Initial Management of Head Injury - sample

PART I

Epidemiology2 CHAPTER 1 Epidemiology of Acute Head Injury

CHAPTER 1

Epidemiology of Acute Head Injury 3 Head Injury: The Magnitude of the Problem

3 Defi nition of Head Injury

3 Incidence of Head Injury

3 Classifi cation of Head Injury

4 Causative Factors

4 Changing Patterns of Head Injury

5 Organisation of Head Injury Care

7 References

EPIDEMIOLOGY OF ACUTE HEAD INJURY CHAPTER 1 3

Head Injury: The Magnitude of the ProblemIn developed and in many developing countries, trauma is the

leading cause of death in the population aged under 45 years. In

view of the young age of most victims, more productive years of

life are lost from trauma than from cardiac and cerebrovascular

disease or from cancer.1 Head injuries account for nearly half

the trauma deaths. Although most trauma deaths prior to

hospital admission are due to chest and multiple injuries, head

injury is responsible for the majority of trauma deaths after

hospital admission.2,3 Head injury is also the most common

cause of permanent disability after injury and such disability

may manifest even in patients with less severe degrees of head

injury.4–6

Hence, head injury poses a major public health problem

worldwide. It results in great personal loss and imposes a

tremendous burden on health-care systems through disability

and costs of care, as well as on society through the years of

productive life lost. In the US, an estimated 1.5–2.0 million

people experience a head injury each year; nearly 250 000 of

these patients require hospitalisation and approximately 52 000

die. Long-term disability affects an estimated 70 000–90 000

people annually. The economic consequences are considerable.

Lifetime medical care costs of head injuries in the US in 1985

were estimated to total US$4.5 billion, including US$3.5 billion

in hospital costs alone.7–10

In low- and middle-income countries (LMIC), trauma is

an increasingly important cause of death and disability. It has

recently been estimated that the economic burden of trauma for

11 countries in South-East Asia is approximately US$11 billion

per year.11 In these countries, large shifts of rural populations

to urban areas and a rapid increase in the use of motor vehicles

are outpacing efforts at injury prevention and organisation of

trauma care.12,13 The multiple costs of head injury are more

burdensome in these emerging economies.

Defi nition of Head InjuryHead injury may be broadly defi ned to include any of

following:15,16

1. a documented history of a blow to the head

2. evidence of injury to the scalp in the form of swelling,

abrasion or contusion

3. evidence of a fracture in a skull X-ray (or computed

tomography (CT) scan) or evidence of brain injury in a

CT scan performed immediately after trauma

4. clinical evidence of a fracture of the skull base

5. clinical evidence of a brain injury (loss or impairment of

consciousness, amnesia, neurological defi cit, seizure)

The scalp, skull and brain can be injured independently and only

a proportion of patients with a head injury sustain a concomitant

brain injury. Conversely, a small number of patients without

initial clinical evidence of an injury to the brain may develop

serious complications, such as intracranial haemorrhage, brain

swelling, meningitis or epilepsy. Consequently, some patients

without clinical evidence of an initial injury to the brain may

need evaluation at emergency departments, and even hospital

admission, making a considerable impact on the health-care

system.14

Incidence of Head InjuryEpidemiological data are of paramount importance in planning

effective preventive measures, planning and providing care for

the acutely injured and rehabilitation for disabled survivors.

Reliable statistics on head injury are diffi cult to obtain from

routinely collected data from hospital admissions because of

poor identifi cation or categorisation of organ-specifi c injuries.

In addition, estimates of the frequency of head injuries from

deaths and discharges in hospital statistics do not include

deaths at the site of the injury and omit patients transferred

after initial assessment.13 Epidemiological factors also depend

on geographic, demographic and socioeconomic factors which

vary with time. In many countries, the overall incidence of

head injury is diffi cult to determine because most statistics are

derived from specifi c locations and minor head injuries tend

to be under-reported. Hence, data from one country cannot be

used as the basis for planning head injury care in another and

the data from a given location need to be updated constantly.

The epidemiological parameters of head injury (in adults) from

diverse locations are given in Table 1.1. The mean incidence rate

of hospitalised and fatal head injury for Europe is reported to be

235 per 100 000 population, similar to the average rate of three

reports from Australia, but much higher than that reported for

the US (103 per 100 000) and India (160 per 100 000).17–21

The incidence of head injury, based on hospital admissions,

is mostly reported from developed countries and is unlikely

to apply to developing countries. Each year in the UK, 1500

per 100 000 population attend an accident and emergency

department with a head injury, 300 are admitted to hospital

and nine die; head injury is implicated in approximately half of

all trauma deaths.22 It has been estimated that for each patient

admitted to hospital with a head injury, approximately three to

four patients with minor head injury are seen and discharged

from emergency departments.23

Classifi cation of Head InjuryHead injury can be classifi ed as outlined below.

By severity of brain injury The most commonly used

modality for classifying brain injury severity is the

post-resuscitation Glasgow Coma Scale (GCS).28

Traditionally, head injury has been classed by severity

as mild (GCS 13–15), moderate (GCS 9–12) or severe

(GCS ≤ 8). Based on this classifi cation, studies of the

head-injured population in high-income countries

have estimated the incidence among different subsets as

follows: severe head injury 5%; moderate head injury

4 PART I EPIDEMIOLOGY

Causative FactorsIn general, the main causes of head injury are road accidents,

falls and assaults. However, there is considerable variation in

the distribution of causes in different countries. Road accidents

are responsible for the majority of head injuries in most

countries.32 World Health Organization (WHO) data show that,

in 2002, nearly 1.2 million people worldwide died as a result

of road traffi c injuries (an average of 3242 people dying each

day). The type of road user accounting for most road fatalities

varied in different countries: in Australia, Netherlands and

the US, most were motor car users; in Malaysia and Thailand,

most were motorcyclists; and in India and Sri Lanka, most

were pedestrians. Between 20 million and 50 million people

globally are estimated to be injured or disabled each year from

traffi c-related injuries. Head injury accounted for a signifi cant

proportion of such deaths and disability.33,34

Falls are an important cause of head injury, especially among

young children and the elderly. Assault is a more common

cause in economically depressed and densely populated inner-

city areas.35 The importance of civil strife (prevalent for long

periods in some areas of the world) is probably underestimated

as a cause of head injury because of poor documentation.

The US is unique among developed countries in that, in some

locations, fi rearms have accounted for more head injury deaths

than traffi c accidents since 1990.36

Alcohol is an important contributory factor in road accidents

(affecting pedestrians and drivers), as well as in assaults and

falls. Falls in adults related to alcohol or assault are likely to be

under-reported.

Changing Patterns of Head InjuryIn many developed countries, the trend data for road deaths

from head injury have indicated a decline in recent years,

attributed mainly to the implementation of preventive

measures, such as seat belts, motorcycle and pedal cycle helmets,

laws on alcohol limits for drivers, speed limits and improved car

5%–10%; and mild head injury 85%–90%.23,29 However,

recent studies have demonstrated that patients with

GCS 13 frequently have CT scan abnormalities and develop

intracranial complications requiring surgical intervention,

in a pattern similar to those who are considered to have

moderate head injury.5,30 Hence, in this publication, mild

head injury includes only patients with GCS 14 and 15 at

the time of presentation at the accident and emergency

department. Patients with GCS 13 are considered to have

sustained moderate head injury.

The use of the degree of cerebral concussion and the

duration of post-traumatic amnesia to defi ne injury

severity is discussed in Chapter 4 (Neurologiocal Evaluation)

and Chapter 15 (Sports-Related Head Injury).

International Classifi cation of Diseases (ICD) Code31 This patho-anatomical classifi cation is used for

epidemiological purposes, as well as for hospital record

keeping (see Table 1.2).

Table 1.1 Comparison of selected epidemiological parameters of head injury from different locations (for adults)

Europe22 US20,24,25 Australia17,19,27 East Asia (Taiwan)26 India18

Incidence per 100 000 population (hospitalised patients and deaths)

235 103 226 334 160

Mortality rate per 100 000 population

15.4 18.1 Not reported 38 20

Severity (% mild/moderate/severe)

79/12/9 80/10/10 76/12/11 78/9/13 71/15/13

External cause (% fall/MVA/violence)

37/40/7 21/25/6 49/25/9 23/65/7 59/25/14

MVA, motor vehicle accident.

Table 1.2 International Classifi cation of Diseases (ICD-10)31

Injuries to the Head (S00–S09)S 0-0 Superfi cial injury of the headS 0-1 Open wound of the headS 0-2 Fractures of skull and facial bonesS 0-3 Injuries of joints and ligaments of the headS 0-4 Injury of cranial nervesS 0-5 Injury of the eye and orbitS 0-6 Intracranial injuryS 0-7 Crush injury of the headS 0-8 Traumatic amputation of part of headS 0-9 Other and unspecifi ed injury of head

Sub categorisation of S 0-6: Intracranial injuryS 06-0 ConcussionS 06-1 Traumatic cerebral oedema S 06-2 Diffuse brain injuryS 06-3 Focal brain injuryS 06-4 Epidural haemorrhageS 06-5 Traumatic subdural haemorrhageS 06-6 Traumatic subarachnoid haemorrhageS 06-7 Intracranial injury with prolonged comaS 06-8 Other intracranial injuriesS 06-9 Intracranial injury unspecifi ed


and road design.8,32 In the US, an analysis of national mortality

trends indicated a 22% decline in rates of death associated with

head injury from 1979 to 1992, attributed largely to injury

prevention and improved treatment.8 However, rates for road

deaths may be much higher and rising in LMIC, where such

measures have not yet been implemented and where there has

been a marked increase in vehicular traffi c as a result of rapid

economic growth.37

In many developed countries, there has been an increase in

the incidence of head injury caused by falls, especially in the

increasing elderly population. A recent study from Sweden

reported that falls were the most common cause of head injury

(58%), followed by traffi c accidents (16%) and persons hit by

objects (15%).38

In some parts of the US, the benefi cial effect of a decline

in motor vehicle-related head injury was undermined by a

marked increase in fi rearm-related head injury.8,34,39 Violence is

unfortunately increasing in prominence as a cause of childhood

injury, especially in economically impoverished areas and in

areas of civil strife.40

Organisation of Head Injury Care (Table 1.3)Mortality and morbidity can be signifi cantly reduced by

(i) preventive strategies that reduce the number and severity

of head injuries; and (ii) head injury care systems that aim to

minimise damage to the brain after an injury by optimising:

1. prehospital care and triage

2. initial management at emergency departments

3. urgent evacuation of signifi cant intracranial haematomas

4. high-quality neurointensive care

5. rehabilitation

Instituting these strategies requires reliable data on the

incidence, causation, distribution and degrees of severity

of head injuries in different locations in a country or region

under consideration. Auditing the effi cacy of a head injury care

system may identify preventable lapses in management and is

important in the planning and improvement of care.

In an audit of a state trauma service in the state of Victoria,

Australia (published in 2000), the following lapses were

identifi ed.45

Prehospital phase An inability to intubate, prolonged

accident scene time and no intravenous access.

In the emergency room Inappropriate reception, delay in

arrival of a consultant, lack of neurosurgical consultation,

failure to perform a cranial CT scan, inadequate blood gases

and oxygen monitoring, inadequate fl uid resuscitation,

delayed respiratory resuscitation and delayed despatch to

the operating room.

In the operating room Failure to institute intracranial

pressure (ICP) monitoring, inadequate fl uid administration

and inappropriate anaesthetic technique.

Table 1.3 Organisation of a head injury care system33,41–44

Preventive measures

Public awareness programmes that target:

The behaviour of drivers and pedestrians

Workplace accidents (e.g. construction sites, factories)

Accidental injury at home (especially in children)

Legislative measures

Alcohol control (basal alcohol concentration < 100 µg/dL in most countries)

Speed limits

Use of safety devices (seat belts, airbags, restraints for infants; helmets for motor cyclists, cyclists, construction workers)

Improved infrastructure

Road design, warning devices, speed limits

Improved safety in vehicles

Seatbelts, air bags, infant restraints

Side impact protection

Firearm registration (to reduce the general availability of fi rearms)

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Advanced trauma systems developed in developed countries

depend on teamwork involving multiple specialties, proper

sequence and timing of interventions and adequate supporting

equipment, resources and personnel. Such systems may not be

easily adapted to LMIC.51,52 Therefore, a head injury care system

in a given locality must take into account the local conditions,

as well as fi nancial and manpower resources. A study in Latin

America showed that prehospital trauma care can be improved

signifi cantly by instituting simple, low-cost measures such as

Prehospital Basic Trauma Life Support training for emergency

medical personnel, increasing sites of dispatch of emergency

medical personnel, use of oropharyngeal airways, suction,

administration of oxygen, intravenous fl uid resuscitation

and cervical collar immobilisation. Implementation of such

measures nearly halved the deaths en route, did not increase

mean time spent at the accident site and increased costs only

minimally.53 In LMIC with limited health care resources, the

institution of preventive measures, organisation of prehospital

care, triage and optimal initial management in emergency

departments will have a substantial impact on the outcome of

trauma.33

6 PART I EPIDEMIOLOGY

In the intensive care unit Failure to institute ICP

monitoring.

Although programmes that provide optimal care for head

injuries of all degrees of severity will reduce mortality and

morbidity, the most profound impact of such programmes has

been the improved management of moderate and mild head

injuries.46,47 Mild injuries are much more common and yet

some patients with mild injury develop life-threatening, but

remediable, complications. Appropriate triage of these patients

is extremely important, particularly when CT scanning and

neurosurgical expertise are scarce.

