer was not experienced in airway without causing further coughing and
management and may not have had the drugs to straining.
effect adequate sedation and paralysis. Once Upon CT scan this patient was found to have a
capnography was undertaken, the end-tidal CO2 was left occipital fracture, underlying thin EDH and left
54╯mmHg, equating to an arterial PaCO2 in the high frontal lobe contusion. Fortunately both of these could
50s. This level of hypoventilation is not acceptable be managed non-operatively. He eventually was
for a patient with a severe traumatic brain injury. awoken, extubated and made a good recovery.
5 • Emergency department management • A. Initial assessment and treatment 71

suspected head injury may require intubation as a BOX 5.2â•… Canadian CT head rule17
secondary airway protection during procedures
requiring sedative anaesthesia, such as reducing and CT head rule is required only for patients with minor
splinting long-bone fractures and relocating dislo- head injuries* with any one of the following:
cated joints. Patients with suspected head injury who High risk (for neurological intervention):
are combative also require intubation. The comÂ� • GCS score <â•›15 at 2 hours after injury
bative or agitated patient requiring therapeutic and • suspected open or depressed skull fracture
diagnostic procedures (including cervical immobili- • any sign of basal skull fracture (haemotympanum,
sation and CT head respectively) may require con- ‘racoon’ eyes, cerebrospinal fluid
otorrhoeaâ•›/â•›rhinorrhoea, Battle’s sign)
siderable sedation. This is best delivered and titrated • vomiting >â•›two episodes
where the head-injured patient is concurrently intu- • age >â•›65 years
bated and receiving ventilatory support.14–16 If it is Medium risk (for brain injury on CT):
anticipated that general anaesthesia will be required • amnesia before impact >â•›30 minutes
for concomitant injury and the patient is haemody- • dangerous mechanism (pedestrian struck by motor
namically stable, intubation is more conveniently vehicle, occupant ejected from motor vehicle, fall
undertaken prior to CT imaging. from height >â•›3 feet or five stairs)
*Minor head injury is defined as witnessed loss of
consciousness, definite amnesia or witnessed disorientation
IMAGING in a patient with a GCS score of 13–15.

CT head remains the current investigation of choice

following head injury. CT identifies skull fractures,
macroscopic intracranial anatomy, and the presence
and mechanical effects of intracranial haemorrhage. and neurosurgical intervention.17 Importantly, the
CT does not demonstrate neural pathways or neural medium risk criterion ‘dangerous mechanism’ fea-
function. tures components consistent with a major trauma
Indications for CT scanning for patients with callout. Using this guideline, in major trauma, a
cranial trauma include: mild head injury (loss of consciousness and GCS
• GCS 14 or less 15) would mandate CT head.
• GCS 15 with: Head-injured patients with a normal CT head, a
– documented loss of consciousness GCS of 15 and no other indications for admission
– history of seizure can be discharged. Similarly, patients with no indi-
– amnesia for injury cation for CT head and no other indication for
– focal neurological deficit admission may be safely discharged home.
– signs of basal or calvarial skull fracture Where there is no CT scanner available, a skull
– exclusion of penetrating skull injury X-ray is performed. Patients with identified fracture
– headache should be kept under observation in hospital for
– repeated vomiting 8–24 hours because they are at risk of a delayed
– elderly patients intracranial haematoma.
– concurrent anticoagulation therapy or co- 
– shunt-treated hydrocephalus.
Transfer of the neurotrauma patient to CT for Non-survivable head injury (NSHI)
scanning entails some risk. The trauma team needs One of the objectives of senior emergency depart-
to accompany the patient to CT. Tubes and lines may ment, neurosurgical and intensive care medical staff
be dislodged and must be secured. Monitoring is the exclusion of NSHI as soon as possible. Per-
devices must be visible to the trauma team during sistence with advanced medical care in patients
scanning. Drugs and equipment that will allow the unlikely to survive their brain insult is futile and
ongoing management and resuscitation of the patient unethical. Precious resources such as blood products
must accompany the patient. may be wasted. Staff may be exposed to sharps in
The Canadian CT head rule (Box 5.2) is one unnecessary procedures, and managing patients
attempt to develop guidelines by weighting various whose outcome is futile is distressing for both staff
risk factors by the likelihood of CT abnormality  and families. The recognition that a patient has

suffered an NSHI and the decision to manage the ‘a trauma-induced alteration in mental status that
patient conservatively should be made at a senior may or may not involve loss of consciousness’.19
and multidisciplinary level. The World Health Organization Centre Task
Good clinical evidence for NSHI must be gath- Force’s definition of mild TBI is as follows:
ered and confirmed with functional diagnostic tests. MTBI is an acute brain injury resulting from
For example, GCS 3 with fixed and dilated pupils,18 mechanical energy to the head from external
craniocerebral dissociation (see Chapter 6) and physical forces. Operational criteria for clinical
massive cervical vascular disruption all carry grim identification include:
outcomes. Drugs, alcohol, hypotension and hypo-
thermia may all contribute to deep coma and will 1. One or more of the following: confusion
require due consideration before the final decision or disorientation, post-traumatic amnesia
is made by senior staff that the TBI is irreversible. for less than 24 hours andâ•›/â•›or other
Hypotension due to haemorrhagic shock should transient neurological abnormalities such
usually be treated before making the determination as focal signs, seizure, and intracranial
of NSHI. lesion not requiring surgery; andâ•›/â•›or
Physiologically, Cushing’s reflex may be present. 2. Glasgow Coma Score of 13–15 about
Bradycardia, and otherwise inexplicable hyperten- 30 minutes after injury or later upon
sion in a patient with GCS 3 and a brain injury is a presentation for healthcare.
pre-fatal event, signalling direct disruption of basic
These manifestations of MTBI must not be due to
autonomic pathways and centres in the pons and
drugs, alcohol or medications, or caused by other
injuries or treatment for other injuries (e.g.
Radiologically, CT scanning should be performed
systemic injuries, facial injuries or intubation),
to confirm or exclude cerebellar herniation, efface-
caused by other problems (e.g. psychological
ment of cerebral sulci and effacement of the fourth
trauma, language barrier or co-existing medical
ventricle. Cerebral angiography with CT scanning
conditions) or caused by penetrating
should confirm lack of cerebral blood flow.
craniocerebral injury.20
Senior medical staff in at least two specialties,
including neurosurgery, should be consulted Patients who have a GCS of 15 and present after
promptly, while time and space should be allowed sustaining a brief loss of consciousness require
to break the distressing news to families and to careful appraisal and examination. Given the gener-
debrief medical and nursing staff. Many non- ally young age of this cohort, the inherent recurrent
survivable head injuries are the result of motor risk of future head injury from sport, assault or
vehicle accidents, assault or falls from a height. The motor vehicle accidents and the recognised lifetime
police and coroner’s office will often have early risk of malignancy from radiation from tomography,
involvement. All deaths occurring in emergency guidelines have been devised for the early obser�
departments are reviewed at a senior level, so vation and management of minor head injuries 
detailed and accurate notes are mandatory. (see Appendix L, ii). CT scanning should still be
Once it has been decided that the patient has performed according to the indications described
NSHI, the independent organ transplant team may above. Emergency department observation units or
become involved, but it should be emphasised this hospital trauma units are ideally placed to further
is a separate process from the determination of non- risk-stratify patients susceptible to concussive brain
survivability (see Chapter 18). injury requiring intensive rehabilitation to ensure
prompt return of functioning. Box 5.3 describes the
Mild head injury management of patients with mild TBI. Patients
Mild head injury is also called minor head injury, with mild TBI and a normal CT brain should be
mild TBI and concussion. Mild head injury has been observed and assessed for amnesia using tests 
defined as GCS 13–15.7 However, there is concern such as the Abbreviated Westmead Post-traumatic
that the GCS is too insensitive an instrument to Amnesia Scale21,22 (see Appendix G). If patients
describe mild TBI. More recently there has been a are neurologically normal after 4 hours, fully alert
trend to reclassify mild TBI as GCS 14–15 and with no ongoing headache, amnesia, confusion,
minimal TBI as GCS 15.9 Concussion was defined behavioural problems or other symptoms, they are
by the American Academy of Neurology in 1997 as discharged. Observation of patients with TBI should
5 • Emergency department management • A. Initial assessment and treatment 73

BOX 5.3â•… Management of mild TBI

• Minimum of hourly observations should be taken

for 4 hours post-injury. These observations
– alertness / behaviour / cognition
– pupillary reactions
– vital signs.
• Serial neurological observations should be
continued on any mild TBI patients who fail to
improve clinically at 4 hours post-injury or who
are found to have an abnormal CT head scan.
• Assessment for post-traumatic amnesia (PTA)
should be performed on any mild TBI patients
who fail to improve clinically at 4 hours post-
injury or who are found to have an abnormal CT
scan requiring hospital admission.

continue until they are clinically not intoxicated

(irrespective of blood alcohol levels), safe for dis-
FIG 5.5â•… Axial CT scan showing large left-sided
charge and risk-stratified for concussive head injury.
extradural haemorrhage with cerebral compression.
Patients failing these screens should be considered Note the concave (lens) shape of the haematoma.
for admission and rehabilitation. Discharge planning
must be comprehensive, involve timed follow-up,
written instructions and adequate time off work. The
family physician (GP) should be involved in the
follow-up. The presence of certain risk factors place common (about 10% of EDHs) and may arise from
some patients with mild TBI in a higher risk cate- a tear in the transverse venous sinus underlying a
gory for which CT scan and admission are indicated skull fracture. CT findings are diagnostic—a concave
(see Box 5.2). (lens-shaped) collection of blood. Larger haemato-
mas will cause shift of midline brain structures (Fig
Extradural haematoma 5.5). The aim of treatment is to perform the ABCs
Extradural haematoma (EDH) may occur after focal of trauma, prevent secondary brain injury and ensure
head blunt trauma, such as an assault with a blunt prompt neurosurgical consultation and referral.
instrument, or a strike to the head during sport. Typi- Moderate to large EDHs should be evacuated
cally, there is an initial loss of consciousness, normal urgently and generally have good outcomes. The
function after awaking and then a period of increas- neurosurgeon may decide to observe a small EDH.
ing drowsiness that without imaging and surgical Patients can deteriorate rapidly from an expand-
intervention may progress to coma and death. The ing EDH. Initially there is worsening headache,
interim period of alertness is called the lucid inter- drowsiness and confusion. The patient will develop
val. The classic scenario is the football player who coning as the haematoma enlarges. The temporal
is knocked out on the field, awakes from his injury, extradural haematoma will cause uncal herniation,
continues to play, goes home to sleep and is later transtentorial herniation and compression of the
found unconscious and unable to be roused. midbrain and third cranial nerve. This will cause an
EDHs collect between the dura and the skull. ipsilateral dilated unreactive pupil and usually a
Bleeding is usually arterial, most commonly from contralateral hemiparesis. The latter is due to com-
the middle meningeal artery. The collection of blood pression of the ipsilateral cerebral peduncle (the
is focal and usually forms a solid clot in the temporal corticospinal tract that crosses over lower down 
region and extending into the frontal or parietal in the medulla). Less commonly there may be an
regions. An EDH in the posterior fossa is much less ipsilateral hemiparesis due to compression of the

opposite peduncle against the tentorial edge. This is

called Kernohan’s phenomenon and is a false local-
ising sign. As the compression increases, the patient
may develop a Cushing reflex, with a rise in blood
pressure and a fall in pulse rate. As the coning pro-
gresses, both pupils dilate and become unreactive.
This is a very late development and considerably
worsens the prognosis. The Cushing reflex may not
occur if the patient is shocked from other injuries.
A posterior fossa epidural will tend to cause an early
compromise of the level of consciousness, breathing
and circulation because of tonsillar herniation with
compression of the medulla.
The life-saving procedure for EDH is craniotomy
or a rapid craniectomy and evacuation of clot (see
Chapter 8). Mild hyperventilation is recommended
only as a temporising measure in the presence of
acute lateralising deficits such as a blown pupil or
hemiparesis. Similarly, mannitol (1╯g╛/╛kg bolus IV)
may be indicated as a temporising measure to FIG 5.6â•… Axial CT scan showing an acute left subdural
prevent progression of life-threatening intracranial haematoma with underlying left hemisphere swelling
and midline shift to the right. Note the convex shape of
pressure.23 Urgent access to the operating theatre is the haematoma following the curve of the cortical
crucial, and every minute of time saved until surgery surface.
is critical to a good outcome in those patients who
are deteriorating.
There is usually minimal underlying brain tissue
damage in an EDH, so provided the haematoma is The skull is usually fractured. Intracerebral haema-
evacuated before the patient has coned the recovery toma may also develop. SDHs form beneath the
is usually very good (5–10% mortality). dura and compress the underlying brain tissue,
which in high-energy injuries is often severely
Delayed extradural haematoma (DEDH)
injured (Fig 5.6). SDHs are associated with more
This is not present on the initial CT but is seen on
extensive primary brain injury and a high mortality
a subsequent CT and comprises 9–10% of all EDHs
(>â•›30%). Clinical suspicion should be raised in high-
in some series. The risk factors are a vigorous resus-
energy mechanisms as above, with an abnormal
citation with a surge in blood pressure, rapid reduc-
GCS, seizure activity or focal neurologic signs.
tion in ICP (e.g. after evacuation of a contralateral
The high-energy SDH occurs not infrequently in
collection) and coagulopathy. There is often a skull
the presence of other injuries (i.e. in multiple
fracture, and DEDH has been reported infrequently
trauma). Urgent craniotomy and evacuation of the
after mild head injury. The ICP level may not ini-
acute SDH is required to save life and to optimise
tially reflect the development of DEDH and the
outcome. The neurosurgeon confers with the trauma
clinical deterioration may also occur late. There
team and the trauma surgeon to determine the timing
should be a high index of suspicion, particularly in
of the craniotomy in relation to the resuscitation of
the patient deteriorating after an initial non-surgical
a multiple-injured patient. Life-threatening haemor-
CT scan.
rhage beyond the head will have to be stopped as a
priority, but it may be possible to undertake the
Acute subdural haematoma craniotomy at the same time as a laparotomy or
Acute subdural haematomas (SDHs) occur as a thoracotomy when both are critical.
result of high-speed incidents, such as a motorcycle In the multiple-injured high-speed accident
accident, a motor vehicle rollover, pedestrians hit by victim with a GCS <â•›9, priority is still given to the
a vehicle or a fall from a height. Blood vessels on ABCs of trauma care, with special emphasis on
the surface of the brain are torn by a shearing mech- securing an airway by intubation, identifying and
anism and the brain itself may be torn and bleeding. controlling external bleeding, splinting fractures,
5 • Emergency department management • A. Initial assessment and treatment 75

reversing other causes of shock such as pneumotho- may develop a large, acute SDH, particularly if they
rax and maintaining a systolic blood pressure above are taking an anticoagulant.
100╯mmHg. After the initial chest and pelvic X-rays, Reversal of coagulopathy in patients may be
the priority for imaging is CT of the head and neck, required to cease progression of intracranial bleed-
to identify collections that can be evacuated in ing and also to aid in the neurosurgical evacuation
theatre promptly (within an hour of arrival). of the haematoma. Temperature and acidosis also
Subdural haematoma may also occur from rela-
tively low-energy trauma in high-risk patients. These
include patients over the age of 60 years, patients
on anticoagulants or antiplatelet agents, and alcohol-
ics. These patients pose a deceptively ‘normal’ clini-
cal risk group. SDHs are not infrequent findings on
CT in these patients in the investigation of falls,
confusion or focal neurologic deficits. There may be
a history of previous head injuries. The presence of
an atrophic brain with a widened CSF space between
the brain and skull also renders the elderly and alco-
holics more vulnerable to SDH. Elderly patients
(>â•›60 years) who have a fall from a standing position
or from a bed and strike their head on the ground


A 66-year-old woman with a past history of left

clinoid meningioma presented following a fall down
some stairs, resulting in a head injury with altered
conscious state. In the ED she had a GCS of 14. In FIG 5.7â•… Axial CT scan showing large, post-traumatic
the CT scanner her GCS dropped to 10, and she was intracerebral haemorrhage in the left temporal lobe with
intubated. The CT scan revealed a large intracerebral an overlying thin acute subdural haemorrhage.
haemorrhage in the left temporal lobe extending into
the parietal lobe, with an overlying acute subdural
haematoma (Figs 5.7 and 5.8).
An urgent craniotomy was performed and the
haemorrhages evacuated. No source for the
haematoma was identified. Cervical spine precautions
were continued until the cervical spine was cleared.
Postoperatively she made a good recovery but had a
residual right-sided hemiparesis.
It is important to determine whether an intracerebral
haemorrhage such as this precedes the head injury
or is caused by it. The size and site of the
haemorrhage may give some clue (e.g. hypertensive
ICH is typically in the capsulo-ganglionic region but
the ICH in this woman was centred in the temporal
lobe). An MR scan may also be helpful in identifying
underlying pathology, such as an arteriovenous
malformation (AVM), aneurysm or tumour. A CT
angiogram is also helpful to exclude an underlying
AVM or aneurysm. It was performed in this case and
no vascular pathology was identified. We presume,
therefore, that this haemorrhage was caused by the
fall. It is also important to check for a clotting
abnormality as a possible aggravating factor and
there was none in this case. FIG 5.8â•… Axial CT scan showing the intracerebral
haemorrhage extending into the parietal lobe.

affect clotting time, so in general terms patients patient with a closed head injury is deteriorating
should be normothermic and acidosis should be with focal signs or is having focal seizures following
avoided by the resuscitative measures outlined an initial CT scan which showed contused areas of
above. Specific warfarin reversal may be achieved brain or a small haematoma. The prognosis is poor
by the judicious intravenous use of vitamin K if the haematoma is large and remains untreated. If
(usually 5–10╯mg), fresh frozen plasma (FFP) (150– the haematoma is greater than 3╯cm and contributing
300╯mL) and prothrombinex (25–50╯IUâ•›/â•›kg╯IV).24,25 to the raised ICP, consideration should be given to
The aim of reversal should be an aPTT╯<╛60 and evacuating it (see Chapter 8).
INR╯<╛2.0. The INR is a logarithmic measure of
bleeding time and efforts to reduce it below 1.5 may Cerebral contusion and contrecoup injury
prove futile (see Chapter 16). Focal brain injury, or cerebral contusion with bleed-
Antiplatelet agents are commonly prescribed in ing, commonly occurs in association with SDHs 
highly functioning middle aged and elderly patients. and less so with EDHs. Contusion of the brain is 
Control of bleeding in these patients is particularly not uncommon in falls and may occur alone as 
challenging and may involve platelet transfusion a result of a fall from standing. On CT, the area 
even with a normal platelet count.26 Early consulta- most damaged is opposite to the area of the skull
tion with a haematologist is advised (see Chapter 16). struck. This is a contrecoup injury. When the head
Subacute subdural haematoma is moved and then stops suddenly, as in a fall with
a head strike, the brain is accelerated against the
By definition, subacute subdural haematoma devel- opposite inner skull wall. The opposite area of the
ops 4–14 days after a head injury. It presents with brain affected (contrecoup) is often more severely
headache, deterioration in conscious level (often injured than the part striking (coup) because of 
with focal neurological signs) or a seizure. The CT this acceleration. A common scenario is that of 
scan often shows an isodense SDH (i.e. roughly the ‘one punch can kill’, where a young man may be
same density as brain) that contains bloody, watery punched and lose consciousness and the occiput
fluid. impacts the ground, resulting in a contrecoup injury
Chronic subdural haematoma to the frontal lobes (Fig 5.9) and severe secondary
brain swelling.
Chronic subdural haematoma develops between 10
days and 3–6 months after a head injury that is often
trivial. It particularly affects the very young and the
very old, because the subarachnoid space is rela-
tively large and therefore the bridging veins more
susceptible to rupture when the brain suddenly
moves following trauma. By the time it develops, the
patient may have forgotten the original injury and
may present with neurological signs, unexplained
coma or a change in behaviour. Always consider the
diagnosis in a patient with unexplained coma. A
chronic subdural haematoma is a great mimicker and
may present with chronic headache, focal neuro�
logical signs, dementia, epilepsy and, in an infant,
enlarging head size (see Chapters 8 and 12). The CT
scan shows a hypodense collection of varying thick-
ness over the hemisphere that may contain some
more acute elements (i.e. haemorrhages of different
ages and, in some cases, membranous septations and
loculations). Midine shift may be present.

Intracerebral haematoma (ICH)

An intracerebral haematoma is difficult to recognise
without a CT scan. It should be suspected if the FIG 5.9â•… Contrecoup injury.
5 • Emergency department management • A. Initial assessment and treatment 77

FIG 5.11â•… Axial CT scan showing diffuse axonal injury,

with basal cisterns obliterated, loss of grey–white
differentiation, loss of subarachnoid space and the
FIG 5.10â•… An axial CT scan showing severe contusion presence of diffuse subarachnoid haemorrhage.
in the right frontal and temporal lobes.

Contusions may evolve over the first few days often lifelong. The mortality is high (>â•›30%). Every
following the injury (Fig 5.10). The small haemor- effort must be made to prevent and correct second-
rhages become larger and more confluent (joined ary brain injury. ICP monitoring is instituted early
together), and the amount of oedema surrounding in DAI, and in many neurosurgical centres the neu-
them greatly increases. The neurological state of the rosurgery staff put these monitors in place under
patient may deteriorate as a result and require surgi- local anaesthesia in the emergency department (see
cal decompression (see Chapter 8). Chapter 8).

Diffuse axonal injury Traumatic subarachnoid haemorrhage

Diffuse axonal injury (DAI) (Fig 5.11) results from Traumatic subarachnoid haemorrhage (SAH) is rel-
high-speed injuries, particularly those involving a atively common after closed head injury; its patho-
rotation of the head with an angular accelera- physiology is described in Chapter 3. It may be
tionâ•›/â•›deceleration. The pathophysiology is of DAI isolated or associated with other acute bleeding such
described in Chapter 3. CT scan may demonstrate as intracerebral haematoma and SDH. It is identified
cerebral swelling and small haemorrhages (pete- by CT scan (Fig 5.12a–d). An underlying cause for
chiae), which particularly occur at the grey/white the haemorrhage other than trauma will need to be
interfaces (i.e. just beneath the cerebral cortex), considered, depending on the patient’s history and
around the corpus callosum and in the posterior part the distribution of the haemorrhage. Examples of
of the midbrain. This is caused by shearing forces causes are a ruptured intracranial aneurysm or, less
at the time of injury. The CT features are described commonly, haemorrhage from a brain tumour or
in Chapter 3. arteriovenous malformation (AVM) that would
The patient with DAI is usually comatose from cause intracerebral haemorrhage as well. A CT
the time of the injury or shortly afterwards. These angiogram (CTA) is a rapid screen for aneurysmal
injuries may be devastating and result in a prolonged SAH or AVM. Basal SAH may be due to trauma in
coma, prolonged period of anterograde amnesia, and and around the carotid canal and cavernous sinus
multiple cognitive and physical deficits that are and may indicate carotid or vertebral artery trauma

FIG 5.12aâ•… Subarachnoid haemorrhage (arrow) in the FIG 5.12bâ•… Basal subarachnoid haemorrhage with
left sylvian fissure. adjacent air bubbles.

FIG 5.12câ•… Basal sub-arachnoid haemorrhage (arrow) FIG 5.12dâ•… Subarachnoid haemorrhage in the gyri of
in the pre-pontine cistern. the hemispheres.

if the SAH is in the posterior fossa. This should be transcranial Doppler, careful fluid and blood pres-
discussed with the neurosurgeon and radiologist to sure management and calcium channel blockers.
decide on the appropriate investigations. Traumatic
SAH patients will be at risk of cerebral vasospasm Penetrating TBI
with higher grades of SAH shown on CT scan and Penetrating TBI is uncommon in most Western
are often managed in the ward or ICU, in the same countries. A self-inflicted gunshot wound (GSW) in
way as aneurysmal SAH patients, with regular a suicide attempt is the commonest mechanism of
5 • Emergency department management • A. Initial assessment and treatment 79

injury and has a high mortality rate. High-velocity as a result of posterior fossa or posterior supratento-
penetrating TBI inflicted by a second party is more rial haemorrhage and/or contrecoup contusion. A
common in urban environments where there is a low threshold for observation and CT scanning is
flourishing illicit drug trade and in war zones. mandated.
Penetrating brain injury may be broadly divided The patient may have been involved in an acci-
into high- and low-velocity injuries. High-velocity dent and sustained the TBI as the result of collapse
penetrating injuries from firearms frequently dem- from a vasovagal episode, an arrhythmia or an
onstrate catastrophic brain tissue damage and poor unwitnessed epileptic seizure. An underlying
clinical outcomes. The high-energy pressure waves medical cause should be considered, depending on
generated by the missile as it traverses the brain are the circumstances of the injury.
poorly tolerated by the brain and not infrequently
cause injury to critical areas such as the basal ganglia Inadequate examination
and brainstem. These injuries, as well as the special
Low-velocity penetrating injury of the skull may 
case of bomb-blast injury with penetrating frag-
be missed in a cursory examination without ade-
ments of metal and other foreign bodies, are
quate imaging in patients with scalp lacerations.
described in Chapter 15.
Similarly, focal trauma from seemingly innocuous
Low-speed penetrating injuries are commonly
mechanisms may result in delayed TBI and EDH
the result of assault with a weapon such as a knife
formation from bleeding from a meningeal artery.
and may present with minimal or no clinical deficits.
Deterioration in the neurological status may mean
The skull is breached and so the underlying brain
that the patient requires urgent investigation and
may be lacerated. Clinical signs may not be present
treatment. An accurate, thorough examination is
or may be delayed. There should be a high index of
important to establish a baseline. In the paralysed,
suspicion of penetrating injury or facial fractures
sedated, ventilated patient, the pupils, pulse and
with secondary skull penetration, and careful exami-
blood pressure that are monitored closely, because
nation of the scalp and head should be performed.
the remainder of the neurological examination
Identifying skull penetration is necessary even in
cannot be determined. Changes for the worse will
patients who are clinically well, as a pitfall in care
necessitate a CT scan and neurosurgical review.
may be the local repair or even conservative man-
Eyelid swelling can occur rapidly over several
agement of an open brain injury that, once closed,
minutes and render it very difficult to examine the
may progress to a brain abscess. Clinical estimates
eyes. Therefore, the eyes and pupils require careful
of skull fractures in these patients are poor, so there
examination before the lids become too swollen.
should be a low threshold for CT scanning. If metal
Penetrating eye injuries can easily be missed.
or a weapon is in situ on presentation, it should not
be removed until after imaging and neurosurgical
review. The Glasgow Coma Score
The Glasgow Coma Score (GCS) is the most 
successful and widely used trauma score. The GCS
PITFALLS IN ASSESSMENT is predictive of outcome and mortality and is incor-
AND MANAGEMENT porated into other trauma scoring systems, such as
the Revised Trauma Score (RTS) and the Trauma
Inadequate history Score and Injury Severity Score (TRISS) analysis
Not infrequently, the details of the events at the time methodology.27,28 The GCS has been subject to sta-
of injury are unclear. The patient may be amnesic, tistical analyses and the important conclusion is that
confused or unconscious. Pre-hospital information the motor component of the GCS alone is predic-
regarding the circumstances and mechanism of tive.29 Two scenarios where the motor score of the
injury and the patient’s medical history and medica- GCS is not reliable are the intubated paralysed
tion have a significant bearing on the cause of the patient and the quadriplegic patient.
injury and its subsequent evolution. This informa- The verbal component of the score is biased
tion must be actively sought. against dominant hemisphere brain lesions, which
Note the mechanism of the injury. A fall onto  affect the ability to perceive or create speech. Limi-
the back of the head may seem initially well  tations due to culture or deafness may also bias
tolerated, but these patients can deteriorate rapidly against the verbal component of the GCS.

Intoxication and drowsiness, as well as facial Patients with multiple trauma

injuries such as fractures or burns, or eye injuries The management of multiple-injured trauma patients
may affect the eye component of the GCS. is prone to errors. Clinicians and trauma teams may
While reliability of the GCS is high from one be focused or distracted by one aspect of care.
rater to another, individual clinicians have a duty of Patients with TBI may be at high risk of errors of
care to perform and document the GCS scores them- omission during trauma resuscitation.
selves. In asymmetrical observations, incorrect Careful examination for neurologic deficits and
recording of the worst observation has been shown early examination of the pupillary reflexes is critical
to occur, with arbitrary lowering of the recorded and should be done and documented at the earliest
GCS in up to 25% of cases. opportunity as discussed above. It is vital that the
neurosurgery team are informed early about CNS
High-risk patients
injury and the multidisciplinary head and neck team
As discussed, there are cohorts of high-risk patients consulted early about complex head and neck inju-
in whom TBI may not be clinically apparent from ries (see Chapter 8).
examination findings or presenting history.
Chronic alcoholics are at risk of missed chronic
and acute-on-chronic SDHs. Assuming that an
altered conscious state in this population is due  1. The approach to head-injury management is
only to intoxication is particularly risky. The elderly team based and multidisciplinary.
not infrequently suffer significant head injuries from 2. The aim of care in the emergency department is
minor mechanisms. Clinicians should be mindful the identification and treatment of life threats
that anticoagulant and platelet inhibitor therapy is and the prevention of secondary brain injury, as
common, placing active middle-aged and elderly well as the early identification and communica-
people at risk of TBI from falls, motor vehicle acci- tion of non-survivable head injuries.
dents or sporting injuries. 3. Become confident assessing the conscious state
The young child or infant with a TBI may dete- with the Glasgow Coma Scale.
riorate rapidly from cerebral swelling or intracranial 4. Head injury tends to evolve, whether isolated or
haematoma (see Chapter 12). associated with multiple trauma. Patients must
be assessed neurologically as a baseline, then
Diagnostic imaging observed and reassessed. Changing signs means
The CT scan room is a transitional diagnostic area changing pathology, and action is required.
that may pose significant clinical risk without proper 5. Adequate oxygenation, blood pressure, low
patient screening. A focused, thorough neurologic normal PaCO2 and normal blood glucose should
assessment should occur before the patient attends be maintained.
the CT scanner. In particular, attention should be 6. The patient with severe TBI is time-critical.
given to pupil reflexes for patients with suspected Urgent, efficient and effective treatment will
TBI. Clinicians should also seek to document any save lives and lessen morbidity. Every second
focal or evolving neurologic deficits prior to CT counts. Do not delay in calling the neurosurgeon.
scan of the brain and neck. 7. The immediate priority in severe TBI is estab-
Patients may suffer an indirect brain injury from lishing a secure airway, providing adequate ven-
trauma to the vessels of the head and neck. Vaso- tilation and correcting or preventing hypoxia
spasm, dissection, traumatic aneurysm formation or and hypotension.
disruption of the carotid or vertebral arteries may 8. All patients with a severe TBI (GCS <â•›9) should
result in focal deficits or dense functional deficits. be intubated.
There should be a high index of suspicion for vas- 9. A CT head scan should be obtained as soon as
cular injury in patients with penetrating trauma and the patient is stable enough.
cervical seatbelt bruising. 10. The cervical spine should be considered unsta-
Patients with unexplained loss of consciousness, ble and immobilised until cleared or until surgi-
focal neurologic deficits or seizure activity should cal stabilisation.
have contrast angiography at the time of the CT scan 11. Decide whether craniotomy is indicated. If there
to exclude major areas of ischaemia and focal, poten- is rapid deterioration, unequal pupils or lateral-
tially reparable, vascular injuries (see Chapter 7). ising signs, and a significant mass lesion on CT,
5 • Emergency department management • B. Maxillofacial injuries 81

surgery by the general surgeon in the remote any first responder is made and, if required and
location may be indicated. To aid this decision, feasible, elimination of the source of risk or removal
teleradiology and discussion with a neurosur- of the patient from that danger is then undertaken.
geon are advised (see Chapter 8). Once a safe environment has been assured, assess-
12. Mannitol reduces the ICP prior to surgery or ment and care of the patient begins using EMST/
transfer for surgery. ATLS® protocols. These protocols have been dis-
13. Seizure prophylaxis should be considered in cussed earlier in this chapter, but as maxillofacial
selected patients, and seizures should be treated injury can have specific relevance to several of these
vigorously. protocols, these will be discussed in more detail.
14. Intoxicated patients should be considered for
cerebral imaging or observed until clinically AIRWAY MANAGEMENT AND
15. Up-to-date notes, communication with family CERVICAL SPINE
members and debriefing of staff are hallmarks The first priority with any seriously injured patient
of excellent care. is to ensure a patent airway, while keeping in mind
16. Gunshot wounds to the head are commonly fatal, the need to protect and stabilise the cervical spine.
but patients can be selected for aggressive treat- Injury to the facial skeleton can cause airway
ment (e.g. GCS >â•›5, reactive pupils). The neuro- obstruction through:
surgeon should be involved at an early stage. • fractured or avulsed teeth
17. With mild head injury, if there are ongoing • displaced or broken dentures
symptoms and signs, including post-traumatic • intraoral or pharyngeal haemorrhage
amnesia (PTA), or additional risk factors, obser- • bilateral mandibular fractures causing a loss of
vation for at least 4 hours, CT head scan and anterior tongue support
admission are required. • the presence of foreign bodies in the oropharynx
(such as mouthguard, food, vomit, dirt, grass,
Treatment requires removal of any loose object in
Injury to the maxillofacial region is common in the mouth, stabilisation of the mandible and estab-
patients with significant head injury. Particularly in lishment and protection of a patent airway (jaw
frontal impacts, the facial skeleton will initially thrust, Guedel airway, endotracheal intubation, sur-
absorb the energy of any blow and protect the skull gical airway, as required).
base and calvaria from direct injury. In many ways, Any retrieved tooth or denture fragments should
the face can be considered to be the skull’s very  be retained and documented to allow cross-
own ‘crumple zone’. Low-energy (or low-velocity) referencing later during a formal examination of the
injuries tend to cause simple fractures to single dentition and occlusion. This will help minimise the
bones and are not usually associated with direct risk of a missing tooth or fragment being overlooked
head injuries. Classic examples include a displaced and creating a more distal airway obstruction
zygoma fracture from a head clash in contact sport (trachea or bronchus).
or a fractured mandible from a fistfight on Saturday
night. Higher-energy (or higher-velocity) injuries
that overwhelm the face’s ability to absorb the
energy tend to cause more comminuted fractures to Once an airway has been established and ventilation
multiple facial bones. They can lead to significant confirmed, attention turns to the maintenance of cir-
injury to the skull base, calvaria and brain, and are culation and the control of any haemorrhage. Rapid
associated with cervical spine injury, ocular injury exsanguination from maxillofacial injury is very
and significant soft-tissue injury. These situations unlikely, but significant ongoing blood loss can
tend to arise in motor vehicle accidents, industrial occur. Bleeding into the oral cavity or pharynx caused
accidents, gunshot wounds and blast injury. by comminuted midface fractures can initially cause
The initial management of a patient with maxil- airway obstruction and the first priority is estab�
lofacial injuries is the same as for any seriously lishing a patent airway, as previously discussed.
injured patient. At the scene, a rapid assessment  However, once this has been achieved, attention 
of the possibility of further harm to the patient and must be turned to stopping ongoing haemorrhage.

The management of nasal, oral or pharyngeal BOX 5.4â•… Symptoms of maxillofacial injury
bleeding can be quite challenging and needs to be
approached in a logical manner. Firstly, adequate • Pain
blood volume and circulation needs to be main- • Numbness (trigeminal nerve territory)
tained at all times. Secondly, a clotting profile needs • Double vision, blurred vision, visual loss
to be established and any abnormalities corrected. If • Malocclusion
• Trismus (inability to fully open jaw)
possible, ask the patient whether she or he is cur-
rently taking any anticoagulant medication. Even
aspirin, which is commonly self-prescribed, can
cause prolonged bleeding in this setting. Despite BOX 5.5â•… Signs of maxillofacial injury
these concerns, most midfacial bleeding will stop
with no further intervention. Soft tissues
However, if bleeding is persistent, then attempts • Swelling
• Bruising/ecchymosis
need to be made to control the haemorrhage. For • Lacerations, degloving injury
bleeding from the nose or nasopharynx, nasal • Soft-tissue crepitus
packing can be applied. This is described in the Skeleton
section on epistaxis later in this chapter. • Tenderness
If bleeding continues, attempts should be made • Displacement
• Mobility
to reduce any known facial fractures (usually maxil- • Bony crepitus
lary or midface fractures). This can be attempted in • TMJ dysfunction
a closed manner, but may require a formal surgical Nerves
approach, open reduction and internal fixation. If the • Visual disturbance (CN II)
patient is unconscious and intubated, the trauma • Ophthalmoplegia, diplopia (CN III, IV, VI)
• Pupillary disturbance (CN II, III)
specialist can place the gloved index finger under • Sensory loss (CN V)
the palate and lift a mobile depressed midfacial • Facial weakness (CN VII)
segment forwards into better alignment. Bleeding Fluids
that is not controlled by these manoeuvres requires • Epistaxis/septal haematoma
embolisation of the source vessel by an interven- • Subconjunctival haematoma
• CSF otorrhoea or rhinorrhoea
tional radiologist. These are often high-energy inju- • Salivary leak (parotid gland, parotid duct)
ries that have resulted in significant comminution of
the facial bones and associated soft-tissue trauma. TMJ = temporomandibular joint; CN = cranial nerve.

SECONDARY SURVEY motor and sensory nerves, the globe and its function
Once the patient has been stabilised, a more thor- (discussed above), the occlusion and the function of
ough assessment of the entire patient is undertaken. the jaw, and a thorough dental examination.
Of particular relevance at this point is the associa- Wherever possible, a full medical history should
tion between facial injury, head injury, cervical be obtained from the patient or relatives. Informa-
spine trauma and ocular injury. It is common for tion that should be sought includes current medica-
these patients to require input from specialists in tion, known allergies, tetanus status, current health
neurosurgery, orthopaedics (spine), ophthalmology, issues, previous facial injury and a dental history
ENT, maxillofacial surgery, and dentistry, and it is (orthodontics, restorative work, extractions).
imperative that all specialties develop a close Inspection can reveal swelling, bruising or lac-
working relationship. This enables appropriate com- erations that can indicate an underlying bony injury.
munication, timely referral and coordinated treat- Overall, the face may exhibit the classic hallmarks
ment to occur. of facial fracture, including a ‘saddle-nose defor-
The symptoms and signs of maxillofacial injury mity’ (naso-orbito-ethmoid (NOE) fracture or
are multiple (Boxes 5.4 and 5.5). Symptoms that can midface fracture), ‘raccoon eyes’ (periorbital or
be described by conscious patients include pain, base-of-skull fracture), or ‘dishpan facies’ (impacted
numbness, blurred or double vision, visual loss and midface fractures). Epistaxis can be present in a
malocclusion. Examination should involve an simple nasal fracture or a complex panfacial injury.
assessment of the bony structures in the face, the CSF rhinorrhoea or otorrhoea indicate an associated
5 • Emergency department management • B. Maxillofacial injuries 83

base-of-skull fracture and communication with the BOX 5.6â•… Dental assessment
dural cavity.
Each bone in the facial skeleton should then be • Number of teeth
firmly palpated. For each bone, establish any dis- • Lost, loose, fractured teeth
placement, step defect, comminution, mobility or • Third molars
crepitus. Frontal bone injury will be identified by a • Teeth in the line of fractures
• Dentoalveolar fracture segments
boggy swelling and the presence of a palpable • Occlusion, malocclusion
depression. Zygomatic injury classically presents • Dental caries
with a step deformity in the infraorbital rim. NOE • Orthodontics
fractures can cause deformity and mobility of the • Restoration
medial canthus. Nasal fractures present with visible • Edentulous
deformity, palpable fractures and bony mobility.
Maxillary fractures are usually impacted and
cause a shortened midface and malocclusion. Mobil- and re-established. A traumatic malocclusion is
ity of these fractures is established by manipulating present when this pre-existing occlusal relationship
the upper jaw with the right hand while stabilising the is altered. Patients will complain that their teeth
forehead with the left hand, and can be elicited at the ‘don’t meet properly’ and examination will reveal
Le Fort I, II, or III level.30,31 Mandibular fractures areas of premature contact or open bite.
are indicated by intraoral lacerations, mobility of the Dental examination begins with counting the
fracture segments, step defects and malocclusion. number of teeth and establishing whether any have
been lost or damaged acutely. If so, the location of
DENTAL EXAMINATION the missing fragments needs to be determined. Iden-
tify mobile teeth, teeth in the line of fractures and
Examination for injuries to the teeth and supporting the state of the third molars. Identify dentoalveolar
alveolar bone in these patients is often overlooked fracture segments, their mobility and viability.
in those without dental training or experience in Assess the occlusion and the presence of any trau-
managing these injuries but is an essential part of matic malocclusion. Assess general dental health
any assessment of a maxillofacial injury. The maxilla (indicated by the presence of dental caries and asso-
and mandible are both tooth-bearing bones; any ciated gingival disease) and evidence of previous
injury to them will affect the occlusion and can  dental restoration (fillings, crowns, bridges,
be associated with dentoalveolar injury. Accurate implants) or orthodontic manipulation. Of course,
treatment of these injuries requires an understanding the presence of an edentulous mandible or maxilla
and re-establishment of the pre-injury occlusal needs to be documented as well (Box 5.6).
Adults have 32 teeth, with eight in each quadrant
(two incisors, one cuspid, two bicuspids and three
molars). By convention,32 the teeth are numbered The gold standard form of investigation for facial
from 1 (central incisor) through to 8 (third molar) in fractures is now CT scanning with 3D reconstruction.
each quadrant. Quadrants can be identified by These reconstructed images give an excellent overall
description (e.g. upper right, lower left) or by impression of the fracture patterns, but also allow
number (1 is the upper right quadrant, with the more detailed inspection of the fractures on the two-
others numbered in a clockwise direction). By these dimensional axial, coronal or sagittal views. In the
means, the left maxillary lateral incisor can be called severely injured patient, scanning of the face, brain
the upper left lateral incisor, the upper left 2, or the and cervical spine (as well as the thorax and abdomen,
22 (pronounced two-two, not twenty-two). if required) can be carried out at the same time. It is
The occlusion is the relationship of the maxillary important to note at this point that images need to be
teeth to the mandibular teeth. Malocclusion describes obtained from the cranial vertex to the mentum to
an incorrect relationship between opposing teeth allow complete assessment of the facial skeleton.
andâ•›/â•›or the dental arches. Most people have some Additional information about the occlusion and
degree of malocclusion prior to any injury, but this dentition can be obtained by performing an OPG
is still referred to as their ‘normal’ occlusion, and it (orthopantomogram) scan, which provides a pan-
is this ‘normal’ occlusion that needs to be identified oramic view of the jaws and teeth. This can be

performed only in alert and cooperative patients, as spine or a vision-threatening globe injury can further
they are required to sit up and place their head in delay or alter the management plan for maxillofacial
the apparatus for approximately one minute. trauma. Open lines of communication between
However, it gives a much clearer view of the man- various specialties are clearly paramount in these
dible and the teeth and can help with diagnosis of situations, so that care is appropriately coordinated.
dental injury and disease. The description of facial fractures can be brief,
but still convey sufficient information to visualise
the injury, understand its severity and plan surgical
DIAGNOSIS AND TREATMENT access and sequencing of repair. For this purpose,
To this point, efforts have been directed at stabilis- the facial skeleton can be divided into regions based
ing the patient, dealing with life-threatening prob- on the bones involved, and their critical compo-
lems and acquiring as much information as possible nents. Clinically, the facial skeleton consists of the
about the injuries sustained. Eventually, the injuries frontal bone (which has anterior and posterior
need to be diagnosed and a problem list compiled. tables), the nose, paired zygomatic bones and orbits,
Once this has been achieved, a management plan a left and right NOE segment, a left and right
can be formulated with input from all involved maxilla, a left and right mandible and corresponding
specialties. condylar segments, and the dentoalveolar region.
Maxillofacial injury repair is usually of a lower By using this framework, all facial fractures can
priority in the patient with multiple injuries. Atten- rapidly be described by referring to each region and
tion is first given to the management of head injury, the degree of displacement and comminution. Max-
thoracic and abdominal injury, and orthopaedic illaryâ•›/â•›midface fractures are usually described by
(long-bone) injury. Treatment of an unstable cervical referring to the pattern of the fracture lines, as first


FIG 5.13â•… Le Fort classification of maxillofacial fractures. (From Smith JA et al33, a. Table 13.6. b. Fig 13.17.)
a. Frontal views
I Horizontal maxillary fracture (between teeth and face—stable infraorbital rim)
II Pyramidal-type fracture (movement of the medial section of the infraorbital rim)
III Craniofacial dysjunction (movement of the whole infraorbital rim and maxilla)
b. Lateral views
I Horizontal maxillary fracture (between teeth and face—stable infraorbital rim)
II Pyramidal type fracture (movement of the medial section of the infraorbital rim)
III Craniofacial dysjunction (movement of the whole infraorbital rim and maxilla)
5 • Emergency department management • C. Blunt injury of the neck 85

described by Rene Le Fort in 1901,29,30 and can be

at multiple levels (Fig 5.13a & b). Thus, a low-
velocity injury to the right cheekbone can be
described as a minimally displaced fracture of the
right zygoma, whereas a high velocity panfacial
injury can be described as a bilateral Le Fort I and
II injury, with extensive comminution and displace-
ment, with extension into the anterior table of the
frontal bone and involvement of the left NOE
segment, an associated left zygomatic fracture and
segmental fracture of the mandibular symphysis.
Further information can be conveyed by referring
to the mechanism of injury and associated soft-tissue
trauma. High-energy impacts and penetrating inju-
ries cause greater destruction of bone and soft tissue
than low-velocity blunt injuries, are usually more
complicated to repair and are more likely to have
suboptimal results functionally and cosmetically.
The surgical approaches, techniques of repair, out-
comes and potential complications of maxillofacial FIG 5.14â•… Extensive surgical emphysema in the neck
injuries are discussed in greater detail in Chapter 8. (black areas) and CT angiogram after blunt trauma.


Blunt trauma to the neck often occurs in association Airway obstruction due to injuries of the larynx,
with head injuries. The pharynx and larynx can both trachea or pharynx is a frequent cause of death in
be injured. The mechanisms include lateral displace- patients who suffer head trauma. The patient’s
ment of the central neck structures with tearing of airway and breathing need to be assessed in the
soft tissues, posterior compression of the larynx primary survey and an adequate airway needs to be
onto the vertebral column with haematoma and assured. The relocation of major fractures of the
crush injury, or explosive rupture of the pharyngeal upper or lower jaws may be necessary to allow the
wall from compression of the air in the lumen at the patient to breathe. The mouth and pharynx need to
time of impact. Degenerative changes of the spine be cleared of blood and foreign bodies such as dis-
with anterior osteophyte formation may increase the placed teeth or dentures. Early endotracheal intuba-
risk of trauma to the pharyngeal wall. tion should be performed if necessary, and may in
Subcutaneous gas (surgical emphysema) is evi- some trauma systems be undertaken by paramedics
dence of injury to the wall of the pharynx or larynx. before transfer to hospital.
The neck will swell and crepitus may also be pal- If the larynx is not able to be accessed via the
pable. A large volume of gas can pass into the neck mouth, a life-saving airway can be established with
and may extend from the scalp to the upper chest a cricothyroidotomy and insertion of some form of
wall (Fig 5.14). The site of injury and air leak may tube, preferably one designed for the purpose. This
be very small. will provide only a temporary airway until a trache-
Haematomas may involve the lumen of the larynx ostomy can be performed.
at the level of the vocal folds or below, the supra-
glottis, and the walls of the hypopharynx and oro-
pharynx. Bruising may range from minor submucosal
ecchymosis to haematomas large enough to obstruct Suspected or established injury to the wall of the
the airway. pharynx is usually treated conservatively, at least
Major crush injuries to the larynx and trachea initially. The patient is kept nil by mouth and 
may occur and the cricoid cartilage may even be covered with parenteral broad spectrum antibiotics.
completely torn away from the trachea without any A nasogastric or other feeding tube should not be
breach of the overlying skin. inserted as extraluminal passage is likely in the

presence of a defect in the pharyngeal wall. The

patient is also instructed not to blow the nose or
perform other manoeuvres that may force air through
the defect. Careful observation for signs of infection 
or collection or abscess formation in the neck is
The surgical emphysema usually resolves over a
period of days. A radiological contrast study of
swallowing is performed after three or more days.
If no leak outside the pharynx is identified, the
patient is allowed to take oral fluids and then a soft
diet for a period of days. Normal eating is resumed
when the pharynx is fully healed.

The leak of cerebrospinal fluid (CSF) from the nose
after head injury is due to a breach of the bony skull
base and dura of the anterior or middle cranial fossa. FIG 5.15â•… Fracture through the roof of the ethmoid
Fractures of the frontal, ethmoid and sphenoid sinus, with fluid in the anterior ethmoid cell.
sinuses may lead to a leak from the anterior fossa.
Fractures of the temporal bone are frequently com- required to fracture the bone. Pneumocephalus is
plicated by a leak of CSF from the middle fossa via often seen with fractures of the anterior skull base.
the external ear or occasionally down the eustachian Intrathecal radiological studies are not now gener-
tube to the nose. ally performed.
Any drainage of watery fluid from the nose after Most leaks will settle within a few days. Complex
a head injury is likely to be due to a CSF leak. The fractures or those with significant displacement 
rate of flow will usually increase with bending of bone fragments are less likely to resolve and
forward or with straining. There may be a salty taste. therefore require surgical management. Increasing
A low-pressure headache due to the leak may be pneumocephalus is another indication for early
relieved by lying down. When the CSF is mixed intervention. Meningitis or pseudomeningocele may
with blood and dries on the bedclothes, the blood occur months or years after an injury to the skull
dries first and the CSF seeps more peripherally base, and the responsible defects will need to be
forming a paler stain around the blood clot, called corrected surgically (see Chapter 8).
the ‘halo sign’.
Examination of the nasal cavity, with or without
an endoscope will usually identify the leak, but not
its exact site. If there is enough fluid to collect, it
should be sent for beta-2 transferrin estimation. This Head injuries are frequently associated with injury
protein is only found in CSF, vitreous humour and to the nose and other facial bones, and significant
perilymph, and a positive test on nasal fluid con- epistaxis may ensue. The trauma may be blunt or
firms a leak of CSF. sharp, and from an anterior or lateral direction.
The cribriform plate of the ethmoid bone, which Bleeding may come from:
forms the bony roof of the nasal cavity, is the com- • direct trauma to the external nose, with bleeding
monest site for a leak, as this bone is very thin. Other from the anterior nasal and anterior ethmoidal
sites are the roof of the ethmoid sinuses (Fig 5.15), arteries
the posterior wall of the frontal sinuses, and the roof • midfacial fractures, with bleeding from the nasal
or lateral walls of the sphenoid sinuses. septal, posterior ethmoidal and sphenopalatine
The site and size of fractures of the skull base arteries
will usually be well shown on high-resolution CT • fractures of the lateral and central skull base, with
scans. Multiple defects may be seen, due to the force involvement of the internal carotid artery.
5 • Emergency department management • E. Epistaxis 87

The ethmoidal arteries are distal branches of the If the bleeding is from the nasopharynx or poste-
internal carotid artery. All other significant blood rior nasal airway, it will require the placement of
supply to the nose and nasal cavity originates from some form of posterior pack (Fig 5.16b). The sim-
the external carotid artery. plest way to do this in the emergency department is
The patient may have facial lacerations as well to use a Foley catheter, ensuring that it is accurately
as signs of facial fractures, including swelling and placed in the lumen of the nasopharynx and inflated
deformity. There may also be evidence of a fracture with no more than 8╯mL of saline. Facial and neck
of the lateral skull base with bleeding from the ear. fractures, however, open the possibility of passage
Active nasal bleeding needs to be assessed and of the catheter to the anterior cranial fossa, orbit and
managed promptly. Signs of significant blood loss deep upper neck, which must be avoided. If poste-
also need to be sought and the patient resuscitated rior packing is required, this is performed prior to
appropriately. anterior nasal packing.
CT scans are necessary to assess the facial skel- The technique entails anaesthetising the anterior
eton, and it should be remembered that the force nasal cavity if the patient is alert and there is enough
required to fracture the facial bones is often enough time. This can be done with pledgets soaked in xylo-
to injure the cervical spine as well. caine in adrenaline or cocaine solutions. The Foley
catheter is gently inserted through the nose until its
Control of blood loss tip is seen in the oropharynx. The balloon is then
The nose is examined with the aid of a headlight and injected with 5–8╯mL of normal saline and the cath-
suction to identify the site of bleeding, whether it is eter is tractioned forwards to impact the inflated
anterior, midlevel, posterior or from multiple sites. balloon into the choana of the nasopharynx, thus
If bleeding is anterior, it may be possible to cau- stopping bleeding backwards into the pharynx. The
terise the vessel definitively, or it may require the assistant holds the catheter forwards and the anterior
placement of an anterior pack such as ribbon iodo- nasal cavity is also packed to stem all bleeding from
form gauze or commercially available packs such as that side of the nose. Forward tension is kept on the
the Rapid Rhino® into both nasal airways in an catheter, which is then clamped with a haemostat
attempt to tamponade the source of bleeding (Fig clamp or similar instrument. The clamp sits across
5.16a). In addition, local vasoconstrictive agents can the rim of the nostril to maintain the traction. The
be used. nostril is protected from the clamp with gauze or

FIG 5.16aâ•… Anterior nasal packing in situ.


foam rubber padding. The second side of the nose maxillofacial section of this chapter (Section B) and
is treated similarly if bleeding is bilateral. Chapter 8.
The balloon can be left inflated for 24 hours and
then unclamped and deflated, but left in position for
a further 24 hours in case bleeding re-starts. The
anterior pack can be removed after 2–4 days as Injury to the external ear is commonly seen in asso-
required. ciation with head injuries. Blunt injury may cause a
The patient should be treated with broad spec- haematoma of the auricle (haematoma auris). It may
trum antibiotics while the packs are in place to also cause bruising or rupture of the tympanic mem-
prevent infective complications, including toxic brane owing to the piston effect that occurs when
shock syndrome. Nasal packing may cause breath- the column of air in the external auditory canal is
ing difficulties, especially posterior packing, which forced onto or through the drum.
may distort the soft palate. The volume of fluid used
in the balloon should be just enough to stop bleeding
into the pharynx. Patients with nasal packs need to
be closely observed and additional airway support In a haematoma auris blood accumulates between
provided if necessary. the perichondrium and the cartilage, causing a loss
In cases of massive nasal or pharyngeal bleeding, of vascularity to the cartilage. It may also be com-
where the patient has survived transfer to the emer- plicated by infection, via any small breach in the
gency department and has been intubated, packing overlying skin. If left untreated, the cartilage will
of the pharynx via the mouth as well as anterior necrose and result in significant deformity in the
nasal packing may be enough to stop the blood loss form of a ‘cauliflower ear’.
while the extent of all injuries is being assessed  Haematomas of the auricle need to be drained 
and definitive management begun. Embolisation  in an aseptic fashion. An incision is made in the 
of the major bleeding source(s) may be required. skin in one or more areas, usually along a ridge or
Massive bleeding from the internal carotid artery  hollow of the external ear. The blood is aspirated
in the skull base is likely to be incompatible with and a soft rubber drain tube is inserted. The ear is
survival. Epistaxis is further discussed in the padded with sterile cotton wool, taking care not to

FIG 5.16bâ•… Posterior nasal packing in situ.

5 • Emergency department management • G. Fractures of the temporal bone 89

cause pressure areas on the skin, and a slightly firm

dressing is applied to prevent re-accumulation of 
the haematoma. The dressing is left for approxi-
mately 3 days. The drain can then be removed and
the ear padded again for 1–2 days if necessary. Any
re-collection of blood is formally drained again in
the same way.

Blunt trauma occurring to the ear may cause a
rupture of the tympanic membrane and even disrup-
tion of the ossicular chain. This will cause conduc-
tive hearing loss. A severe pressure injury may
rupture the seal of the round or oval windows,
leading to sensorineural hearing loss. Hearing should
be assessed clinically and with tuning forks, and an
audiogram performed early, especially if sensori-
neural hearing loss is suspected.
Middle ear injuries with only conductive loss can
be treated expectantly. The ear is examined under a
microscope to assess the extent of injury and to
ensure the canal is patent. Blood clot is otherwise
left in the canal, and the ear is protected from water.
Antibiotic drops are used only if infection is sus-
pected. Quinolone preparations are the least likely
to be ototoxic and are preferred in the presence of
an open middle ear.
Most traumatic perforations will close within
6–12 weeks. Delayed repair of the drum can be
performed for defects that do not heal.
FIG 5.17â•… Line diagram of the facial nerve in temporal
TYPES OF FRACTURE into the cerebellopontine angle of the posterior
Fractures of the temporal bone or lateral skull base cranial fossa and into the internal auditory canal. 
are classically described as being longitudinal or At the lateral end of the canal, it curves forward to
transverse, based on their orientation to the long axis the geniculate ganglion, then backwards into the
of the temporal bone, which sits at approximately middle ear as the horizontal segment. It next curves
45 degrees to the anterior–posterior plane. There is inferiorly into the vertical segment and exits the
a smaller group of fractures in which the tympanic temporal bone via the stylomastoid foramen (Fig
bone that forms the anterior wall of the external 5.17). The facial nerve is easily injured in these
auditory canal is fractured because the head of the fractures. The ossicular chain and internal carotid
mandible has been forced posteriorly. As fractures artery may also be damaged.
of the temporal bone often have a complex pattern, In longitudinal fractures (Fig 5.18), the force
an alternative classification is based on whether the passes through relatively weaker parts of the skull
inner ear is involved or not. base, namely the external auditory canal, middle ear
The facial nerve has a complicated course through and eustachian tube. This spares the inner ear and is
the temporal bone. It passes from the brainstem  less likely to sever the facial nerve. Bruising and

FIG 5.18â•… CT scan of a longitudinal fracture with FIG 5.19â•… CT scan of a transverse fracture through the
separation of ossicular chain. inner ear.

compression injuries of the nerve may still occur. it open. We generally do not attempt to clean the 
The tympanic membrane is usually torn and the ear canal in the first few days, apart from what is
ossicular chain may be disrupted. required to ensure that the canal is patent. The clot
In transverse fractures (Fig 5.19), the inner ear acts as an early dressing and can be removed after
is usually involved. The fracture may pass through 1–2 weeks.
one or more of the cochlea, the vestibular apparatus Further examination will depend on whether the
and the internal auditory canal. Facial nerve injuries patient is conscious and able to cooperate. Facial
are generally more severe. movement on each side must be assessed, if possi-
The bony roof of the middle ear and mastoid is ble. A complete paralysis that is seen immediately
often fractured, and CSF leak is common in both after the injury may indicate that the nerve has been
types of fracture, either from the external ear (CSF disrupted. If the face is seen to move after the injury,
otorrhoea) or down the eustachian tube to the nasal it is certain that the nerve has not been disrupted and
cavity. any delayed palsy can generally be managed con-
servatively with confidence.
The hearing must be assessed. Simple speech and
SYMPTOMS AND SIGNS whisper testing may be enough to ensure that hearing
The classical early sign of a fracture of the lateral remains in an ear. The tuning fork tests are very
skull base is bleeding from the external auditory useful in this situation. The Weber lateralises to the
canal. This should be assessed in all cases of head side of a conductive hearing loss and away from a
injury. Other sources of blood in the ear canal should sensorineural loss. The Rinne test compares air and
be excluded, such as lacerations of the scalp or bone conduction. Bone will be perceived louder
pinna. CSF may also be seen issuing from the canal, than air in a conductive loss, but air louder than 
and this can be profuse on occasions. A halo sign bone in normal hearing or with a sensorineural loss
(as described above) may be seen on the pillow if (Fig 5.20).
the CSF is mixed with blood. Dizziness or vertigo are commonly experienced
The ear canal must also be assessed to ensure that after head injury. Benign positional vertigo (BPV)
it has not been crushed from in front. If this has is very common, even after minor head trauma. Sig-
occurred, early intervention is required with dilation nificant vertigo will be present if the inner ear has
of the bone fragments and sterile packing to splint been damaged.
5 • Emergency department management • G. Fractures of the temporal bone 91

FIG 5.20â•… Rinne and Weber tuning fork tests: AC = air conduction; BC = bone

External signs of trauma may be seen around the a few days. A sterile dressing can be applied, and
ear, depending on the mechanism of injury. Bruising the ear is protected from water. Antibiotic drops 
over the mastoid may appear after 3–4 days, due to are used only if the ear becomes infected. The
blood exiting the mastoid fracture line (Fig 5.21a), patient is regularly reviewed by the ENT surgeon to
which produces the Battle’s sign (Fig 5.21b). ensure that all the ear-related injuries are dealt with
High-resolution axial and coronal CT scans allow
full assessment of the site and extent of fractures of Early assessment of facial movement is very impor-
the temporal bone and skull base. The middle and tant and must be performed in detail as soon as
inner ear structures, facial nerve canal and carotid possible. Partial weakness suggests a compressive
canals must be examined. CT angiography is a very injury, and parenteral steroids may be used if there
useful adjunct to assess injury to the internal carotid is no contraindication. Partial facial paralysis involv-
artery. ing only one segment of the face suggests injury to
Formal audiometry should be performed as soon a peripheral branch of the nerve. Facial lacerations
as practicable, depending on the patient’s general will need to be explored and nerve repair performed
state, the effects of the head injury and all other  as necessary.
injuries. Air and bone conduction and speech dis- A total paralysis that is present immediately after
crimination should all be assessed. Impedance testing the injury or that is present as soon as the patient can
should not be performed in the presence of a recently be assessed (such as after endotracheal extubation)
damaged ear canal or tympanic membrane. is highly likely to indicate a severe nerve injury and
possible division of the nerve. In such a case, where
the fracture is seen to involve the facial nerve canal
MANAGEMENT on CT scan and the facial nerve is unable to be elec-
The clot is left undisturbed in the ear canal early on, trically stimulated with tests such as electroneurog-
once the patency of the canal is assured. Bleeding raphy or maximal nerve excitability, exploration is
is usually short-lived. CSF leaks mostly settle within generally indicated. The timing of surgery will

FIG 5.21aâ•… Fracture in the left mastoid bone resulting

in Battle’s sign. (Parrillo JE et al34, Fig 67.1a.)