The publication of practice guidelines for head injury

care (such as those of the Brain Trauma Foundation43, the

Neurosurgical Society of Australasia48 and the European Brain

Injury Consortium49) has been very useful in standardising

head injury management. However, a recent study in the US

revealed that only 16% of the trauma centres surveyed were

in full compliance with the guidelines of the Brain Trauma

Foundation.50

Table 1.3 (cont)

Organisation of a trauma-care system

Patient retrieval by a well-designed EMS, with adequately trained EMS personnel, a well-equipped ambulance service acting in coordination with police and other emergency services; the EMS should provide:

Immediate basic resuscitation at the scene of an accident

Proper triage of the injured

Rapid and safe transfer to an appropriate institution as determined by the nature and severity of the injury

A streamlined referral system based on available resources at trauma care institutions in the region and their proximity

A three-level organisation of trauma care institutions:

Level 3 centres (rural hospitals), with basic care facilities, provide initial resuscitation and safe transfer

Level 2 centres (community trauma centre, district hospital), with a well-designed emergency department with ATLS-trained staff, emergency operating theatre facilities, the services of a General Surgeon, an Orthopaedic Surgeon, an Anaesthetist and, optimally, a CT scan facility and, in some level 2 centres, the services of a Neurosurgeon, provide initial care of head injury if a Neurosurgeon is available on-site or, if a Neurosurgeon is not available, immediate management of life-threatening extracranial injury, initial resuscitation and evaluation of patients with head injury (those patients requiring neurosurgical care are transferred to a level 1 centre)

Level 1 centres (regional trauma centres, teaching hospital), with, in addition to facilities available at a level 2 centre, 24 hour availability of CT scanning, a 24 hour neurosurgical service with an operating theatre for emergency neurosurgery, a well-equipped Neurosurgical Intensive Care Unit, observation wards, facilities for head injury rehabilitation, educational and research programmes, provide comprehensive management of all aspects of head injury

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EMS, emergency medical service; ATLS, advanced trauma life support.


References1. Rockett IRH, Smith GS. Injury related to

chronic disease: international review of premature mortality. Am J Public Health 1987;77:1345–7.

2. Daly K, Thomas P. Trauma deaths in the south west Thames region. Injury 1992;23:393–6.

3. Demetriades D, Murray J, Charalambides K, et al. Trauma fatalities: time and location of hospital deaths. J Am Coll Surg 2004;198:20–6.

4. Kraus JF. Epidemiology of head injury. In: Cooper PR, ed. Head Injury, 3rd edn. Baltimore: William Wilkins, 1993:1–25.

5. Shackford SR, Mackersie RC, Holbrook TL, et al. The epidemiology of traumatic death: a population-based analysis. Arch Surg 1993;128:571–5.

6. Masson F, Thicoipe M, Aye P, et al. Epidemiology of severe brain injuries: a prospective population-based study. J Trauma Infect Crit Care 2001;51(3):481–9.

7. Max W, Mackenzie EJ, Rice DP. Head injuries: costs and consequences. J Head Trauma Rehabil 1991;6:76–91.

8. Sosin DM, Sniezek JE, Waxweller RJ. Trends in death associated with traumatic brain injury, 1979 through 1992: success and failure. JAMA 1995;273:1778–80.

9. Sosin DM, Sniezek JE, Thurman DJ. Incidence of mild and moderate brain injury in the United States, 1991. Brain Inj 1996;10:47–54.

10. Thurman D, Guerrero J. Trends in hospitalization associated with traumatic brain injury. JAMA 1999;282:954–7.

11. Asian Development Bank. Report of Asian Development Bank, 2002. Manila: Asian Development Bank, 2003, http://www.adb.org

12. Murray CJL, Lopez AD. Mortality by cause for the eight regions of the world: global burden of disease study. Lancet 1997;349:1269–76.

13. Sethi D, Zwi AB. Traffi c accidents: another disaster? Eur J Public Health 1999;9:65–7.

14. Jennett B. Epidemiology of head injury. Arch Dis Child 1998;78:403–6.

15. Brookes M, Macmillan R, Cully S, et al. Head injuries in accident and emergency departments. How different are children from adults. J Epidemiol Community Health 1990;44:147–51.

16. Jennett B, Macmillan R. Epidemiology of head injury. BMJ 1981;282:101–4.

17. Badcock K. Head injury in South Australia: incidence of hospital attendance and disability based on a one-year sample. Community Health Studies 1998;XII:428–36.

18. Gururaj G, Sastry Koeluri V, et al. Neurotrauma Registry in the NIMHANS. Bangalore: National Institute of Mental Health and Neurosciences, 2004.

19. Hillier S, Hiller J, Metzer J. Epidemiology of traumatic brain injury in South Australia. Brain Inj 1997;11:649–59.

20. Langlois J, Rutland-Brown W, Thomas K. Traumatic brain injury in the United States: emergency department visits, hospitalizations, and deaths. Atlanta: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control, 2004.

21. Tagliaferri F, Compagnone C, Korsic M, et al. A systematic review of brain injury epidemiology in Europe. Acta Neurochir (Wien) 2006;148(3):255–68.

22. Hutchinson PJ. Future perspectives in the acute management of head injury. Br J Surg 2003;90:769–71.

23. Miller JD. Head injury. J Neurol Neurosurg Psychiatry 199356:440–7.

24. Torner J, Choi S, Barnes T. Epidemiology of head injuries. In: Marion D, ed. Traumatic Brain Injury. New York: Thieme, 1999:9–28.

25. Kraus J, McArthur D. Brain and spinal cord injury. In: Nelson M, Tanner C, eds. Neuroepidemiology: from principles to practise. New York: Oxford University Press, 2004:1291–306.

26. Chiu W, Yeh K, Li Y, Gan Y, et al. Traumatic brain injury registry in Taiwan. Neurol Res 1997;19:262–4.

27. Tate R, McDonald S, Lulham J. Incidence of hospital-treated traumatic brain injury in an Australian community. Aust NZ J Public Health 1998;22:419–23.

28. Jennett B, Teasdale GM. Assessment of coma and impaired consciousness: a practical scale. Lancet 1974;ii:81–4.

29. Ruff RM, Marshall LF, Crouch J, et al. Predictors of outcome following severe head trauma: follow-up data from the Traumatic Coma Data Bank. Brain Inj 1993;7(2):101–11.

30. Stein SC, Ross SE. Minor head injury: a proposed strategy for emergency management. Ann Emerg Med 1993;22:1193–6.

31. World Health Organization. The International Statistical Classifi cation of Diseases and Health Related Problems, ICD-10, 2nd edn. Geneva: WHO, 2005.

32. Jennett B. Epidemiology of head injury. J Neurol Neurosurg Psychiatry 1996;60:362–9.

33. Report of the Injury Control Unit. Kuala Lumpur: Ministry of Health, Malaysia, 1996.

34. World Health Organization. World Report on Traffi c Injury Prevention, 2004. Geneva: World Health Organization, 2004, http://www.who.int/world-healthday/./infomaterials/world_report

35. Cooper KD, Tabbador K, Hauser WA, Shulman K, Feiner C, Factor PR. The epidemiology of head injury in the Bronx. Neuroepidemiology 1983;2:70–88.

36. Langlois JA, Rutland-Brown W, Thmoas JE. Traumatic brain injuries in the United States: emergency deparment visits, hospitalizations and deaths. Atlanta: National Centre for Injury Prevention & Control, 2006, http://www.cdc.gov/ncipc/pub-res/TBI_in_US_04/TBI%20in%20the%20US_Jan_2006.pdf

37. Hung C, Chiu W, Tsai C, et al. Epidemiology of head injury in Hualien County, Taiwan. J Formos Med Assoc 1991;262:1227–33.

38. Andersson EH, Bjorklund R, Emanuelson I, et al. Epidemiology of traumatic brain injury: a population based study in western Sweden. Acta Neurol Scand 2003;107:256–9.

39. Masson F, Vecsey J, Salmi LR, et al. Disability and handicap 5 years after a head injury: a population-based study. J Clin Epidemiol 1997;50:595–601.

40. Meyer AA. Death and disability from injury: a global challenge. J Trauma 1998;44:1–12.

41. American College of Surgeons Committee on Trauma. Resources for optimal care of the injured patient. Chicago: American College of Surgeons, 1999.

42. Fearnside MR, Simpson DA. Epidemiology. In: Reilly P, ed. Head Injury. London: Chapman & Hall, 1997:1–23.

43. Bullock RM, Chesnut RM, Clifton GL, et al. Guidelines for the management of severe head injury. J Neurotrauma 2000;17:449–627.

44. Sampalis JS, Lavoie A, Boukas S, et al. Trauma center designation: initial impact on trauma-related mortality. J Trauma Injury Infect Crit Care 1995;39:232–9.

45. Rosenfeld JV, McDermott FT, Laidlaw JD, et al. The preventability of death in road traffi c fatalities with head injury in Victoria, Australia. J Clin Neurosci 2000;7:507–14.

46. Klauber MR, Marshall LF, Luerssen TG, Frankowski R, Tabaddor K, Eisenberg HM. Determinants of head injury mortality: importance of the low risk patient. Neurosurgery 1989;24:31–6.

47. Maas AIR, Dearden M, Servadei F, et al. Current recommendations for neurotrauma. Curr Opin Crit Care 2000;6:281–92.

48. The Royal Australian College of Surgeons. Guidelines for the Management of Acute Neurotrauma in Rural and Remote Locations. Melbourne: The Royal Australian College of Surgeons, 2000, http://www.nsa.org.au/documents/Neurotrauma.pdf

49. Maas AIR, Dearden NM, Teasdale GM, et al. EBIC-Guidelines for management of severe head injury in adults. Acta Neurochir (Wien) 1997;139:286–94.

50. Hesdorffer DC, Ghajar J. Predictors of compliance with the evidence-based guidelines for traumatic brain injury care. A survey of United States trauma centers. J Trauma Injury Infect Crit Care 2002;52:1202–9.

51. Sethi D, Aljunid S, Saperi SB, et al. Injury care in low and middle income countries: identifying potential for change. Inj Control Safety Promotion 2000;7:153–67.

52. Kirsch TD. Emergency medicine around the world. Ann Emerg Med 1998;32:237–8.

53. Arreola-Risa C, Mock CN, Lojero-Wheatly L, et al. Low-cost improvements in prehospital trauma care in a Latin American city. J Trauma 2000;48(1):119–24.

PART II

Basic Principles10 CHAPTER 2 Pathophysiology of Acute Non-Missile Head Injury

33 CHAPTER 3 Intracranial Pressure

CHAPTER 2

Pathophysiology of Acute Non-Missile Head Injury 11 Introduction

11 Phases of Acute Head Injury

11 Biomechanics of Head Injury 11 Impact Injury 13 Inertial Injury 14 Diffuse Axonal Injury 14 Cranial Injury by Static Loading

14 Primary Brain Injury 14 Focal Injuries 16 Diffuse Brain Damage

18 Evolution of Primary Brain Injury 18 Damage to Parenchymal Cells 19 Damage to the Cerebral Vasculature

21 Secondary Brain Injury 21 Traumatic Intracranial Haematomas 25 Post-traumatic Brain Swelling 26 Focal Brain Damage Secondary to Brain Shifts and Herniations

26 Secondary Brain Insults 26 Secondary Insults due to Extracranial Causes

27 Ischaemic Brain Damage Following Acute Head Injury

28 Mechanisms Contributing to Repair of Damage from the Initial Injury

28 Role of Genetic Profi le in Determining the Outcome of Head Injury

29 Summary

30 References

PATHOPHYSIOLOGY OF ACUTE NON-MISSILE HEAD INJURY CHAPTER 2 11

INTRODUCTIONThe pathophysiological changes following acute head

injury are complex. The injury may be caused by different

mechanisms, often in combination. Changes following

injury occur at the molecular, biochemical, cellular

and macroscopic levels. They are dynamic and may be

adversely infl uenced by events occuring after the initial

injury.

Phases of Acute Head InjuryAcute head injury is a progressive process.

The initial, or primary, injury is caused by the mechanical

deformation of brain tissue and blood vessels at the moment of

injury. At a macroscopic level, there may be gross disruption of

brain tissue; at a microscopic level, there may be damage to the

brain parenchymal cells (neurones, axons, glial cells) and the

microcirculation (arterioles, capillaries and venules).

The primary injury may evolve over hours or days through

a series of inter-related biochemical and metabolic changes,

infl ammatory reactions and progressive structural damage to

neurones, glia and the cerebral vasculature. The consequences

of these dynamic changes include cellular swelling, cell death

by necrosis and apoptosis, intracranial haemorrhage, brain

swelling, raised intracranial pressure and cerebral ischaemia.

Hence, the pathophysiological changes in acute head injury can

be considered at three levels (Fig. 2.1).

Secondary injury refers to the delayed effects of events

initiated by the injury. The term may be applied to the evolving

deleterious effects of the primary injury referred to above but in

clinical terms secondary injury is generally applied to the effects

of post-traumatic intracranial haematomas, brain swelling

and increased intracranial pressure and, in the later stages, to

hydrocephalus and infection.

Secondary brain insults are systemic events occurring

after injury that have the potential to add to the damage to

neurones, axons and the cerebral vasculature, already rendered

susceptible by the primary injury. The principal secondary

insults are hypoxia, hypotension, hypercarbia , hyperpyrexia

and electrolyte imbalances. There is increasing evidence that

the primary injury stimulates reparative processes. Therefore,

the magnitude of any head injury is determined by the total

effects of the primary and secondary brain injury, as well as

secondary brain insults, and may be modifi ed by reparative

processes (Fig. 2.2).1

Biomechanics of Head InjuryThe effects that an injury has on the brain and its coverings

tissues may be analysed in terms of the forces applied. Impact

loading refers to the direct effects that contact has on the head;

for example, when the moving head strikes an object and is

prevented from moving after impact. Impact loading results

primarily in injuries at the site of impact. Inertial loading refers

to the effects of acceleration or deceleration on the brain; for

example, when a pedestrian is struck on the body by a moving

vehicle and the head is set in sudden motion or in a high-speed

motor vehicle collision, when the body of the driver is stopped

by the steering wheel and the head continues to decelerate. The

pattern of brain injury is affected by the subsequent motion

within the cranium. This is invariably a combination of linear

(translational) motion and angular motion.

Most injuries are caused by a combination of impact and

inertial forces. Biomechnical analysis has lead to a greater

understanding of the effects of different types of impact and,

hence, to advances in methods of protecting the brain.

For clinical purposes, it is useful to consider injury in terms

of focal and diffuse components.