FIG 5.21bâ•… Battle’s sign. (Parrillo JE et al34, Fig 67.1b.)

depend on the other injuries and the patient’s general

condition, but should be done sooner rather than
later. Good results have been reported in cases of possible as long as the stapes footplate remains
nerve grafting, even many months after injury. mobile. Standard tympanoplasty techniques are
The middle ear is explored and the status of the
ossicular chain assessed. If the only abnormality is
The management of hearing loss can usually be a dislocated incus, it can be removed, re-shaped and
delayed until all other injuries have been treated. A re-positioned between the malleus and stapes. More
full assessment of the hearing in both ears is complex injuries can be managed with insertion of
performed. partial or total ossicular replacement prostheses.
Sensorineural hearing loss is generally not ame- Complete or near complete correction of the con-
nable to surgical treatment. Partial loss of more than ductive hearing loss can be achieved. This surgery
a mild level is usually helped significantly with a can be combined with other corrective surgical pro-
hearing aid. Total loss may be managed with hearing cedures on the ear if necessary.
aid systems that re-route sounds from the deaf to the
hearing ear. Bilateral severe-to-profound hearing
loss may require the insertion of a cochlear implant
on one or both sides. CSF leak from the ear after a lateral skull base frac-
Most cases of temporal bone fracture will have ture is very common and can be profuse on occa-
some conductive hearing loss early on, which is due sions. In most cases, it settles spontaneously. A leak
to blood in the external canal or middle ear space. that continues over more than 4–5 days with loss of
Significant persistent conductive hearing loss with significant volumes of fluid may resolve with the
the preservation of good inner ear hearing can be insertion of a lumbar drain for 3 or more days. Per-
treated with a hearing aid, but surgery is also sisting leaks may need to be addressed surgically.
5 • Emergency department management • H. Eye injuries 93


A 36-year-old male was found unconscious near a approach. The fracture was seen to involve the lateral
railway station early in the morning by passers-by. He mastoid cortex and crossed the vertical facial nerve
was retrieved by ambulance and did not require canal. A cortical mastoidectomy was performed, and
airway support. On arrival in the emergency the nerve was exposed with removal of multiple bone
department he was breathing spontaneously, was fragments. The nerve had been severed completely.
responsive to painful stimuli and had no localising Contraction of the proximal and distal ends had left a
neurological signs. He had a bruise over the right nerve defect of approximately 1╯cm. The middle ear
temple and some other minor abrasions. There was a was also explored. The incus had been dislocated
thin blood-stained discharge from the right ear. laterally, with separation of its joint with the stapes
Otoscopic examination revealed an open ear canal head and rotation of the long process into the
with a slit-like perforation of the postero-superior part tympanic membrane.
of the tympanic membrane. The severed ends of the facial nerve were
A CT brain scan showed a longitudinal fracture of debrided. A 15╯mm segment of the ipsilateral sural
the right temporal bone that did not involve the inner nerve was harvested from the lateral side of the ankle
ear. The fracture passed through the vertical segment and inserted between the ends of the facial nerve as
of the facial nerve canal. The rest of the trauma a cable graft. Two 9â•›/â•›0 nylon sutures were used to
series revealed no other fractures and particularly no anastomose each end in the facial nerve canal and
injury to the cervical spine or facial skeleton. the whole area was covered with a sheet of
Initial assessment of facial movement and hearing temporalis fascia.
was not possible because he was unconscious. After The incus was retrieved, drilled to shape and
24 hours he regained consciousness and was noted inserted between the malleus handle and the head of
to have a complete facial palsy on the right side with the stapes. The tympanic membrane perforation was
normal movement on the left. The tuning fork tests repaired with an underlay graft of fascia.
revealed the Weber lateralising to the right and a The patient had a gold weight inserted in the
negative Rinne (bone conduction greater than air upper right eyelid by the ophthalmologist as a
conduction) on the right. separate procedure.
After a further 48 hours, a formal audiogram was Hearing was tested 3 months after the surgery
successfully completed and showed a maximal and showed near-complete resolution of the
conductive hearing loss with near-normal bone conductive hearing loss.
conduction on the right and good perception of the Some recovery of facial movement was seen
spoken word. The hearing on the left side was 7 months after the repair. Eighteen months
normal. The facial nerve was unable to be stimulated postoperatively the patient had a near normal
on the right with electroneurography. A normal appearance at rest, indicating good muscle tone. He
response was seen on the left. was able to move the middle third of the face, had
The complete facial palsy present as soon as it some elevation of the angle of the mouth and had
could be assessed after the injury, the site of the good active eye closure. After a further 12 months
fracture and the inability to stimulate the nerve he developed some mild synkinesis of the right side
electrically suggested a severe injury of the nerve. A of the face, indicating only mild, aberrant nerve
decision was made to explore the nerve via a mastoid re-growth.

H. EYE INJURIES • traumatic optic neuropathy

• blunt ocular injury: (a) hyphaema, (b) vitreous
ASSESSMENT OF THE EYES haemorrhage, (c) blunt retinal injury (commotio
AND ORBIT retinae)
It is important to consider significant eye injury in • penetrating ocular injury.
any patient with facial injuries, especially those with
periorbital bruising or lid laceration. Early assess- Orbital fractures
ment of the patient with head and facial injuries to Orbital fractures may be diagnosed clinically by the
exclude significant eye or orbital injuries is impor- presence of periorbital bruising, bleeding from the
tant. Important eye and orbital injuries to exclude are: nose, facial (infraorbital nerve) numbness, abnormal
• orbital fractures: (a) orbital wall fractures (espe- ocular movements, proptosis or, less commonly,
cially floor and medial wall), (b) zygoma frac- acute enophthalmos. On examination there is gener-
tures, (c) orbital haemorrhage ally periorbital bruising. Unless there is associated

globe or optic nerve involvement, the visual acuity anteriorly, where it is defined by the orbital septum
is usually normal. There may be abnormal eye (which is a strong fascial sheath attached to the
movements, especially limitation of up-gaze due to arcus marginalis). When there is significant haemor-
entrapment of inferior rectus. There may be accom- rhage in the orbit, a compartment syndrome may
panying infraorbital nerve numbness, but this sign ensue, leading to visual loss through either optic
is often hard to detect in a patient with significant nerve, or more rarely, direct globe ischaemia. Para-
facial bruising. In large orbital floor fractures there doxically when there are significant orbital floor or
may be acute enophthalmos, but in general enoph- medial wall fractures, there is less likelihood of a
thalmos is a late sign in orbital floor fracture, only compartment syndrome, as the orbit is able to
occurring when the orbital oedema or haemorrhage decompress into the maxillary or ethmoid sinus.
has settled. The definitive diagnosis of orbital wall Vision-threatening orbital haemorrhage can be
fracture is made by radiology. CT scanning of the recognised by a combination of tense expanding
orbit reveals the fractures of the medial wall or floor, proptosis, haemorrhagic chemosis and evidence of
generally with accompanying opacity of the adja- optic nerve compromise. If awake, the patient may
cent ethmoid or maxillary sinus. describe severe pain and visual loss. More often, the
Zygoma fractures may occur in isolation or in patient is unconscious or sedated and the optic nerve
combination with orbital wall fractures. In an iso- compromise is recognised by the presence of a rela-
lated zygoma fracture, the cheek is depressed. There tive afferent pupil defect. In this setting it is impor-
may be an associated trismus due to involvement of tant to rule out significant globe injury or rupture.
masseter or the temporalis tendon. The eye is in the The CT scan may reveal an extraconal or intra-
normal position and there is no abnormality of conal haemorrhage.
vision or eye movement.
Traumatic optic neuropathy
Orbital haemorrhage The optic nerve may be injured directly (direct trau-
Significant orbital haemorrhage generally occurs in matic optic neuropathy) or more commonly indi-
the setting of severe facial injuries (Fig 5.22). The rectly (indirect traumatic optic neuropathy). Most
orbit is surrounded by bone in all directions except commonly the visual loss in traumatic optic neu-
ropathy occurs at the time of the injury. The patient
complains of sudden (usually unilateral) visual loss.
In an unconscious patient, the optic neuropathy is
recognised by the presence of an afferent pupil
In patients with traumatic optic neuropathy, apart
from the afferent pupil defect and the accompanying
head or orbital injury, the examination is generally
normal. Acutely, the optic nerve head nearly always
appears normal. It is uncommon for the imaging to
reveal direct evidence of optic nerve swelling or
haemorrhage. Indirect traumatic optic neuropathy
should be considered and looked for in all patients
with significant facial or head or orbital injury.

Blunt ocular injury

The important ocular injuries to suspect and exclude
in a patient with blunt ocular trauma are hyphaema,
vitreous haemorrhage and blunt retinal injury (com-
motio retinae).
Hyphaema may be diagnosed by the presence of
FIG 5.22â•… Coronal CT scan showing orbital a layer of blood on the iris or in the angle inferiorly.
haemorrhage with a fractured depressed right orbital Sometimes the blood is circulating and the entire
floor. anterior chamber appears red or cloudy. Vitreous
5 • Emergency department management • H. Eye injuries 95

a b
FIG 5.23â•… Anteroposterior (a) and lateral (b) plain X-ray views of an orbital foreign body showing cranial

haemorrhage is diagnosed by the presence of blood excluded in elderly patients who have fallen and
in the vitreous obscuring the view of the retina or knocked their eye or head.
optic nerve. In any patient with a vitreous haemor- In any patient with penetrating orbital or globe
rhage, penetrating trauma should also be considered injury, an associated intracranial injury must be sus-
and excluded. Commotio retinae is diagnosed by the pected and excluded (Fig 5.23a & b).
appearance of retinal pallor and swelling and occa-
sional haemorrhage. Commotio retinae usually
occurs in the setting of significant ocular injury and EARLY MANAGEMENT
its signs are best seen after the acute hyphaema and Orbital fractures
vitreous haemorrhage have resolved.
Unless there are vision-threatening features, orbital
wall fractures do not require emergency department
Globe rupture or penetrating eye injury
treatment. Secondary orbital cellulitis is uncommon.
Early recognition and repair of globe rupture or pen- If there is a history of sinusitis or dirty penetrating
etration is important for the long-term visual prog- orbital trauma, antibiotics to prevent orbital celluli-
nosis. In general, clinical assessment is all that is tis should be started. Coverage against Streptococ-
required to exclude significant eye injury. cus and Staphylococcus aureus is required. Usually
Important clinical signs of globe rupture are: a combination of a second- or third-generation ceph-
• haemorrhagic chemosis alosporin (e.g. ceftriaxone 1╯g 12-hourly) and a spe-
• loss of red reflex cific anti-Staphylococcus drug (e.g. vancomycin 1╯g
• irregular or displaced pupil 12-hourly) is used. Patients should be advised
• unexplained deep anterior chamber against blowing their nose for 7 days, as increasing
• unexplained visual loss or afferent pupil defect. the intrasinus pressure can lead to further escape of
In some patients with haemorrhagic chemosis air and sinus organisms into the orbit.
and a poor view of the posterior pole, it may be
impossible to exclude penetrating eye injury without
surgical exploration. Globe rupture may occur with Orbital haemorrhage
relatively minor trauma in patients who have had Minor orbital haemorrhage (without signs of globe
previous intraocular surgery (most commonly cata- or optic nerve compromise) requires no treatment.
ract surgery) and should always be suspected and Vision-threatening orbital haemorrhage should be

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identification of cognitive impairment in patients with 3rd ed. Philadelphia: Mosby; 2007.
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Psychiatry. 2008;79(10):1100-1106. FURTHER READING
23. Sakellaridis N, Pavlou E, Karatzas S, et al. Comparison
of mannitol and hypertonic saline in the treatment of Anderson L, Kahnberg K-E, Pogrel MA, eds. Oral and
severe brain injuries. J Neurosurg. 2011;114(2): maxillofacial surgery. 1st ed. Chichester: Wiley-
545-548. Blackwell; 2010.
24. Ivascu FA, Howells GA, Junn FS, et al. Rapid warfarin Batterbury M, Bowling B. Ophthalmology: an illustrated
reversal in anticoagulated patients with traumatic colour text. 2nd ed. Edinburgh: Churchill Livingstone;
intracranial hemorrhage reduces hemorrhage 2005.
progression and mortality. J Trauma. 2005;59(5): Behrbohm H, Kaschke O, Nawka T, et al. Ear nose and
1131-1139. throat diseases: with head and neck surgery. 3rd ed.
25. Baker RI, Coughlin PB, Gallus AS, et al. Warfarin New York: Thieme; 2009.
reversal: consensus guidelines, on behalf of the Kanski JJ, Bowling B. Clinical ophthalmology: a systematic
Australasian Society of Thrombosis and Haemostasis. approach. 7th ed. Edinburgh: Saunders; 2011.
Med J Aust. 2004;181(9):492-497. Lee KJ. Essential otorhinolaryngology: head and neck
26. Ivascu FA, Howells GA, Junn FS, et al. Predictors of surgery. 9th ed. New York: McGraw Hill Medical;
mortality in trauma patients with intracranial 2008.
Injury to the spine and spinal cord
Susan M Liew, Arvind Jain,
Jeffrey V Rosenfeld, Jin W Tee, Patrick Chan

A. SPINAL INJURY 1.╇ History

• Age and mechanism of injury should either
This section sets out the diagnosis, investigation and make you think of a specific condition (e.g. an
management of vertebral column injuries. It focuses elderly patient with a head strike and Type II dens
on the cervical spine, but the principles detailed fracture) or a group of diagnoses (e.g. high-speed
below can be applied to the entire spine. rollover motor vehicle accident and a facet or
The cervical spine is divided into anatomicalâ•›/â•›  burst fracture). Remember also that children have
functional segments: the occipito-atlanto-axial junc- a different spectrum of injuries in the cervical
tion (C0–C2), the subaxial cervical spine (C3–C6) spine (see SCIWORA under Traumatic Spinal
and the cervicothoracic junction (C7–T1). Cord Injury: Special Conditions).
• Certain associated injuries should alert you to
EPIDEMIOLOGY the probability of other injuries. For example, a
The overall prevalence of traumatic cervical spinal head injury, which will have taken precedence in
injury is 3.7% in a meta-analysis of all trauma litera- assessment, has a higher rate (said to be up to
ture from 1986 to 2008.1 In this study, the preva- 16%) of a concurrent cervical spine, especially
lence of cervical spinal injury in alert patients was ‘minor’ C0â•›/â•›foramen magnumâ•›/â•›occipital condyle,
2.8%, while the prevalence of the same injury in C1 or C2 injury.
clinically unevaluable patients was 7.7%. Instability • Associated neurological symptoms and signs
was present in 41.9% of traumatic cervical spine may help you to localise a level but more impor-
injuries. Up to 55% of traumatic spinal cord injuries tantly will alert you to the urgency of treatment.
are caused by cervical spine injuries.2 • Certain other co-morbidities, such as ankylosing
spondylitis or a degenerative (older) spine, should
CLINICAL ASSESSMENT alert you to the possibility of a seeming mismatch
between mechanism and severity of injury (e.g.
In orthopaedic surgery, the priority is ‘save the the ankylosing spondylitic three-column fracture
limb’, and in spine surgery we may need to ‘save after a simple fall: see Radiological diagnosis: CT
the cord’. However, preventing further damage to scan, below). It is obviously important to know
neurological structures is the key objective. Acute about other co-morbidities, as these can have an
spinal cord injury is discussed later in this chapter. impact on your treatment plan (e.g. the patient on
This section sets out the most relevant clinical warfarin who needs operative treatment).
information that will need to be obtained rapidly by
doctors treating the patient with spine injury and
conveyed succinctly to the consultant orthopaedic 2.╇ Examination
surgeon or neurosurgeon, so that timely decisions • You will need help to maintain spinal precautions
can be made about the management. Urgent stabili- while completing a full examination, as this
sation of the neck with traction devices or surgery necessitates removing the collar while the head
may be required. is held and while the patient is logrolled.
6 • Injury to the spine and spinal cord • A. Spinal injury 99

• At the early stage, when the patient may still be Association (ASIA) assessment chart (Fig 6.1
in the emergency department, tenderness is not and Appendix F) is useful for this task. Subtle
a particularly good or useful discriminator, as nerve root injuries may easily be missed while
many patients will already have a significant looking at other injuries and it is wise to
amount of analgesia in their system and this can re-examine the patient for a specific neurologi-
cloud the assessment. You should make a note of cal sign if you find something on the imaging
whether tenderness is present and its location. (e.g. a facet fracture).
Midline tenderness is more significant than lateral • Look for features that may influence the
tenderness. It is not possible to elicit tenderness operative decisions, such as the condition of
in the intubated patient. You need to maintain a the overlying skin and soft tissues. This should
high index of suspicion for spine injury, depend- include an examination of the operative site
ing on the mechanism of injury and co-morbidities. before surgery so there are no unexpected find-
• A thorough neurological examination is essenÂ� ings (Fig 6.2).
tial and you must know your dermatomes and
myotomes. We recommend you choose one key 3.╇ Investigations
muscle per myotome to test for as part of your Confirm the diagnosis and assess technical issues
examination routine. The American Spinal Injury relevant to the treatment:

FIG 6.1â•… American Spinal Injury Association (ASIA) Standard Neurological Classification of Spinal Cord Injury.
(Courtesy American Spinal Injury Association: International Standards for Neurological Classification of Spinal Cord Injury, revised 2011; Atlanta,
GA. Reprinted 2011.) (Continued over)

Muscle Function Grading ASIA Impairment (AIS) Scale Steps in Classification

The following order is recommended in determining the
classification of individuals with SCI.
0 = total paralysis A = Complete. No sensory or motor function
is preserved in the sacral segments S4-S5. 1. Determine sensory levels for right and left sides.
1 = palpable or visible contraction B = Sensory Incomplete. Sensory but not 2. Determine motor levels for right and left sides.
motor function is preserved below the Note: in regions where there is no myotome to test, the motor
neurological level and includes the sacral level is presumed to be the same as the sensory level, if testable
2 = active movement, full range of motor function above that level is also normal.
segments S4-S5 (light touch, pin prick at S4-S5:
motion (ROM) with gravity or deep anal pressure (DAP)), AND no motor 3. Determine the single neurological level.
eliminated function is preserved more than three levels below This is the lowest segment where motor and sensory function is
the motor level on either side of the body. normal on both sides, and is the most cephalad of the sensory
3 = active movement, full ROM against C = Motor Incomplete. Motor function is and motor levels determined in steps 1 and 2.
gravity preserved below the neurological level**, and 4. Determine whether the injury is Complete or Incomplete.
more than half of key muscle functions below the (i.e. absence or presence of sacral sparing)
single neurological level of injury (NLI) have a If voluntary anal contraction = No AND all S4-5 sensory
4 = active movement, full ROM against muscle grade less than 3 (Grades 0-2). scores = 0 AND deep anal pressure = No, then injury is
gravity and moderate resistance in a COMPLETE. Otherwise, injury is incomplete.
D = Motor Incomplete. Motor function is
muscle specific position. preserved below the neurological level**, and at 5. Determine ASIA Impairment Scale (AIS) Grade:
least half (half or more) of key muscle functions Is injury Complete? If YES, AIS=A and can record ZPP
(lowest dermatome or myotome on
5 = (normal) active movement, full below the NLI have a muscle grade > 3.
NO each side with some preservation)
ROM against gravity and full E = Normal. If sensation and motor function as
resistance in a muscle specific tested with the ISNCSCI are graded as normal in Is injury
all segments, and the patient had prior deficits, motor Incomplete? If NO, AIS=B
position expected from an otherwise
then the AIS grade is E. Someone without an (Yes=voluntary anal contraction OR
unimpaired peson. initial SCI does not receive an AIS grade. motor function more than three levels
YES below the motor level on a given side,
5* = (normal) active movement, full **For an individual to receive a grade of C or D, i.e. motor if the patient has sensory incomplete
incomplete status, they must have either (1) voluntary anal classification)
ROM against gravity and sufficient sphincter contraction or (2) sacral sensory sparing with
resistance to be considered normal sparing of motor function more than three levels below the Are at least half of the key muscles below the
motor level for that side of the body. The Standards at this
if identified inhibiting factors (i.e. time allows even non-key muscle function more than 3 levels
single neurological level graded 3 or better?
pain, disuse) were not present. below the motor level to be used in determining motor
incomplete status (AIS B versus C). NO YES
NT= not testable (i.e. due to
NOTE: When assessing the extent of motor sparing below
immobilization, severe pain such that the level for distinguishing between AIS B and C, the motor AIS=C AIS=D
the patient cannot be graded, level on each side is used; whereas to differentiate between
AIS C and D (based on proportion of key muscle functions If sensation and motor function is normal in all segments, AIS=E
amputation of limb, or contracture with strength grade 3 or greater) the single neurological Note: AIS E is used in follow-up testing when an individual with
of >50% of the range of motion). level is used. a documented SCI has recovered normal function. If at initial
testing no deficits are found, the individual is neurologically
intact; the ASIA Impairment Scale does not apply.

FIG 6.1â•… Continued

FIG 6.2â•… The surprise finding of knife wounds upon examination of the posterior
neck and the trunk.
6 • Injury to the spine and spinal cord • A. Spinal injury 101

• The cervical spine should be cleared or an injury

diagnosis made (see below). Many hospitals have
developed their own imaging pathways, depend-
ing on their resources and systems (see below).
• Further investigations will need to be done to
assess the patient’s fitness for surgery andâ•›/â•›or
check for other co-morbidities.
Clinical case studies 6.1, 6.2 and 6.3 will aid
pattern recognition.


A 68-year old female felt dizzy while getting up to go

to the toilet in the middle of the night and collapsed,
hitting the back of her head on the floor. She was
neurologically intact, with some mild upper midline
neck tenderness. A single plain lateral cervical X-ray
appeared normal, but the sagittal CT reconstruction
showed the fracture (Fig 6.3)
The history alone should alert the doctor to the
possibility of a dens fracture. The vast majority of
patients with dens fractures have no neurological
impairment. Dens fractures may not be seen on the
lateral cervical X-ray but are more often diagnosed on
the odontoid ‘open mouth’ view. They may also be
missed on the axial CT cuts, especially if the axial
cuts are not fine enough, as this is in the plane of
the injury. In some cases, the fracture may be seen
only on the sagittal CT reconstruction.

FIG 6.3â•… CT sagittal reconstruction image of a Type II

dens fracture.

A 70-year-old male overbalanced and fell off a

stool when reaching for something in an overhead
cupboard, hitting his forehead on the cupboard door.
He had a laceration on his forehead and complained
of weakness and dysaesthesia in both upper limbs.
Examination revealed muscle weakness of grade 3–5
in his hands, but normal shoulder power. A lateral
X-ray and a CT scan (Fig 6.4) showed no bony
injury, but there were generalised degenerative
With the history alone the doctor should already
be considering the triad of spinal canal stenosis,
hyperextension injury and central cord syndrome.
A dens fracture should also be considered. The
examination findings confirmed that the patient had
developed a central cord syndrome. The plain X-rays
and CT scans show spinal canal stenosis, with
contributions from a congenitally narrow canal with
short pedicles and superimposed degenerative
changes (facet osteophytes, ligamentum flavum
hypertrophy, disc dessication). The MRI (Fig 6.5)
shows a spinal cord injury and loss of space for
cerebrospinal fluid (CSF) around the swollen cord. FIG 6.4â•… CT sagittal reconstruction image of a
degenerative spine.

clearance practices that were relevant to all emer-

gency centres, from the smallest rural centre to the
largest major trauma centre (Fig 6.6a). This simple
algorithm was further developed in the Victorian
State Trauma Service cervical spine clearance policy
(see <www.health.vic.gov.au/trauma/publications/
cervical_spine_guidelines.pdf>). Some trauma cen�
tres, a significant number of smaller hospitals and
hospitals in the developing world still rely solely on
plain radiographs, but whether the health service
uses plain X-rays or CT, the principles of the algo-
rithm are still applicable. It should be remembered,
however, that an algorithm is just a guide and not a
substitute for thorough clinical assessment and good
clinical judgment.
There are two evidence-based guidelines for
clearing the cervical spine: the National Emergency
X-Radiography Utilization Study (NEXUS) guide-
lines (Box 6.1) and the Canadian Cervical Spine
FIG 6.5â•… T2-weighted MRI sagittal reconstruction Rules (CCR) (Fig 6.6b). These are discussed in
image of a central cord injury. The arrow indicates Stiell et╯al who favour CCR for alert patients in
spinal cord signal change.
stable condition.3
There should be a high index of suspicion for
cervical spine injury in patients who present with
CASE STUDY 6.3 minor mechanisms of injury but have degenerative
spine disease, regardless of their level of pain. We
A 20-year old male had his neck wrenched to the have recently shown that there is a higher risk of
side when he collided with another player while discoligamentous injury in this group.4 As a result
going up for a mark during a football game. He of the increasing longevity of the population, the
developed immediate pain down his arm, with
numbness and pins and needles going down his numbers of such cases are increasing in frequency.
arm to his thumb. He did not think he had any
weakness. By the time he reached hospital a few
hours later the symptoms had largely resolved;
he just had some residual numbness at the tip of In many major trauma centres, plain X-ray has been
his thumb. A CT scan and an MRI scan were
superseded by CT, but X-ray is still a very useful
With the history alone the doctor should be technique as it is less expensive, has a smaller 
considering a ‘stinger’—a traction neuropraxia of a radiation dose and is often quicker and more acces-
nerve root. C5–6 is a common level for this injury, sible than CT. The various imaging modalities each
being the most mobile segment of the cervical spine.
The natural history is usually resolution of mainly
sensory symptoms over 24 hours and the MRI is
normal. BOX 6.1â•… The National Emergency
X-Radiography Utilization Study (NEXUS)

CLEARANCE OF THE CERVICAL SPINE Cervical spine radiography is indicated for patients
with trauma unless they meet all of the following
All trauma patients should be treated with a high criteria:
index of suspicion for a suspected cervical spine • No posterior midline cervical-spine tenderness
• No evidence of intoxication
injury. This involves taking spinal precautions, • A normal level of alertness
including laying trauma patients flat in a hard collar • No focal neurologic deficit
until the cervical spine is investigated and cleared • No painful distracting injuries
of any injury. We developed an algorithm to reflect
6 • Injury to the spine and spinal cord • A. Spinal injury 103

FIG 6.6aâ•… Algorithm for the assessment of the cervical spine in trauma.

FIG 6.6bâ•… Canadian Cervical Spine Rules. These apply to alert (GCS = 15) and stable
trauma patients where cervical spine injury is a concern.

have their strengths and weaknesses, which are  injuries (which will display mal-alignment of the
discussed below. The relevant radiological features spinous processes) may be seen, but the diagnosis
to identify are fractures, mal-alignment, markers of will usually already have been made on the lateral
(ligamentous) instability, and spinal cord pathology. X-ray. The odontoid, or open-mouth view (Fig 6.9),
will usually show all three types of odontoid fracture
Plain X-ray very well and is helpful for assessing the stability of
The traditional five-views series is now rarely per- atlas (Jefferson-type) fractures (Fig 6.10). The two
formed, but an adequate lateral film (Fig 6.7) is oblique views (Fig 6.11) will show facet injuries
useful in ruling out the vast majority of significant quite well and can also be useful for assessing align-
injuries. An adequate lateral film should extend to ment across C7–T1, if this area is not shown clearly
T1. If you cannot see down to T1, a swimmer’s  by the lateral andâ•›/â•›or swimmer’s view.
view may be required. A lateral X-ray is also used The assessment of the cervical radiograph should
to follow the progress of healing by checking the be done systematically by examining ABCDEF in
alignment of the spine during treatment. The antero- turn, as follows:
posterior view (Fig 6.8) adds only a little more infor- Alignment (Fig 6.12)
mation: lateral mass fractures and unilateral facet Bones (Fig 6.13)
6 • Injury to the spine and spinal cord • A. Spinal injury 105

FIG 6.7â•… X-ray of normal cervical spine: lateral view.

FIG 6.8â•… X-ray of normal cervical spine: anteroposterior


FIG 6.10╅ X-ray of unstable Jefferson fracture: >╛9╯mm

FIG 6.9â•… X-ray of normal cervical spine: odontoid view. of displacement of lateral masses.

a b

FIG 6.11â•… X-ray of normal cervical spine: a. left oblique view; b. right oblique view.

Cartilage and intervertebral disc spaces (Fig CT scan

6.14) Each pathology you can identify on X-ray is more
Dens (odontoid process) (Fig 6.15) readily seen on CT, which has now become the
Extra-axial soft tissues (pre-vertebral soft tissues) imaging modality of choice for a complete assess-
(Fig 6.16) ment of acute bony injuries. The images are acquired
Facet joints (Fig 6.17) in the axial plane (Fig 6.19), but the advent of sagit-
Lateral flexion-extension views (Fig 6.18) are not tal reconstructions (Fig 6.20) has made things easier
required in the acute assessment of trauma and to interpret. The interval of the slices should be
should only ever be done actively by the patient and 3╯mm or less for accuracy, otherwise the scan may
not with someone else holding the patient’s head. miss fracture lines parallel to the slice. It makes
These views can still be useful when there is a sus- assessing the three columns described by Denis5
pected subacute ligamentous injury, providing there (anterior, middle and posterior: Fig 6.21) straight-
is minimal pain. The patient must have a good range forward. Any injury involving two or more columns
of motion for the X-ray to be meaningful, and so it should be considered unstable. During later follow- 
is more useful as a follow-up investigation. up of the patient, CT is excellent for assessing bony
6 • Injury to the spine and spinal cord • A. Spinal injury 107


FIG 6.12â•… Assessment of cervical radiograph: FIG 6.13â•… Assessment of cervical radiograph: vertebral
alignment. A = anterior vertebral line. B = anterior spinal bodies, lateral masses, facet joints and spinous
line. C = posterior spinal line. D = spinous processes. processes.

FIG 6.14â•… Assessment of cervical radiograph: FIG 6.15â•… Assessment of cervical radiograph: dens
intervertebral disc space. (odontoid process). Note that the distance between the
odontoid process and the anterior arch of the atlas
(small oval outline) is normally <╛3╯mm.
FIG 6.16â•… Assessment of cervical radiograph: anterior FIG 6.17â•… Assessment of cervical radiograph: facet
border of the prevertebral soft tissues (long line). joints.

a b

FIG 6.18â•… X-ray of normal cervical spine: a. normal flexion view; b. normal extension view.
6 • Injury to the spine and spinal cord • A. Spinal injury 109

FIG 6.20â•… CT scan of normal cervical spine: sagittal

FIG 6.19â•… CT scan of normal cervical spine: axial
(mid-spine) view: a. vertebral body; b. cut through the
vertebral body and the facet joints.

union and for checking the position of any implants patient may have also been scanned to rule out 
or fusion mass. CT is particularly useful at C0–2 head, pelvis, thoracolumbar spine and abdominal
(the occipito-atlanto-axial area) and at C7–T1, trauma.
which are difficult levels to assess on plain X-ray.
CT cannot, however, assess stability in the erect MRI scan
posture and pick up the ‘unstable’ facet fracture seen MRI clearly shows the spinal cord, neural structures,
by one vertebrae slipping forward on another. One soft tissues and ligaments. The sagittal plane of
drawback is the amount of radiation delivered, imaging is a useful image for the clinician. A further
which is higher than the amount for a plain radio- advantage of MRI is that there is no radiation expo-
graph. This may be acceptable for an isolated assess- sure for the patient. MRI is also an excellent modal-
ment of the cervical spine, but the accumulated ity to assess the soft-tissue structures and, along
radiation dose may be of concern by the time a with CT, has supplanted the requirement for acute

FIG 6.21â•… Anterior, middle and posterior columns: a. the entire vertebral segments, showing the annulus fibrosis
(AF) of the intervertebral disc, the anterior longitudinal ligament (ALL), the posterior longitudinal ligament (PLL), the
interspinous ligament and the supraspinous ligament (SSL); b. the anterior column, comprising the anterior half of
the vertebral body and adjacent disc and the ALL; c. the middle column, comprising the posterior half of the
vertebral body and disc and the PLL; d. the posterior column, comprising the facet joints, laminae, spinous
processes, interspinous ligaments and the SSL.

flexion–extension images to assess for instability. ‘neck strain’: usually no abnormality or only mild
The clinical significance of lesions in the soft tissues oedema in the soft tissues and interspinous liga-
and ligaments is still under investigation. MRI ments is seen on the MRI scan.
remains the second-line examination after CT but is When assessing the MR images, it is helpful first
definitely indicated if the patient has neurological to examine the T2-weighted image (Fig 6.23), where
symptoms or signs. MRI should be done urgently in the CSF signal is white, as this provides the best
the case of a suspected spinal cord injury, particu- contrast for examining the ligaments such as the
larly if there is progressive neurology. It is also anterior longitudinal ligament (ALL), the posterior
useful in ruling out or confirming significant liga- longitudinal ligament (PLL) and the ligamentum
mentous, disc or facet capsule injury, which may be flavum, which show up as dark lines and will be
suspected by ‘widening’ on the CT scan (Fig 6.22). discontinuous if ruptured. The T2-weighted image
MRI is also done on an outpatient basis when there will also show any oedema in the spinal cord as a
is persistent midline cervical tenderness. The vast high-intensity signal. Secondly, the short T1 inver-
majority of these patients have ‘whiplash’ injury or sion recovery (STIR) image (Fig 6.24) should be
6 • Injury to the spine and spinal cord • A. Spinal injury 111

FIG 6.22â•… a. Sagittal CT scan showing widened facet
joint (arrow). b. Axial MRI (STIR) showing widened
discâ•›/â•›facet due to disrupted discâ•›/â•›capsule (arrow).

FIG 6.23â•… MRI of normal cervical spine: T2-weighted FIG 6.24â•… MRI of normal cervical spine: STIR image.


It is easy to memorise a list of treatments for a 
given condition, but having clinical perspective,
understanding the underlying principles and making
rational decisions are what makes a good clinician.
The clinician may not have encountered the particu-
lar spinal injury previously, but should be able to
work from first principles and then consult more
experienced practitioners at the earliest opportunity.
Pattern recognition is also very helpful in assessing
these injuries.
A categorisation of cervical injuries is presented
with an emphasis on the clinical perspective, includ-
ing the significance of the injury, what should not be
missed and the recommended treatment. Many inju-
a ries may be treated by external stabilisation in an
orthosis or brace. If a cervical hard collar is not avail-
able at the scene of the accident, the head may need
to be immobilised in the neutral position between
two sandbags and taped to the spine boardâ•›/â•›trolley.
See Chapter 8 for a discussion of particular orthosesâ•›/â•›
braces. Unfortunately, space does not permit more
detail on the epidemiology and pathophysiology, but
further information can be found in any spinal injury
textbook (see Further Reading at the end of this

Occipital condyle (C0) fracture

Classification: Anderson and Montesano6 types
I–III (Fig 6.26).
Mechanism: Compression or distraction.
Perspective: Most of these are bony injuries and
most are undisplaced (if they are displaced most do
not survive). If the risk of displacement is high, the
potential for severe neurological deficit is high. The
high-grade lesions are usually associated with severe
traumatic brain injury.
Treatment options: Orthosis, posterior occipitocer-
vical fusion.

FIG 6.25â•… MRI of cord haematoma STIR whiplash: Atlanto-occipital (C0–1) dislocation
a. T2-weighted image; b. T1-weighted image.
Classification: Traynelis8 types I–III (Fig 6.27).
Mechanism: Distraction or extension with rotation.
examined. Oedema around the disc and ligamentous Perspective: This is a very unstable, ligamentous
ruptures, facet capsule injuries and erector spinae injury and the commonest cause of death in high-
tears will display a high-intensity signal. Lastly, if velocity trauma. It is measured by the Powers ratio
there is a cord injury, haematoma will show up as (Fig 6.28), but most often identified by seeing dis-
an additional high signal in the T1-weighted image traction between C0 and C1 and sometimes C2.
(Fig 6.25). Once diagnosed, the patient should be immobilised
6 • Injury to the spine and spinal cord • A. Spinal injury 113

FIG 6.26â•… Anderson and Montesano classification of occipital condyle fractures. (Based on Canale ST & Beaty JH,7 Fig 35-25.)

FIG 6.27â•… Traynelis classification of occipitocervical dislocation. (Based on Traynelis VC et al8, Fig 2.2.)

intact, resulting in the rotation of C1 on C2, with the

dens being the axis of rotation. Traumatic atlanto-
axial subluxation or dislocation in the sagittal
(flexion–extension) plane is exceedingly uncom-
mon, because for this to occur the alar ligament must
be ruptured. It is much more common in rheumatoid
arthritis due to inflammatory destruction of the alar
Treatment options: Cervical traction reduction,
then halo-thoracic vest, posterior C1–2 fusion.

Atlas (C1) fracture

Classification: Jefferson11 types I–III (Fig 6.30).
Mechanism: Axial compression.
Perspective: This is a burst injury of C1. While it is
FIG 6.28â•… Powers ratio. (Based on Hosalkar HS41.) a bony injury, in the most unstable case (type III) the
alar ligament is rendered unstable because of the
position of the fractures (see Fig 6.10). This is
uncommon, but if it does not heal or stabilise with a
immediately with a halo-thoracic vest. Cervical trac- strong soft-tissue scar, atlanto-axial subluxation in
tion should NOT be used. flexion–extension movements may occur.
Treatment options: Posterior occipitocervical Treatment options: Orthosis, halo traction, poste-
fusion. rior C1–2 fusion.

Atlanto-axial (C1–2) rotatory subluxation Odontoid (C2) fracture

Classification: Fielding and Hawkins10 types I–IV Classification: Anderson and D’Alonzo12 types
(Fig 6.29). I–III (Fig 6.31).
Mechanism: Rotation. Mechanism: Flexion (anterior displacement) or
Perspective: This is uncommon in trauma and is extension (posterior displacement).
much more commonly seen presenting as torticollis Perspective: The type II injury is very common in
in children. While it is a ligamentous injury, the elderly patients and notable for its high bony non-
most important ligament (the alar ligament) remains union rate. However, the rate of a ‘stable fibrous

FIG 6.29â•… The Fielding and Hawkins classification of atlanto-axial subluxation. (Based on Canale ST and Beaty JH,7 Fig 35-23).

FIG 6.30â•… Jefferson classification of atlas fractures: a. Axial view of stable Jefferson
fracture (transverse ligament intact); b. Axial view of unstable Jefferson fracture
(transverse ligament ruptured). (Based on Canale ST and Beaty JH,7 Fig 35-26a & b.)

FIG 6.31â•… Anderson and D’Alonso classification of dens fractures. (Based on Canale ST and Beaty JH,7 Fig 35-1.)
6 • Injury to the spine and spinal cord • A. Spinal injury 115

union’ with non-operative treatment is quite high. Perspective: In principle this is a great classification
Hence, treatment is very controversial because it for allowing us to understand these injuries because
raises the question of ‘does it matter?’, if the func- it is mechanistic, but it is difficult to remember and
tional outcome is reasonable. This is especially per- impractical to use in clinical practice. It provides 
tinent in the elderly patient with this injury, where us with a framework for understanding the most
fibrous healing is common. Lastly, a warning: common injury patterns. Injuries are most common
‘beware the os odontoideum’ (Fig 6.32), which may at the C5–6 level. This makes sense, as it is the most
mimic a type II fracture although it is thought to be mobile part of the cervical spine.
most likely due to a developmental anomaly.
Treatment options: Orthosis, halo-thoracic vest,
anterior C2 screw, posterior C1–2 fusion.

Traumatic spondylolisthesis of C2
(hangman’s fracture)
Classification: Levine and Edwards13 types I–III
(Fig 6.33).
Mechanism: Combinations of extension with com-
pression, flexion with distraction, or flexion with
Perspective: This is actually not a common injury
in hanging! Type III, with dislocation of the C2–3
facet joints and rupture of the C2–3 disc, is what this
injury was named after, as the C2 slides forward on
C3. It is the most unstable type and the least common!
The rest are mainly bony injuries across the pedicles
that heal very well with non-operative treatment if
they are not or only minimally displaced.
Treatment options: Halo vest, anterior C2–3 cervi-
cal discectomy and fusion, posterior C2–3 open
reduction and fusion.

Fractures and dislocations in the

subaxialâ•›/â•›lower cervical spine (C3–C7)
Classification: Allen and Ferguson14: six mecha-
nisms. FIG 6.32â•… CT scan of os odontoideum.

FIG 6.33â•… Levine and Edwards classification of hangman’s fracture. (Based on Canale ST
and Beaty JH,7 Fig 35-33.)

FIG 6.35â•… CT scan of an endplate-only, or crush,

fracture: sagittal view.
FIG 6.34â•… Radiograph of a teardrop fracture: lateral

compressionâ•›/â•›wedge fractures through to the two-

column stage 3 burst fracture (Fig 6.36a & b), which
The six mechanisms are as follows: usually occurs at C5, C6 or C7. The burst fracture
1.╇ Compressive flexion stages 1–5 can sometimes be treated in a halo-thoracic vest but
These are exemplified by the stage 4 or 5 teardrop often requires surgical treatment (anterior partial
fracture (Fig 6.34), which usually occurs at C4, C5 and fusion).
or C6. The fracture fragment is actually larger than 3.╇ Distractive flexion stages 1–4
a teardrop! The plane of injury extends out through These are exemplified by stage 2 or 3 unilateral (Fig
the posterior elements, either through the ligaments 6.37) or stage 4 bilateral facet dislocation (Fig 6.38),
and facets or through the bone as facet or pedicular which usually occurs at C5–6 or C6–7.
fractures, making it a three-column, very unstable Dislocated facets (Fig 6.39a) are described as
injury. This injury is always accompanied by com- ‘perched’ when the facet joint is distracted and the
plete quadriplegia, which virtually never recovers. two edges are sitting tip to tip (Fig 6.39b), or
Remember you are seeing only the resting position ‘jumped’ when the inferior facet above has ‘jumped’
of the spine after the bones have gone back into place; over and in front of the superior facet below, and
there has obviously been significant displacement at can become ‘locked’ (Fig 6.39c) in that position. As
the time of injury. The teardrop fracture requires a rule of thumb, if you see a 25% slip forward of
surgical treatment (anterior corpectomy and fusion). one vertebrae on another, you should assume a uni-
Corpectomy is an excision of the vertebral body. lateral facet injury until proven otherwise, and like-
2.╇ Vertical compression stages 1–3 wise a bilateral injury if there is a 50% slip. We
These are exemplified by a one-column endplate- consider a bilateral facet joint dislocation with
only fracture (Fig 6.35), and from anterior normal or near normal (e.g. nerve root only)
6 • Injury to the spine and spinal cord • A. Spinal injury 117

FIG 6.37â•… CT scan of a unilateral facet dislocation:
a. sagittal view; b. axial view.
FIG 6.36â•… CT scan of a burst fracture: a. sagittal view;
b. axial view.

FIG 6.39aâ•… CT scan of facet dislocation: sagittal view.

neuro�logy to be a surgical emergency because the
spine is very unstable and the patient has so much
to lose if the vertebrae displace more. However,
before any treatment at all, a MRI is mandatory to
check for loose disc fragments—if there are any,
there is a risk that any reduction manoeuvre (closed
or open) will send the fragments back into the canal
and compress the cord. This situation requires surgi-
cal removal of the disc before any reduction, whether
this is by a closed manipulation technique or by an
open approach. The open operation requires an addi-
tional posterior approach and manual reduction of
the facets under vision, a technique followed by
fixation and fusion. This is a so-called ‘front and
back 360-degree’ operation. If there is no loose disc
fragment, reduction may be undertaken closed (in
b traction or with manipulation), and treatment can
continue with a halo-thoracic vest or an anterior or
FIG 6.38â•… CT scan of bilateral facet dislocation: posterior fusion.
a. sagittal view; b. axial view.
6 • Injury to the spine and spinal cord • A. Spinal injury 119

FIG 6.39bâ•… CT scan of facet dislocation: perched facet.

4.╇ Compressive extension stages 1–5

FIG 6.39câ•… CT scan of facet dislocation: jumped facet.
These are exemplified by isolated undisplaced
lamina, pedicle or facet fractures, through to the
stage 5 fracture–dislocation (Fig 6.40). A fracture–
dislocation is the most potentially unstable of all of the stenosis (narrowness) of the spinal canal can
injuries, because even after reduction there is no be narrowed even more if there are associated
inherent stability. Think about the modicum of sta- degenerative changes. These should be considered
bility afforded by reduced but unbroken facets. as very unstable three-column injuries until instab�
These injuries require anterior and posterior fusion. ility can be ruled out, because of the stiffness and
5.╇ Distractive extension stages 1–4 long lever arms of the surrounding spine in these
These are exemplified by the anterior opening of a conditions. Any patient with ankylosing spondylitis
disc ‘fracture’ in patients with ankylosing spondyli- and a cervical spine fracture should be immobilised
tis (Fig 6.41), diffuse idiopathic skeletal hyperosto- immediately in a halo-thoracic brace in their ‘normal’
sis (DISH) or Forrestier’s disease, or disc rupture in position (of neck ankylosis). Sometimes these inju-
degenerative cervical spines. Unfortunately these ries can be treated in a halo-thoracic vest alone but
are often associated with neurological injury because they often require anterior ± posterior fusion.

a b
FIG 6.40â•… Fracture–dislocation: sagittal view. a. Lateral radiograph; b. MRI scan.

6.╇ Lateral flexion of the spinous process that can also occur in the
These injuries are very rare and represented by an upper thoracic spine. Treatment is symptomatic.
asymmetric vertebral body crush with unilateral 2. transverse process fracture with extension into
facet injury. the foramen transversarium (Fig 6.43). The con-
Of all the unstable injuries in the subaxial spine, troversy is not about treatment of the fracture
the commonest is a facet fracture, followed by facet (symptomatic) but about any occult injury to the
dislocations, then burst and then teardrop injuries. vertebral artery. Most major trauma centres have
Most of these require surgical treatment, apart from a protocol for further angiographic investigation
the undisplaced facet fracture, which heals very well when any of these fractures are detected (see
in a halo-thoracic vest, because once the bone heals Chapter 7). If there is any evidence of vertebral
completely it will be as strong as normal bone. artery injury, the patient should be anticoagulated
to prevent the occurrence of stroke, which is rare
Stable injuries in the subaxial–lower but devastating when it does occur.
cervical spine (C3–C7)
Other bony injuries include spinous process and Ligamentous injuries in the subaxialâ•›/â•›lower
transverse process fractures, which can be treated cervical spine (C3–C7)
with an orthosis. Two special cases to mention Anterior longitudinal ligament and disc ruptures
include: (Fig 6.44) have been mentioned above, but it should
1. C6 or C7 spinous process (clay shoveller’s) frac- be emphasised that they are very uncommon in the
ture (Fig 6.42), a hyperextension avulsion fracture normal spine. They occur when the affected spinal
6 • Injury to the spine and spinal cord • A. Spinal injury 121

a b

FIG 6.41â•… CT scans of ankylosing spondyltic ‘disc fracture’: a. mid-sagittal view, showing opening of the C56 disc
space (arrow); note the ankylosis of the vertebrae and fusion of the dens to the arch of atlas; b. lateral sagittal view,
showing extensive fracture at C56 of the vertebral body and posterior elements (arrow); c. further lateral sagittal
view, showing fracture across the facet joint (arrow).
FIG 6.43â•… CT scan of a transverse processâ•›/â•›lateral
mass fracture extending into the foramen

FIG 6.42â•… CT scan of a ‘clay shoveller’s fracture’:

sagittal view (arrow).

FIG 6.45â•… CT scan of late posterior instability after

ligamentous injury: sagittal view.

FIG 6.44â•… MRI (STIR) of disc rupture: sagittal view.

6 • Injury to the spine and spinal cord • B. Traumatic spinal cord injury 123

4. Have a high index of suspicion for cervical spine

injury in the patient with a degenerative spine.
5. An adequate cervical spine X-ray must show the
vertebrae down to the level of T1.
6. Use CT scans to delineate bony injury.
7. Use MRI to delineate soft tissue and spinal cord
8. Bony injuries heal well.
9. Ligamentous injuries do not heal as well as bony
injuries and may develop late instability.


Traumatic spinal cord injury (SCI) is a severe
disease process and can result in significant morbid-
ity, disability and mortality. In Australia, there are
14.9 new cases of traumatic SCI reported per million
population aged 15 years and older.15 This amounts
to approximately AU$2 billion spent per year for
FIG 6.46â•… MRI (STIR) of ‘whiplash’: sagittal view. treatment of this population.16 The USA spends
almost five times as much, at US$ 9.7 billion a year,
for about 11,000 new cases of SCI a year.17 Causes
segment is the ‘weakest’ part of the spine due to in a descending order include motor vehicle acci-
adjacent stiff (ankylosed) arthritic segments. dents, assaults, falls and recreational activities.18
Remembering that ligaments never heal to their
original strength and that the adjacent ankylosed PATHOPHYSIOLOGY
arthritic segments do not change, these injuries
usually require anterior fusion because of the risk of Primary traumatic injury of the spinal cord occurs
late instability when they do not heal or heal poorly. with direct compression, tearing or stretching of the
Isolated ruptures of the ligamentum flavum ± neural elements and disruption of the blood supply
interspinous ligament are not very common either. of the spinal cord due to fractured and displaced
The challenge is to predict which patients may bone fragments, disc material and ligament injuries.
develop late instability (Fig 6.45) because the healed This leads to varying components of spinal cord
soft tissue is not strong enough. The patients at risk haemorrhage, oedema, infarction and mechanical
of this are those with a degree of ligamentous laxity. discontinuity. Secondary injury to the spinal cord
‘Whiplash’ is non-medical term that describes  results from systemic hypoxia and hypotension.
the acceleration–deceleration injury associated with These cause ischaemia of the spinal cord. Cellular
neck pain. It used to be a diagnosis of exclusion but processes are set in train, which ultimately result in
now includes ‘findings’ such as high intensity on the loss of neurons and their connections within the cord
STIR MRI (Fig 6.46), which is thought to represent and brain.
muscle oedema. Why some patients have persistent
pain is largely unknown but thought to be multifac- EVALUATION AND DIAGNOSIS
torial, and the treatment remains symptomatic.
Traumatic SCI should be suspected in an individual
with multi-system trauma andâ•›/â•›or sensory or motor
KEY POINTS symptoms and signs. These patients should be
1. Listen to the patient—a good history puts you at treated with full spinal precautions and rigid cervical
least halfway to the diagnosis. collars while the primary and secondary trauma
2. Examine the patient and you are three-quarters surveys are carried out.
there (and will have no surprises!). Hypoxia and hypotension must be corrected vig-
3. Use investigations to confirm your diagnosis and orously in a patient with suspected SCI, because an
prepare your patient for surgery. incomplete or partial lesion of the spinal cord may

be aggravated or the patient with an incomplete provides the clinician with a tool for assessing a
lesion may be or tipped to a complete SCI. patient’s initial neurological status and predicting a
Loss of sympathetic innervation of the cardiovas- patient’s functional outcome, a scheme for grading
cular system from a T6 or higher cord lesion will a treatment’s efficacy and a communication tool.
result in loss of vascular tone and a reduced cardiac The ASIA scale (see Fig 6.1 and Appendix F)
venous return, causing hypotension. There is also an features two main components: a motor and a sensory
associated relative bradycardia. This is known as evaluation. The scale assesses the motor function of
neurogenic shock. The patient has a warm and pink 10 muscles on each side of the body from C5 to T1
well-perfused periphery. Inotropic support and ade- spinal segments in the upper limbs and from L2 to
quate volume loading and maintenance are crucial S1 spinal segments in the lower limbs. These are
at this point to ensure adequate end-organ perfusion. graded from 0 to 5 and are as follows:
The cord lesions above C5 will compromise dia- 0 total paralysis
phragm function and result in excessive use of the 1 muscular contraction only
accessory muscles of respiration such as the inter- 2 full range of movement with gravity
costals and the large neck muscles, which can be eliminated
seen contracting along with shallow breathing. The 3 full range of movement against gravity
male patient may also have priapism, which is mani- 4 full range of movement against gravity but
fested as a prolonged erection of the penis due to weaker than full strength
loss of autonomic function. 5 normal motor activity
Neurogenic shock should not be confused with In addition, the left and right sides are scored sepa-
spinal shock, in which the functions of the spinal rately with each limb receiving a maximum total of
cord shut down such that the patient has a flaccid 25; a score of 100 represents a person without motor
paralysis with areflexia below the level of the injury deficit. The ASIA scale also assesses light touch and
to the cord. These patients may have complete or pinprick sensation from C2 to S4–6 at key sensory
partial recovery of their neurological deficits. This points, utilising a numeric scale from 0 to 2, as
improvement may take place even up to three weeks follows:
after the initial trauma. If the descending tracts are 0 absent sensation
transected or irreparably damaged, the spinal shock 1 abnormal sensation
phase transitions to one of permanent spasticity, 2 normal sensation
hyperreflexia and a neurogenic bladder. The scale assesses the two sensory modalities of
A full neurological examination is carried out as light touch and pinprick sensation separately, thus
part of the secondary survey. This includes assess- assessing the dorsal columns and spinothalamic
ment of the upper and lower limb tone and motor systems, respectively. The system has a total of 28
function, anal sphincter tone and power (voluntary dermatomes, with the left and right sides graded
contraction of the sphincter around the gloved finger individually, thus making 224 points for a patient
in the rectum), and presence of reflexes including without sensory deficit.
limb reflexes, perineal reflexes and the bulbocaver- The ASIA impairment scale describes the func-
nosus reflex. The bulbocavernosus reflex is present tional impairment of a patient as a result of their
when there is anal contraction on manual compres- spinal cord injury. It is a tool used in follow-up testing
sion of the glans penis. of a patient to quantify improvement of neurological
An individual has suffered a complete cord lesion function. The level of SCI is based on the most caudal
if the bulbocavernosus reflex is present without any level with normal function. An injury can be broadly
sensory or motor function. In a complete cord lesion classified into complete or incomplete SCI.
the anal sphincter is atonic, with no voluntary con- A patient assessed as ASIA A has a complete SCI
traction. The sensory system is examined for a without preservation of any motor or sensory func-
sensory level with light touch and pinprick, and the tion caudal to the injury level without sacral sparing
perianal and perineal region is also examined. (absent voluntary anal contraction and presence of
The American Spinal Injury Association (ASIA) perianal anaesthesia [S4–S5]). ASIA B is an incom-
score19 was developed to aid and document the extent plete SCI with preservation of some sensation but no
of SCI (see Fig 6.1). It is currently the most widely motor function caudal to the level of injury. ASIA C
utilised scale because it is both accurate and reliable, and D are incomplete spinal cord injuries with partial
with a low inter-rater and intra-rater variability. It motor and sensory preservation caudal to the level of
6 • Injury to the spine and spinal cord • B. Traumatic spinal cord injury 125

FIG 6.47â•… Four common spinal cord syndromes.

injury. If the grading of half of the myotomes caudal having pre-existing cervical canal stenosis second-
to the level is less than 3 of 5 in terms of motor score, ary to degenerative change. The hallmark of this
the injury is classified as ASIA C; if it is greater than condition is the fact that the upper limbs are affected
3 of 5, then the patient is classified as ASIA D. ASIA more than the lower limbs. There is flaccid paralysis
E denotes a normal neurological status. and loss of pain and temperature sensations in the
upper limbs due to anterior horn damage with inter-
ruption of the more deeply placed cervical fibres of
SPINAL CORD SYNDROMES the anterolateral corticospinal tract. The lower limbs
The total absence or partial presence of motor or are spastic if the lumbar fibres of the lateral cortico-
sensory function more than three segments below spinal tract are involved. Sacral fibres are more
the level of injury defines a complete or incomplete superficial and have pial vessels supplying them
SCI. Four common incomplete spinal cord syn- and, as such, are likely to be spared.
dromes are discussed below (Fig 6.47).
Anterior cord syndrome
Central cord syndrome Anterior cord syndrome is due to anterior cord com-
Central cord syndrome is usually caused by a sudden pression andâ•›/â•›or infarction caused by anterior spinal
cervical hyperextension mechanism, with patients artery occlusion. This results in paraplegia if the

FIG 6.48aâ•… CT scan of the cervical spine, showing a FIG 6.48bâ•… MRI of cervical spine, showing the C7
traumatic C7 burst fracture with 40% loss of height of burst fracture with acute oedema within the body. The
the vertebral body. Fracture retropulsion causes 40% loss of height is appreciated with compression of
significant cervical canal stenosis. There is some the anterior part of the cord causing significant oedema
pre-vertebral soft tissue swelling at C7. and cord signal change centred at C7. Prevertebral soft
tissue hyperintensity signifying swelling is evident from
C6 to T2.

affected segments are lower than T1, or quadriplegia dorsal column interruption. There is loss of pain and
if the affected segments are higher than C7. There temperature sensation on the contralateral side, with
is also dissociated sensory loss, with loss of pain and interruption of crossed anterolateral spinothalamic
temperature sensation and preserved two-point dis- tracts.
crimination, proprioception and vibration denoting
an intact posterior column. IMAGING
Posterior cord syndrome Patients with suspected SCI require urgent imaging
Posterior cord syndrome causes burning pain and to delineate the pathology and to formulate a treat-
paraesthesia in the neck, upper arms and torso, with ment plan. A lateral cervical spine X-ray is obtained
mild paresis of the upper extremities. as part of the initial series in the resuscitation area.
Multislice CT of the spine allows assessment of
Brown-Séquard syndrome spinal column alignment and stability (Fig 6.48a).
Brown-Séquard syndrome is due to hemicord injury MRI of the neural elements is used acutely to define
or transection, and causes paralysis and loss of touch the injuries in the spinal cord and spinal nerves (Fig
and proprioception sense below the level of the lesion 6.48b). It also enables the clinician to determine
on the ipsilateral side, with lateral corticospinal and whether there is injury to the ligaments and disc.
6 • Injury to the spine and spinal cord • B. Traumatic spinal cord injury 127

halo-thoracic vests (this technique is described in

the section on spinal cord injury in Chapter 8).

Medical therapies
The mainstay of medical management for acute
traumatic SCI is the maintenance of the cord perfu-
sion by correcting shock, maintaining an adequate
blood pressure and achieving adequate oxygenation
of the spinal cord by ensuring adequate airway and
ventilation. Supportive therapies recommended at
present are as follows:
• An adequate airway and ventilation are obtained
to correct and prevent hypoxia. The patient
receives supplemental oxygen and may require
intubation at an early stage if there is inadequate
tidal volume and the arterial blood gases show
hypoxia and hypercapnia with a respiratory
• Intravenous (IV) access is obtained. Inotropic
and intravascular volume support are adminis-
tered to ensure maintenance of adequate perfu-
sion thresholds.
• A nasogastric tube is placed in the stomach to
prevent gastric and bowel distension, because
gastric stasis and paralytic ileus are common after
• The bladder is catheterised to prevent enlarging
bladder with urinary retention and overflow
FIG 6.48câ•… Postoperative CT scan of the cervical incontinence.
spine of the patient in Fig 6.48a and b, showing
a decompression of the spinal canal with a C7
• Deep venous thrombosis prevention is imple-
corpectomy and iliac crest graft in situ with plate and mented with pneumatic compression stockings,
screw augmentation. consideration of subcutaneous low-molecular
weight heparin and inferior vena caval (IVC) filter.
• Regular pressure care prevents pressure sores and
• Physiotherapy prevents atelectasis and pneumo-
nia as well as limb muscle contractures.
There has been considerable preclinical and clini-
Management principles for traumatic SCI are cal research into using methylprednisolone to treat
directed at preventing secondary injury. The spine is secondary SCI, animal studies having shown benefit,
immobilised, taking care when moving the patient with significant neurological recovery following
to maintain spinal column stability. Second, medical traumatic SCI. The timing and dose are clearly criti-
treatment is administered to prevent or lessen sec- cal factors. Its use in human SCI remains controver-
ondary cord injuries and to anticipate and treat the sial. The National Acute Spinal Cord Injury Study
complications of SCI. Third, surgery is directed at (NASCIS) trials are large, prospective, randomised
decompression of the acutely injured spinal cord and trials that have been carried out to elucidate the effec-
stabilisation of fracture dislocations of the spine  tiveness of steroids, in particular methylprednisolone
(Fig 6.48c). in the treatment of SCI. To date they have shown
Some unstable fracture dislocations of the cervi- small statistical benefits in terms of neurological
cal spine require traction using skull tongs such  recovery that have not been translated into significant
as the Crutchfield or Gardner-Wells tongs to reduce functional recovery, with severe adverse effects
the deformity prior to surgery or placement of reported in the trials.

TABLE 6.1â•… Findings of the National Acute Spinal Cord Injury Study (NASCIS) trial22–27

Trials Intervention Outcomes

NASCIS I 330 patients were randomised to • No differences in clinical improvement were observed between the
(1984) receive either 25╯mg or 250╯mg two groups.
of methylprednisolone sodium • The high-dose group demonstrated a significantly higher incidence of
succinate (MPSS) every 6 hours for wound infection (Pâ•›=â•›0.01) and a trend towards increase sepsis,
10 days after a 100╯mg bolus. pulmonary emboli and death (not statistically significant).
NASCIS II 487 patients were randomised to • No differences were observed in neurologic outcomes between the
(1990) receive either high-dose MPSS, three groups.
naloxone or a placebo given • Twice as many pulmonary emboli and wound infections were seen in
through a 24-hour period after SCI. the steroid group compared with controls (not statistically significant).
• In post-hoc analyses, patients treated with MPSS within 8 hours of
their SCI showed a statistically significant improvement in motor and
sensory scores at 6 months, but this effect persisted for motor scores
only at 1 year.
• While a mean improvement of 5 points on the motor grading scale
was reported for total right-sided scores, when distributed over two or
three muscle groups, an improvement of 1–2 points in an individual
muscle, particularly one of grade 0 strength, becomes of questionable
functional significance.
NASCIS III 499 patients were randomised to • There were no differences between any of the groups with respect to
(1998) receive either 24 hours of MPSS, primary outcome measures such as motor, sensory or functional
48 hours of MPSS or 48 hours of independence measure (FIM) scores at the 1-year endpoint.
tirilazad mesylate. • In post-hoc analyses, patients treated with the 48-hour MPSS
protocol between 3 and 8 hours after injury had slightly better motor
scores than the 24-hour MPSS group at 6 weeks and 6 months.
• Statistically significant neurologic recovery was attained, but
differences in FIM recovery were relatively small and represented
self-care and mobility rather than actual locomotion.
• Severe pneumonia afflicted twice as many patients, while severe
sepsis was contracted by four times as many patients in the 48-hour
MPSS group compared with the 24-hour group. Six times as many
patients died from respiratory complications in the 48-hour MPSS
group (Pâ•›=â•›0.056).