Impact InjuryA direct impact to the cranium results in local distortion and

propagation of stress waves from the area of impact through

successively deeper layers of the cranium (i.e. scalp–skull–

meninges–brain parenchyma), the degree of distortion of the

tissue and the depth of propagation of the stress waves being

determined by the velocity of impact. Impact injury usually

involves energy of a high magnitude acting directly on the skull

for a short duration (approximately < 50 msec).1

Cascades of cellular, biochemical, metabolic, inflammatory changes, immunological reactions Ischaemic changes, cellular

swelling, cell death (necrosis andapoptosis)

Macroscopic changes (focal or diffuse damage) Contusions, haematoma, brain swelling, brain shifts and herniations

Microscopic changes

Neurones, glia

Axonal injury

Changes in the microcirculationCapillary damage, hypoperfusion,oedema, hyperaemia,haemorrhage, ischaemia

▲ Figure 2.1 Spectrum of the pathophysiological changes after acute head injury

12 PART II BASIC PRINCIPLES

▲ Figure 2.2 Overlapping phases of head injury

▲ Figure 2.3 Effects of direct impact injury from a blunt object with a restricted area of impact. Fragments of bone separate from the rest of the cranium and are driven below the level of the surrounding bone, resulting in a depressed fracture (black arrow). The underlying dura may become lacerated and the underlying brain may be damaged, resulting in a focal contusion (open arrows).

Depending on the characteristics of the injury, such as the

energy of impact and the nature of the impacting surface,

several patterns of damage may result, as described below.

Scalp haematoma The dermal and subcutaneous layers

can distribute the force of an impact and reduce its effects

up to a point without structural damage. However, when

the force exceeds the capacity of the scalp to dissipate

the energy, a scalp haematoma or a scalp laceration will

result.

Linear skull fracture When the skull is impacted over a large area, skull deformation may result, with inward and outward bending. With a moderate force of impact, or if the skull is more resilient, as in an infant, inward and outward bending of the skull may occur without fracture. However, signifi cant inbending of the more mature, rigid skull will result in a linear fracture.

Impact forces can propagate stress waves through the surrounding bone and result in a skull fracture remote from the impact site. Thus, fractures in the base of the skull may result from an impact to the skull vault.2

Depressed fracture When the impacting force is distributed over a relatively small area, such as from a blow by a hammer, a fragment or fragments of bone may separate from the cranium and are driven inwards to a depth equivalent to or more than the thickness of the skull, resulting in a depressed fracture. The underlying dura may either remain intact or be lacerated. The underlying brain may be contused (Fig. 2.3).

Penetrating injury High-energy impact from an object

with a very small surface area (especially a sharp, pointed

object) may lead to deep penetration of the cranium

through very narrow rents in the scalp and cranial bone, as

well as penetration of the dura, and may result in a cerebral

contusion or intracerebral haematoma (Fig. 2.4).

Extradural haematoma The inward and outward bending

of the skull can strip the dura from its attachment to the

inner table of the skull, creating a potential space. If the

dural separation or an overlying skull fracture damages a

meningeal vessel (most commonly the middle meningeal

artery, but also meningeal veins or dural sinuses), an

extradural haematoma (EDH) can result (Fig. 2.5).

▲ Figure 2.4 Impact from a sharp, pointed object resulting in a penetrating injury. Deep penetration can occur through a very narrow rent in the cranial bone, resulting in penetration of the dura and small fragments of bone being driven into the underlying brain with contusion of the underlying brain (black arrow). An intracerebral haematoma may also result (white arrowheads).

Inertial InjuryContre coup contusions See Fig. 2.6a–d.

A direct impact can result in movement of the skull and the

brain in a direction away from the impacting force. The brain

lags behind the skull because of its inertia, and because it is

surrounded by cerebrospinal fl uid (CSF), and then continues

to move once the skull has stopped. During such differential

movement, the brain can be damaged at points remote from

the impact (e.g. by the irregular surfaces of the fl oor of the

anterior and middle cranial fossae and the lesser wing of the

sphenoid), resulting in contre coup contusions, typically located

in the frontal and temporal poles and the orbital surfaces of the

frontal lobes (Fig. 2.6a–d). Contre coup contusions may also occur

in the lateral and inferior surfaces of the temporal lobes, as well

as in the cortex above and below the Sylvian fi ssure.7

Another mechanism for contre coup injury may be the effect

of relative movement between the skull and the brain, leading

to pressure changes in the brain parenchyma, typically at the

poles of the brain (especially in the frontal and temporal poles).

Negative pressure is created at the onset of movement, when

the brain lags behind the skull, and positive pressure is created

when the still-moving brain impacts the stationary skull. When

such pressure change strains exceed the tolerance of the brain

parenchyma and vasculature, contre coup contusions and ICH

can result.


▲ Figure 2.5 Direct impact injury leading to an extradural haematoma (EDH). Direct impact can result in a sub-galeal haematoma in the scalp (black arrow). The inward and outward bending of the skull can result in a skull fracture, which is usually located directly beneath the scalp haematoma. The dura may become stripped from the inner table of the skull and an EDH (open arrow) results from a tear in a meningeal vessel.

▲ Figure 2.6 Contre coup contusions after a direct impact injury. (a) An impact to the occipital region results in differential movement between the brain and the rough, irregular surfaces of the fl oor of the anterior cranial fossa and the temporal fossa (open arrows). (b) Such motion can lead to cerebral contusions involving the inferior surfaces of the frontal lobes and the temporal poles (black arrowheads). (c, d) Computed tomography scans showing an area of impact over the right parieto-occipital region (white arrow) leading to contre coup contusions in the frontal lobes (white arrowheads).

d

c

a

b


▲ Figure 2.8 Effects of compression. Forces of compression can lead to signifi cant deformation of the skull and extensive comminuted fractures of the skull vault (black arrowheads) that may extend to the skull base (curved arrows).

Primary Brain InjuryFocal Injuries

CEREBRAL CONTUSIONSContusions may result from focal impact or diffuse acceleration–

deceleration forces. Stress waves propagating from the area of

impact may deform brain tissue directly underneath. When such

strains exceed the tolerance of brain tissue and its vasculature,

there is a disruption of the brain tissue and vasculature that

results in a direct cerebral contusion (coup contusion; i.e. a

contusion directly beneath the site of impact. This is seen most

clearly in contusions that develop beneath a fracture Fig. 2.9

(‘fracture contusions’).

Contusions may also be associated with diffuse injury and

are most commonly located in the frontal pole, orbital surface

of the frontal lobe, the temporal pole and inferior and lateral

surfaces of the temporal lobe. Contusions are often multiple

and may be associated with other lesions, such as acute SDH,

EDH and diffuse axonal injury (DAI).

A contusion may be localised to the cerebral cortex or may

extend deeper to involve the underlying white matter (Fig. 2.10a).

Contusional damage may also extend over the surface of

the cerebral cortex and there may be associated subarachnoid

haemorrhage (SAH). The severity of a contusional injury may

be judged by the surface extent and depth, as well as whether

the damage is solitary or multiple.4

The damage to the vasculature principally involves

capillaries. Disruption of larger blood vessels at a site of impact

can result in an acute SDH (termed ‘complicated SDH’) or an

ICH (Fig. 2.9).

A typical cerebral contusion consists of a central area of

haemorrhage admixed with areas of non-haemorrhagic necrosis

and partly damaged, oedematous brain (Fig 2.10a). With time, this

central area becomes surrounded by a zone of pericontusional

Acute SDH Acute SDH can result from the tearing of veins

that bridge the brain and venous sinuses or the dura

(uncomplicated acute SDH). Less commonly, an acute

SDH can result from the rupture of a cortical artery

(Fig. 2.7a, b).

Diffuse Axonal Injury (discussed later)

▲ Figure 2.7 Relative movement between the skull and the brain can result in the tearing of veins that bridge the brain and venous sinuses or, less often, cortical arteries (inset, curved arrows), resulting in acute subdural haematoma.

Cranial Injury by Static LoadingThis uncommon injury occurs when compressive forces are

exerted on the stationary head (e.g. a wheel of a vehicle or a

heavy weight compressing the head against the fl oor). Such

forces occur over a longer duration (> 200 msec) compared with

impact forces and usually lead to signifi cant deformation of the

skull, extensive comminution of the skull vault and fractures

of the skull base (Fig. 2.8). The degree of brain injury and the

risk of development of an extra-axial haematoma depend on

the force. Because there is no diffuse injury, consciousness may

be preserved, even in the presence of extensive injury to the

cranium.3


▲ Figure 2.10 Cerebral contusion. (a) A computed tomography (CT) scan demonstrating typical features in a cerebral contusion: location at the cortical surface and involvement of the grey matter at the crests of the gyri. There is a central area of haemorrhage (white arrow) admixed with areas of low density (black arrow) representing non-haemorrhagic necrosis or partly damaged, oedematous brain and a zone of pericontusional oedema (white arrowhead). (b) A CT scan performed within the fi rst 24 hours after a head injury, showing a small contusion (black arrow) in the basal portion of the left frontal lobe. (c) A repeat CT scan performed 72 hours later showing a marked increase in the size of the contusion due to an increase in the haemorrhagic component (black arrow), as well as an increase in the surrounding oedema (white arrowhead).

b

c

a

▲ Figure 2.9 Effects of direct impact injury from a blunt object, with a broad area of impact. (a, b) The inward and outward bending of the skull can lead to a linear fracture. The (a) compressive (small black arrows) and (b) tensile (small open arrows) strains created can damage the brain parenchyma and its vasculature, resulting in (c) a direct cerebral contusion (white arrowheads) and a contusion-related acute subdural haematoma (large black arrow). (d) Computed tomography (CT) scan showing a cerebral contusion underneath a comminuted fracture (white arrows).

a

b

c

d


Herniation contusions occur when the medial parts of the

temporal lobe impinge on the free edge of the tentorium or the

cerebellar tonsils make contact with the foramen magnum at

the time of injury.

Gliding contusions are haemorrhagic lesions in the cerebral

cortex and subjacent white matter that typically result from

shearing injuries and are now considered to be part of the

vascular damage associated with diffuse injuries.2

CEREBRAL LACERATIONSCerebral lacerations resemble contusions, except that the pia-

arachnoid on the surface of the involved area in the cerebral

cortex is disrupted. Lacerations of the frontal and temporal

lobes are usually associated with other lesions, such as ICH

and acute SDH. This combination is termed a ‘burst’ frontal or

temporal lobe and the SDH is termed a ‘complicated SDH’.1

Cerebral lacerations may also result from a penetrating

injury of the cranium and depressed skull fractures when the

sharp edges of the in-driven bone may disrupt the underlying

cortex and the pia-arachnoid covering.

Diffuse Brain DamageThe most important cause of diffuse brain damage is shearing

force, which affects all components of the brain, in particular

axons and the cerebral vasculature.2,18 Minor strains cause

transient stretching of the axons and cerebral vasculature.

The typical clinical manifestation of minor diffuse injury is a

momentary loss of consciousness followed by recovery. Axons

subjected to severe strain may undergo immediate disruption,

this process being termed primary axotomy. However, most

axons subjected to shearing strain do not undergo immediate

disruption. Some may undergo progressive swelling followed

by secondary axotomy from 4 hours to several days after

injury. Others, less severally injured, may be able to repair the

cytoskeletal damage.19–21

Axonal injury may be focal or widely distributed in the white

matter of the cerebral hemispheres (diffuse axonal injury)

(Fig. 2.11). Severe shearing strain also leads to diffuse vascular

injury. Diffuse brain injury is often associated with ischaemic/

hypoxic injury and brain swelling.

DIFFUSE AXONAL INJURYIn mild forms of DAI, microscopic foci of axonal damage are

typically distributed in the white matter of the parasagittal

cortex and the corpus callosum. However, with increasing

severity of injury (increased velocity of injury), such foci are

also demonstrated in the internal capsule, the thalami, the

cerebellum and in the ascending and descending tracts of the

brain stem1,3,19,22 (Fig. 2.11a, b). In the more severe forms of DAI,

areas of axonal damage may be suffi ciently large to be visible

on magnetic resonance imaging (MRI) as non-haemorrhagic

lesions.23

Adams et al.24 proposed of a grading system for DAI. In

Grade 1 DAI, abnormalities are limited to histological evidence

of axonal damage throughout the white matter without focal

concentration in either the corpus callosum or in the brain stem.

oedema. In some instances, a traumatic ICH may develop within

a cerebral contusion. Blood fl ow is characteristically absent in

the central core of the contusion and is reduced in the zone

of pericontusional oedema, where autoregulation is impaired

(vasoparalysis). Therefore, the zone of partially damaged cells

at the periphery of a contusion is vulnerable to any further

reductions in perfusion by a reduction in mean arterial pressure,

increased intracranial pressure or vasoconstriction following

hypocapnia as a result of hyperventilation.5,6

EVOLVING CHANGES IN CONTUSIONSA contusion may increase progressively in size, beginning hours after the injury (Fig. 2.10b, c). This may occur as a result of increased bleeding and/or swelling, as outlined below.

Enlargement of the haemorrhagic component The haemorrhagic component of the contusion can enlarge by coalescence of small haemorrhages or delayed haemorrhage secondary to vascular damage. Yamaki et al. demonstrated that the haemorrhagic component of cerebral contusions reaches a maximum 12 hours after the injury in 84% of patients, although some patients may be at risk of delayed haemorrhage for a longer period.8 Kaufmann assessed the risk of delayed haemorrhage within a contusion to be maximal in the fi rst 3–4 days after injury.9 Coagulopathy associated with injury to the brain parenchyma may contribute to the risk of delayed haemorrhage.9 A high incidence of bleeding into the contusions has been reported to occur in alcoholic patients and patients on anticoagulant therapy.10

Increased swelling of the central core of the contusion as well as in the pericontusional zone Partially damaged brain parenchymal cells in the core, as well as in the pericontusional zone, may swell (cytotoxic oedema). In the necrotic areas of the contusion, macromolecules are degraded into smaller molecules, leading to an increase in tissue osmolarity, drawing water from the intravascular compartment into areas of contusion necrosis (osmolar oedema).11 Swelling in the central area of a contusion may lead to compression of the pericontusional zone, resulting in further ischaemia and swelling. Swelling in the pericontusional area may reach a maximum around 48–72 hours after injury.8,12

The mass effect of cerebral contusions from delayed haemorrhage and swelling usually peaks around 3–5 days (although it may range from 24–48 hours to 7–10 days, even, rarely, up to 3 weeks after an injury).13,14 Usually after the fi rst week there is a slow reduction in the volume of the contusion owing to a reduction in swelling, liquefaction and resorption of the haemorrhagic component.