TABLE 6.2â•… Methylprednisolone dosing for acute SCI

more consistent than any suggestion of clinical
benefit (Tables 6.1 and 6.2).
Methylprednisolone Time after SCI The Canadian Neurosurgical Society, the Cana-
dosing 0–3 hours 3–8 hours dian Spine Society and the Canadian Association of
Loading 30╯mg╛/╛kg 30╯mg╛/╛kg Emergency Physicians have adopted their commit-
(over 15╯min) (over 15╯min) tee’s recommendation that a high-dose, 24-hour
Maintenance 5.4╯mg╛/╛kg╛/╛hr 5.4╯mg╛/╛kg╛/╛hr infusion of methylprednisolone started within 8
Duration 24 hours 48 hours hours after an acute closed SCI is not a standard
Note: Steroids are not recommended if more than 8 hours have elapsed treatment nor a guideline for treatment but, rather, a
since the SCI.
treatment option, for which there is weak level II
and III evidence.21
In the Alfred Hospital, Melbourne, we do not
recommend the use of methylprednisolone for
The American Association of Neurological Sur- patients with acute SCI. Other therapies, including
geons (AANS)â•›/â•›Congress of Neurological Surgeons Tirilazad, Naloxone and GM-1 ganglioside, have yet
(CNS) Joint Section on Disorders of the Spine and to show significant benefits in traumatic SCI and are
Peripheral Nerves Guidelines Committee20 con- currently not recommended for routine use.
cluded that the administration of methylpredniso-
lone for either 24 or 48 hours is an option in the Surgery
treatment of patients with acute spinal cord injuries It has been proposed that early decompression and
that should be undertaken only with the knowledge stabilisation will lessen secondary injury to the
that the evidence suggesting harmful side effects is injured spinal cord. However, the timing of surgical
6 • Injury to the spine and spinal cord • B. Traumatic spinal cord injury 129


A 23-year-old woman was a passenger involved in a

high-speed motor vehicle accident. She presented as
a tetraplegic who was in neurogenic and spinal shock
(ASIA A). She had a burst fracture of C4 (Fig 6.49a
& b) with retropulsion of the posterior vertebral body
causing spinal cord compression.
Figure 6.49a depicts cord signal change secondary
to contusion and oedema. Note the ‘step’ in the
alignment of the vertebrae at C3–4 that compromises
the spinal canal, and the swelling of the spinal cord
in the narrowed spinal canal. Note also the presence
of the endotracheal tube and the smaller nasogastric
tube posterior to it. Prevertebral swelling is displacing
the oesophagus and trachea forwards.
The patient had decompression of the spinal canal
performed with a C4 corpectomy (i.e. removal of the
fractured vertebral body) (Fig 6.49c) and replacement
of the C4 vertebral body with an iliac crest graft,
supplemented with plate and screw fixation. The
surgery was performed within 24 hours after her
admission. She did not recover any neurological
function but the surgery enabled early mobilisation
and she was discharged to a specialised SCI
rehabilitation centre a week later.

b c
FIG 6.49â•… Cervical spine of a 23-year-old woman with a traumatic C4 vertebral body fracture and spinal cord
compression and damage: a. preoperative MRI; b. pre-operative CT scan; c. postoperative CT scan.

decompression and internal fixation of the injured modest hypothermia (33°) was used for 48 hours to
spine remains controversial. Advances in MR treat acute traumatic SCI in 14 patients.29 The results
imaging, intensive care management and the techni- showed an improvement of one or more Abbrevi-
cal aspects of complex spine surgery have resulted ated Injury Scale (AIS) grades without any adverse
in the more frequent performance of decompression effects when compared to the normothermic group.
and fixation of the spine, even for patients with Cappuccino et╯al recently reported on an American
complete cord lesions. This enables rapid mobilisa- Football player who suffered a C3â•›/â•›4 fracture dislo-
tion of the patient and the commencement of early cation with spinal cord compression; the player went
rehabilitation. Complications of the bedridden, from an ASIA A rating, or complete cord injury,
immobilised patient are thus avoided. below the deltoids (bulbocavernosus reflex was
It remains to be determined whether acute surgery present during initial assessment, indicating that
improves neurological outcome in humans with spinal shock was over) to an ASIA D rating 4 months
acute SCI. Results from animal studies have shown after admission. Spinal cord decompression and
that neurological outcomes are improved with surgi- spinal column fixation was completed 7 hours post-
cal decompression.28 Instrumentation and surgical injury and he was treated with 48 hours of systemic
techniques to decompress and internally fix the hypothermia (33–35°).34 Despite these findings,
spine have advanced considerably in the last decade, there is no level 1 or 2 evidence guiding this treat-
and spinal surgeons are more willing to operate soon ment. Further clinical trials are eagerly awaited to
after the patient with acute cord injury is admitted. judge the efficacy of this promising therapy.
Spine surgeons will decompress an incomplete
SCI earlier than a complete injury because there is Cell transplantation
potential for greater gain. Preliminary data from the The spinal-cord-injured community is seriously
Surgical Treatment of Acute Spinal Cord Injuries seeking a biological ‘cure’ for SCI. Intense experi-
(STASCIS) trial have indicated that decompression mentation is currently proceeding in animal models
within 24 hours of injury may improve the outcome of SCI. The biology of repair of the human spinal
in patients with isolated SCI.29 cord is incredibly complex and simply placing cells
Early surgery for patients with traumatic central into a chronic SCI where there is chronic atrophy,
cord syndrome secondary to pre-existing spinal cystic degeneration and scarring will be unlikely to
canal stenosis or intervertebral disc disease (without produce significant gains in function. The small-
acute prolapse), however, is still a controversial animal research cannot automatically be extra-
topic with no clear guidelines.30 At present, treat- polated to humans. Combination strategies of cell
ment options include early decompression (within implantation, with growth factors produced by the
24 hours) and delayed decompression (6 weeks to 3 transplanted cells and various biomaterials as scaf-
months). Results from the STASCIS trial are eagerly folding for the grafted cells, may all be required for
awaited to guide treatment of this entity. some repair to succeed. Strategies to reduce second-
ary inflammation and gliosis are clearly relevant.
Immunological rejection is also a consideration when
FUTURE THERAPIES allogenic cells are transplanted. The optimal time for
transplantation remains uncertain and controversial.
Hypothermia There may be significant spontaneous improvement
Hypothermia is a potentially neuroprotective therapy in the first few months following the injury, which
for acute SCI. Hypothermia affects mechanisms could be adversely affected by the grafting proce-
involved in the pathophysiology of secondary cord dure. However, it may be preferable to do the surgery
injury (for example, slowing spinal cord tissue in the early stages following the injury before per�
metabolism) and lessens spinal cord inflammation manent scarring has developed. In addition, many
by reducing oedema, leucocyte accumulation, anti- ethical challenges are involved when embryonic or
oxidant release and apoptosis.31 Numerous animal precursor cells are to be transplanted in humans.35
studies of traumatic SCI treated with systemic hypo- Neural transplantation, variously using embry-
thermia have yielded positive outcomes, including onic neural precursor cells, embryonic stem cells,
functional recovery.32,33 amniotic-derived stem cells, bone-marrow stem
Levi AD et╯al performed a phase 1 clinical trial cells and olfactory ensheathing cells, has been taking
of safety and outcome, in which endovascular place in patients with chronic SCI for a number of
6 • Injury to the spine and spinal cord • B. Traumatic spinal cord injury 131

years. Many of these patients are desperate and SPECIAL CONDITIONS

become medical tourists willing to spend large sums
of money to secure an improvement in their plight. Spinal cord injury without radiographic
There are anecdotal reports of improvements but abnormality
few patients have been entered into well-constructed Spinal cord injury without radiographic abnormality
clinical trials. A number of clinical trials are under (SCIWORA) was defined in 1982 as objective signs
way; so far, the results have shown slight benefits in of myelopathy as a result of trauma with no evi-
some patients. dence of fracture or ligamentous instability on plain
X-rays and CT.36,37,38 It is a term that is not often
Electrical stimulation of paralysed limb used, especially in adults, because of the widespread
Two kinds of electrical simulation are being devel- use of magnetic resonance imaging (MRI) for
oped experimentally and may have roles in the trauma spine imaging. It is still used, however, in
future: direct electrical stimulation of limb muscles paediatric spinal trauma, especially in those less
with implanted electrodes on the peripheral nerves, than 9 years of age.
and stimulation of the spinal cord by implanted SCIWORA is hypothesised to occur in children
multi-electrode arrays that may be connected directly owing to their ligamentous hyperelasticity and bony
to the motor cortex of the patient’s brain. immaturity, which allow traumatic distraction and
compression of the cord, causing potential cord
REHABILITATION ischaemia. There can also be a delay in presentation
of up to 4 days (late or delayed SCIWORA). On the
Once the acute injuries have been stabilised, the SCI other hand, SCIWORA occurring in the adult popu-
patient is transferred to a spinal rehabilitation unit. lation is probably due to long-standing spinal steno-
An intensive rehabilitation program is paramount sis and intervertebral disc disease.39
for successful reintegration into the community and At present, there is no evidence that SCIWORA
for a positive long-term outcome. Most patients with dictates any need for urgent decompressive surgery.
incomplete spinal cord injuries will return to inde- The current recommendation is for conservative
pendent living following rehabilitation. Complete treatment with a rigid collar until there is no evi-
spinal-cord-injured patients, however, are less likely dence of instability of the spinal column and the
to achieve independent living. The rehabilitation  neurological impairment has stabilised.
literature recommends individualised multidisci- One meta-analysis showed that of 109 paediatric
plinary care and treatment programs to help with  patients with SCIWORA, about a third had com-
the complications of SCI (Box 6.2). Programs are plete neurological recovery. In total, about half will
available for respiratory conditioning, bowel and improve either partially or completely.38 MRI find-
bladder continence, sexual dysfunction, chronic ings of complete spinal cord transection and major
pain and long-term intrathecal analgesic administra- haemorrhage have extremely poor prospects of
tion, and functional retraining involving orthotics recovery. MRI findings of minor haemorrhage or
and adaptive equipment. Intramuscular Botox (botu- isolated cord oedema improve to a mild level of
linum toxin) and Intrathecal Baclofen are also used neurological deficit in 40% and 75%, respectively.
to treat severe ongoing spasticity. Those with normal MRI findings all attained full
neurological recovery.36 In a study of 189 patients
with SCIWORA, patients with complete SCI had
BOX 6.2â•… Traumatic SCI rehabilitation little chance of recovery (1 patient out of 19), while
95% of 170 patients with incomplete SCI attained
• Autonomic dysreflexia full neurological recovery.40
• Ventilator dependency and recurrent respiratory
tract infections High quadriplegia
• Gastric stasis and constipation An upper cervical SCI may result in a high quadri-
• Bladder and bowel incontinence and sexual plegia with a complete cord lesion at C0 to C4 while
• Pressure ulceration the patient probably remains conscious and aware.
• Pain, contracture, spasticity and skeletal deformities These patients pose an early management and ethical
• Dependence for activities of daily living dilemma. They are often young. They will be intu-
bated soon after arrival to assist with their

FIG 6.50bâ•… MRI of cervical spine STIR: sagittal image

showing near complete transection of the craniocervical
FIG 6.50aâ•… CT scan of cervical spine: sagittal image junction with cord and medulla haemorrhage. Oedema
showing a subtle bony fragment just above the tip of extends superiorly to the pontomedullary junction and
the dens. There is perhaps a slight angulation of the inferiorly to C7. There is an anterior epidural
anterior part of the arch to the tip of the dens. haematoma extending down from C2 to T2, with the
cord displaced posteriorly at these levels. There is also
damage to the posterior ligaments between C0–C1 and
C1–C2, with the hyperintensities seen at those areas.
Note the significant paraspinal tears throughout.

respiration. An early MRI scan usually shows a

severe SCI, often with extensive cord swelling, Craniocervical dissociation causing spinal
haemorrhagic infarction and an associated fracture cord transection
dislocation. These patients have minimal prospect Spinal cord transection at the craniocervical junction
of making any functional recovery and will very is associated with disruption of the atlanto-occipital
likely have a permanent complete quadriplegia, with ligaments and membrane, and a subluxation and
the need for permanent respiratory support. Man- distraction of the cervical spine away from the skull
agement of these patients is controversial and (Fig. 6.50a). At times, the occipital condyles may be
requires much discussion between family, medical fractured and displaced. This injury can be seen
staff, nursing staff and sometimes lawyers and ethi- clearly on a lateral cervical spine X-ray. An urgent
cists regarding diagnosis and prognosis. It is our MRI scan shows a complete transection of the cord
usual practice to inform the relatives of the futility at the craniocervical junction, with surrounding
of treatment once the diagnosis is confirmed on MRI haemorrhage (Fig 6.50b & c). These patients usually
scan and it is clear that the patient is not showing die at the scene because they cannot breathe, but
any signs of recovery. The patient is then palliated with very prompt first aid and paramedic care they
with eventual extubation. sometimes make it to the emergency room. They
6 • Injury to the spine and spinal cord • B. Traumatic spinal cord injury 133

4. Administration of methylprednisolone for either

24 or 48 hours is an option in the treatment of
patients with acute spinal cord injuries that should
be undertaken with the knowledge that the evi-
dence of morbidity from steroid administration
may outweigh any clinical benefit.
5. The optimal timing of surgery for acute SCI is
uncertain. Surgeons are moving towards early
decompression and stabilisation. Trial results are
6. SCI rehabilitation is essential for maximal recov-
ery and the successful reintegration of a spinal-
cord-injured patient into the community.
7. Spinal cord repair strategies show some early
promise but remain experimental and should be
conducted within clinical trials.

1. Milby AH, Halpern CH, Gui W. Prevalence of cervical
spine injury in trauma. Neurosurg Focus. 2008;25(2):
2. Sekhon LH, Fehlings MG. Epidemiology,
demographics, and pathophysiology of acute spinal
cord injury. Spine. 2001;26(suppl):S2-S12.
3. Stiell IG, Clement CM, McKnight RD, et al. The
Canadian C-spine rule versus the NEXUS low-risk
FIG 6.50câ•… MRI of cervical spine: T2 axial image criteria in patients with trauma. NEJM. 2003;349(26):
showing a haematoma within the anterior half of the 2510-2518.
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Cervical spine magnetic resonance imaging in alert,
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midline tenderness and negative computed tomography
results. Ann Emerg Med. 2011;58(6):521-530.
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three-column spine concept in acute spinal trauma.
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7. Canale ST, Beaty JH. Campbell’s operative
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SUMMARY 8. Traynelis VC, Marano GD, Dunker RO, et al.
Traumatic atlanto-occipital dislocation. Case report.  
1. Traumatic SCI is a severe disease process and  J Neurosurg. 1986;65(6):863-870.
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3. Correction of cardiovascular and respiratory 11. Jefferson E. Fracture of the atlas vertebra. Report of
four cases and a review of those previously recorded.
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normal blood pressure and blood gases is a key odontoid process of the axis. JBJS (Am). 1974;
goal. 56(8):1663-1674.

13. Levine AM, Edwards CC. Treatment of injuries in the methylprednisolone for the treatment of acute spinal
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Vascular injury
Jeffrey V Rosenfeld, Jin W Tee, Peter Hwang, Anoop Madan

also causes the formation of a thrombus, which may

A. BLUNT CAROTID AND VERTEBRAL lead to thromboembolism and transient ischaemic
ARTERY INJURIES attacks, or strokes. Figure 7.2 shows the pathology
Blunt carotid and vertebral artery injuries (BCVI) of a blunt vascular trauma injury.
are extracranial or intracranial cerebrovascular inju-
ries that are directly attributable to a known direct PRESENTATION
high-energy non-penetrating impact or torsional The clinical presentation of symptomatic BCVI
force.1 BCVI occurs in about 1% of all blunt force includes headache andâ•›/â•›or neck pain, Horner’s 
trauma patients.2 Motor vehicle accidents are the syndrome, cranial nerve palsies, cervical bruit, 
most common cause of cervical BCVI, accounting brain ischaemia, arterial haemorrhage from the 
for 41–70% of cases with other common causes ears, mouth or nose, spinal cord ischaemia or haem-
including assaults, motor vehicles versus pedestrian, orrhage.3,6 Patients with clinically silent BCVI are
falls and hanging.1 A morbidity rate of 32% and those with mild grades of BCVI due to distracting
mortality rate of 20% have been reported.3 injuries and intubated patients in whom a thorough
neurological examination is not possible. Table 7.1
PATHOPHYSIOLOGY illustrates the features of high-risk patients who
require consideration for BCVI screening with a
BCVI typically results from extreme cervical hyper-
sixteen-slice or greater computed tomographic cer-
extension or rotation, a direct vascular blow, intra-
vical and cerebral angiogram (CTA) or a four-vessel
oral trauma or direct laceration from bony fracture
digital subtraction cerebral angiogram (DSA).
fragments.4 Spine injuries are a common source of
BCVI, with the majority of vertebral artery injuries
being due to subluxations and foramen transver-
sarium fractures.5 BCVI leads to formation of trau- This is a controversial topic upon which there is no
matic pseudoaneurysms, vascular dissection andâ•›/â•›or consensus. The best evidence at present recommends
a decrease in vascular calibre (Fig 7.1). that BCVIs with luminal narrowing and dissection
Pseudoaneurysms, or false aneurysms, are blow- are considered for treatment with antithrombotic
outs in the arterial wall due to traumatic rupture of agents such as aspirin (100–150╯mgâ•›/â•›d) or heparin
the vessel wall. The wall of a false aneurysm con- (activated partial thromboplastin time, APTT, 50–
sists of a connective tissue capsule rather than the 75). For those in whom anticoagulation is to be com-
wall of the artery. Arterial dissection of the carotid menced, conversion to warfarin with an international
andâ•›/â•›or vertebral arteries may occur following an normalised ratio (INR) of 2 to 3, for 3 to 6 months is
intimal tear due to blunt force. A false channel is recommended.7 Following this, lifelong aspirin is
then created between the inner and outer layer of the usually recommended. This may be difficult to imple-
vessel. Entry of blood here may lead to vessel nar- ment for all patients, as many have discrete contra-
rowing or occlusion. This dissection flap may also indications to anticoagulation and antiplatelet agents,
continue distally and be very difficult to treat. BCVI especially patients with traumatic brain injuries.
7 • Vascular injury • A. Blunt carotid and vertebral artery injuries 137

FIG 7.1â•… Illustrations

showing: a normal
vessel with intact tunica
adventitia (outer layer),
tunica media (middle
layer) and tunica
intima (inner layer);
a vascular dissection;
and a traumatic

TABLE 7.1â•… Risk factors for which screening for

BCVI should be considered7

Asymptomatic with significant

Symptomatic blunt head trauma

Any neurologic Severe traumatic brain injury

abnormality that is with Glasgow Coma Scale
unexplained by a score ≤â•›8
diagnosed injury
Blunt trauma patients Petrous bone fracture
presenting with epistaxis
from a suspected arterial
source after trauma
Neck pain • Lefort II or III facial fractures
• Cervical spine fracture
particularly those with
fracture of C1 to C3;
fracture through the foramen
• Cervical spine fracture with
subluxation or rotational

Traumatic aneurysms should be treated with endo�

vascular or surgical intervention, as their natural
history is one that precludes resolution without 
treatment. The endovascular approach includes the
use of stents and coils, which are usually introduced
via the femoral artery in the groin. Flow-restoring
surgery should be considered for patients with neu-
rological deficits with high-grade to total vascular
occlusion, except if significant established infarc-
tions are evident on imaging. Hence, the need for
rapidity in investigations and treatment.
In 2007, the Alfred Hospital BCVI Workgroup
published the Alfred Hospital Suspected Blunt 
FIG 7.2â•… Pathology of a blunt vascular traumatic injury.

FIG 7.3â•… The Alfred Hospital Suspected Blunt Cerebrovascular Injury Protocol. NIHSS = National Institutes of
Health Stroke Scale. (Based on <http://intranet.alfredhealth.org.au/assets/contentfiles/312/BCVIprotocol.pdf>)
7 • Vascular injury • A. Blunt carotid and vertebral artery injuries 139

CASE STUDY 7.1 Cerebrovascular Traumatic Injury Protocol (Fig

7.3). It is based on the Denver grading scale (Table
A 32-year-old woman developed a dense right-side 7.2) for BCVI severity and complications. It is a
hemiplegia two days after a high-speed motor vehicle useful aid in decision making for a complex problem.
accident. Magnetic resonance imaging (MRI) of the
brain revealed left-side cerebral hemispheric infarcts.
MR angiography showed a left internal carotid artery SUMMARY
(ICA) dissection. A digital subtraction angiogram
was then performed and showed severe dissection 1. BCVI is an infrequent injury but may have a
of the ICA, commencing approximately 1.5╯cm from devastating outcome.
the origin. In addition, a small pseudoaneurysm 2. Patients with high-risk injury patterns should
was seen along the anterior aspect. The woman have screening CT angiograms of the cervical
subsequently had successful stenting of the severely and intracranial vasculature.
dissected left ICA with the pseudoaneurysm (Fig
7.4a–c). She was discharged for stroke rehabilitation 3. Recognition and therapy may prevent the occur-
after a short inpatient stay. rence and extension of ischaemia and infarction
from cerebral hypoperfusion, provided there are
no contraindications.

A 27-year-old man was involved in a high-speed TABLE 7.2â•… Denver BCVI grading8
motor vehicle accident eight months ago. He had Grade Radiological signs
a CT angiogram (CTA) of his vertebral and carotid
arteries, as he had a petrous temporal bone fracture. 1 Luminal irregularity or dissection with <â•›25%
He was otherwise neurologically intact. The CTA stenosis
showed a 7╯mm pseudoaneurysm on the right 2 Dissection with >╛25% narrowing or raised
infrapetrous ICA (Fig 7.5a). The decision was made intimal flap
to treat him electively. He had successful coiling of 3 Pseudoaneurysm
the pseudoaneurysm and remained neurologically
intact (Fig 7.5b & c). 4 Complete occlusion
5 Transaction with free extravasation of contrast

FIG 7.4bâ•… Stent insertion along the dissection segment

FIG 7.4aâ•… Proximal ICA dissection (red arrow). (red arrow).

FIG 7.4câ•… Contrast flowing through stent, denoting

successful therapy. (The red arrow indicates the area FIG 7.5aâ•… Traumatic pseudoaneurysm (red arrow) on
of dissection.) the right infrapetrous ICA.

b c

FIGS 7.5b & câ•… Coiled pseudoaneurysm (red arrows), with good flow through the ICA.
7 • Vascular injury • B. Traumatic caroticocavernous fistula 141


FISTULA Barrow and associates15 developed the current clas-
A traumatic caroticocavernous fistula (CCF) results sification system of caroticocavernous fistulas in
from an abnormal communication between the arte- 1985, as follows:
rial and venous systems within the cavernous sinus. • Type A: direct connection between the intracav-
In the context of head injury, this usually occurs ernous internal carotid artery and the cavernous
after a significant trauma that causes fracture of the sinus. These are usually high-flow and high-
skull base into the cavernous sinus. This damages pressure fistulas. Most traumatic CCFs belong to
the carotid artery and as a result arterial blood under this category.
high pressure enters the cavernous sinus, impeding • Type B: dural shunt between intracavernous
the normal venous return of the cavernous sinus and branches of the internal carotid artery and the
causing engorgement of the draining veins of the cavernous sinus.
cavernous sinus (the superior and inferior ophthal- • Type C: dural shunt between meningeal branches
mic veins). This can manifest most dramatically as of the external carotid artery and the cavernous
a sudden conjunctival engorgement and redness of sinus.
the eye on the same side. • Type D: combination of types B and C, with dural
CCFs may also occur following surgical damage, shunts between internal and external carotid
rupture of an intracavernous aneurysm or in asso� artery branches and the cavernous sinus.
ciation with connective tissue disorders, vascular • Types B, C, and D tend to be lower-flow and
diseases and dural fistulas.9–13 Most CCFs are of lower-pressure fistulas, with a slower progression
spontaneous origin and unknown aetiology. CCF of signs and symptoms.
has also been reported secondary to blunt trauma The four types of caroticocavernous fistulas are
after functional endoscopic sinus surgery.14 shown diagrammatically in Figure 7.6.

FIG 7.6â•… Diagrammatic representation of the four types of caroticocavernous fistulas,

as described in the text. ICA = internal carotid artery; ECA = external carotid artery.
(Based on Karadag R et al16, Fig 1.)

CLINICAL PRESENTATION All patients should have a complete ophthalmo-

logic workup, including visual acuity, pupillary
Although CCF is not a lethal disease, its symptoms function, intraocular pressure, fundoscopy (direct
can be disabling. Pain is the symptom that patients and indirect) and gonioscopy.
often find the most intolerable.
Patients usually present with sudden or insidious
onset of redness in one eye, associated with pro� DIAGNOSIS
gressive proptosis, which is frequently pulsatile.  • Suspicion of CCF should be investigated
A bruit may be heard over the orbit. Other ocular radiologically.
manifestations include ophthalmic venous hyperÂ� • An MRI head with MR venogram and MR angio-
tension and orbital venous congestion, corneal expo- gram, or a CT head and orbit with CT angiogram
sure, chemosis, arterialisation of episcleral veins, and venogram (see Fig 7.9c) can be performed in
diplopia, cranial nerve palsy (III, IV, V, VI), central most trauma centres. These modalities have the
retinal vein occlusion, retinopathy and glaucoma advantage of being non-invasive, and may dem-
(Fig 7.7a & b). onstrate proptosis, swelling of extraocular muscles
Left untreated, CCF will eventually lead to per- and dilation of the superior ophthalmic vein.17
manent visual loss and ophthalmoplegia. The other • Orbital ultrasound study is also a useful investi-
eye may also be affected if the fistula enlarges. gative tool, and can demonstrate increased pulsa-
tile flow in the ophthalmic veins.
• The gold standard for diagnosis is a percutaneous
catheter selective cerebral angiogram of both the
internal and external carotid arteries (see Figs
7.8 and 7.9). This enables detailed study of the
anatomy and pathophysiology of the CCF, and
also enables endovascular treatment.

Medical therapy
Patients with acute vision loss andâ•›/â•›or paralysis of
cranial nerves resulting in ophthalmoplegia may
benefit from the administration of high-dose gluco-
corticosteroids (e.g. dexamethasone IV 12╯mg bolus,
a then 4╯mg q.i.d.) , while awaiting definitive diagnos-
tic studies and treatments.

Surgical therapy
The definitive management of a CCF is obliteration
of the fistulous connection, with restoration of
normal arterial and venous flow. This is achieved
usually via an endovascular approach.18,19 After
complete delineation of the fistulous tract with an
angiogram, an endovascular approach is made to
close the fistula.
Type A CCFs are usually approached through 
the internal carotid artery. A detachable balloon is
b deployed to occlude the fistula while maintaining
patency of the internal carotid artery. Venous
FIG 7.7â•… A well-established caroticocavernous fistula. approaches through the internal jugular vein and the
On examination, there was pulsatile proptosis with a
bruit over the orbit. Note the proptosis, gross chemosis, petrosal sinus may allow access to the fistula from
eyelid oedema and congestion. a. Front view. b. Lateral the venous side. Platinum detachable coils have also
view showing the gross degree of proptosis. been used for the same effect.
7 • Vascular injury • B. Traumatic caroticocavernous fistula 143

Type B, C, and D fistulas have smaller fistulous CCF in the developing world
connections and usually are not amenable to the In countries where interventional radiology is not
same treatment approaches as Type A CCFs. Carotid available, the treatment of CCF becomes surgical.
self-compression for 20–30 seconds four times per ‘Trapping’ the fistula by ligation of the internal
hour may lead to thrombosis of the fistula. Patients carotid artery in the neck (provided there is adequate
are instructed to compress the carotid artery on the crossflow from the contralateral side on an angio-
side of the lesion using their contralateral hand. gram) and ligation of the supraclinoid internal carotid
Should the patient develop cerebral ischaemia artery, if possible below the origin of the ophthalmic
during the compression, the contralateral hand artery, are usually enough to close the fistula.
would be affected, releasing the compression.
If compression is not effective or if a more rapid
intervention is indicated, selective endovascular OUTCOME AND PROGNOSIS
embolisation of the fistula through the external Patients with CCF generally have a good prognosis.
carotid artery is usually effective. Traumatic CCFs are not associated with a high inci-
Some CCFs may require an endovascular dence of spontaneous resolution. Persistent lesions
approach through the superior ophthalmic vein. This respond well to intervention. The risk of non-
requires surgical exposure of the vein via a small ophthalmologic neurological complications is not
upper eyelid incision to allow placement of the significant; however, persistent untreated lesions
catheter. may cause significant visual complications.
Direct surgical exposure and obliteration of 
the fistula has been described. This rarely is  CASE STUDY 7.3
done because endovascular approaches are usually
successful. However, a persistent CCF may require A patient presented with chemosis and proptosis of
such surgery via a skull base approach with dis� the right eye, which developed 12 days after severe
closed-head injury (Figs 7.8a–g).
section and opening of the cavernous sinus to 
Figures 7.8a and b show a direct high-flow
close the fistulous connection. This is a complex  carotid-cavernous fistula (CCF) between the internal
and difficult endeavour even for the experienced carotid artery (white arrow) and cavernous sinus.
neurosurgeon.20 Reflux of contrast is seen into the superior ophthalmic
Severely refractory fistulas can be treated by sur- vein (black arrow) responsible for the ocular
symptoms. Abnormal early contrast opacification is
gical or endovascular sacrifice of the internal carotid
also seen of the superior (black arrowhead) and
artery. This should be preceded by a balloon trial inferior (white arrowhead) petrosal sinus (IPS) to the
occlusion test (BTO) to see if the patient has suffi- transverse-sigmoid sinus (curved black arrow) and
cient collateral flow and can tolerate the occlusion. through to the internal jugular vein. Also note the
Failure of BTO may necessitate an extracranial-to- shunting into the contralateral cavernous sinus
(curved white arrow) through the intercavernous
intracranial bypass procedure, with a vein or arterial
sinus and drainage into the pterygoid venous plexus
graft. (black dashed arrow). The reduced calibre of the
supraclinoid ICA and reduced intracranial flow is due
to the sump effect of the fistula.
Patients require a follow-up angiogram to check for
recurrence of the fistula or the opening of alternative CASE STUDY 7.4
fistulous pathways. Further endovascular treatments
may then be required. A 76-year-old female patient presented after a fall with
severe head strike (Figs 7.9a–h). On examination
The complications in untreated CCFs are visual there was bilateral mild proptosis, moderate chemosis
loss, cranial nerves paralysis, ophthalmoplegia, and and 6th cranial nerve palsies. Interestingly, she was
the cosmetic concerns of chemosis and proptosis. known with left intracavernous internal carotid artery
The complications of endovascular treatment (ICA) aneurysm which was incidentally discovered
include the known complications of cerebral angi- when bilateral intracranial ICA aneurysms were
clipped 13 years previously. Presumptive diagnosis of
ography (e.g. stroke, arterial dissection, thrombo� rupture of intracavernous ICA aneurysm, resulting in
embolism). Arterial and venous compromise may bilateral carotid cavernous fistulae (CCF) secondary to
also occur, causing cerebral or retinal ischaemia and trauma, was confirmed on imaging.

a b
FIGS 7.8a & bâ•… Selective angiograms in mid-arterial phase of the right internal carotid artery (ICA): a. frontal view;
b. lateral view.

c d
FIGS 7.8c & dâ•… Transarterial endovascular treatment of CCF in the same patient: c. unsubtracted lateral view of a
selective angiogram of the right ICA; d. corresponding subtracted image. A 7.5â•›×â•›10╯mm detachable silicone balloon
(Balt Extrusion, Montmorency, France) has been deployed (white arrow) with almost total exclusion of the CCF, apart
from residual opacification of the IPS (black arrow).
7 • Vascular injury • B. Traumatic caroticocavernous fistula 145

FIG 7.8eâ•… Simultaneous transvenous coil embolisation of residual CCF in the same patient: subtracted lateral view,
showing addition of fibered coils (Vortex, Target Therapeutics/Boston Scientific, Fremont, CA) (black arrow) through a
microcatheter (white arrow) in the right IPS via a guide catheter in the right internal jugular vein.

f g

FIGS 7.8f & gâ•… Selective angiograms of the right internal carotid artery 10 weeks after transarterial and
transvenous endovascular treatment of a right caroticocavernous fistula with a detachable balloon and coils:
f. frontal view; g. lateral view. There is persisting total occlusion of the fistula, with calibre and flow restoration of
the supraclinoid ICA. The inset shows that the detachable silicon balloon (white arrow) has deflated spontaneously.

a b

FIGS 7.9a & bâ•… Selective left internal carotid angiogram: a. frontal view in early arterial phase; b. frontal view in
late arterial phase. There is instant opacification of the left cavernous and intercavernous sinus (white arrow) on
injection of the left ICA (black arrow). Subsequent contrast is seen in the right cavernous sinus (black arrow head)
with reflux into cortical veins (white arrow heads) normally draining into the cavernous sinus. This is an ominous
sign requiring emergent treatment to reduce the risk of subarachnoid haemorrhage.