Even small contusions that initially appear relatively innocuous have the potential to enlarge and cause increased intracranial pressure. Sudden and catastrophic deterioration may occur in patients who initially appeared relatively neurologically intact (the ‘talk and die’ or ‘talk and deteriorate’ category).15 Contusions in the temporal fossa and those involving both frontal lobes are most likely to lead to such deterioration.16,17


is related to the level of consciousness immediately after the

injury, the duration of the post-traumatic unconscious state

and the outcome from head injury. Patients who sustain severe

DAI may succumb in the early stages after injury or survive

with severe impairment.

Concussion is a clinical term that implies immediate but

transient impairment of the conscious state after a head injury,

followed by complete recovery of consciousness. Magnetic

resonance imaging and post-mortem pathological studies have

found evidence of axonal injury in deep white matter tracts

and in the brain stem in patients who had made an apparently

complete recovery from concussion.18,23 These lesions may

be the basis for persistent symptoms and neuropsychological

sequelae in some patients after a typical concussional injury. In

a patient who recovers from concussion without any sequelae,

the disturbance of axonal function may have been transient or

the degree of permanent injury too small to detect.14 Clinical

grading of concussion is discussed in Chapter 18.

DIFFUSE VASCULAR INJURYThe cerebral blood vessels are more resistant to shearing

strain than axons. The effects of damage to the cerebral

microvasculature has already been described. Severe forms of

diffuse vascular injury may be evident as multiple petechial

haemorrhages and are often found in patients who die within

minutes of a closed head injury.25 Tissue tear haemorrhages

associated with DAI that are small (< 2 cm in diameter),

discrete and located in typical sites (corticomedullary junction,

deep white matter, basal ganglia and posterolateral midbrain)

are also a form of diffuse vascular injury.

Grade 2 DAI is defi ned by a wider distribution of axonal injury

accompanying a larger focus of axonal damage in the corpus

callosum, whereas Grade 3 DAI is characterised by diffuse

damage to axons associated with larger foci of axonal damage

in both the corpus callosum and brain stem. Haemorrhage

may occur in the larger foci of axonal damage in the corpus

callosum and brainstem as a result of diffuse vascular damage

(Fig. 2.11c).24

Diffuse axonal injury disrupts the neuronal interconnections

between the cerebral cortex and the brain stem reticular

formation. Disruption of these interconnections contributes to

impairment or loss of consciousness in patients who sustain

head injury. With progressively severe injury, the extent and

depth of axonal injury increases.18 Hence, the severity of DAI

a

b

▲ Figure 2.11 Diffuse axonal injury. (a) Shearing forces in the brain (curved arrows) created by angular motion. (b) Foci of microscopic diffuse axonal injury distributed throughout the parasagittal white matter in the cerebral hemispheres (open arrows), in the corpus callosum, typically in the splenium (black arrow), and in the dorsolateral aspect of the midbrain (black arrowhead). (c) Computed tomography scan showing a haemorrhagic focus of axonal damage (a ‘marker’ lesion) in the deep white matter (white arrow).

c

Evolution of Primary Brain InjuryDamage to Parenchymal CellsThe forces associated with the primary injury may immediately

and irreversibly destroy some neurones, axons and glial cells.

In partially damaged cells and axons, complex biochemical

and metabolic events are initiated, which may lead to cellular

swelling and delayed cell death over a period of minutes to

days.21 These events initiated by mechanical deformation are

extremely complex and incompletely understood. They include

the following.

Excitotoxic cascade In this scenario, mechanical deformation

of the neuronal cell membrane results in depolarisation,

major ionic fl uxes and the release of excitatory amino

acids, such as glutamate. There is an effl ux of intracellular

potassium and an infl ux of extracellular sodium and

calcium. The entry of sodium and calcium is accompanied

by water. The excess potassium in the extracellular space is

taken up by astrocytes, which swell.21,26 The infl ux of calcium

into the neurone activates enzymes, including calpains,

which destroy the internal architecture (cytoskeleton) of

the cell, interfere with mitochondrial energy production

and trigger the release of free radicals. Free radicals initiate

cell membrane lipid peroxidation, further disruption of

ionic permeability, further cellular swelling and, fi nally,

cell death through both necrotic and apoptotic processes

(Fig. 2.12).21,26

Infl ammatory cell responses Trauma-induced cytokine

release and leucocyte accumulation in the injured brain


Initial injury

Release of excitatory amino acid neurotransmitters (glutamate, aspartate)

Injury induced cell membrane depolarisation

Opening of gated ion channels

Increased influx of calcium into the cell

Increased influx of sodiumchloride and water into the cell

Efflux of intracellular potassium into the extracellular space

Activation of proteases (calpains), lipases

Destruction of cellular cytoskeleton

Delayed cell death Cellular swelling (cytotoxic oedema)

Swelling of glial cells, extrinsic compression of capillaries, ischaemia

▲ Figure 2.12 Excitotoxic cascade. The sequence of deleterious events in brain parenchymal cells, triggered by the excitotoxic cascade and their consequences.21,26,27


tissue suggest that infl ammation may contribute to traumatic

cellular and vascular injury.28 Intra- and perivascular

accumulation of polymorphonuclear leucocytes occurs

approximately 24 hours after injury. This is followed by a

delayed phase of infl ammation dominated by macrophage

infi ltration, peaking at approximately 3–5 days.29 The

macrophages can secrete a range of factors, including

cytokines, tumour necrosis factor and interleukin (IL)-1 and

IL-6, which may contribute to the release of free radicals and

increase capillary permeability by changing the blood–brain

barrier. Conversely, some aspects of the neuroinfl ammatory

response may be involved in promoting repair.30,31

Metabolic changes Cerebral oxidative metabolism (cerebral

metabolic rate for oxygen (CMRO2)) remains depressed

by approximately 50% in comatose head injury patients

for the fi rst 2 weeks after a severe head injury. The degree

of depression has been shown to be correlated with long-

term outcome.32 Changes in glucose metabolism after

acute head injury follow a triphasic pattern. An early,

brief hyperglycolytic phase may refl ect increased energy

demands in attempting to reverse ionic imbalances. This is

followed by a ‘metabolic depression’ phase that may last up

to 30 days after injury. The third stage is gradual recovery.33

In damaged regions of the brain, lactate levels increase as a

result of anaerobic metabolism.

CONSEQUENCES OF THE EVOLUTION OF CELLULAR DAMAGE

Vulnerability of Partly Damaged CellsPartially damaged cells are more vulnerable to secondary brain

insults. Brain parenchymal cells need a high rate of energy

production to maintain cell integrity and the ionic gradients

needed for impulse generation. The oxygen and glucose

requirements of brain tissue are higher than those of most

other organs and energy stores are limited. These features

account for the extreme vulnerability of brain parenchymal

cells to ischaemia. Any further insults to partially damaged

cells in the immediate postinjury period, particularly hypoxia,

focal ischaemia or reduced cerebral perfusion pressure, may

accelerate the adverse cascades of changes and result in cell death.

Ischaemia may also occur as a result of vasoconstriction that

follows severe hypocapnia (reduced PaCO2) or vasospasm.

Ischaemia is also aggravated by the increased metabolic

demands of injured cells as a result of seizures or pyrexia. It is

important to realise that most secondary ischaemic insults

in the early postinjury period are preventable.

Cerebral OedemaAccumulation of water in neurones and glial cells results

in cellular swelling (cytotoxic oedema). This is considered

to be one of the principal factors contributing to increased

intracranial pressure in the early postinjury period.34,35

Cytoprotective TherapyAs knowledge developed of the sequential changes following

head injury, several pharmacological ‘neuroprotective’ agents

were developed and underwent clinical trials. These included

free radical scavengers, glutamate antagonists and calcium

channel blockers. None has proven benefi cial at the time of

printing. Clearly, a proven ‘neuroprotective’ therapy would be a

major breakthrough in head injury management.36

Damage to the Cerebral VasculatureDamage to the cerebral microvasculature may lead to:

(i) narrowing and distortion of the capillary lumen by swelling

of capillary endothelial cells, extrinsic compression of capillaries

from swollen glial cells, increased leucocyte adherence to

capillary endothelium and sludging of red cells; (ii) disruption

of the blood–brain barrier, resulting in transendothelial passage

of water, ions and protein-rich fl uid into the extracellular space

(vasogenic oedema); (iii) pericapillary haemorrhage, which

may coalesce and enlarge, contributing to the progression of

the haemorrhagic component in cerebral contusions; and

(iv) loss of autoregulation or vasoparalysis, with vasodilatation

and hyperaemia (congestive brain swelling) (Fig. 2.13a, b).26,35

a

(b) b

▲ Figure 2.13 Effects of progression of the initial injury in the microcirculation. (a) Uninjured capillary. (b) Changes in the injured capillary leading to reduced fl ow in the microcirculation, including narrowing and distortion of the capillary lumen by swelling of capillary endothelial cells (open arrows), extrinsic compression by swollen glial cells (large black arrows), leucocyte adherence to the capillary endothelium (small black arrow) and sludging of red cells (black arrowheads).

CONSEQUENCES OF DAMAGE TO THE MICROVASCULATURE

Reduction of Regional Cerebral Blood Flow (Hypoperfusion)Pathological changes in the microvasculature and surrounding glial cells can contribute to regional post-traumatic hypoperfusion.2 The loss of endogenous vasodilators (such as nitric oxide) and liberation of vasoconstrictors (such as endothelin-1) are also thought to contribute to early post-traumatic hypoperfusion.38,39

There may be a signifi cant global reduction in cerebral

blood fl ow during the early postinjury period (especially in the

fi rst 6–8 hours) after severe head injury. There may also be focal

reductions in blood fl ow around cerebral contusions and in the

cerebral hemisphere underlying acute SDH.5,21,26,37,40–42 Current

investigations suggest heterogeneity in the degree of perfusion

in different regions of the brain after acute head injury.43

Injured brain cells are particularly vulnerable to any

reductions in perfusion, contributing to the common occurrence

of ischaemic cell change in patients after severe head injury.17

Brain Swelling and Increased Intracranial PressureExtracellular oedema (vasogenic oedema) may result from increased capillary permeability due to disruption of the blood–brain barrier.28 Hyperaemic brain swelling may also result from vasoparalysis and vascular engorgement (hyperaemia). Vasogenic oedema and hyperaemia can contribute to post-traumatic brain swelling (and, hence, increased intracranial pressure) in the later stages of acute head injury.

Impairment of AutoregulationAutoregulation is the capacity of the cerebral microvasculature to adjust cerebral blood fl ow in response to changes in cerebral perfusion pressure or changes in cerebral metabolism. The ability of the cerebral arterioles to change their calibre is termed vasoreactivity.

PRESSURE AUTOREGULATIONThe cerebral perfusion pressure (CPP) is the net force driving arterial blood into the cranial cavity:

CPP=MAP–ICPwhere MAP is mean arterial blood pressure and ICP is

intracranial pressure.In the uninjured brain, pressure autoregulation maintains

a constant cerebral blood fl ow (CBF) within a range of CPP between 50 and 150 mm Hg. An increase in CPP leads to vasoconstriction of the arterioles. Conversely, a reduction in CPP leads to vasodilatation.

METABOLIC AUTOREGULATIONNormally, CBF is coupled to the cerebral metabolic rate; CBF is diminished in patients who are in deep coma, in whom the cerebral metabolic rate is reduced. Conversely, CBF increases with seizures or pyrexia when there is an increase in cerebral metabolism. If CBF falls, there is a fall in tissue oxygen, a fall in pH and an increase in tissue carbon dioxide levels. These metabolic changes stimulate vasodilatation and increase CBF.

In a signifi cant proportion of patients with severe head

injury, cerebral autoregulation is impaired. The impairment

of autoregulation is most evident in the immediate postinjury

phase and may improve over time.44–48 The loss of the capacity to

increase cerebral perfusion in the face of threats such as hypoxia

and hypotension contributes to the increased vulnerability of

the injured brain to secondary insults.28,49 The distribution of

impairment of autoregulation in the cerebral vasculature may

be asymmetric, with the more damaged portion of the brain

demonstrating greater impairment.45,46,48

Impaired autoregulation has also been demonstrated in

patients after mild and moderate head injury, emphasising

the importance of maintaining an adequate cerebral perfusion

pressure (CPP) even in patients with less severe injury.21,50

The deleterious consequences of impaired autoregulation

are further discussed in Chapter 3.

CARBON DIOXIDE REACTIVITYArteriolar calibre, and hence CBF, is sensitive to changes in

the pH in the perivascular spaces of the arterioles and, thus,

to changes in arterial CO2 levels. Hypercarbia leads to a fall

in pH, arteriolar dilatation and an increase in cerebral blood

volume and CBF (potential for increased intracranial pressure).

Hypocapnia leads to an increase in pH, arteriolar constriction

and a decrease in CBF (potential for ischaemia). In most patients

with severe head injury, CO2 reactivity is temporarily disturbed,

but returns to normal within 24 hours. The vulnerability to

hypocapnia is especially signifi cant because the damaged vessels

in the ischaemic areas of the contusions may retain reactivity to

changes in PaCO2 even though pressure autoregulation is lost.5,6

Marion et al.51 demonstrated that CO2 reactivity was increased

in the hemisphere underlying acute SDH. Patients with severe,

persistent impairment of CO2 reactivity die or remain severely

disabled.52

CONSEQUENCES OF DAMAGE TO LARGER INTRACRANIAL VESSELS

Haemorrhage

Extradural haematoma From injury to dural vessels

(middle meningeal artery and vein, other meningeal

vessels or the dural venous sinuses).

Acute subdural haematoma From rupture of bridging

veins, that extend between the dural venous sinuses or less

commonly arteries between the dura and brain surface, the

sylvian veins.

Contusion/laceration-related acute SDH From rupture

of cortical arteries or venules, most often with injuries to

frontal, temporal poles (‘burst lobes’).