FIG 7.9câ•… This 3D reconstruction of CTA illustrates the
CCF (black arrow) in relation to the neurocranium.
7 • Vascular injury • B. Traumatic caroticocavernous fistula 147

d e
FIGS 7.9d & eâ•… Selective left internal carotid angiogram: d. lateral view demonstrates CCF with additional reflux
anteriorly into superior ophthalmic vein (white arrow) and posteriorly (black arrow) into inferior petrosal sinus (IPS);
e. lateral unsubtracted view during emergent treatment under general anaesthesia shows a balloon microcatheter
(HyperGlide 4â•›×â•›15╯mm, ev3 Neurovascular, Irvine, CA) over microguide wire (white arrow heads) positioned in the
intracavernous segment of the left ICA. Note previous aneurysm clips rostral to the fistula.

f g

FIGS 7.9f & gâ•… Selective left internal carotid angiogram: f. lateral view before occlusion; g. unsubtracted view after
occlusion with embolisation coils Detach 11 (Cook, Bloomington, IN) (white arrow) and Onyx® (Onyx 34, ev3
Neurovascular, Irvine, CA) (black arrow). These were delivered through a microcatheter (Progreat 2.8F, Terumo
Interventional Systems, Somerset, NJ) positioned transvenously through the right IPS (black arrow heads), while the
balloon microcatheter was intermittently inflated in the left ICA (white arrow heads).

FIGS 7.9h & iâ•… Selective left internal carotid angiogram: h. unsubtracted and magnified frontal view (The
microcatheter is in the right IPS [black arrow heads], while the balloon microcatheter was in the left ICA [white
arrow heads]). i. Selective left internal carotid angiogram after total occlusion of CCF with preservation of the vessel,
which was confirmed with Dyna CT. The patient’s chemosis and proptosis resolved over the next few days, while the
bilateral 6th cranial nerve palsies gradually reversed over two months.

C. PENETRATING INJURY TO be excluded. Stable patients with evidence of pen-

THE CERVICAL CAROTID AND etrating neck injury should be investigated with
plain X-rays, CT and CTA. Imaging of the patient
swallowing with contrast, flexible endoscopy and
A detailed discussion of this topic is outside the rigid endoscopy should be performed if there is sus-
scope of this book. An overview is presented. picion of aerodigestive tract damage despite a nega-
tive multislice CT. A conventional angiogram is still
PRESENTATION AND EVALUATION the gold standard for vascular examination; however,
a CTA is gradually supplanting it, especially in the
Most penetrating neck injuries are caused by sharp emergency setting.
objects and gunshot wounds. Tissue damage caused
by sharp objects is usually less than that caused by
missile penetrating wounds or fragments from bomb
blast. Nonetheless, a trauma patient with severe Direct pressure is immediately applied to exsangui-
haemorrhage from a penetrating cervical injury is at nating vascular injuries in the neck. Blind clamping
high risk of shock and death in a matter of minutes should be avoided. Early airway management and
if the bleeding site is not controlled. Indications for the ability to perform a surgical airway are crucial
immediate surgical intervention include an expand- to the successful management of severe penetrating
ing haematoma, exsanguination, shock, airway com- neck injuries. An immediate referral to a vascular
promise and massive subcutaneous emphysema.21 surgeon with immediate transfer to the operating
Asymptomatic patients without indications for room for exploration and repair is mandatory. If 
surgery should be evaluated for signs of vascular the injury is in the high-cervical region, endo�
injury such as vascular bruits and thrills, an expand- vascular intervention may be necessary to gain
ing or pulsatile haematoma, irregular or poor pulse control of the haemorrhage. A thoracotomy and
volume, and neurological impairment. Pharyngo- clavicle division or disarticulation may be required
oesphageal and laryngotracheal injury should also for access in some situations where the penetration
7 • Vascular injury • C. Penetrating injury to the cervical carotid and vertebral arteries 149

has injured blood vessels in the root of the neck or 14. Karaman E, Isildak H, Haciyev Y, et al. Carotid-
upper thorax. cavernous fistula after functional endoscopic sinus
If a major vein division in the neck is severed, surgery. J Craniofac Surg. 2009;20(2):556-558.
15. Barrow DL, Spector RH, Braun IF. Classification and
direct pressure should be applied over the laceration. treatment of spontaneous carotid-cavernous sinus
In addition to blood loss, these patients are also fistulas. J Neurosurg. 1985;62(2):248-256.
susceptible to air embolism, which may be fatal. 16. Karadag R, Bayraktar N, Kirbas I, et al. Unilateral,
Surgery for lacerations involving the great veins of indirect spontaneous caroticocavernous fistula with
the neck includes unilateral ligation, which has been bilateral abduction palsy. Indian J Ophthalmol.
proved to be safe.22 2011;59:336-337.
17. Bacon KT, Duchesneau PM, Weinstein MA.
Demonstration of the superior ophthalmic vein by high
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1. Fusco MR, Harrigan MR. Cerebrovascular dissections: 18. Debrun GM, Vinuela F, Fox AJ. Indications for
a review. Part II: blunt cerebrovascular injury. treatment and classification of 132 carotid-cavernous
Neurosurgery. 2011;68(2):517-530. fistulas. Neurosurgery. 1988;22(2):285-289.
2. Hughes KM, Collier B, Greene KA, et al. Traumatic 19. Serbinenko FA. Balloon catheterization and occlusion
carotid artery dissection: a significant incidental of major cerebral vessels. J Neurosurg. 1974;41(2):
finding. Am Surg. 2000;66(11):1023-1027. 125-145.
3. Hwang PY, Lewis PM, Balasubramani YV, et al. The 20. Dolenc VE. Extradural approach to carotid parasellar
epidemiology of BCVI at a single state trauma centre. fistulae. In: Microsurgical anatomy and surgery of
Injury. 2010;41(7):991-996. Epub 2010 Apr 2. the central skull base. Wien: Springer-Verlag; 2003:
4. Crissey MM, Bernstein EF. Delayed presentation of 106-115.
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trauma. Surgery. 1974;75(4):543-549. Learning the lessons from conflict: prehospital cervical
5. Cothren CC, Moore EE, Ray CE, et al. Cervical   spine stabilisation following ballistic neck trauma.
spine fracture patterns mandating screening to rule   Injury. 2009;40(12):1342-1345.
out blunt cerebrovascular injury. Surgery. 2007;141: 22. Nair R, Robbs JV, Muckart DJ. Management of
76-82. penetrating cervicomediastinal venous trauma.  
6. Biffl WL. Diagnosis of blunt cerebrovascular injuries. Eur J Vasc & Endovasc Surg. 2000;19:65-69.
Curr Opin Crit Care. 2003;9:530-534.
7. Bromberg WJ, Collier BC, Diebel LN, et al. Blunt
cerebrovascular injury practice management guidelines: FURTHER READING
the Eastern Association for the Surgery of Trauma.  
J Trauma. 2010;68(2):471-477. Bagheri SC, Khan HA, Bell RB. Penetrating neck injuries.
8. Biffl WL, Moore EE, Offner PJ, et al. Blunt carotid Oral Maxillofacial Surg Clin N Am. 2008;393-414.
arterial injuries: implications of a new grading scale.   Barkana Y, Stein M, Scope A, et al. Pre hospital
J Trauma. 1999;47:845-853. stabilization of the cervical spine for penetrating
9. Hieshima GB, Cahan LD, Mehringer CM. Spontaneous injuries of the neck—is it necessary? Injury.
arteriovenous fistulas of cerebral vessels in association 2000;305-309.
with fibromuscular dysplasia. Neurosurgery. 1986; Hirshberg A, Mattox KL. Top knife: the art and craft of
18(4):454-458. surgery. Harley: TFM Publishing; 2005. Chapter 14,
10. Dandy WE, Follis Jr RH. On the pathology of ‘The neck. Safari in tiger country’, pp 199-214.
carotid-cavernous aneurysms (pulsating exophthalmos). McNeil JD, Chiou AC, Gunlock MG, et al. Successful
Am J Ophthalmol. 1941;24:365-385. endovascular therapy of a penetrating Zone III internal
11. Hamby WB. Carotid-cavernous fistula. Springfield, Ill: carotid injury. J Vasc Surg. 2002;187-190.
Charles C Thomas; 1966. Rathlev NK, Medzon R, Bracken ME. Evaluation and
12. Newton TH, Hoyt WF. Dural arteriovenous shunts in management of neck trauma. Emerg Med Clin N Am.
the region of the cavernous sinus. Neuroradiology. 2007;679-694.
1970;1:71-81. Tisherman SA, Bokhari F, Collier B, et al. Clinical practice
13. Walker AE, Allegre GE. Carotid-cavernous fistulas. guideline: penetrating Zone II neck trauma. J Trauma.
Surgery. 1956;39:411-422. 2008;64:1392-1405.
Operative surgery
Jeffrey V Rosenfeld, Vince Cousins, Anthony Hall,
David Morgan, Susan M Liew, Arvind Jain

The purpose of this chapter is not to offer a compre- imaging findings and the extent of intracranial
hensive description of all aspects of the operative injury. Urgent surgery is indicated in all patients
surgery, because this can be found in the standard with a deteriorating level of consciousness, pupil-
textbooks. This chapter aims to describe the prin- lary abnormalities, hemiparesis and when CT scan
ciples and strategies of operative surgery for head reveals an intracranial haematoma causing cerebral
and neck trauma in order to give the non-surgeon compression, midline shift and effacement of the
some appreciation of what the surgeon’s tasks and basal cisterns.1 Expanding haematomas in the middle
challenges are in the operating room. Postoperative cranial fossa are particularly dangerous because of
care is discussed in Chapter 10. the rapid midbrain compression that develops as the
The neurosurgeon, ear, nose and throat (ENT) uncus of the temporal lobe herniates. In general, all
surgeon, ophthalmologist, maxillofacial surgeon, acute traumatic extra-axial (i.e. external to the brain)
plastic surgeon and general trauma surgeon need to haematomas 1╯cm thick or greater warrant urgent
develop a close working relationship and to work as evacuation. An acute subdural haematoma (SDH) or
a multidisciplinary team in managing patients with extradural haematoma (EDH) >5╯mm in thickness
head and neck trauma. Clearly, there are many inju- with midline shift in a comatose patient (Glasgow
ries that primarily involve individual practitioners, Coma Score [GCS] 8 or less) should be evacuated
such as penetrating eye injury or extradural haema- urgently. Surgical decompression of a thin acute
toma, but there are also many injuries that involve convexity SDH 3╯mm or less associated with marked
multiple systems and multiple specialties, where the hemispheric swelling and a large midline shift may
best results are obtained by working as a cohesive not benefit from evacuation. The role of decompres-
team. The orthopaedic or neurosurgical spinal sive craniectomy in this group is controversial.
surgeon will also be part of the team if the cervical Many neurosurgeons would opt to place an intracra-
spine is traumatised. nial pressure (ICP) monitor or ventriculostomy in
Some procedures have been described in greater these patients and control the brain swelling medi-
detail because if no neurosurgical services are avail- cally. The CT would need to be repeated to check
able the practitioner may have to perform the emer- for enlargement of the SDH. If raised intracranial
gency neurosurgery, such as a burr hole, craniotomy pressure becomes intractable in these patients due to
or craniectomy, to save a patient’s life. increasing brain swelling despite medical therapy, a
craniectomy and evacuation of the thin subdural
haematoma may be indicated.
A. NEUROSURGERY Another somewhat uncertain group of patients
INDICATIONS FOR EMERGENCY are those with an acute extradural or subdural hae-
matoma 5–10╯mm thick who have a GCS of 9–13.
If surgery is not undertaken, they need to be observed
The most important factors for deciding whether to very closely for any deterioration. Patients who can
proceed with surgical evacuation of an intracranial be managed in an intensive care setting with fre-
haematoma are the patient’s neurological status, the quent neurological examination include those with
8 • Operative surgery • A. Neurosurgery 151

a GCS of 9–13, stable or improving level of con- respirations. Similarly, in patients over the age of 
sciousness, no focal deficits and normal basal cis- 75 with a GCS of 5 or less, a non-operative course
terns on CT scan with no appreciable midline shift. is often taken, given their almost uniformly poor
Any deterioration warrants a repeat CT scan or, in outcome with or without surgery (see further discus-
some cases, urgent surgery. Another group of sion in Chapter 13 on the elderly with traumatic brain
patients who warrant initial conservative manage- injury). All other patients with surgical mass lesions,
ment are those with an interhemispheric or tentorial even those with a post-resuscitation GCS of 3 but at
SDH without neurological deficit. least one reactive pupil, warrant urgent operative
There is controversy as to when to evacuate intra- intervention. A significant, albeit small, portion of
cerebral haematomas and haemorrhagic contusions, such patients make a satisfactory recovery. Addition-
and whether such removal is helpful in controlling ally, in some patients a low GCS may be due to
intracranial pressure and improving outcome. These intoxication, hypothermia, drugs, postictal state or
haematomas often develop significant cerebral other causes of a decreased level of consciousness.
oedema around them over the first few days after the Discussion with a neurosurgeon is recommended
injury and this oedema may significantly worsen the to aid decision making.
ICP levels. Contusions may also ‘blossom’ (increase
in size and prominence) over several days. Early
surgical removal of large intracerebral haematomas
and extensive cerebral contusions provides early Antibiotics and the prevention of infection
control of ICP and helps to prevent the cascade of Great care should be taken to maintain sterility
secondary events that lead to delayed intracranial throughout the surgery. Neurosurgical infection is
hypertension with the oedema surrounding the always serious and easily becomes life-threatening.
lesion. Some of the factors to be weighed up by the Contaminated cranial wounds need adequate debride-
neurosurgeon considering surgery include the size ment, and antibiotics should be administered to any
of the lesion, its depth from the cortical surface, patient with a compound skull fracture. There is
exact location, the presence of associated lesions evidence that prophylactic antibiotics prevent post-
and the patient’s neurological status and ICP. operative infection in ‘clean’ neurosurgery. Antibiot-
Cortical contusions over 2╯cm in diameter should ics are administered intravenously just prior to or at
generally be removed if there is significant mass induction, and theoretically the one dose is enough.
effect and ICP is difficult to control medically. Frontal Continuance postoperatively is unnecessary unless
pole and temporal lobe haematomas or contusions the wound is compound. The combinations of flu-
2╯cm in diameter or more with significant mass effect, cloxacillin or cloxacillin and gentamycin, or a single
basilar cistern impingement and midline shift over cephalosporin such as cephalothin or ceftriaxone are
5╯mm should also be removed if ICP management is suitable alternatives. In the developing world, peni-
problematic. An initial conservative approach is war- cillin and chloramphenicol are often used.
ranted, however, when ‘eloquent’ cortex is involved,
such as lesions in or near the dominant temporal lobe, Anticonvulsants
the sensorimotor or visual cortex. An expectant
course is also indicated in comatose but neurologi- There is evidence that post-craniotomy epilepsy is
cally stable patients with small lesions associated prevented by using prophylactic anticonvulsants for
with <5╯mm of midline shift and open basal cisterns one week. A loading dose of phenytoin is given
on CT scan. Similarly, lesions confined to the deep before surgery or intraoperatively (10╯mg╛/╛kg). Phe-
white matter or basal ganglia are best managed nytoin is the drug of choice because it can be given
without surgery. ICP should be carefully monitored intravenously. A depressed fractured skull with cor-
and controlled by medical means. If such measures tical laceration, an intracerebral haematoma or an
fail, the patient can be considered for surgery. acute subdural haematoma all place the patient at
There are situations where the dismal clinical higher risk of ongoing seizures.
status of the patient warrants a non-operative course
despite the presence of radiographic surgical lesions. Steroids
Such cases include the adult patient who after resus- The use of dexamethasone or other steroids do not
citation remains flaccid with a GCS of 3, non-  improve the outcome of brain injury and are not
reactive and dilated pupils, and without spontaneous indicated.

Preparation for surgery by cetrimide or Betadine. Be careful not to get alco-

the neurosurgical team holic solution anywhere near the eyes. Scalp wounds
The close and frequent observation of the patient can bleed heavily and should be closed rapidly in a
should continue up to the time of surgery. Informed multiple-trauma patient. The quickest way to do this
consent is obtained for the surgery; this will be from is by using skin staples.
the patient if possible, or from the next of kin if the A dressing with scalp bandage is applied to
patient is unconscious. If it is a life-saving operation provide ongoing pressure to the wound. If there is
and no next of kin is available the surgery will more time available to close the wound formally and
proceed without consent. it is more than 2╯cm in length, it should be closed
The patient is kept nil by mouth. Oxygen is in two layers with interrupted absorbable suture
administered if the patient is not intubated. such as 3/0 Vicryl to the galea and subcutaneous fat
The patient is discussed with the anaesthetist and and an interrupted or continuous layer of nylon to
the intensive care physician (if the patient is likely the skin. Wounds less than 2╯cm length could be
to need postoperative ICU care) as soon as possible closed with a single layer of nylon or staples. Large
so that they can assess the patient. The patient is also areas of scalp loss such as in degloving injuries will
discussed with the general trauma surgeon, ortho- require plastic surgery involvement. Advancement
paedic surgeon and other relevant surgical special- flaps or rotation flaps may be required for immediate
ties (such as ENT, plastics or maxillofacial) to coverage. More complex, free vascularised flap
determine the sequence and priority of the surgery reconstructions are performed as secondary proce-
and whether any of the procedures can be performed dures when the vascularity and health of the existing
simultaneously. For example, it is possible to scalp is compromised.
perform the insertion of an ICP monitor or a crani-
otomy at the same time as a laparotomy, thoractomy Burr holes
or other procedure if the urgency requires it. Indications
The haemoglobin level, white cell count includ- 1. Suspected intracranial haematoma.
ing platelets and clotting tests are checked (see 2. Access for insertion of intracranial pressure
Chapter 16). Electrolytes, blood sugar and liver monitor.
function are checked.
Correction of clinical or laboratory-screentest- Strategy
based coagulopathy is commenced (see Chapter 16). In the absence of a CT scanner, the burr hole is made
Blood products are grouped and held. overlying the suspected haematoma. However, if the
Blood and blood products are crossmatched if the site of the haematoma is unknown, three burr holes
patient is anaemic and there is likely to be excessive are made on each side of the head, starting on the
blood loss such as in a large EDH or SDH operation most likely side, until the collection is located. The
in the setting of multiple trauma. entire scalp is shaved and prepared unless the side
is obvious.
The first burr hole is made over the suspected site
OPERATIVE PROCEDURES of the collection, which for most extradural haemato-
mas is in the temporal region on the side of the scalp
Closure of scalp wounds contusion and swelling, andâ•›/â•›or on the side of pupil-
The scalp is shaved, prepared with antiseptic solu- lary dilatation and sluggishness. The temporal burr
tion and infiltrated with 0.5% bupivicaine and hole is placed approximately at the mid-zygomatic
1/200,000 adrenaline. point, approximately 3–4╯cm above the zygoma. If
Scalp wounds in patients with traumatic brain the haematoma is found at this site, frontal and pari-
injury (TBI) should be palpated with a gloved index etal burr holes are made. The frontal burr hole is
finger to detect any underlying skull fractures. The made just behind the hairline in the mid-pupillary
wound should be irrigated with antiseptic solution. line, and the parietal burr hole is made over the pari-
Betadine should be used to wash out the wound etal eminence (the most prominent part of the parietal
when there is a compound fracture so that no alco- bone). Figure 8.1 shows the sites for burr holes.
holic antiseptic skin preparation makes contact with If an extradural haematoma is present, the dark
the brain. If the wound is heavily contaminated, it semi-solid blood will be obvious when the skull is
can be scrubbed with a scrubbing brush using  breached, and some fresh bleeding may flow from
8 • Operative surgery • A. Neurosurgery 153

a b

FIG 8.2â•… Diagrams showing adjacent burr hole with

(a) perforator and (b) conical burr.

occipital protruberance (inion) in the midline of 

the skull posteriorly. The sigmoid sinus beneath the
mastoid bone and two finger breadths behind the
external auditory canal should also be avoided.
In the absence of CT, the three burr holes are
FIG 8.1â•… Sites for burr holes. repeated on the contralateral side if no haematoma
is located and the presence of a haematoma on the
contralateral side is a possibility.
the burr hole. A craniotomy or craniectomy for Method
drainage of the epidural haematoma is then carried A burr hole is a basic component of all cranial neu-
out (see below). The presence of a subdural haema- rosurgery that can stand alone or form part of a
toma will give the dura a bluish colour and will craniotomy (Fig 8.2). The scalp is shaved, prepared
make it tense. If a subdural collection is a possibil- and infiltrated with 0.5% bupivicaine and 1/200,000
ity, the dura should be opened, and if a subdural adrenaline.
collection is present, a craniotomy will be necessary. A linear 3╯cm incision is made, the periosteum is
If there is no collection and the patient has a primary separated off the skull with a sharp periosteal eleva-
brain injury with cerebral swelling, the dura will be tor subjacent to the wound, and a small self-retaining
tense and usually pale. When the dura is opened to retractor is inserted. The skull perforator is used to
exclude a collection, swollen and sometimes necrotic create a conical opening in the skull, which will
brain matter will swell out of the burr hole. eventually create a small hole through the inner
When CT is available, the craniotomy should be table to reveal the blue or white dura beneath. If you
centred over the major component of the haema- are not sure when the perforator is through the skull,
toma, that is frontal, temporal or parietal. The tem- you will feel it pass freely through into the cancel-
poral craniotomy will usually require an inferior lous bone and then it becomes more difficult to cut
extension with craniectomy technique, because an the bone as it passes through the firm inner table.
extradural haematoma in this location often extends The base of the hole is probed with fine forceps until
to the floor of the middle cranial fossa and even the bone gives way in the base. You should avoid
beneath the temporal lobe, as the rupture of the undue pressure, as the inner table is traversed for
middle meningeal artery may be at the level of the fear of cracking the skull and plunging. The conical
floor of the middle cranial fossa. or cylindrical burr is used to convert the conical
Posterior fossa burr holes and craniectomy are opening into a cylindrical opening. When the burr
performed if a posterior fossa extradural haema�toma becomes difficult to turn it is usually through the full
is seen on CT. The surgeon must stay away from the thickness of the skull.
transverse sinus, which runs in an imaginary line In the adult skull, some pressure must be exerted,
continuous with the zygomatic arch to the external particularly when the outer table of the skull is

perforated, but then pressure should be reduced. The delay in gaining access. The cleaner environment of
squamous temporal bone and the child’s skull in the operating theatre and its equipment is advanta-
general are quite thin: care should be taken not to geous. The insertion of the ICP monitor, if indicated
press too hard on the brace in these situations or it in a patient with multiple trauma and severe TBI,
may plunge through the skull and into brain. If no should be done in the operating theatre at same time
brace, perforator or burr is available, a bone gouge as other general or orthopaedic surgery, if these are
and large mallet, a trephine or even a carpenter’s urgent and require immediate attention. This enables
brace and bit are worthwhile alternatives in a des- the anaesthetist to monitor and control the ICP
perate situation. Opening the skull and evacuating a during the procedure. This is preferable to waiting
haematoma can be life-saving. until the other procedures are finished, during which
Bipolar coagulation is used to coagulate the time the patient may have had uncontrolled ICP,
exposed dura, which is then lifted with a sharp dural which will worsen the prognosis. Alternatively, as
hook and incised with a scalpel (15 or 11 blade) in mentioned above, the neurosurgeon may place an
a cruciate pattern and the edges further diathermied. ICP monitor at the time of craniotomy for evacua-
Control of bleeding from the edge of the bone can tion of a haematoma, because these patients may
usually be achieved with small pieces of Surgicel develop brain swelling or a re-bleed postoperatively,
impacted beneath the bone edge. If this fails, use a and ICP monitoring in a sedated patient will detect
curved dissector, such as a Watson Cheyne dissector, the silent rise in ICP, necessitating a repeat CT scan.
and pass it beneath the bone and diathermy under ICP monitors are usually in place for 2–5 days
the bone against the dura. Bone wax may also be and occasionally for 10–14 days. The timing of
impacted along the bone edge. removal depends on the resolution of the brain
swelling, contusion and the intracranial hyperten-
Intracranial pressure monitor sion (see Chapter 9).
Indications The landmark for placement of the frontal burr
1. Neurological2: a severe TBI (GCS ≤8 after car- hole or twist drill opening is just behind the hairline
diopulmonary resuscitation) with an abnormal in the mid-pupillary line with the eye in a neutral
CT scan or with a normal scan but with ≥2 of the position. An alternative vertical measure is 10╯cm
following three factors: above the inion. Usually the right side is chosen to
• age >40 years avoid any injury to the dominant hemisphere.
• Systolic blood pressure (SBP) <90╯mmHg
• decerebrate or decorticate posturing on motor External ventricular drain
examination (unilateral or bilateral). (ventriculostomy) (EVD)
An abnormal scan is one with haematomas, con- A ventricular catheter is placed in the frontal horn
tusions, brain swelling, midline shift, brain her- of the lateral ventricle (Fig 8.3). The advantage of
niation or compressed basal cisterns. inserting the intraventricular catheter is that cerebro-
2. Multiple systems injuries with altered level of spinal fluid (CSF) can be vented to reduce ICP and
consciousness, where the patient is likely to be it thus becomes a therapeutic device as well as a
sedated or to receive high ventilatory pressures monitoring device. The ICP being measured is the
or large fluid volumes in the ICU. ventricular ICP, which differs from the parenchymal
3. Following the craniotomy, to remove a mass ICP by a few millimetres. The disadvantages are
lesion, such as a haematoma or contusion. that: (a) the catheter becomes blocked if the ven-
Relative contraindications to the insertion of an tricles are small due to a swollen brain; (b) infection
ICP monitor are: is a higher risk than with the parenchymal monitors
• an awake patient if the catheter is left in situ more than five days; and
• coagulopathy, including acute coagulopathy of (c) the catheter may not be placed accurately and
severe trauma and disseminated intravascular may lie outside the ventricle. The catheter is con-
coagulopathy (DIC), which is frequently seen in nected to a closed drainage system, with the height
severe TBI. Coagulopathy should be corrected of the tubing set at the opening pressure of CSF
before an ICP monitor is inserted. drainage (15–20╯cm H2O). CSF either vents as the
ICP monitors are often placed in the emergency pressure drops to this opening pressure or does not
room or ICU, but it is preferable that they be placed drain if the ICP is below this pressure. Continuous
in the operating theatre, provided there is no undue drainage is not advisable because the ventricle may
8 • Operative surgery • A. Neurosurgery 155

FIG 8.3â•… Ventricular catheter placed in the right frontal FIG 8.4â•… Codman parenchymal ICP monitor.
horn. Note the small acute-on-chronic subdural
haemorrhage on the left side.

close down over the catheter and block it. A pressure diameter. The monitor may take the form of an elec-
transducer is placed on a three-way tap so that the tric strain gauge (Codman, Codman and Shurtleff
ICP can be measured, except during venting. Inc) (Fig 8.4), an air-filled plastic balloon (Spiegel-
External ventricular drains should be inserted in berg) or a fibreoptic catheter (Camino, Integra).
hospitals where neurosurgical staff are available for Combined strain gauge monitors within a ventricu-
the following reasons. lar catheter are also commercially available but 
1. It is technically challenging to place the catheter are not often used. The intraparenchymal monitors
in the frontal horn of the ipsilateral lateral are placed 2–3╯cm into the brain parenchyma and
ventricle. brought out through a separate stab incision in the
2. Complications of the insertion are possible, scalp to minimise the infection risk. The disadvan-
including haemorrhage and infection. tages of intraparenchymal ICP monitors are drift of
3. The ongoing management of the patient with the the baseline over time, technical failure of the
catheter in situ may require intermittent unblock- device, issues of MR compatibility and inability to
ing or revision in the OR for more accurate siting. vent CSF. Brain oxygen monitors such as the Licox
4. There is a requirement for neurosurgeons to (Integra), microdialysis catheters and cerebral blood
manage the ongoing surgical needs of the patient flow measuring catheters may also be passed through
in concert with the ICU team. the twist drill anchoring device into the brain or
If intensive care is available without any neuro- through separate twist drill openings.
surgical support, we suggest that a parenchymal
monitor be used. Preferably the patient should be sent The ‘classical’ method of craniotomy
to a centre where neurosurgical care is available. The high-speed compressed air or electric cranio-
tome is used to rapidly perform a craniotomy in
Parenchymal monitor most neurosurgical operating rooms. However, the
Commercial kits are available with all the instru- remote surgeon should learn to open the skull using
ments necessary to perform a twist drill opening in the brace and Gigli saw. This simple but effective
the skull, penetrate the dura and place an parenchy- instrument was first used for symphysiotomy in
mal ICP monitor. The drill is held perpendicular to obstructed labour and is often still used for complet-
the skull. The opening is approximately 0.5╯cm in ing a limb amputation. The recommended scalp

a b

FIG 8.5â•… Craniotomy flap: a. frontotemporoparietal flap; b. parietal flap; c. frontotemporal flap.

incision for the frontotemporoparietal region is a The recommended craniotomy technique is a

‘question-mark’ incision commencing just above free-flap craniotomy where the pericranium and
and in front of the tragus, extending posteriorly muscle are stripped off the skull, and the bone flap
above the earlobe and then turning upwards and is completely freed by joining all of the burr holes
forwards into the frontal region just beyond the hair- using the Gigli saw (Fig 8.6a–c). The burr holes are
line (Fig 8.5a). An inverted U-shaped flap is used placed 4–6╯cm apart in positions that will create a
for a parietal collection (Fig 8.5b). Figure 8.5c polygonal craniotomy. A plane is then developed
shows a frontotemporal craniotomy. between the dura and the inner table of the skull at
8 • Operative surgery • A. Neurosurgery 157

FIG 8.6â•… Using a Gigli saw. a. The Gigli saw is being passed between burr holes
attached to the guide. b. The Gigli has passed through the distant burr hole and is
attached to the hook on the guide. c. The guide has been removed and the hooked
handles have been attached to each end of the Gigli saw, which is ready to make a cut
between the two burr holes.

each of the burr hole sites using a smooth periosteal guide. Once the blade has passed through the burr
elevator or a Penfield or Watson Cheyne dissector. hole towards which the guide is directed, it is
The leading edge of the dural guide with the Gigli detached from the hook on the guide and attached
saw attached to the hook on the instrument is then to the handle with the hook, as is the other end of
passed in the epidural plane between adjacent burr the saw blade. The surgeon then grips both handles
holes, with the assistant holding the saw blade taught and progressively cuts the bone until the burr holes
so that the blade easily passes along the path of the are joined, using a back-and-forth sawing motion

with arms spread apart and the Gigli saw angled Strategy
backwards to create a bevelled edge. This manoeu- The single burr hole overlying the collection is
vre is repeated between each burr hole pair until the enlarged either by craniectomy or by craniotomy.
flap is completely freed. The bone rongeurs can be For the inexperienced surgeon, a craniectomy is
used to extend the burr holes if required. The assis- preferable because it is more rapid. If a temporal
tant must place a finger on the flap for the last cut craniotomy is performed, a craniectomy is extended
so that the bone flap does not flip out and onto the inferiorly, if necessary, to follow the haematoma
floor. If access to the middle cranial fossa is required onto the floor of the middle cranial fossa beneath the
in order to remove an extension of the haematoma, temporal lobe dura. The clot is usually semi-solid
a craniectomy can easily be used to extend the expo- and cannot be removed adequately through a single
sure inferiorly. burr hole. The enlarged opening is necessary. The
In a time-critical situation where the patient clot is completely evacuated.
shows signs of coning due to a suspected epidural A headlight is helpful to check the areas beyond
haematoma, the remote surgeon should perform a the bone edge, particularly inferiorly under the tem-
burr hole and craniectomy rather than a craniotomy poral lobe dura. The bleeding is often coming from
using a Gigli saw. The craniectomy is performed by a single meningeal artery on the dura and it is impor-
nibbling away the bone piecemeal using rongeurs tant to locate this bleeding point and either under-
until the haematoma is adequately deroofed. This run it with silk or use diathermy.
will commit the patient to a delayed cranioplasty General dural ooze is often a problem following
(see below). the removal of a large haematoma, particularly one
that has been present for several hours, and this
Extradural (or epidural) haematoma (EDH) bleeding is controlled with a combination of Surgi-
cel, diathermy, gelfoam and the essential dural
There has usually been a blow to the head with a hitching sutures around the edge. Dural hitching
local scalp haematoma, and underlying skull frac- sutures pass from the dura up through small holes
ture. The patient will deteriorate neurologically and drilled at the bone edge or up to the pericra-
may cone rapidly. This will result in focal neurologi- niumâ•›/â•›muscle near the bone edge. The dura is then
cal signs, including a dilated pupil on the ipsilateral pulled tightly up towards the bone, with some surgi-
side. If there is time or availability, CT is recom- cal or gelfoam passed extradurally under the bone
mended (Fig 8.7a–c). The surgeon should perform edge to further quell the bleeding. A drain is placed
a craniotomyâ•›/â•›craniectomy overlying the haema- in the extradural space. This should be a closed
toma and evacuate the clot, which is often semi- drainage system, with a low-pressure suction drain
solid, and control the bleeding by under-running the or a passive drain if the suction drain is unavailable.
meningeal artery bleeding point with silk or by If no closed drainage system is available and the
using diathermy. A drain should be placed in the wound is very oozy, an open Penrose or rubber drain
epidural space. If no CT is available, a burr hole is will suffice. The opening in the skull to remove a
initially placed over the most likely site (usually collection is often too small when performed by an
temporal region) and the burr hole enlarged if this inexperienced surgeon and only part of a haema-
is the site of the extradural. Further burr holes are toma is evacuated. The surgeon should try to perform
made in the frontal and parietal regions on that side, a craniotomy which encompass the collection as
and then on the opposite side, until the collection  seen on the CT scan. Working with a neurosurgeon
is found. The dura is opened at each site to exclude can help the non-neurosurgeon to appreciate flap
a subdural haematoma. Posterior fossa EDHs are size and positioning.
uncommon (about 5% of all EDHs) and would
require posterior fossa burr holes and craniectomy, Prognosis
which is best done in the prone position. The mortality rate from acute extradural haematoma
Indications should be around 5–10%, but if the patient has no
1. Deteriorating conscious state post head injury lucid interval or presents late, with a poor conscious
and extradural haematoma identified on CT or state, and bilateral neurological signs, particularly
suspected on clinical grounds. extension to pain or no response to pain, or fixed,
2. Exploratory burr holes performed and extradural dilated pupils, the mortality rises significantly. Time
haematoma identified. is critical in extraction of an extradural haematoma.
8 • Operative surgery • A. Neurosurgery 159

a b

FIG 8.7â•… CT scans showing examples of extradural haemorrhage: a. right posterior temporal extradural
haematoma—note the overlying scalp haematoma, brain swelling with obliteration of the basal cisterns and multiple
small haemorrhages typical of diffuse axonal injury; b. large left frontoparietal extradural haemorrhage—note the
overlying scalp haematoma; c. large left frontal extradural haematoma—note the associated severe midline shift and
ventricular distortion and compression underlying the haematoma.