Intracerebral haematoma From rupture of deeply situated

perforating vessels in the brain parenchyma.

IschaemiaVascular injury and ischaemia may also follow stretching

and distortion of brain vessels as a result of mechanical


b

a

▲ Figure 2.14 Extradural Haematoma (EDH). (a) A computed tomography (CT) scan demonstrating an EDH, typically located directly beneath the area of impact, as indicated by the overlying scalp haematoma. (b) A CT scan with bone window settings demonstrating a skull fracture (white arrowhead).

displacement (brain shift or herniations caused by intracranial

hypertension) or as a result of vasospasm secondary to

traumatic subarachnoid haemorrhage.2 Ischaemia may also

occur from damage to major extracranial vessels (e.g. traumatic

dissection, stenosis or thrombosis of the internal carotid artery

with distal embolisation) or primary traumatic occlusion of the

middle cerebral artery.53

Secondary Brain InjuryTraumatic Intracranial Haematomas

EXTRADURAL HAEMATOMAExtradural haematoma has been reported in up to 4% of all patients who have a computed tomography (CT) scan after acute head injury and in approximately 9% of all patients who are unconscious at admission. Most EDH occur in the second or third decade, when the dura is less densely adherent to the overlying cranium than in the newborn and elderly and, therefore, more easily stripped from the cranium after an impact. Hence, EDH is rare in the newborn and elderly, in whom the dura is tightly adherent to the cranium.54–56

An EDH is usually located directly beneath the point of impact and is associated with a skull fracture in 66%–95% of instances (Fig. 2.14).55 However, in children < 15 years of age, an EDH may occur without skull fracture because the skull is more pliable and can deform without fracturing. Although a blow to the head or a fall has the most potential to cause EDH, motor vehicle accidents, being more common mechanisms of head injury, account for nearly 50% of all EDH. In infants and young children, most EDH result from falls.56

Most EDH occur in the temporal or temperoparietal region (62%–80%), with the frontal area (7%–18%), posterior fossa (4%–11%) and vertex being less common sites.55

The anterior or posterior branches of the middle meningeal vessels are the source of bleeding in approximately 80% of EDH. In vertex and posterior fossa haematomas, a dural venous sinus, diploic veins or other meningeal vessels may be the source. Usually the EDH is confi ned to the area where the dura was stripped at the initial impact. However, brisk and continued arterial bleeding may produce rapidly increasing pressure within the EDH, resulting in progressive stripping of the dura and a rapidly expanding EDH.54

Associated LesionsIntradural lesions, in particular acute SDH and cerebral contusions, are associated with 27%–38% of EDH.54 The incidence of associated lesions is much higher (50%–70%) in patients who are comatose.57 Associated lesions may signifi cantly infl uence the clinical picture and outcome.

Posterior Fossa EDHExtradural haematoma is the most common traumatic intracranial lesion in the posterior fossa and is most often seen during the second and third decades of life.58 There is usually an impact injury in the occipital region and a fracture crossing the transverse, sigmoid or confl uence of sinuses.


SUBDURAL HAEMATOMASubdural haematomas are classifi ed as acute, sub-acute or chronic depending on time of presentation after injury. Acute SDH presents within 48 hours, subacute SDH presents between 48 hours and 2 weeks, whereas chronic SDH presents after 2 weeks.59

Acute Subdural HaematomaAcute SDH has been reported in 11% of all patients with acute

head injury and in 21% of those with severe head injury.57

The mechanism of injury responsible for the development

of an SDH differs between age groups, with motor vehicle-

related accidents (MVA) being the mechanism in a majority

of younger patients and falls accounting for most SDH in the

older age group (> 65 years). In comatose patients, MVA are the

mechanism of injury in 53%–75% of SDH.57 Cerebral atrophy

with an increase in the potential subdural space increases the

risk of acute SDH in chronic alcoholics and the elderly.

The usual source of bleeding is a ruptured bridging vein,

although at times a cortical artery may be the source (Fig. 2.7).2

When SDH is associated with a cerebral laceration, damaged

pial vessels contribute. When a surface artery is the source of

bleeding, rapid deterioration of consciousness may occur,

similar to the common presentation of an EDH.60

LESIONS ASSOCIATED WITH ACUTE SDH

Unilateral hemisphere ischaemia and swelling Brain

compression caused by the SDH may lead to ischaemia

in the microcirculation and brain swelling (Fig. 2.15).42

Venous compression may also be a factor. The force that

generates the SDH may also be responsible for hemisphere

damage and swelling. In some instances, the acute SDH

may be very thin, but may be accompanied by signifi cant

unilateral hemisphere swelling that accounts for most of

the mass effect.

Diffuse axonal injury, cerebral contusions and intracerebral haematomas (ICH) Acute SDH may be

accompanied by DAI, cerebral contusions and ICH.

‘Burst lobe’ Complicated acute SDH is associated with a

laceration of the frontal or temporal lobe and intracerebral

bleeding (‘burst lobe’). Solonuik et al. described that 28%

of cases of traumatic ICH are associated with an acute

SDH.16

Patients with acute SDH and coexistent unilateral

hemisphere swelling and/or associated lesions often

present with a severe degree of neurological impairment

and have the potential for further deterioration. This

underscores the need for early intensive management

once an acute SDH is detected.

Subacute SDHSubacute SDH becomes symptomatic between 48 hours and

2 weeks after injury. These lesions are usually not accompanied

by signifi cant associated injury. The haematoma undergoes

degradation and is usually a mixture of semisolid and fl uid

blood at the time of presentation.

Chronic SDHChronic SDH becomes symptomatic 2 weeks or more after

trauma and is more commonly seen in the elderly or chronic

alcoholics. Chronic SDH is also liable to occur in patients with

coagulopathy, chronic epilepsy and those with CSF shunts. The

head injury may be of a minor nature or, indeed, there may

be no history of a head injury. A chronic SDH is thought to

originate from a small asymptomatic SDH that becomes

enclosed in a membrane containing numerous fragile, enlarged

capillary vessels (macrocapillaries). Continued bleeding and

escape of plasma from these fragile capillaries is thought to

contribute to gradual enlargement of the haematoma.13 Several

layers of membranes may develop and haematomas of different

stages of evolution may be evident in one location. Absorption

of fl uid into the haematoma by osmotic mechanisms may also

play a role in enlargement of the lesion.

Subdural hygromaThis is a collection of CSF that accumulates in the subdural

space as a result of tear in the arachnoid allowing CSF to enter

the subdural space in a valvular fashion. Effusion of fl uid from

injured vessels in the meninges or in the underlying parenchyma

may also play a role.61,62 The fl uid in a subdural hygroma is

usually clear and xanthrochromic, although at times it may be

blood stained.

INTRACEREBRAL HAEMATOMASA typical traumatic ICH is a well-defi ned, homogeneous

collection of blood within the brain parenchyma in contrast

with a cerebral contusion, which is an ill-defi ned, heterogeneous

lesion comprising areas of haemorrhage, partially damaged

brain parenchyma and necrotic brain. However, this distinction

is not always clear because a contusion with a predominantly

haemorrhagic component may appear as a traumatic ICH.

Traumatic ICH have been reported in approximately 15% of

patients with fatal head injury.63 Solonuik et al.16 reported that

28% of traumatic ICH was associated with SDH and 10% with

EDH. Most cases of traumatic ICH result from direct rupture

of small vessels within the parenchyma secondary to a contre

coup injury. Hence, traumatic ICH are often multiple and most

frequently (in 80%–90% of cases) occur in the white matter of

the frontal and temporal regions. As a result of the common

biomechanical mechanisms involved in their production, ICH

may be associated with lobar contusions and SDH, the ‘burst

lobe’.33,64,65


▲ Figure 2.15 Acute subdural haematoma (AcSDH). A computed tomography scan demonstrating an AcSDH with ischaemia and swelling of the underlying cerebral hemisphere, contributing to a signifi cant mass effect.

a

b

▲ Figure 2.16 Intracerebral haematoma (ICH) secondary to penetrating injury. (a) A computed tomography scan with ‘bone’ window settings demonstrating a narrow area of disruption of the cranium (white arrow) by a penetrating injury; there is also evidence of air in the subdural space (white arrowhead). (b) ‘Brain’ window settings showing an ICH (white arrow).


Traumatic Basal Ganglia HaematomasIntracerebral haematomas occur in the thalamus and basal ganglia in approximately 3% of patients with severe closed head injury.66 These haematomas are often associated with diffuse axonal injury and are thought to result from shearing of deep penetrating branches of the anterior choroidal and lenticulostriate arteries.67 They are often associated with a poor prognosis.

POST-TRAUMATIC INTRAVENTRICULAR HAEMORRHAGEPost-traumatic intraventricular haemorrhage has been reported in as many as 25% of patients with severe head injury. Parenchymal haemorrhages and basal ganglia haemorrhages may extend into the ventricular system. Intraventricular haemorrhage in the absence of parenchymal or basal ganglia haemorrhages is due to tearing of veins in the fornix, septum pellucidum or the choroids plexus and is an indicator of a shearing injury.68,69

TRAUMATIC SUBARACHNOID HAEMORRHAGETraumatic SAH (tSAH) usually results from shear injury to

vessels in the subarachnoid space. In the Traumatic Coma Data

Bank Study of patients after severe head injury, 39% showed

CT scan evidence of tSAH as hyperdense collections of blood in

the cerebral sulci, Sylvian fi ssures and basal cisterns. The risk of

mortality rose nearly twofold when tSAH was evident in the CT

scan.70 In addition, tSAH may occur at sites of contact injury as

a result of disruption of superfi cial vessels.

HAEMATOMAS IN THE CEREBELLUM AND BRAIN STEMTraumatic haematomas in the cerebellum and brain stem are

uncommon, being detected in approximately 3% of patients

who have CT scans after acute head injury.71

CEREBELLAR HAEMATOMASIntraparenchymal haematomas of the cerebellum may develop

within areas of cerebellar contusions (which are often a result

of direct impact) or may develop after a delay in areas of

the cerebellum that appear normal on the initial CT scans.72

Traumatic cerebellar haematomas in children which are often

associated with an occipital fracture.73

BRAIN STEM HAEMATOMATwo types of traumatic brain stem haematomas have been

described:72,73 (i) those associated with diffuse axonal injury,

usually located in the dorsolateral part of the upper brain

stem; and (ii) secondary brainstem haemorrhages or Duret’s

haemorrhages caused by brain stem compression and distortion

associated with increased ICP and brain herniation, usually

located centrally in the pons or midbrain. Blumbergs also

described brain stem contusions, lacerations in relation to skull

base fractures and disruptions at the mesencephalic–pontine,

pontomedullary and medullocervical junctions.74

An ICH may also develop beneath the site of impact (e.g.

adjacent to a linear or depressed fracture) or as the result of a

penetrating injury (Fig. 2.16a, b).

The mass effect secondary to a traumatic ICH may increase with time due to perilesional swelling or from continued bleeding. Delayed ICH may develop in regions that appear normal in an early CT scan, underlying the need for repeat scanning in patients with severe head injury, even when the initial scan was normal, whenever there is unexpected deterioration (see Chapter 5, Radiological Evaluation).

PROGRESSION OF INTRACRANIAL HAEMORRHAGIC LESIONS AND DEVELOPMENT OF NEW HAEMORRHAGEAcute head injury is a dynamic process and progressive changes that can lead to an increase of the mass effect and intracranial pressure. These changes are: (i) enlargement of existing mass lesions; (ii) development of new mass lesions; and (iii) progression of brain swelling.

French and Dublin75 demonstrated that 52% of patients with acute head injury developed new lesions or progression of known lesions in follow-up CT scans. Gentleman et al.76 demonstrated delayed traumatic intracranial haematomas in 15%–20% of patients with severe head injury. A mass effect secondary to evolution of existing lesions or the development of new lesions is the most common cause of sudden neurological deterioration in patients who may be relatively intact at initial assessment.77–79

Delayed Lesions with Diffuse Brain InjuryIn a recent study of patients with moderate and severe head

injury whose initial CT scan showed evidence of a diffuse injury,

one of six showed evidence of deterioration in a subsequent CT

scan. A new mass lesion was evident in 74% of patients who

showed CT evidence of deterioration, worsening prognosis.80

Delayed Lesions After Normal Initial CT ScansThe incidence of delayed lesions after a normal initial CT scan,

is low (4%–9%) in current studies of comatose patients when

high-resolution CT scanners are used.80,81

Mechanisms responsible for delayed haemorrhage in

patients with acute head injury include the following.82–87

Delayed rupture of blood vessels partially damaged during initial injury This may be precipitated by an increase

in intravascular pressure secondary to vasodilatation

following loss of autoregulation or as a result of hypoxia or

hypercarbia. Surges in blood pressure in restless patients

or restoration of blood pressure in a hypotensive patient

may also contribute.

Release of tamponade effect This may follow a rapid

decrease of ICP after surgical removal of a large

intracranial haematoma or administration of a bolus dose

of intravenous mannitol or excessive CSF drainage.

Coagulopathy secondary to brain injury This is discussed

in the next section of this chapter.

Disseminated coagulopathy Disseminated coagulopathy

may occur after severe trauma or as a result of premorbid

coagulopathy (e.g. due to anticoagulant medication,

alcohol intoxication or liver dysfunction).

The lesions most likely to show delayed enlargement are cerebral contusions, ICH and EDH.73,88

Delayed enlargement of EDH Approximately 25% of EDH enlarge in the postinjury period, within a mean interval of 8.2 hours from injury to reaching their fi nal size (range

6–36 hours after injury).89–91 Approximately 8% of EDH appear after an initially negative CT study.92

Delayed enlargement of acute SDH Delayed development of acute SDH is considered rare, with some small acute SDH reported to disappear or decrease in volume.88 However, delayed enlargement of acute SDH has been reported after restoration of blood pressure in hypotensive patients and after evacuation of large traumatic intracranial haematoma.83 Acute SDH in the posterior fossa may enlarge during the fi rst 4 days after injury, especially when it is associated with parenchymal cerebellar injury.93

Delayed enlargement of cerebral contusions Most cerebral contusions increase in size or appear as new lesions during the fi rst 12 hours (Fig. 2.13b, c).88 The maximal mass effect due to new haemorrhage and swelling usually occurs at 3–5 days, although this may range from the fi rst 24–48 hours to 10 days or, rarely, even up to 3 weeks after an injury.8,12–14 Statham et al.17 demonstrated that most patients with bifrontal contusions show evidence of progression by 3 days postinjury, but some deteriorate as late as 9 days after injury.