Mannitol can be used to gain an extra half-hour to Acute subdural haematoma

an hour, by reducing intracranial pressure. Beyond These patients have usually had a high speed decel-
this time, the haematoma may expand to fill the eration and a significant primary brain injury. They
space left by the shrinkage of the brain following are usually significantly impaired at the time of
osmotic diuretic administration. injury and then deteriorate further. Urgent CT is


This is a 37-year-old gentleman with a past history of 4. In the posterior fossa, there was mild compression
asthma who was assaulted when heavily intoxicated of the posterior left cerebellar hemisphere.
and fell with an occipital head strike. He had a 5. Associated right frontotemporal contrecoup injury
2-minute period of loss of consciousness (LOC). He with multiple small inferior right frontal lobe
was agitated on arrival and was intubated. He was haemorrhagic contusions, a couple of small right
noted to have been moving all limbs, with equal and inferior temporal lobe contusions and small
reactive pupils. volume right frontal traumatic subarachnoid
CT scan (Fig 8.8a) showed: haemorrhage with a thin subdural bleed,
1. Non-depressed left occipital bone fracture, measuring 5╯mm in maximal depth.
which extended towards the foramen magnum 6. Moderate oedema in the compressed left occipital
and into the superior left anterolateral occipital lobe, but otherwise grey–white╯differentiation was
condyle. preserved.
2. Associated large left parieto-occipital EDH, which 7. No subfalcine, uncal or transtentorial herniation.
measured 3.2╯cm in internal depth maximally, The patient was taken to the operating theatre for
6.9╯cm in mediolateral dimensions supratentorially evacuation of the EDH and insertion of an ICP
and 1.7╯cm in thickness in the posterior fossa. monitor (Figs 8.8b–f). He recovered well with a
3. Positive mass effect results in sulcal effacement of residual right-sided homonymous hemianopia.
the left parietal and occipital╯lobes, with There was no other deficit or complication. The
compression of the occipital horn and trigone of postoperative scan is shown in Figure 8.8g. The
the left lateral ventricle. patient was discharged to his family 8 days later.

FIG 8.8aâ•… CT showing extradural haemorrhage.

FIG 8.8bâ•… Linear excision with bone exposed.

FIG 8.8câ•… Extradural haemorrhage exposed. FIG 8.8dâ•… Extradural haemorrhage removed.

FIG 8.8eâ•… Dural hitching suture being inserted. FIG 8.8fâ•… Bone flap replaced and anchored with mini
plates. Note the extradural drain tube and the Codman
ICP monitor.

advised. The underlying brain is usually swollen,

with midline shift, and the subdural is usually
located over the convexity extending under the tem-
poral andâ•›/â•›or frontal lobes (Fig 8.9a). There may be
a bursting injury of the brain where it has impacted
and torn on the sharp edge of the sphenoid wing at
high speed. These injuries are technically challeng-
ing, even for an experienced neurosurgeon. It would
be preferable for the surgeon to have had some neu-
rosurgical experience.
Nevertheless, if the patient is rapidly deteriorat-
ing and there is not enough time to seek definitive
care, the surgeon should act.
Figure 8.9b shows the brain three days after
1. SDH >1╯cm thickness (>5╯mm in children).
2. Deteriorating conscious state following trauma,
or comatose since time of injury.
3. Focal neurological signs suggesting mass lesion.
4. Dilated pupil on ipsilateral side or bilaterally
dilated pupils.
FIG 8.8gâ•… CT scan of extradural haematoma A CT scan should be obtained and will show the
evacuated. acute subdural collection and frequently midline
shift. Thin subdurals may not require evacuation but
will need to be followed closely with repeat CT scan
to detect enlargement.

a b
FIG 8.9â•… CT scans showing: a. large acute right frontoparietal subdural haematoma (SDH) with underlying
hemisphere swelling and midline shift; b. appearance 3 days postoperatively, with evacuation of the SDH. Note the
return of the midline structures.
8 • Operative surgery • A. Neurosurgery 163

FIG 8.10aâ•… CT scan showing a thin acute left SDH FIG 8.10bâ•… Position of the scalp flap.
with midline shift. Arrows indicate the subdural

FIG 8.10câ•… Bone flap removed and dura exposed. Note FIG 8.10dâ•… Dura being opened to release the semi-
the temporalis muscle retracted forwards of the solid and liquid subdural haemorrhage.

Strategy is lifted with the scalp flap, a free bone flap is raised
A rapid, large craniotomy andâ•›/â•›or craniectomy is andâ•›/â•›or craniectomy performed, any extradural hae-
performed, the haematoma evacuated and the active matoma is evacuated and the dura is opened widely
bleeding controlled. Further mannitol may be and rapidly to allow the brain to swell uniformly
administered intraoperatively or postoperatively if (Figs 8.10c & d). Meningeal bleeders are secured
the brain is particularly swollen. An ICP monitor is and the subdural haematoma is evacuated, including
inserted and the dura closed if possible. The bone beyond edges of craniotomy (Fig 8.10e). A head-
flap is usually left out because of the brain swelling light and malleable brain retractor should be used
that is already present or is likely to develop post- for gentle retraction of the brain away from the dura
operatively. These patients will all require neuro- on all sides of the craniotomy. Non-viable brain
intensive care treatment. tissue is removed.
Active bleeding from the sagittal sinus region is
Method difficult to control, but the best way is to use crushed
A generous scalp flap is raised overlying the region muscle (e.g. temporalis) andâ•›/â•›or large segments of
of trauma (Figs 8.10a & b). The temporalis muscle surgical or gelfoam impacted over the sagittal sinus

FIG 8.10eâ•… Subdural completely exposed. FIG 8.10fâ•… Subdural haematoma evacuated. Note the
acute haemorrhage continuing to flow from the sagittal
sinus region due to torn bridging veins.

FIG 8.10gâ•… Dura replaced over the brain. Note the EVD FIG 8.10hâ•… Scalp closed and ICP monitors in position.
and Codman ICP monitors inserted in the frontal lobe. Note also the subgaleal drain tube posteriorly.

and bridging veins to tamponade the haemorrhage subdural haematoma because of the impact of this
(Fig 8.10f). Do not attempt to extend the craniotomy part of the brain against the sharp edge of the sphe-
up to the sagittal sinus, because the bleeding is likely noid wing and the adjacent bone (bursting injury of
to become uncontrollable. Cortical bleeders are con- the brain).
trolled with bipolar coagulation or Weck clips, and Once haemostasis is obtained, an attempt is made
non-viable macerated brain is removed (e.g. tempo- to achieve a watertight closure of the dura. (Fig
ral lobectomy). If bipolar coagulation is not avail- 8.10g). The subdural space may be drained with
able, standard diathermy on coagulation mode could low-suction drains or passive, closed drains if there
be used. Surgicel or Avitene is placed over the is ongoing ooze or a large potential space between
oozing brain surface. The application of Weck tita- the brain and the skull. Suction drains placed here
nium vascular clips is also helpful to stop bleeding can be harmful because of aggravation of the 
from larger cortical vessels. brain shift. The bone flap is usually left out (see
The underside of the frontal lobe and temporal below). A subgaleal drain is placed if there is
pole as well as the peri-Sylvian region are the areas ongoing ooze of concern. The scalp is closed (Fig
most commonly contused and damaged in an acute 8.10h).
8 • Operative surgery • A. Neurosurgery 165

The non-neurosurgeon may wish to leave the

dura open if haemostasis has not been secured. At
least this may prevent a compressive mass lesion
developing until the patient reaches the neurosur-
geon for a more definitive procedure. Control of
massive progressive brain swelling is challenging
for experienced neurosurgeons. This ‘malignant’
brain swelling continues unabated, despite measures
to correct it. Under the edges of the craniotomy
should be examined again to exclude a distant sub-
dural haematoma, particularly under the temporal
lobe, and consideration should be given to needling
the brain with a brain needle and aspirating to make
sure there is no large, expanding intracerebral hae-
matoma. The lateral ventricle can also be tapped. FIG 8.11aâ•… Lateral skull X-ray showing small
Debridement of necrotic brain can sometimes help depressed parietal fracture.
this situation. The surgeon should check that end-
tidal CO2 or PaCO2 levels are adequately controlled
and that the patient is being ventilated satisfactorily,
and then elevate the head end of the table. If all of
these are negative and the brain continues to swell,
the outlook is very poor and usually the patient will
not survive. The wound is then closed rapidly. The
dura is laid over the brain without closing it. (Dural
closure is impossible in this situation.) The tempo-
ralis muscle is repaired with a few holding sutures
and the scalp is closed.
The bone flap should be placed in a sterile plastic
bag or container, which is then placed in ice and sent
with the patient to the neurosurgical centre, where
it will be stored in the refrigerator at –70°C. As an
alternative, the general surgeon may place the bone
in a subcutaneous pocket in the abdominal wall (see
below). The bone may need to be cut into smaller FIG 8.11bâ•… Lateral skull X-ray showing comminuted
fragments to fit into this cavity. The repair of the depressed frontoparietal fracture.
skull defect usually occurs several weeks to months
following the injury, when the brain swelling has
subsided and the patient is generally stable. an elevator to be passed under the depressed area.
The fracture fragments are elevated and the haema-
Compound depressed fracture of the skull toma is evacuated. Sometimes further burr holes and
(Figs 8.11a–f) craniectomy are required to remove impacted frag-
If the depressed fracture is part of the haematoma ments. The dura may be intact and is left undis-
evacuation, it can be elevated at the time, and incor- turbed unless there is an underlying haematoma that
porated in the craniectomy. The wound edges may requires evacuation. If the dura is torn, the opening
require debridement. The bone fragments are is widened to inspect the brain beneath. In more
removed and all foreign material is removed and major injuries, the contaminated brain is debrided,
washed out. The wound can be irrigated with Beta- the superficial fragments of bone and foreign mate-
dine. Beware of using alcoholic antiseptic prepara- rial are removed, and haemostasis is obtained with
tions on the scalp in this situation, as they may enter bipolar coagulation and Surgicel. The deep, hidden
the wound and damage the exposed brain beneath. fragments of bone or foreign material are not usually
A burr hole is placed at the edge of the fracture line retrieved, particularly if the operator is inexperi-
if the fragments are impacted, and this will enable enced. The dura is repaired to be watertight and this

FIG 8.11dâ•… CT scan: bone windows showing

depressed fracture involving sagittal sinus.

FIG 8.11câ•… Anteroposterior skull X-ray showing the

same fracture as in Figure 8.11b.

often requires a pericranial patch. Monofilament

non-absorbable suture such as Prolene is suitable for
this repair.
If the bone fragments are heavily contaminated,
or the wound has been open for more than 4 hours,
the bone fragments should not be replaced, and the
wound can usually be closed in layers. However, if
there is a sizeable soft-tissue defect, or gross con-
tamination and the question of viability of tissue
remain following debridement, the wound should be
packed and left open for delayed repair; but the dura
does need to be closed to be watertight in this situ- FIG 8.11eâ•… CT scan: brain windows showing the
ation, to prevent meningitis from developing. same injury as in Figure 8.11d. Note that this is a
Depressed fractures in the midline are treacher- treacherous injury because of the involvement of the
sagittal sinus and an inexperienced surgeon should not
ous surgical problems because of the possible attempt to elevate this fracture.
involvement of the sagittal sinus. Removing frag-
ments from the sagittal sinus may cause torrential
haemorrhage and air embolism (Figs 8.11d–f). Only ball rather than fracturing fragments completely.
the most experienced surgeons should venture into These fractures can usually be levered back to a
this region. In most cases, these fractures can remain normal-shaped skull by passing a small elevator like
depressed over the sinus. Depressed fractures in a Watson Cheyne dissector through a small side hole
infants deform the skull like a deformed ping-pong at the edge of the fracture.
8 • Operative surgery • A. Neurosurgery 167


This is a 66-year-old athletics meet official who

presented after being struck by an athletics hammer
in the right temporal region. She had a GCS of 3 at
the scene, with a dilated right pupil. Her CT brain
scan (Fig 8.12a & b) showed an open right-sided
frontotemporal depressed skull fracture. She also had
associated extra-axial and intra-axial haemorrhages.
There was also evidence of right-sided uncal
herniation. She was brought immediately to the
operating theatre, where the depressed skull fracture
was elevated, extradural and subdural haemorrhages
were evacuated, the open wound was debrided and
the bone was left out. She was managed in the ICU
with routine TBI protocols. She was found to have
loss vision in her right eye and suffered a third
cranial nerve palsy once extubated. She was
otherwise intact. She returned for a cranioplasty 3
months later. She remains functionally independent a
year later.

FIG 8.11fâ•… CT scan: sagittal view showing the same

injury as in Figure 8.11e.

a b
FIG 8.12â•… Depressed fracture of the right temporal bone region with underlying extradural haemorrhage and
temporal and frontal lobe contusion: a. axial CT scan, brain windows; b. axial CT scan, bone windows.

Gunshot wound to the brain patient is in a remote location. The principles of this
Selection of patients with a gunshot wound (GSW) emergency surgery are described below and must
to the head for surgery depends on the likely prog- include adequate cleaning and decontamination of
nosis. A significant haematoma, GCS 5 after resus- the wound, debridement, securing haemostasis and
citation, pupils reacting, or single hemisphere lesion obtaining a watertight closure.
would all favour surgery3 (see Chapter 15). This If the patient is deemed suitable for surgery, the
surgery should preferably be performed by a neuro- head is shaved to examine the entire scalp for entry
surgeon, unless there is a large haematoma and the and exit wounds. These wounds are debrided so that

primary closure will still be feasible, unless the defect exploration is required at the remote centre, the
is so large or so contaminated that delayed primary same principles are followed as outlined in the
closure will be indicated. The skin incision is fash- above sections. The patient should be placed on
ioned with the GSW either in the middle of the flap prophylactic antibiotics. The patient’s family should
or included in the middle of a sigmoid incision. A be warned that the patient may die following removal
bone flap or craniectomy is performed to gain ade- of the foreign body if it passes through major vas-
quate exposure of the injured brain and to decom- cular territory.
press the brain. Brain swelling is often a major The neurosurgeon should have a good idea of
problem with these injuries. The superficial loose which blood vessels the knife may have injured. A
bone fragments are removed, along with debris and preoperative angiogram (as well as CT) may be nec-
hair and the bullet track is followed into the brain essary to show this and help with the planning of
substance, using irrigation and forceps to remove the surgery. The neurosurgeon should have vascular
further debris. If the bullet is easily retrieved, it  instruments available, including aneurysm clips and
is removed and placed in a container for forensic microinstruments. If the patient is clinically well
analysis. Haematoma in the trajectory of the bullet  and the blade has already been removed, the wound
is evacuated, and any sizeable vessel bleeding is is debrided and closed. If the weapon is still in situ,
controlled with Weck titanium clips andâ•›/â•›or bipolar it should be removed under general anaesthesia and
coagulation. The brain is irrigated with hydrogen the track debrided in a similar way to the gunshot
peroxide solution and can be irrigated with Betadine wound to the head, by raising a bone flap and then
as well, including the cerebral wound. The exit following the track of the stab wound, if possible. A
wound is then treated in a similar way. An ICP moni� craniectomy may be performed around the blade
tor (preferably including a ventriculostomy catheter) with a drill and the blade gently removed. The blade
is inserted to aid postoperative management. should not be rocked in the bone to remove it. If it
The preoperative skull X-ray or CT will give an looks like a clean stab, then it would be better to
indication as to how much metal is intracranial. perform a very superficial inspection and not follow
These fragments should not be followed deep into the wound deeply into the brain. Only a heavily
the brain unless there is significant necrotic tissue contaminated wound should be followed. Any
and further debris along the track. If in doubt about obvious haematoma is extracted. The dura is then
what is viable and what is non-viable, it is better to closed to be watertight.
leave the tissue rather than take it. A superficial If the patient has a fixed neurological deficit, this
cerebral debridement will usually suffice. The dura is unlikely to be altered by the surgery. If the patient
should be closed to be watertight, even if a pericra- is clinically deteriorating before reaching the operat-
nial patch is necessary. Then the wound is closed, if ing room, this would imply a progressively enlarg-
possible. Brain swelling is managed in a similar way ing haematoma; or if the deterioration is more
to that in other head-injury patients, and a generous sudden, a thromboembolic episode due to vessel
craniectomy, or leaving a craniotomy flap out, may injury is likely. An enlarging haematoma with pro-
be necessary to allow for the swelling to occur, to gressive deterioration can be dealt with by evacua-
minimise a rise in intracranial pressure. Broad spec- tion of the haematoma.
trum intravenous antibiotics, including aerobic and If on removing the blade the patient subsequently
anaerobic cover, are administered. deteriorates, this would imply that a vessel or vessels
have been pierced and, on removing the foreign
Stab wound to the head body, haemorrhage is occurring. It could prove very
Unless there is rapid deterioration with an intracra- difficult to manage this problem without adequate
nial haematoma seen on CT scan, the patient should investigation and instrumentation, and it may lead
be transferred for neurosurgical management. The to the death of the patient. However, there is no
blade is left in situ for the journey, as it may be alternative but to remove the foreign body under
tamponading major blood vessels, venous sinuses or controlled conditions, preferably with an experi-
even the cavernous sinus. Ideally, a cerebral angio- enced neurosurgeon performing the surgery with the
gram should be performed before surgery to define necessary vascular instruments. If the blade involves
any vascular injury. There is a significant incidence the intracavernous or proximal intracranial carotid
of the formation of a delayed ‘false’ aneurysm, or artery, proximal control should be obtained by
pseudoaneurysm following such injuries. If urgent exposing the internal carotid artery in the neck.
8 • Operative surgery • A. Neurosurgery 169

Decompressive craniectomy management of the ICP is failing. The neuro�

There are several scenarios for the application of surgeon may perform an extensive bifronto-
decompressive craniectomy (DC) in patients with temporo-parietal craniectomy to decompress the
TBI. The DC opens the closed cranial compartment, brain (Fig 8.13). This is a major procedure with
allowing the brain to expand out of the confines of a significant complication risk and may not nec-
the skull; this will lower the ICP. This follows the essarily improve outcome. It remains controver-
Monro-Kellie doctrine (see Chapter 3). Larger-sized sial. A randomised trial of early craniectomy for
craniectomies are more effective at reducing ICP diffuse TBI has recently demonstrated worse out-
than small openings. The dura is usually opened and comes in the patients having bifronto-temporo-
expanded using pericranium or temporalis fascia, or parietal craniectomy compared to those having
patched with artificial dura, and this further reduces medical management in ICU.5 The results of this
the ICP. A technique of unilateral and bifrontal cra- trial do not apply to all timings and all types of
niectomy has been described to try to standardise craniectomy, but caution should be exercised
the techniques.4 when considering this operation for patients 
with DAI and refractory elevated ICP. Some 
Scenarios neurosurgeons are advocating unilateral crani�
1. The non-neurosurgeon has raised a rapid craniec- ectomy for predominantly unilateral swelling of
tomy to gain access to an underlying haematoma. the hemisphere or even in cases of bilateral
The bone is not replaced because it is in pieces, diffuse swelling, although there is no evidence
but the underlying brain remains decompressed. base for the latter approach. The timing and
2. The neurosurgeon has performed a unilateral cra- trigger for decompressive craniectomy for diffuse
niotomy or craniectomy and made a decision to swelling with intracranial hypertension remain
leave the bone flap out because of brain swelling controversial.
or because brain swelling is likely. This scenario 4. The military surgeon performs a craniectomy in
often follows the evacuation of an acute SDH and a remote setting to manage a patient with bomb-
there is underlying hemisphere swelling with blast injury to the brain. These injuries cause
midline shift (see Fig 8.10). severe brain swelling and an urgent craniectomy
3. The patient has a diffuse axonal injury (DAI) may save life (see Chapter 15). Air transport of
with generalised brain swelling, and the medical the patient also makes it easier to control ICP in

a b
FIG 8.13â•… a. CT scan, scout view, showing extensive frontotemporoparietal craniectomy; b. axial CT scan showing
extensive craniectomy.

transit. These craniectomies have been very large If there is more acute bleeding and if what looks
when performed by military neurosurgeons (see like semi-solid clot on the background of a chronic
Chapter 15). collection on CT scan is a subacute subdural haema-
toma, a small craniotomy may be preferred by the
Anterior cranial fossa fracture neurosurgeon. This gives good access to the entire
convexity and allows for evacuation of the clot and
This is described in other sections of this chapter, as all the subdural fluid. The cavity can also be fully
follows: irrigated and membranes more completely removed
• For frontal sinus fracture, see Ear, nose and than can be achieved through burr holes.
throat (ENT) surgery and Maxillofacial injuries.
• For CSF rhinorrhoea, see Ear, nose and throat
(ENT) surgery. Cranioplasty
• For orbital fracture, see Maxillofacial injuries. If a craniectomy has been performed, a reconstruc-
• For orbital apex fracture, see Maxillofacial inju- tion of the skull will be required when the brain
ries and Ocular injuries. swelling has receded, the primary wounds have fully
• For transcranial dural repair, see Maxillofacial healed and there is minimal chance of infection,
injuries. with the patient free from systemic infection fevers
• For transnasal endoscopic repair, see Ear, nose or raised white cell count. Thus, it may be several
and throat (ENT) surgery. weeks to months before the skull reconstruction
takes place.
Middle cranial fossa fracture, If the wound was clean and uncontaminated and
CSF leak and repair the bone is in one of several main pieces, these can
See Ear, nose and throat (ENT) surgery in this be joined with mini-plates and replaced. The bone
chapter. can be stored in the refrigerator at –70°C, or in a
subcutaneous cavity created for it in the iliac fossa
(usually the left, so that it is not confused with an
Chronic subdural haematoma appendicectomy scar).
This condition is described in the Chapter 5. Chronic If the bone is too contaminated or comminuted
subdural haematoma (Figs 8.14a–d) will require from the original injury, it is discarded and alterna-
evacuation if it is symptomatic and is causing raised tive reconstructive techniques are utilised. This may
intracranial pressure, with mass effect and midline be acrylic (methyl methacrylate) plastic fashioned at
shift on the CT scan. Clotting abnormalities are the time of the surgery if the defect is relatively
reversed as much as possible preoperatively. If the small. Newer hydroxy-apatite materials are also
patient is elderly and frail, the procedure can be increasingly being used because they form a matrix
done with a single twist drill opening in the skull, for new bone to grow in to them.
with an infant feeding tube passed into the subdural Alternatively, if the defect is large, the cranio-
space to relieve the pressure. Most patients can tol- plasty flap made of acrylic andâ•›/â•›or titanium is fash-
erate general anaesthesia, which is preferred to local ioned preoperatively based on the CT scan showing
anaesthesia. the defect. Cranioplasty manufacturers use com-
Our usual approach is to perform two burr holes puter programs to reconstruct the flap accurately in
over the collection (often frontal and parietal, as this the exact shape of the defect. In the developing
drains a convexity chronic SDH). The subdural world where these materials are not available, seg-
space is drained of bloody fluid, with internal mem- ments of rib can be sectioned longitudinally and
branes being breached so that deeper loculated col- placed in the defect. In young children the adjacent
lections can also be released. The subdural cavity is skull can be split into layers, with one half filling the
then irrigated with warm Ringer’s solution or saline donor site and the other half being used to fill the
until the efflux is clear. A non-suction, closed drain- defect. This is known as ‘split skull’ cranioplasty.
age system is placed in the subdural space and the The operation is fairly straightforward and
drainage bag placed dependently below head level. involves raising the scalp over the defect using the
The patient is nursed flat for several days until the original scar. The existing bone edge and dura are
drainage slows and the brain has expanded to fill the defined. Sometimes the temporalis muscle needs to
subdural space. be separated from the dura, to which it adheres in
8 • Operative surgery • A. Neurosurgery 171

a b

c d
FIG 8.14â•… Axial CT scans showing chronic subdural haematomas: a. hypodense collection; b–d. collection of
mixed densities with septation and membrane formation.

the absence of the bone. The construct is fashioned to be performed at the same time as the cranioplasty,
to fit the defect and is fixed in position, usually using or a ventricular drain placed temporarily so that the
mini-plates and screws. The temporalis is replaced cranioplasty can be performed without the brain
and the scalp is closed in the usual two layers. A bulging out of the craniectomy site. A shunt is then
subgaleal drain may be required if there is sufficient inserted soon after the cranioplasty as a secondary
ooze. The patient is covered with perioperative anti- procedure.
biotics and great care is taken to maintain sterility
throughout the procedure. Special considerations for resource-limited or
If the patient has hydrocephalus and also needs remote environments
the cranioplasty, a CSF shunt diversionary proce- The decision for the general surgeon to perform
dure such as a ventriculoperitoneal shunt may have emergency neurosurgery depends on:

1. the distance and time to definitive neurosurgical

2. the rate of deterioration of the patient
3. CT findings
4. skills of the surgeon
5. consultation advice provided by the neurosur-
geon in the trauma centre
6. interaction with a trauma centre via tele�
The initial management of the severely head-
injured patient should be the same, whether it is in
a major teaching hospital or a rural district hospital.
The definitive management of severe head injury,
however, can become problematic in remote loca- FIG 8.15aâ•… From left to right: Raney scalp clip
tions where neurosurgical services are not available. applicator (with a Raney clip in its applicator); double-
The Neurosurgical Society of Australia has pub- hook scalp retractor; malleable brain strip retractor;
lished guidelines for the management of acute neu- Metzenbaum dissecting scissors.
rotrauma in remote locations because the transfer
distances are so large in Australia.6
If a patient with a surgically amenable intracra-
nial haemorrhage, in particular extradural haema-
toma, cannot be transferred to a neurosurgeon within
2 hours, on-site surgery must be considered. This
decision is best made in consultation with the accept-
ing neurosurgeon and must take into account the
experience of the surgeon at the scene. A patient
who has the classic picture of deterioration after
initial lucidity, unilateral pupillary dilatation and
contralateral hemiparesis with evidence of a skull
fracture should not wait longer than 2 hours for
definitive management. Practitioners who are FIG 8.15bâ•… From top to bottom: bayoneted forceps;
involved in trauma management in remote locations Lane’s toothed forceps (heavy); Gillies toothed forceps
should become familiar with the techniques required (fine); Adson toothed forceps (fine).
for burr holes and craniotomy in preparation for just
such an eventuality.

The instruments normally required to perform emer-
gency neurosurgery are shown in Figures 8.15a–k,
and are divided in to the major groupings for neuro�
surgery as described in the following sections:

General instruments
• Needle holders.
• Scalpel blades and holders.
• Metzenbaum dissecting scissors (Fig 8.15a).
• Mayo curved scissors.
• Bayoneted forceps (Fig 8.15b): non-toothed
FIG 8.15câ•… From top to bottom: Dakin syringe (CR
forceps to diathermy bleeding points and manipu- Bard Inc, Covington, GA, USA); two standard wide-bore
late tissue. The diathermy is touched on the side neurosurgical suckers; three Rhoton suckers (5 Fr, 7 Fr
of the forceps. 10 Fr).
8 • Operative surgery • A. Neurosurgery 173

FIG 8.15eâ•… From top to bottom: brain needle (with

stylet in situ); blunt hook; sharp hook.

FIG 8.15dâ•… From left to right: MacDonald’s dissector;

Watson Cheyne dissector; sharp straight (broad)
periosteal elevator; sharp curved (narrow) periosteal
elevator; smooth periosteal elevator.

FIG 8.15fâ•… Hudson brace with small and large

perforators and conical burrs.

FIG 8.15hâ•… Bone rongeurs, left to right: Wilms, which

FIG 8.15gâ•… Gigli saw showing the saw blade attached have thin longer blades; Horsley, which have broad
to a hook on either end and the dural guide. blades.

FIG 8.15iâ•… Power tools. From left to right: craniotome FIG 8.15k (part 1)â•… The Kerrison rongeur. From top to
with footplate; matchstick burr. bottom: 5╯mm Kerrison rongeur; 2╯mm Kerrison
rongeur; pituitary rongeur (angled).

FIG 8.15jâ•… Gardner-Wells skull tongs. FIG 8.15k (part 2)â•… Enlarged view of ends of Kerrison
rongeurs. From top to bottom: 5╯mm; 2╯mm.

• Bipolar bayoneted forceps with 1–1.5╯mm tip. bleeding in and on the brain itself. The unipolar
These are essential for neurosurgery. It is possible diathermy tends to char widely and stick on the
to do many neurosurgical procedures with stan- brain, which does not quell the haemorrhage
dard unipolar diathermy, but bipolar diathermy when the forceps are removed, and may make it
will be advantageous, particularly for stopping worse.
8 • Operative surgery • A. Neurosurgery 175

• Vessel clips (Weck, Ligaclips): useful to clip • Smooth periosteal elevator (Fig 8.15d): to strip
dural or cerebral vessels, particularly if deeply periosteum on the inside of the skull.
placed or if diathermy is unavailable. • Hudson brace (Fig 8.15f) with posterior fossa
• Standard suckers (Fig 8.15c): these come in extension.
varying sizes from 5 Fr to 10 Fr. • Cranial perforator: to make the conical opening
• Crile class haemostatic forceps (no. 20). of the burr hole (Fig 8.15f).
• Fine-toothed forceps (Fig 8.15b): Adson or • Conical or round burr: to make the cylindrical
Gillies type. burr hole (Fig 8.15f).
• Lane’s heavy-toothed forceps (Fig 8.15b). • Gigli saw (Fig 8.15g) (The set comes with two
• Dakin syringe, plastic disposable (CR Bard Inc, hooks which are attached to the loops at either
Covington, GA 30014, USA) (Fig 8.15c). end of the saw blade and the dural guide is used
• Irrigation fluid: Ringer’s solution is preferable to draw the saw blade through between the burr
because it is the most physiological, but saline holes. The loop at the end of the saw blade
can be used if Ringer’s is unavailable. The brain attaches to the small hook on the dural guide.)
or spinal cord and neural structures should be • Bailey (De Martel) guide (quantity 2): to pass the
kept moist during operative procedures. The fluid Gigli saw under the bone (Fig 8.15g).
is irrigated through a chip syringe or a Dakin • Gigli saw blades (quantity 10, disposable): to cut
syringe. An ordinary plastic syringe will suffice, the bone flap (Fig 8.15g).
if the above is not available. Do not irrigate the • Gigli saw handles (quantity 2): used to hold the
brain directly with penicillin solution because it Gigli saw at each end (Fig 8.15g).
is highly epileptogenic. • Bone rongeurs (Horsley, Wilms): used to remove
• Fibreoptic headlight: very helpful for seeing into pieces of bone (Fig 8.15h).
deep recesses. • Bunnell hand drill (used if no high-speed cranio-
tomeâ•›/â•›drill is available): for drilling holes in the
Scalp instruments bone edge to place dural hitching sutures and to
• Raney scalp clip applicator (Fig 8.15a): for apply- fix the bone flap to the cranial edge using thin
ing plastic clips to the edge of the scalp for haemo- wire or sutures (e.g. heavy silk).
stasis (Omni Medical Designs, Livonia MI, USA). • Power tools: used to cut a cranial bone flap (foot
• Dandy haemostatic forceps (quantity of 20): used plate and rapidly rotating cylindrical cutting saw
to turn back galea and obtain scalp haemostasis blade) and to drill away segments of bone with
if Raney clips are not available. high-speed rotating burrs (Fig 8.15i). Power tools
• Self-retaining retractors. will make neurosurgical exposure much easier
• Double-hook scalp retractor (Fig 8.15a): used to but are not essential. These are driven by com-
retract a dissected scalp flap. It is attached to the pressed air or electricity.
galeal layer, and to the adjacent drape by rubber Brain instruments
elastic bands wrapped around a haemostat forcep.
• Malleable brain strips: to elevate or retract the
Dissectors brain (Fig 8.15a).
• Brain needle (Fig 8.15e): to pass from the surface
• Penfield dissector no. 3: to lift dura away from of the brain to cannulate the ventricle or other
inner table. fluid-filled spaces in the brain.
• Macdonald’s dissector (Fig 8.15d). • Rhoton suckers (5 Fr, 7 Fr, 10 Fr) (Fig 8.15c):
• Watson Cheyne dissector (Fig 8.15d). suckers with a gentle bulbous tip to use on and
• Blunt hook (Fig 8.15e): to dissect in and around in the brain.
small spaces (e.g. nerve root in canal).
• Sharp hook (Fig 8.15e): to tent up a membrane Spinal instruments
(e.g. dura or arachnoid or for fine sharp • Gardner-Wells skull tongs (Fig 8.15j): to attach
dissection). to the skull for cervical traction and immobilisa-
tion of cervical spine fracture (see Cervical spine
Bone instruments injuries in this chapter).
• Sharp periosteal elevator (Fig 8.15d): to strip • Angled bone punches (Kerrison or Cloward) of
periosteum on the outside of the skull. varying size (2╯mm, 3╯mm, 4╯mm): used to

remove small amounts of overhanging bone edge artificial airway. Once in the operating theatre, the
bone from the skull (Fig 8.15k, parts 1 and 2). surgeon and anaesthetist will need to decide on the
• Nerve root retractor (Krayenbühl): to retract best course of action. It is recommended that an
spinal nerve roots. experienced anaesthetist is involved, as emergency
• Pituitary rongeurs of varying angle for grasping airway provision can be very challenging.
and removing pieces of tissue, particularly disc A trial of intubation is undertaken without muscle
material (Fig 8.15k—part 1). paralysis. This may be performed with breathing the
patient down with inhaled anaesthetic agents or with
HAEMOSTATIC AGENTS IN an awake intubation over a fibreoptic endoscope. If
there is any significant doubt about the potential
NEUROSURGERY success of these techniques, or if they have failed,
The haemostatic agents commonly used in neuro- an awake tracheostomy is usually a safer option. The
surgery are listed below. patient is supported, the neck is infiltrated with local
• Surgicel (Johnson & Johnson) is cellulose mesh anaesthetic and a rapid formal tracheostomy is per-
and is very useful to stop haemorrhage on moist formed. A cricothyrotomy is the default procedure
surfaces. It is left in situ. and can be converted to a tracheostomy once an
• Gelfoam (The Upjohn Company) is a gelatin airway is established and the patient is fully
sponge and is used to fill dead space and act as a anaesthetised.
buttress to quell haemorrhage: for example, when Formal endoscopic examination of the pharynx,
placed between the dura and the bone edge and larynx and upper trachea can then be performed.
held in place with sutures. It is not directly Disruptive injuries of the larynx and trachea are
haemostatic. repaired via an open approach. The framework is
• Avitene sponge (Alcon, Puerto Rico) is a fibril- reconstructed, as much mucosa as possible is pre-
lary material made of collagen and is very effec- served and repaired, and the lumen stented (splinted)
tive in stopping haemorrhagic ooze. for six weeks or more above the tracheostomy. Later
• Cottonoids are flat squares (patties) and long rect- revision procedures and scar removal may also be
angular strips (linteens) of matted cotton to which required. These are usually done via an endoscopic
strings are attached, so that they can easily be approach.
retrieved from deep spaces. These protect the
brain from the trauma of instruments abrading its Pharyngeal injury
surface as they pass. They are placed over bleed- If there is ongoing leakage of air or fluid into the
ing points and compressed over the area with a tissues of the neck or formation of an abscess, open
Surgicel or Gelfoam applied to the bleeding drainage and formal repair of the defect will be
surface. If Cottonoids are not available, wet necessary. A passive drain is left in the neck until all
gauze placed over the brain and kept moist is an drainage resolves.
alternative. Swallowing studies to ensure healing and a grad-
• Bone wax (Ethicon) is helpful in stopping con- uated return to normal diet will be employed here
tinued ooze from cancellous bone. It is pressed as well.
onto the cut face of the bone using the index
finger, interposed with gauze, a smooth periosteal CSF rhinorrhoea
elevator, or a Watson Cheyne dissector. CSF rhinorrhoea may emanate from the frontal,
ethmoid and sphenoid sinuses or from the eusta-
B. EAR, NOSE AND THROAT (ENT) chian tube (i.e. middle ear origin), and the diagnosis
SURGERY and management are discussed in Chapter 5.
A CSF leak is shown in Figure 8.16.
Airway management This is discussed under Maxillofacial injuries in this
If the patient’s airway is threatened, but time is avail- chapter.
able for transfer to the operating theatre, this should Ethmoid sinus
occur, but only in the company of doctors who are For complex fractures and intracranial repair, see
adequately equipped and capable of establishing an Maxillofacial injuries in this chapter.
8 • Operative surgery • B. Ear, nose and throat (ENT) surgery 177

in the operating room. An escalating level of inter-

vention is available, depending on the site and
severity of bleeding.
The general anaesthesia may make it easier to
examine and suction the nose to expose the respon-
sible vessel. Diathermy can be used to seal the
vessel permanently. Ongoing bleeding may require
packing, which can be more easily achieved in the
anaesthetised patient. Gauze packs impregnated
with antiseptic or antibiotic and with attached ties
can be placed in the nasopharynx. The ties are
passed through each nasal cavity and tied between
the nostrils across the septum after anterior packs
have been inserted. These can be left for a number
of days if necessary, particularly if the patient has a
FIG 8.16â•… Endoscopic view of a CSF leak. (Courtesy bleeding diathesis.
Dr B Uren.) Pre-existing or new deformities of the nasal
septum may hinder access to the nasal cavity. Septal
repositioning or formal corrective surgery (septo-
plasty) may be required to give access to bleeding
A leak from a single fracture that is easy to localise sites in the mid- or posterior nose. Diathermy and
is well treated with transnasal endoscopic tech- packing techniques can then be used.
niques. If there is doubt concerning the exact site of If bleeding is coming from the posterior nasal
the leak, fluorescein can be injected into the sub- septum or lateral wall of the nose, the sphenopala-
arachnoid space via a lumbar puncture at the time tine artery may need to be ligated (Fig 8.17a–c).
of surgery and a blue light used to confirm the leak This is performed via an endoscopic approach
endoscopically. through the nasal cavity under general anaesthesia.
Leaks through the cribriform plate or roof of the The nose is thoroughly decongested and the artery
ethmoid sinuses will require an an anterior or com- is exposed by raising a mucosal flap at the posterior
plete ethmoidectomy to expose the affected area of end on the middle turbinate, part of which may need
the skull base. The dural defect is plugged or patched to be removed. The artery is mobilised and ligated
with soft tissue such as autologous fat or fascia. with one or more vascular clips. This is usually very
Cartilage or bone can be used to reinforce the repair. effective and additional packing is not required.
The grafts can be secured with tissue glue and Bleeding from the upper nasal cavity is likely to
covered with a free or pedicled nasal mucosal flap, originate from the anterior ethmoidal artery and, to
held in place with absorbable and non-absorbable a lesser extent, the posterior ethmoidal artery. If
packing. ligation is required, it is performed via an external
Sphenoid sinus approach. An incision is made medial to the medial
The sphenoid sinus is adequately exposed via the canthus of the eye and the dissection is performed
nasal cavity and ethmoid sinus. The defect is pre- along the bone of the medial wall of the orbit. The
pared and repaired in a similar way to an ethmoid lacrimal sac is elevated to expose the lacrimal crest.
leak. The cavity of the sinus can then be obliterated The anterior ethmoidal artery is found approxi-
with fat from the anterior abdominal wall. mately 24╯mm posterior to the crest. It is coagulated
A lumbar drain can be used for three days to take with bipolar diathermy. The posterior artery is found
the pressure off repaired leaks. a further 12╯mm posterior and can also be diather-
mied if necessary, but care must be taken as the optic
nerve lies very close behind it. (See Fig 8.17a.)
Multiple vessel ligations are sometimes
If nasal bleeding is not controlled with packing or warranted.
there is ongoing bleeding after the posterior or ante- In a severely compromised patient, with signifi-
rior packs are removed, further intervention may be cant continuing bleeding thought to be from sites
required. This is best done under general anaesthesia supplied by branches of the external carotid artery,

FIG 8.17â•… a. Diagram of the arteries of the nasal septum. b. Diagram of the arteries of the lateral nasal wall. (Based
on Cummings CW36: a. Fig 34.3; b. Fig 34.2.)
8 • Operative surgery • B. Ear, nose and throat (ENT) surgery 179

1. The complete palsy occurred at the time of the

injury (or it is unknown when it occurred due to
the patient’s state of consciousness).
2. The fracture or injury involves the facial nerve
3. The nerve is unable to be stimulated with electri-
cal testing.

Surgical approaches
The surgical approach that is appropriate for a par-
ticular case depends on the state of the hearing in
the ipsilateral ear.
If any hearing is still present in the affected ear,
the inner ear should be preserved. A routine cortical
mastoidectomy is performed to allow access to the
vertical (mastoid) and horizontal (middle ear) seg-
FIG 8.17câ•… Endoscopic view of the sphenopalatine ments of the nerve. The more central segments
artery prior to clipping. Arrow indicates the artery. (labyrinthine and internal auditory canal) are
(Courtesy Dr B Uren.)
explored via a middle cranial fossa craniotomy,
which allows access to the nerve through the roof
of the temporal bone.
ligation of that vessel in the neck may be a life- If the injury or fracture has destroyed the hearing,
saving procedure. The carotid sheath is exposed and a translabyrinthine approach can be employed. In
the external carotid is ligated above its first or second this procedure the mastoid is drilled out to expose
branch to ensure preservation of the internal carotid the vertical and horizontal segments. The labyrinth
artery. is then drilled away to access the two central seg-
If arterial ligation procedures fail to control ments of the nerve.
bleeding, or in patients unfit for anaesthesia or who Facial nerve exploration is performed to establish
have a bleeding diathesis, angiography and emboli- its continuity in the involved segments(s). The nerve
sation of the distal branches of the external carotid is decompressed with removal of the covering bone
artery may be utilised. The facial and internal maxil- and opening of its sheath at the site of the injury.
lary arteries are usually targeted. Embolisation is not This is all that is required if the nerve is in anatomi-
appropriate for the internal carotid artery system in cal continuity or suffered only a minor laceration.
view of the risk of loss of sight and stroke. However, A nerve that has been disrupted needs to be
stenting of carotid injuries is now being increasingly repaired. If the proximal segment can be uncovered
employed by interventional radiologists. and re-routed out of its bony canal to gain length, a
primary microsurgical repair can be performed.
FACIAL NERVE PALSY More commonly, there will be some loss of nerve
length at the site of trauma and a nerve graft will be
Indications for surgery required to replace the missing section. The graft is
Total facial palsy occurring after an injury to the ear usually taken from the sural nerve in the ankle;
or resulting from a fracture of the temporal bone sometimes the greater auricular nerve is harvested
may need to be explored to assess the degree of from the neck.
injury, to decompress it at the site of injury and to Decompression of an injured nerve allows the
repair it if it has been disrupted. The timing of facial best recovery, with the better results achieved in
nerve surgery will depend on the other injuries the cases of lesser compression. Nerves requiring formal
patient may have suffered, particularly those to the repair will never provide normal facial movement,
head and neck, and should be delayed until they but good facial tone, reasonable movement and
have been controlled. complete eyelid closure are generally achieved. The
The nerve should be surgically explored if the improvements seen after surgery take up to two
following criteria are present: years to appear.

C. OCULAR INJURIES need to be disinserted to allow adequate exposure of

the wound. Scleral wounds are closed with 8–0
VISION-THREATENING ORBITAL nylon or Vicryl. Generally wounds are closed ini-
HAEMORRHAGE tially at a recognised landmark (e.g. the limbus).
Prolapsed uveal or retinal tissue may be excised or
In traumatic orbital haemorrhage it is rarely possible reposited, depending on clinical assessment of its
or desirable to explore and evacuate the clot directly. viability. Prolapsed vitreous is excised. After repair
Most often no surgical intervention is required. When of the corneal and scleral wounds, the rectus muscles
there is clear evidence of optic nerve or globe com- are re-attached and the conjunctiva is closed.
promise, the most appropriate surgical management Intracameral antibiotics are given (cefazolin 1╯mg
is to decompress the orbit anteriorly by performing and vancomycin 1╯mg). The conjunctiva is closed
a lateral canthotomy with an inferior cantholysis. with 6–0 plain cat gut (or similar). The patient is
Performance of a canthotomy alone is usually insuf- continued on intravenous antibiotics and the dress-
ficient to decompress the orbit adequately. ing is removed on day 1.
Initially, the canthotomy is performed, either
under local or general anaesthesia. An artery clip is Subsequent management
closed over the lateral canthal tendon with one arm After the primary repair, further surgical procedures
of the artery clip inside the tendon (on the conjunc- are commonly needed. If there has been significant
tival side) and one arm outside (on the cutaneous lens injury, the lens usually becomes rapidly opaque
side). The tendon is crushed for 10 seconds to reduce and intumescent, and its removal is often indicated
subsequent bleeding. The lateral canthal tendon is within the first few weeks. If the posterior capsule
cut horizontally with sharp straight scissors (iris is intact, removal is done either using a standard
scissors or similar). Then the inferior cantholysis is phacoemulsification (in an older patient) or some-
performed. The lateral aspect of the lower lid is times with simple aspiration (especially in a younger
grasped with strong toothed forceps (Adson’s or patient) through a corneal or limbal wound. If there
similar). The lid is pulled away from the eye. The are no signs of infection and if there is adequate
inferior limb of the lateral canthal tendon and the support, a posterior chamber lens is inserted at the
lateral 1╯cm of the orbital septum are incised close time of the lens repair. If there is a posterior capsule
to the orbital margin to free up the lateral 1╯cm of rupture and a mixture of soft lens matter and vitre-
the lower lid. Rarely it may be required to perform ous, generally a vitrectomy and lensectomy are
the same surgery on the upper lid. Usually a second- required.
ary repair is not required. After the surgical repair, Subsequent management of a penetrating injury
the patient is followed to ensure that the visual func- when there has been significant posterior segment
tion returns to normal. injury is complicated. In general, if there is only 
a mild vitreous haemorrhage, it is allowed to 
improve spontaneously. Where there is either a dense
vitreous haemorrhage or a combination of vitreous
General anaesthesia is usually preferred, as it reduces haemorrhage, choroidal haemorrhage and retinal
the risks of further extrusion of intraocular contents detachment, a vitrectomy for removal of vitreous
with the repair and allows for full exploration of the haemorrhage and repair of retinal detachment is indi-
wounds. Simple corneal lacerations are repaired cated. This is usually accompanied by insertion of
with 10–0 nylon. Prolapsed iris is excised if necrotic gas or silicon oil for sustained retinal tamponade.
or dirty and repositioned if it appears viable. Lens Following a severe posterior injury or globe
injuries are usually left at the time of the initial rupture, it may be evident that the eye will not regain
repair and, if needed, secondary cataract can be useful form or any useful vision. In these cases, an
treated later. Wounds extending beyond (posterior early enucleation or evisceration is performed to
to) the limbus require careful exploration and the speed recovery and to reduce the risk of sympathetic
posterior extent of the wound must be identified. In ophthalmia. In the event that after a primary and
general a 360-degree conjunctival peritomy is per- subsequent repair the eye has little visual potential
formed to allow full exposure of the wound(s). and is uncomfortable or is cosmetically unaccept-
Involvement of the thin sclera under the rectus able, a delayed enucleation or evisceration may be
muscles is common, and the rectus muscles may required.
8 • Operative surgery • D. Maxillofacial injuries 181

D. MAXILLOFACIAL INJURIES provide adequate exposure on their own and will

frequently need to be extended, or will require addi-
As discussed elsewhere, injuries of the maxillofacial tional dissection through deeper tissue layers, further
region are usually a secondary management concern putting vital structures at risk. They should therefore
in the head-injured or multi-trauma patient. Once be used with caution. It is often better to close the
life-threatening issues have been treated, attention laceration and to access the injury through the stan-
will then usually turn to the management of any dard approaches.
head injury, thoraco-abdominal injury, or pelvic and
long bone fracture. Unstable cervical spine injuries Coronal approach
and injuries to the globe can further delay treatment The coronal or bitemporal incision is a versatile
of facial fractures. surgical approach to the calvaria and upper regions
Ideally, fracture repair is performed within 10–14 of the facial skeleton, including the zygomatic arch.
days of the initial injury. This allows sufficient time Although a lengthy incision, its main advantage is
for the patient to be stabilised and any significant that most of the scar can be hidden within the hair-
injuries to be treated. Swelling will have started to line. This advantage is lost in those with male-
settle, allowing better visualisation of the facial con- pattern baldness, and the location of the incision
tours and making surgical access easier. Longer should be chosen with care in those with a receding
delays can allow early union of displaced fractures hairline. Once marked, the scalp is incised parallel
to occur, making it more difficult to achieve an ana- to the hair follicles and then elevated in the subga-
tomic reduction. leal plane. This allows the plane of dissection to
Treatment planning will need to take into account extend laterally over the temporalis muscles, leaving
the nature of the injury, the extent of the facial frac- a continuous layer of pericranium and deep temporal
tures, their degree of comminution and displace- fascia on the deep surface. This pericranial layer can
ment, and the patient’s other injuries and overall be elevated as a vascularised flap for coverage of
health. Clearly, the approach taken for a young, fully defects involving the cranial base or the frontal
dentate patient with simple fractures and an excel- sinus. Nearing the supraorbital rims, the plane of
lent prognosis is different from that taken for an dissection is changed to subperiosteal, and dissec-
older, edentulous patient with multiple comminuted tion can then be continued down to the orbit, the
fractures and a poor prognosis. There are no general body of the zygoma and the zygomatic arch. This
rules—each situation needs to be assessed and approach is designed to protect the frontal branch of
treated on its merits. the facial nerve, as well as the supraorbital neuro-
vascular bundle.
PREOPERATIVE PLANNING This approach can also be used when intracranial
access is required in comminuted or depressed
Before beginning any operative repair, several deci-
frontal bone fractures.
sions need to be made. Firstly, what incisions are
required to adequately expose, reduce and fix the Upper eyelid
fractures? Secondly, does the degree of comminu-
This incision allows access to the superolateral
tion and bone destruction necessitate the use of bone
orbital rim and the lateral orbit and is located in a
grafts to adequately stabilise the facial skeleton?
skin crease in the lateral half of the upper eyelid. It
Thirdly, will any form of intermaxillary fixation
may extend more laterally over the orbital rim if
(IMF) be required, and for how long? Finally, what
well hidden in a natural skin crease (a ‘crow’s foot’).
type of airway is desirable to allow the surgical plan
After skin incision, the orbicularis oculi is divided
to be carried out?
and dissection continued in the submuscular plane
to reach the periosteum of the lateral orbital rim.
ACCESS INCISIONS7 This can then be incised and subperiosteal dissection
The standard approaches to incisions in the facial performed to expose the fracture.
skeleton are well defined and allow adequate expo-
sure to all facial bone fractures. Occasionally, lac- Lower eyelid
erations will be present over the site of the fracture Incisions through the lower eyelid allow access to
and these can also be used for access, obviating the the inferior orbital rim, the orbital floor, and the
need for other incisions. However, lacerations rarely medial orbit. Several different incisions have been

described, but they fall broadly into external infraorbital rim, and the zygomatic body and ante-
approaches (via the skin of the lower eyelid) or rior arch. It provides wide exposure through a simple
transconjunctival approaches. and rapid subperiosteal dissection. Complications
External approaches include the subciliary inci- are few, as long as the infraorbital nerve is identified
sion, the mid-lid incision, and the infraorbital (lid– and protected.
cheek junction) incision. Each of these has its The most critical step is correct location of the
advantages and disadvantages, mainly related to the incision within the sulcus, leaving approximately
visibility of the scar and the risk of eyelid malposi- 5╯mm of unattached gingiva on the alveolar side of
tion.8 Essentially, the visibility of the scar decreases the incision to assist wound closure. Straying too
with a higher incision, but the risk of eyelid malposi- laterally near the molar teeth also risks encountering
tion increases. A subciliary incision is analogous to the opening of the parotid duct, and its location
a lower blepharoplasty approach. This skin is incised should be determined before proceeding.
just below the eyelashes and then the orbicularis Once the mucosa has been divided, dissection
oculi is divided inferior to its pretarsal fibres. Dis- proceeds directly to the bony surface, where a sub-
section then continues in the preseptal plane to the periosteal dissection is performed. This can extend
orbital rim. A mid-lid approach is performed through to the infraorbital rim superiorly, the pyriform margin
a relevant skin crease, found approximately 4–7╯mm medially and laterally to the zygomatic arch, where
below the lid margin. The skin is incised along the anterior fibres of masseter will be encountered.
crease, which will descend inferiorly as it progresses These can be divided with sharp dissection to further
laterally. The orbicularis oculi is then divided expose the arch. Further dissection can also be
directly in line with the skin incision and the dissec- carried out along the nasal floor and lateral nasal
tion continued in the submuscular or preseptal plane walls, if required, in the submucosal plane.
down to the orbital rim. Finally, an infraorbital
approach places the incision at the junction of the Lower buccal sulcus
thin eyelid skin and the thicker cheek skin at the An incision involving the entire lower sulcus can
level of the orbital rim, which is then approached expose the mandible from angle to angle, but this is
directly. The periosteum of the rim is then sharply rarely required. More commonly, segments of this
incised and a subperiosteal plane developed. approach are used to access fracture sites, which
Depending on what is required, the orbital rim, often occur on opposite sides of the mandibular
orbital floor or the zygomatic body can be exposed. ‘ring’. Again, the approach requires placement of
Transconjunctival approaches through the lower the incision approximately 5╯mm from the attached
lid have the significant advantage of being able to gingiva, and care must be taken when elevating the
conceal the scar in the conjunctiva, and avoid trans- periosteum near the mental nerve, which exits the
gressing the skin or muscle layers to access the bone in line with the second bicuspid tooth. Exces-
orbital rim and floor. The incision can be extended sive retraction during the procedure also places the
medially, through the region of the caruncle, to nerve at risk of avulsion injury, which can result in
expose the medial orbital wall behind the lacrimal permanent numbness of the lower lip.
system. This approach can be used in isolation and In the anterior sulcus, only the mucosa is divided
is referred to as the transcaruncular approach. The initially to avoid transecting superficial branches of
exposure obtained with these techniques can be the nerve. Once these are identified, the dissection
improved by also performing a lateral canthotomy continues obliquely back to the external surface of
and inferior cantholysis. However, this introduces a the mandible, leaving a suitable cuff of mentalis
skin incision that requires meticulous repair to avoid muscle on the bone to allow re-suspension and
an unwanted canthal deformity. Once the conjunctiva closure at the conclusion. Dissection continues in
has been incised below the lower tarsal plate, dissec- the subperiosteal plane to fully expose the fracture
tion can continue in either a preseptal or postseptal and allow fixation.
plane down to the orbital rim, where a subperiosteal Posteriorly, the incision can extend up along the
dissection is performed to access the fracture. oblique ridge of the mandible, allowing access to the
anterior border of the ascending ramus. Here tem-
Upper buccal sulcus poralis muscle attachments to the coronoid process
This incision, hidden within the mouth, can provide are encountered and can be stripped from the bone.
access to the anterior surface of the maxilla, the Dissection of the masseter off the lateral surface can
8 • Operative surgery • D. Maxillofacial injuries 183

expose the ramus down to the angle, allowing reduc- Other approaches
tion and fixation of fractures in this location. Although this list is not complete, the most common
approaches to the facial skeleton have been dis-
cussed. There are others that can be used in specific
External approaches to the mandible
circumstances, but they are not often employed
It is not always possible, or advisable, to access because of the visibility of the scar or the risk to
mandibular fractures through the mouth. Such  vital structures, or because a better method exists.
circumstances include fractures in the edentulous These include the facelift approach to the temporo-
mandible, fractures involving the superior ramus or mandibluar (TMJ) or posterior zygomatic arch, the
subcondylar region, and significantly comminuted gullwing and direct approaches to the nasal base and
fractures. In these situations, a transcutaneous naso-orbito-ethmoid region, and direct approaches
approach is used to achieve adequate exposure and to the frontal bone through forehead creases. Other
fixation of these more challenging injuries. approaches that are rarely indicated include the
The submandibular (Risdon) incision allows facial degloving approach and the preauricular
access to the angle and body of the mandible, as well approach to the TMJ joint.
as to the subcondylar region. It can be extended Special mention should also be made of the tem-
anteriorly (submental incision) to access the anterior poral, or Gillies, approach to zygomatic fractures.
mandible, and can even continue along the contra- Traditionally, this has been used for blind manipula-
lateral side to expose the mandible widely from tion of displaced zygomatic bone fractures, but it
angle to angle. The incision is placed in a relevant provides no opportunity for fixation in unstable frac-
skin crease approximately 2╯cm below the mandibu- tures. For this reason, it has largely been superseded
lar border. The platysma muscle is subsequently by the upper sulcus approach, as this is hidden in
divided and the deep cervical fascia is encountered. the mouth and can also be used for internal fixation
This is incised at the level of the skin incision to purposes. The Gillies approach is now only consid-
minimise the risk of injury to the marginal mandibu- ered in the setting of an isolated zygomatic arch
lar nerve. Dissection continues deep to the fascia to fracture.
access the lower border of the mandible. The lower
border of the mandible is then accessed by dividing FACIAL BUTTRESSES AND
the pterygomasseteric sling, with care taken anteri-
orly to identify the facial artery and vein. These can
be ligated and divided to improve access. The sub- Structurally, the face consists of lines of thick load-
mandibular gland is also often encountered and is bearing bone (buttresses) interspersed with cavities
retracted as appropriate. Once the periosteum is for the globes, nasal airway, and paranasal sinuses
incised, the bone can be widely exposed in the sub- that are lined with thin, non-structural bone. The key
periosteal plane. to facial fracture treatment is to realign these but-
The retromandibular approach is used to access tresses and so re-establish the correct height, width
the upper ramus and condylar region. Apart from and projection of the face.9 If this is not done cor-
resulting in a visible scar, it requires dissection rectly, the patient is left with a short, wide and flat
through the parotid gland and carries a risk of  face that is the hallmark of inadequately treated
injury to the facial nerve. In addition, the retroman- facial trauma.10
dibular vein may also be encountered during the High-energy maxillofacial injuries can cause
dissection. such significant bony destruction that the integrity
The incision is placed along the posterior border of these buttresses is lost. In these circumstances,
of the mandible, and the skin and subcutaneous bone grafts are usually required to provide enough
layers are divided to reach the parotid fascia. Blunt structur