Delayed traumatic ICH Delayed traumatic ICH (DTICH) is defi ned as an ICH that develops in an area of the brain that was non-haemorrhagic on a previous CT scan.13,56,57 Since the advent of CT scanning, it has been recognised that ICH may develop hours to days or even weeks after an acute head injury, even though an immediate postinjury CT scan may not show their presence.9,94 Although a 3.5% incidence of DTICH has been reported among all head-injured patients, the reported incidence in patients with moderate and severe head injury is 3.3%–7.4%.9,56,76

COAGULOPATHY SECONDARY TO BRAIN INJURYCoagulation consists of conversion of fi brinogen to fi brin by a

cascade of enzymatic changes initiated by tissue and/or vascular

injury. The strands of fi brin trap blood cells (platelets) to form a

clot. Coagulation itself, as well as platelet activity, releases a series

of infl ammatory mediators that promote further coagulation.

Brain tissue is very rich in thromboplastin. The release of

tissue thromboplastin by brain parenchymal damage and the

damaged endothelium of the cerebral vasculature, as well as

platelet activation, can lead to hypercoagulation, fi brinolysis

and a depletion of clotting factors locally in the brain.

The consumption of coagulation factors is refl ected by

changes in coagulation parameters: elevation of prothrombin

time (PT), activated partial thromboplastin time (APTT),

decreased serum levels of fi brinogen and increased serum levels

of fi brin degradation products (FDP) and D-dimer. These

changes are found to peak at about 6 hours after the injury and

return to normal values at 24–36 hours.95

Deleterious Consequences of Coagulopathy Secondary to Brain Injury

Increased risk of post-traumatic haemorrhage Delayed,

as well as progressive, post-traumatic haemorrhage has


been linked to abnormalities of brain injury induced

coagulopathy.86,96

Intravascular microthrombosis and cerebral ischaemia

Microthrombi leading to ischaemic brain damage have

been demonstrated in rats with fl uid percussion injury,

pigs with diffuse axonal injury and in contused brain tissue

removed from patients with acute head injury during

surgical decompression.95

Aggravation of postinjury infl ammatory changes

Blood coagulation can result in an excessive release of

infl ammatory mediators, such as cytokines, which can

damage parenchymal cells and the vascular endothelium

directly, leading to aggravation of ischaemic brain

injury.97

Post-traumatic Brain SwellingBrain swelling implies an increase in ‘brain bulk’. This can

result from an increase in brain tissue water (brain oedema),

an increase in intravascular blood volume (hyperaemia or

vascular engorgement) or a combination of both mechanisms.4

Traumatic brain oedema is considered to contribute most to

post-traumatic brain swelling.35

TRAUMATIC BRAIN OEDEMAThe two principal types of traumatic brain oedema are cytotoxic

oedema (intracellular oedema) and vasogenic oedema.

Cytotoxic (Intracellular) OedemaCytotoxic oedema results from the intracellular accumulation

of water in neurones and glia. Primary damage to parenchymal

cells leads to energy depletion, failure of the active ion pumps

and increased permeability of the cell membrane to sodium

and water, leading to accumulation of sodium and water in the

cells. Cytotoxic oedema can also be aggravated by ischaemia and

hypoxia.98 Astrocytes outnumber neurones and can swell up to

fi ve times their normal size. Hence, glial swelling is considered

the main contributor to cytotoxic oedema.98,99

Vasogenic OedemaVasogenic oedema is the accumulation of fl uid in the

extracellular space. Primary injury to the microvasculature can

lead to disruption of the blood–brain barrier, with increased

capillary permeability and escape of protein-rich fl uid from

the intravascular compartment into the extracellular space.

Vasogenic oedema is seen around cerebral contusions.26

Other important, although less common, mechanisms of

traumatic brain oedema include the following.

Osmotic oedema (osmolar swelling)Osmotic oedema develops as a result of osmotic imbalances

between extracellular and intracellular compartments, leading

to entry of water into cells. Such an imbalance occurs in areas

of contusion necrosis when macromolecules are broken down

into smaller molecules.11,50 Osmotic oedema may also occur as a

result of a reduction in the osmolarity of the extracellular space,

in hyponatraemia.


Interstitial oedema due to obstructive hydrocephalusAn obstruction to CSF outfl ow results in the accumulation of water in the extrcellular space in the periventricular region.

Hydrostatic oedemaHydrostatic oedema may follow an increase in intravascular pressure in an intact vascular bed when loss of autoregulation is combined with high systemic blood pressure or after surgical decompression.

Earlier studies suggested that early post-traumatic brain swelling was mainly due to vascular engorgement and an increase in blood volume. Cellular swelling (cytotoxic oedema) was thought to play a minor role.100,101 However, more recent studies suggest that cytotoxic oedema is the main mechanism of traumatic brain oedema and that cytotoxic oedema can develop during the fi rst 24 hours after injury.26,34,35,98 Diffusion-weighted MRI in patients with severe head injury and early post-traumatic brain swelling demonstrated high levels of water content in brain tissue,102 even in those patients without evidence of ischaemia, indicating that cellular swelling was predominantly responsible for early post-traumatic brain swelling. The blood volume was actually reduced after severe traumatic brain injury. An experimental study with contrast-enhanced MRI demonstrated a lack of blood–brain barrier opening during an early phase of rapid brain swelling after diffuse brain injury, excluding a role for vasogenic oedema in early post-traumatic brain swelling.103

CEREBRAL HYPERAEMIA (VASCULAR ENGORGEMENT)Cerebral vasodilatation or hyperaemia leads to brain swelling as a result of increased volume in the intravascular compartment. Such vasodilatation may be the result of the effects of the initial injury or the result of secondary insults, such as hypoxia, hypercarbia, hyperthermia or seizures. Vascular engorgement can also follow an increase in venous pressure as a result of posture, coughing, straining or high intrathoracic pressure.

DISTRIBUTION OF BRAIN SWELLINGBrain swelling may be focal, unilateral hemispheric or diffuse.

Focal brain swelling This is typically seen around cerebral contusions and intracerebral haematoma (shown in Fig. 2.13a). In the initial stages, the swelling may be predominantly cytotoxic, whereas in the later stages of the injury, vasogenic oedema also plays an important role.104,105

Unilateral hemispheric swelling Swelling of an entire cerebral hemisphere most commonly occurs in association with an acute SDH (less commonly with an EDH or without a mass lesion; shown in Fig. 2.15). When such swelling occurs very rapidly, vascular engorgement may play a role, although eventually the predominant factor responsible appears to be cytotoxic oedema.26

Diffuse brain swelling Diffuse brain swelling may develop after a severe diffuse brain injury or may follow secondary


brain insults, such as hypoxia and hypotension. Diffuse brain swelling is seen in approximately 17% of children with severe head injury.105 In most children, such swelling follows a benign course, unless associated with hypoxia and hypotension.106 Diffuse brain swelling also occurs in approximately 12% of adults after severe head injury.106,107

The deleterious effects of brain swelling include increased ICP, reduced cerebral perfusion, cerebral ischaemia and brain shift, if asymetrical; these aspects will be discussed further in Chapter 3 (Harmful Effects of Increased ICP).

Focal Brain Damage Secondary to Brain Shifts and HerniationsFocal damage may occur secondary to brain shifts and herniations caused by space-occupying haematomas and brain swelling. Such damage includes, most importantly, brain stem compression, focal damage due to compression by brain shifts and focal areas of ischaemia secondary to compression of intracranial arteries. These lesions will be described further in Chapter 3 (Harmful Effects of Increased ICP).

Secondary Brain InsultsSecondary brain insults can occur at any time after the initial injury as a result of systemic or intracranial pathophysiological disturbances (Table 2.1).

Secondary Insults due to Extracranial CausesSecondary brain damage due to extracranial causes is mostly

preventable (see Table 2.1).

HYPOXIA AND HYPOTENSIONHypoxia (PaO

2 < 65 mm Hg, O

2 saturation < 90%, apnoea or

cyanosis before admission) and hypotension (systolic blood

pressure (SBP) < 90 mm Hg in adults) are the most common

extracranial causes of secondary ischaemic brain insults.

Hypotension after acute head injury is most commonly due to

blood loss and should be assumed so until proven otherwise.

However, a small subset of patients has hypotension of

neurogenic origin.108,109

Hypotension may occur at any time after injury, including:

(i) the prehospital period, from the moment of injury to

admission to the Emergency Department; (ii) the early

postinjury period, during management in the Emergency

Department; and (iii) the late postinjury period in the

Intensive Care Unit or in the Head Injury Care Ward. Several

investigations have highlighted the incidence of hypoxia and

hypotension during these different phases and their impact on

the outcome of acute head injury (see Table 2.2).

As noted previously in the section on initial injury and its

progression in this chapter, the injured brain is profoundly

vulnerable to hypotension and hypoxia. Hypotension and

hypoxia also lead to cerebral arteriolar dilatation (hyperaemia),

which, in turn, results in increased ICP.

ANAEMIAAnaemia (haematocrit less than 30%) reduces the oxygen-

carrying capacity of the blood and can contribute to ischaemic

brain injury.116

HYPERPYREXIAEach 1°C increase in temperature results in a 10% increase

in oxygen consumption in the brain, thus increasing the

risk of ischaemic brain damage. Pyrexia also causes cerebral

vasodilatation and increases ICP by 3–4 mm Hg for every 1°C

increase in temperature.117

HYPERGLYCAEMIAThe sympathoadrenal response to trauma can result in an

increase in glucose production. There is experimental evidence

that high serum glucose can exacerbate secondary brain injury

by increasing lactic acid production, changing neuronal pH

and increasing the release of excitatory amino acids.118–120

In patients with severe head injury, hyperglycaemia during the

early postinjury period has been shown to be associated with

poor outcome.121

SEIZURESSeizures can aggravate the neurochemical and metabolic

disturbances in partly damaged brain cells, increase the oxygen

demand of cells and lead to an increase in cerebral blood fl ow

with the risk of increased ICP.

Table 2.1 Types of secondary brain insults

Extracranial insults Intracranial insults

Hypoxia (PaO2 < 60 mm Hg, O

2 saturation < 90%, apnoea or

cyanosis before admission)Hypotension (SBP < 90 mm Hg for adults)Hypocapnia, hypercapniaAcute anaemia (haematocrit < 30%)Hyperpyrexia (temperature > 38°C)Hyponatraemia (serum sodium < 130 mmol/L)Hypoglycaemia, hyperglycaemiaSepsis

Increased intracranial pressure, brain shifts and herniationsIntracranial haematoma• Cerebral contusion• Brain swelling• Hydrocephalus•

Traumatic vasospasmSeizuresIntracranial infection

Meningitis• Brain abscess•

SBP, systolic blood pressure.


Table 2.2 Hypoxia and hypotension after acute head injury

Study Phase Evidence References

131 patients with severe head injury

Prehospital On admission to Emergency DepartmentHypoxia in 27%• Hypotension in 18%•

110

25 patients with acute head injury

Prehospital Hypoxia evident in 44%, associated with poor outcome 111

49 patients with acute head injury

Prehospital Hypoxia in 55%, hypotension in 24%Threefold increase of poor outcome in hypoxic patientsHypotension associated with poor outcome

112

The National Traumatic Coma Data Bank Study of 717 patients with severe head injury

Prehospital, early and late postinjury phases

Prehospital and Early Post-injury Hypotension in 34.6% of patientsLate post-injury hypotension in 32%A single episode of hypotension nearly doubled the risk of mortality. Patients with untreated hypotension in the prehospital phase fared worseHypotension developed only during treatment in the ICU in 16.3% of patients

109, 113


Early postinjury phase

Hypotension in 24% of patientsMortality 65% in hypotensive patientsEven brief episodes of hypotension are associated with poor outcome

114


Early and late postinjury phase (fi rst 24 hours after injury)

Secondary insults occur mostly in the fi rst 24 hours after injuryHypotension is associated with increased mortalityHypoxia is associated with a longer stay in the ICU

115

ICU, intensive care unit.

Ischaemic Brain Damage Following Acute Head InjuryIschaemic brain damage is the predominant pathological

change in patients who die from acute head injury.1,122 The

mechanisms leading to post-traumatic ischaemic brain damage

are listed in Table 2.3.

A global reduction of blood fl ow can occur within the fi rst

few hours after severe brain injury, which is mostly coupled to

a reduction in the cerebral metabolic rate.2,40,41,122 However, in

approximately 30% of patients with severe head injury, the CBF

is reduced to ischaemic levels (< 18 mL/100 g per min).41 It has

been suggested that compromise of the microvasculature is the

most likely cause of early ischaemia in severe head injury.26,124

The role of intravascular microthrombosis in ischaemic brain

damage has already been discussed.

Global ischaemic damage can also result from secondary

insults, such as hypoxia, hypotension, increased ICP (leading

to diminished cerebral perfusion), anaemia, seizures and

hyperthermia, especially in patients in whom the CBF is already

reduced.

MECHANISMS BY WHICH ISCHAEMIA INFLICTS BRAIN TISSUE DAMAGEThe brain is considered to be dependent on aerobic glycolysis

and, hence, an adequate supply of oxygen and glucose, which

Table 2.3 Causes of ischaemic brain damage in acute injury40–42,123

Global ischaemic damage Focal ischaemic damage

Injury to the microvasculature, intravascular microthrombosisHypoxia, hypotensionIncreased ICP

Intracranial haematoma (EDH, SDH, ICH)• Cerebral contusion• Brain swelling•

AnaemiaIncreased metabolic demands (seizures, hyperthermia)

‘Ischaemic penumbra’ around cerebral contusionsHemispheric ischaemia (hemisphere underlying acute SDH)Brain shifts and herniations leading to focal ischaemic damage in the:

Uncus, parahippocampal gyrus• Cingulate gyrus, anterior cerebral artery territory• Posterior cerebral artery territory• Brain stem•

Subarachnoid haemorrhage and vasospasm

ICP, intracranial pressure; EDH, extradural haematoma; SDH, subdural haematoma; ICH, intracerebral haematoma.

again is dependent on adequate perfusion. The reduction in

the cerebral metabolic rate after severe head injury can protect

the injured brain from reduced blood fl ow. Although there is

evidence of increased glucose metabolism in the immediate

postinjury period, increasing the potential for ischaemic

damage, other mechanisms may mitigate the deleterious

effects of reduced blood fl ow. Recent evidence indicates that

lactate released into the extracellular space following glucose

metabolism in the astrocytes and glia may be metabolised

aerobically by the neurones, a phenomenon termed ‘coupled

lactate metabolism’.26,127

However, blood fl ow reduced below a critical ishaemic

threshold can interfere with energy dependent functions,

such as mitochondrial function, cell membrane integrity,

impairment of energy dependant ionic homeostasis in brain

cells and propagation of deleterious biochemical cascades, in a

manner similar to that occurring in partly damaged cells after

the traumatic injury.26

Cerebral ischaemia results in cerebral vasodilatation and

further increases in ICP, a reduction of cerebral perfusion

pressure and further ischaemia. Brain shifts and herniations

secondary to increased intracranial pressure may also result in

further ischaemic damage.

Patients with mild and moderate head injury who suffer

signifi cant ischaemic insults risk adverse outcomes similar to

those with severe head injury.128

FOCAL ISCHAEMIC LESIONSFocal ischaemic lesions include: (i) an ischaemic zone around

cerebral contusions or and ICH; (ii) ischaemia in the hemisphere

underlying an acute SDH (Fig. 2.15); (iii) arterial vascular

territory ischaemia; (iv) venous infarction; and (v) watershed

ischaemia.

Arterial Vascular Territory Ischaemia

Posterior cerebral artery territory This is the most common

arterial vascular territory ischaemia involves the posterior

cerebral artery and is secondary to uncal herniation, which

compresses the artery against the tentorial edge, leading to

a distal ischaemic lesion in the occipital lobe.

Anterior cerebral artery territory Less commonly, the

pericallosal branch of the anterior cerebral artery may be

compressed between the herniating cingulate gyrus and

the free edge of the falx cerebri during lateral transtentorial

herniation, resulting in a distal ischaemic lesion, typically

located along the medial aspects of the frontal and parietal

lobes.

Territory of major intracranial vessels An injury to the

extracranial internal carotid artery, such as a dissection,

may manifest as ischaemia predominantly in the middle

cerebral artery territory. Suspicion of such a lesion is an

indication for an angiographic study of the extracranial

vessels.


Venous InfarctionFractures (especially depressed fractures) overlying a major venous sinus can lead to sinus thrombosis and areas of venous infarction. Such infarcts typically appear as irregular haemorrhages located in the white matter in a non-arterial distribution.73 With superior sagittal sinus thrombosis, such areas of haemorrhagic ischaemia may be located in the parasagittal regions; however, the pattern is quite variable.

Watershed IschaemiaSevere hypotension in the postinjury period can lead to ischaemia of the junctional zones (watershed areas) between the major intracranial vessel territories. These areas are in the frontal parafalcine region (the watershed between the anterior and middle cerebral artery territories) and in the parietal convexity region (the watershed between the middle and posterior cerebral artery territories).73

Mechanisms Contributing to Repair of Damage from the Initial InjuryIntrinsic neuroprotective factors produced by neurones and glia may play an important role in attenuating the effects of the initial injury.129 Neurotrophic growth factors, such as nerve growth factors, brain-derived neurotrophic factor, insulin-like growth factor, glial-derived neurotrophic factor and neurotrophic factor 3, may be upregulated by injury and may aid in recovery. There is experimental evidence that growth factors protect neurones against insults, such as energy loss and glutamate or calcium excess.130

Role of Genetic Profi le in Determining the Outcome of Head InjuryGenetic factors may also play a role in the outcome of head injury. The apolipoprotein E (ApoE) genotype has been demonstrated to infl uence the outcome of head injury. Apolipoprotein E is thought to mediate protective mechanisms against secondary oxidative damage to neurones after head injury. Experimental evidence suggests that ApoE defi ciency may increase vulnerability to increased cerebral cortical lipid peroxidation and protein nitration.21,130 In neuropathological studies of patients who die from head injury, deposits of amyloid β-protein in the cerebral cortex (a pathological marker of injury severity) have been demonstrated predominantly in patients with the APOE ε4 allele. It has also been suggested that, in patients who survive head injury, those with the APOE ε4 genotype are more than twice as likely to have an unfavourable outcome compared with patients without the APOE ε4 genotype, even when other prognostic factors, such as age, coma score and CT fi ndings, are taken into account.21,74


SUMMARYThe initial, or primary, injury results from a mechanical

deformation of brain parenchymal cells, axons and the

microvasculature. The processes initiated by this injury

may continue to damage parenchymal cells, axons and

the microvasculature, progressing over several hours or

days. Secondary brain damage in the form of intracranial

haematoma, brain swelling and increased intracranial

pressure can develop during the course of the injury.

Damaged brain tissue is vulnerable to further ischaemic

insults. This vulnerability is most marked in patients

with severe head injury, but extends across the entire

spectrum of head injury severity. Secondary brain

insults, especially hypoxia, hypotension and increased

ICP, can amplify the primary damage and its progression

by causing ischaemic brain damage. The outcome of

a given injury is determined by a complex interaction

between the severity of the initial injury, the pattern of

progression, the deleterious effects of secondary brain

insults and the processes of healing and repair. There is

an increasing recognition of the role of the genetic profi le

in infl uencing the course of these complex, interacting

processes.


References1. Graham DI, Gennarelli TA. Trauma. In:

Graham DI, Lantos PL, eds. Greenfi eld’s neuropathology, 6th edn. London: Arnold, 1997:197–262.

2. McIntosh TL, Smith DH, Meaney DF, et al. Neuropathological sequelae of traumatic brain injury: relationship to neurochemical and biomechanical mechanisms. Lab Invest 1996;74:315–42.

3. Gennarelli TA. The pathobiology of traumatic brain injury. Neuroscientist 1997;3:73–80.

4. Adams JH, Doyle D, Graham DI, et al. The contusion index: a reappraisal in human and experimental non-missile head injury. Neuropathol Appl Neurobiol 1985;11:299–308.

5. Schroeder ML, Muizelaar JP, Bullock R, et al. Focal ischemia due to traumatic contusion documented by stable, xenon CT, and ultrastructural studies. J Neurosurg 1994;82:966–71.

6. Kent D, Yundt KD, Diringer MD. The use of hyperventilation and its impact on cerebral ischaemia in the treatment of traumatic brain injury. Crit Care Clin 1997;13(1):163–84.

7. Adams J. Brain damage in fatal non-missile head injury in man. In: Handbook of Clinical Neurology, Vol. 13(57). New York: Elsevier, 1980:43–63.

8. Yamaki T, Hirakawa K, Ueguchi T, et al. Chronological evaluation of acute traumatic intracerebral haematoma. Acta Neurochir (Wien) 1990;103:112–15.

9. Kaufmann HH. Delayed posttraumatic intracerebral haematoma. In: Kaufmann HH, ed. Intracerebral haematomas. New York: Raven Press, 1992:173–9.

10. Ramenofsky ML, Subcommittee on ATLS. Advanced trauma life support. Chicago: American College of Surgeons. 1993;

11. Katayama Y, Mori T, Maeda T, et al.: Pathogenesis of the mass effect of cerebral contusions: rapid increase in osmolality within the contusion necrosis. Acta Neurochir Suppl (Wien) 1998;71:289–92.

12. Liau LM, Bergsneider M, Becker DP. Pathology and pathophysiology of head injury. In Youmans JR, ed. Neurological surgery, 4th edn, Vol. 3. Philadelphia: WB Saunders, 1996:1549–94.

13. Gean AD. Concussion, contusion and haematoma. In: Gean AD, ed. Imaging of Head Trauma. New York: Raven Press, 1994:147–206.

14. Teasdale G, Mathew P. Mechanism of cerebral concussion, contusion and other effects of head injury. In Youmans JR, ed. Neurological surgery, Vol. 3. Philadelphia: WB Saunders, 1996:1533–48.

15. Reilly PL, Adams RH, Graham DI, et al. Patients with head injury who talk and die. Lancet 1975;30:375–7.

16. Solonuik D, Pitts LH, Lovely M, et al. Traumatic intracerebral haematomas: timing of appearance and indications for operative removal. J Trauma 1986;26:787–94.

17. Statham PF, Johnston RA, Macpherson P. Delayed deterioration in patients with traumatic frontal contusions. J Neurol Neurosurg Psychiatry 1989;52:351–4.

18. Blumbergs P. Pathology in head injury. In: Reilly P, Bullock R, eds. Head injury. London: Chapman & Hall, 1997:40–70.

19. Povlishock JT. Traumatically induced axonal injury: pathogenesis and pathobiological implications. Brain Pathology 1992;2:1–12.

20. Maxwell WL, Povlishock JT, Graham DL. A mechanistic analysis of nondisruptive axonal injury: a review. J Neurotrauma 1997;14:419–40.

21. Teasdale GM, Graham DI. Craniocerebral trauma: protection and retrieval of the neuronal population after injury. Neurosurgery 1998;43:723–737.

22. Gennarelli TA, Thibault LE, Adams JH, et al. Diffuse axonal injury and traumatic coma in the primate. Ann Neurol 1982;12(6):564–74.

23. Teasdale G, Teasdale E, Hadley D. Computed tomography and magnetic resonance imaging classifi cation of head injury. J Neurotrauma 1992;9(Suppl. 1):S249–57.

24. Adams JH, Doyle D, Ford I, et al. Diffuse axonal injury in head injury: defi nition, diagnosis, and grading. Histopathology 1989;15:49–59.

25. Tomlinson BE. Brain-stem lesions after head injury. J Clin Pathol Suppl (R Coll Pathol) 1970;4:154–65.

26. Bullock MR. Injury and cell function. In: Reilly P, Bullock R, eds. Head injury. London: Chapman & Hall, 1997:121–42.

27. Raghupathi R. Cell death mechanisms following traumatic brain injury. Brain Pathol 2004;14(2):215–22.

28. DeWitt DS, Prough DS. Traumatic cerebral vascular injury: the effects of concussive brain injury on the cerebral vasculature. J Neurotrauma 2003;20:795–814.

29. Holmin S, Söderlund J, Biberfeld P, et al. Intracerebral infl ammation after human brain contusion. Neurosurgery 1998;42:291–8.

30. Bazan NG, Marcheselli VL, Cole-Edwards K. Brain response to injury and neurodegeneration: endogenous neuroprotective signaling. Ann NY Acad Sci 2005;1053:137–47.

31. Graham DI, McIntosh TK, Maxwell WL. Recent advances in neurotrauma. J Neuropathol Exp Neurol 2000;59(8):641–51.

32. Glenn TC, Kelly DF, Boscardin WJ, et al. Energy dysfunction as a predictor of outcome after moderate or severe head injury: indices of oxygen, glucose, and lactate metabolism. J Cereb Blood Flow Metab 2003;23:1239–50.

33. Bergsneider M, Hovda DA, McArthur DL, et al. Metabolic recovery following human traumatic brain injury based on FDG-PET: time course and relationship to neurological disability. J Head Trauma Rehabil 2001;16:135–48.

34. Barzou P, Marmarou A, Fatouros P, et al. Contribution of vasogenic and cellular oedema to traumatic brain swelling measured

by diffusion weighted imaging. J Neurosurg 1997;87:900–7.

35. Marmarou A. Pathophysiology of traumatic brain edema: current concepts. Acta Neurochir Suppl 2003;86:7–10.

36. Marshall LF. Head injury: recent, present, and future. Neurosurgery 2000;47:546–61.

37. Schroeder ML, Muizellar JP, Panos P, et al. Regional cerebral blood volume after severe head injury, in patients with regional cerebral ischaemia. Neurosurgery 1998;42:1276–81.

38. DeWitt DS, Smith TG, Deyo DJ, et al. L-Arginine and superoxide dismutase prevent or reverse cerebral hypoperfusion after fl uid percussion traumatic brain injury. J Neurotrauma 1997;14:223–33.

39. Armstead WM. Role of endothelin-1 in age dependent cerebrovascular hypotensive responses after brain injury. Am J Physiol 1999;277:H1884–94.

40. Bouma GJ, Muizelaar JP, Choi SC, et al. Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischaemia. J Neurosurg 1991;75:685–93.

41. Bouma GJ, Muizelaar JP, Stringer WA, et al. Ultra-early evaluation of regional cerebral blood fl ow in severely head injured patients using xenon-enhanced computerized tomography. J Neurosurg 1992;77:360–8.

42. Schroeder ML, Muizelaar JP, Kuta AJ. Documented reversal of global ischemia immediately after removal of an acute subdural hematoma. J Neurosurg, 1994;80:324–7.

43. Wintermark M, Chioléro R, van Melle G, et al. Relationship between brain perfusion computed tomography variables and cerebral perfusion pressure in severe head trauma patients. Crit Care Med 2004;32:1579–87.

44. Lang EW, Lagopoulos J, Griffi th J, et al. Cerebral vasomotor reactivity testing in head injury: the link between pressure and fl ow. J Neurol Neurosurg Psychiatry 2003;74(8):1053–9.

45. Czosnyka M, Smielewski P, Piechnik S, et al. Cerebral autoregulation following head injury. J Neurosurg 2001;95:756–63.

46. Lee JH, Kelly DF, Oertel M, et al. Carbon dioxide reactivity, pressure autoregulation, and metabolic suppression reactivity after head injury: a transcranial Doppler study. J Neurosurg 2001;95:222–32.

47. Sahuquillo J, Munar F, Baguena M, et al.: Evaluation of CO2 reactivity and autoregulation in patients with post-traumatic diffuse brain swelling (diffuse injury III). Acta Neurochir Suppl (Wien) 1998;71:233–6.

48. Steiner LA, Coles JP, Johnston AJ, et al. Assessment of cerebrovascular autoregulation in head-injured patients: a validation study. Stroke 2003;34:2404–9.

49. DeWitt DS, Jenkins LW, Prough DS. Enhanced vulnerability to secondary ischemic insults after experimental traumatic brain injury. New Horizons 1995;3:376–83.

50. Katayama Y, Kawamata T. Edema fl uid accumulation within necrotic brain tissue as a

cause of the mass effect of cerebral contusion in head trauma patients. Acta Neurochir Suppl (Wien) 2003;86:323–7.

51. Marion DW, Darby D, Yonas H. Acute regional cerebral blood fl ow changes caused by severe head injuries. J Neurosurg 1991;74:407–14.

52. Zwienenberg-Lee M, Muizelaar JP. Clinical pathophysiology of traumatic brain injury. In: Winn HR, ed. Youman’s neurologiocal surgery. Philadelphia: WB Saunders, 2003:5039–64.

53. Mendelow AD, Crawford PJ. Primary and secondary brain injury. In: Reilly PL, Bullock R, eds. Head injury, 2nd edn. London: Hodder Arnold, 2005:73–92.

54. Cooper PR. Post-traumatic intracranial mass lesions. In: Cooper PR, ed. Head injury. Baltimore: Williams & Wilkins, 1993:275–339.

55. Meyer SC, Chestnut RM, Posttraumatic extra-axial mass lesions. In: Tindall GT, Cooper PR, Barrow DL, eds. Current practise of neurosurgery. Baltimore: Williams and Wilkins, 1995:1443–60.

56. Bullock MR, Chesnut R, Ghajar J. et al Surgical management of traumatic brain injury. Neurosurgery 2006;58(Suppl. S2):1–61.

57. Lobato Rd, Rivas JJ Cordobes F, et al. Acute epidural haematoma: an analysis of factors infl uencing the outcome of patients undergoing surgery in coma. J Neurosurg 1988;68:48–57.

58. Chiles BW, Cooper PR. Extra-axial hematomas. In: Loftus CM, ed. Neurosurgical emergencies. Chicago: AANS Publications, 1994:44–8.

59. Graham DI. Neuropathology of head injury. In: Narayan RK, Povlishock JT, eds. Neurotrauma. New York: McGraw Hill, 1996:43–60.

60. Seelig J, Becker D, Miller J, et al. Traumatic acute subdural haematoma: major mortality reduction in comatose patients treated within four hours. N Engl J Med 1981;304:1511–18.

61. Hasegawa M, Yamashima T, Yamashita J, et al. Traumatic subdural hygroma: pathology and meningeal enhancement on MRI. Neurosurgery 1992;31:580–5.

62. Stone JL, Lang RGR, Sugar O, et al. Traumatic subdural hygroma. Neurosurgery 1981;8:542–50.

63. Adams JH, Victor M. Principles of neurology, 5th edn. New York: McGraw Hill, 1993.

64. Crooks DA. Pathogenesis and biomechanics of traumatic intracranial haemorrhages. Virchows Arch A Pathol Anat Histopathol 1991;418(6):479–83.

65. Becker, DP, Doberstein CE, Hovda DA. Craniocerebral trauma: mechanisms, management, and the cellular response to injury. In: Current Concepts. Kalamazoo, MI: Upjohn, 1994:4–47.

66. Cloquhoun IR, Rawlinson J. The signifi cance of haematomas in the basal ganglia in closed head injury. Clin Radiol 1989;40:619–21.

67. Adams JH, Doyle D, Graham DI, et al. Deep intracerebral (basal ganglia) haematomas in fatal non-missile head injury in man. J Neurol Neurosurg Psychiatry 1986;49:1039–43.

68. Karavelis A, Sirmos C. Primary post-traumatic intraventricular haemorrhage. J Neurosurg Sci 1995;39:253–6.

69. LeRoux PD, Haglund MM, Newell DW, et al. Intraventricular haemorrhage in blunt trauma. Neurosurgery 1992;31:678–85.

70. Eisenberg HM, Gary HE, Aldrich EF, et al. Initial CT fi ndings in 753 patients with severe head injury: a report from the NIH Traumatic Coma Data Bank. J Neurosurg 1990;73:688–98.

71. Bernardi RJ, Smith KR Jr. Traumatic hematomas. In: Apuzzo MLJ, ed. Brain surgery: complication avoidance and management, Vol. 2. New York: Churchill Livingstone, 1993:1931–52.

72. d’Avella D, Servadei F, Scerrati M, et al. Traumatic intracerebellar hemorrhage: clinicoradiological analysis of 81 patients. Neurosurgery 2002;50:16–27.

73. Teasdale E, Hadley DM. Imaging the injury. In: Reilly P, Bullock RS, eds. Head injury. London: Chapman and Hall, 1997:167–207.

74. Blumbergs P. Pathology. In: Reilly P, Bullock R, eds. Head injury, 2nd edn. London: Hodder-Arnold, 2005:16–62.

75. French BN, Dublin AB. The value of computerized tomography in the management of 1000 consecutive head injuries. Surg Neurol 1977;7(4):171–83.

76. Gentleman D, Nath F, MacPherson P. Diagnosis and management of delayed traumatic intracerebral haematoma. Br J Neurosurg 1989;3:367–72.

77. Bullock R, Hanemann CO, Murray L, et al. Recurrent hematomas following craniotomy for traumatic intracranial mass. J Neurosurg 1990;72(1):9–14.

78. Kobayashi S, Nakazawa S, Otsuka T. Clinical value of serial computed tomography with severe head injury. Surg Neurol 1983;20(1):25–9.

79. Stein SC, Spettell C, Young G, et al. Delayed and progressive brain injury in closed-head trauma: radiological demonstration. Neurosurgery 1993;32(1):25–30.

80. Servadei F, Murray GD, Penny K, et al. The value of the ‘worst’ computed tomographic scan in clinical studies of moderate and severe head injury. Neurosurgery 2000;46:70–7.

81. Lobato RD, Gomez PA, Alday R, et al. Sequential computerized tomography changes and related fi nal outcome in severe head injury patients. Acta Neurochir (Wien) 1997;139:385–391.

82. Crone KR, Lee KS, Kelly DL Jr. Correlation of admission fi brin degradation products with outcome and respiratory failure in patients with severe head injury. Neurosurgery 1987;21:532–6.

83. Cohen TI, Gudeman SK. Delayed traumatic intracranial hematoma. In: Narayan NK, Wilberger JE, Povlishock JT, eds. Neurotrauma. New York: McGraw-Hill, 1996:689–703.

84. Gudeman SK, Kishore PR, Miller JD, et al. The genesis and signifi cance of delayed traumatic

intracerebral hematoma. Neurosurgery 1979;5:309–13.

85. Fukamachi A, Nagasehi Y, Kohono K, et al. The incidence and development process of delayed traumatic intracerebral haematomas. Acta Neurochir 1985;32:1–13.

86. Kaufman HH, Moake JL, Olson JD, et al. Delayed and recurrent intracranial hematoma related to disseminated intravascular clotting and fi brinolysis in head injury. Neurosurgery 1980;7:445–9.

87. Miner MI, Kaufman HH, Graham SH, et al. Disseminated intravascular coagulation fi brinolytic syndrome following head injury in children: frequency and prognostic implications. J Pediatr 1982;100:687–91.

88. Servadei F, Nanni A, Nasi MT et al. Evolving brain lesions in the fi rst 12 hours after head injury: analysis of 37 comatose patients. Neurosurgery 1995;37(5):899–906.

89. Knuckey NW, Gelbard S, Epstein MH. The management of ‘asymptomatic’ epidural hematomas: a prospective study. J Neurosurg 1989;70:392–6.

90. Smith HK, Miller JD. The danger of an ultra-early computed tomographic scan in a patient with an evolving acute epidural hematoma. Neurosurgery 1991;29:258–60.

91. Sullivan T, Javrik J, Cohen W. Enlargement of conservatively treated epidural haematoma: implications for timing of repeat CT. Am J Neuroradiol 1999;20:107–13.

92. Gean AD. Extra-axial collections. In: Gean AD, ed. Imaging of head trauma, 1st edn. New York: Raven Press, 1994:75–146.

93. d’Avella D, Servadei F, Scerrati M, et al. Traumatic acute subdural haematomas of the posterior fossa: clinicoradiological analysis of 24 patients. Acta Neurochir (Wien) 2003;145:1037–44.

94. Lipper MH, Kishore PRS, Girevendulis AK, et al. Delayed intracranial haematomas in patients with severe head injury. Radiology 1979;33:645–9.

95. Stein SC, Smith DH. Coagulopathy in traumatic brain injury. Neurocrit Care 2004;1:479–88.

96. Mellion BT, Narayan RK. Delayed traumatic intracerebral hematomas and coagulopathies. In: Barrow DL, ed. Head injury. Park Ridge, IL: Amercian Association of Neurological Surgeons, 1992:84–92.

97. Hoots WK. Coagulation disorders in the head-injured patient. In: Narayan RK, Povlishock JT, eds. Neurotrauma. New York: McGraw-Hill, 1996:673–88.

98. Unterberg AW, Stover J, Kress B, et al. Edema and brain trauma. Neuroscience 2004;129:1019–27.

99. Kimelberg HK. Current concepts of brain edema: review of laboratory investigations. J Neurosurg 1995;83:1051–9.

100. Langfi tt TW, Marshall WJ, Kassell NF et al. The pathophysiology of brain swelling produced by mechanical trauma and hypertension. Scand J Clin Lab Invest 1968;102:XIV:B.



101. Langfi tt TW, Weinstein JD, Sklar FH, et al. Contribution of intracranial blood volume to three forms of experimental brain swelling. Johns Hopkins Med J 1968;122:261–70.

102. Marmarou A, Signoretti S, Fatouros PP, et al. Predominance of cellular edema in traumatic brain swelling in patients with severe head injuries. J Neurosurg 2006;104:720–30.

103. Beaumont A, Fatouros P, Gennarelli T, et al. Bolus tracer delivery measured by MRI confi rms edema without blood–brain barrier permeability in diffuse traumatic brain injury. Acta Neurochir Suppl 2006;96:171–4.

104. Lang DA, Hadley DM, Teasdale GM, et al. Gadolinium DTPA enhanced magnetic resonance imaging in acute head injury. Acta Neurochir (Wien) 1991;109:5–11.

105. Aldrich EF, Eisenberg HM, Saydijari C, et al. Diffuse brain swelling in severely head injured children. A report of from the NIH Traumatic Coma Data Bank. J Neurosurg 1992;76:450–4.

106. Todd NV, Graham DI. Blood brain barrier damage in traumatic brain contusion. Acta Neurochir (Wien) 1990;51(Suppl.):296–9.

107. Lang DA, Teasdale GM, Macpherson P, et al. Diffuse brain swelling after injury: more often malignant in adults than children? J Neurosurg 1994;80:675–80.

108. Lobato Rd, Cordobes F, Rivas JJ, et al. Outcome of severe head injury related to the type of intracranial lesion: a computerized tomography study. J Neurosurg 1983;59:762–74.

109. Marshall LF, Bowers-Marshall S, Klauber MR, et al. A new classifi cation of head injury based on computerised tomography. J Neurosurg 1991;75:S14–20.

110. Maas AIR, Hukkelhoven CWPM, Marshall LF, et al. Prediction of outcome in traumatic brain injury with computed tomographic characteristics: a comparison between the

computed tomographic classifi cation and combinations of computed tomographic predictors. Neurosurgery 2005;57(6):1173–82.

111. Chesnut RM. Evaluation and management of severe closed head injury. In Tindall GT, Cooper PR, Barrow DL, eds. Current practise of neurosurgery. Baltimore: Williams and Wilkins, 1995:1401–24.

112. Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993;34:216–22.

113. Silverston P. Pulse oximetry at the roadside: a study of pulse oximetry in immediate case. BMJ 1989;298:711–13.

114. Stocchetti N, Furlan A, Volta F: Hypoxemia and arterial hypotension at the accident scene in head injury. J Trauma 1996;40:764–7.

115. Chesnut RM, Marshall LF, Piek J, et al. Early and late systemic hypotension as a frequent and fundamental source of cerebral ischemia following severe brain injury in the Traumatic Coma Data Bank. Acta Neurochir Suppl (Wien) 1993;59:121–5.

116. Manley G, Knudson MM, Morabito D, et al. Hypotension, hypoxia, and head injury: frequency, duration, and consequences. Arch Surg 2001;136:1118–23.

117. Jeremitsky E, Omert L, Dunham CM, et al. Harbingers of poor outcome the day after severe head injury: hypothermia, hypoxia, hypoperfusion. J Trauma 2003;54(2):312–19.

118. Miller JD, Becker DP. Secondary insults to the injured brain. J R Coll Surg Edin 1982;27:292–8.

119. Chesnut RM. Management of brain and spine injuries. Crit Care Clin 2004;20:25–42.

120. Cherian L. Hyperglycemia increases brain injury caused by secondary ischemia after cortical impact injury in rats. Crit Care Med 1997;25:1378–83.

121. Cherian L. Hyperglycemia increases neurological damage and behavorial defi cits from posttraumatic secondary ischemic insults. J Neurotrauma 1998;15:307–20.

122. Young B, Ott L, Yingling B, et al. Nutrition and brain injury. J Neurotrauma 1992;9(Suppl.):S375–82.

123. Jeremitsky E, Omert LA, Dunham CM, et al. The impact of hyperglycemia on patients with severe brain injury. J Trauma Injury Infect Crit Care 2005;58:47–50.

124. Graham DI, Ford I, Adams JH, et al. Ischaemic brain damage is still common in fatal non-missile head injury. J Neurol Neurosurg Psychiatry 1989;52:346–50.

125. Stein SC, Chen XH, Sinson GP, et al. Intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury. J Neurosurg 2002;97(6):1373–7.

126. Schroder ML, Muizelaar JP, Fatouros P, et al. Early cerebral blood volume after severe traumatic brain injury in patients with early cerebral ischemia. Acta Neurochir Suppl 1998;71:127–30.

127. Zauner A, Bullock R. Biological oxygenation and energy metabolism: part I. Biological

function and pathophysiology. Neurosurgery 2002;51:289–301.

128. Bullock MR Chesnut RM, Clifton GL, et al. Guidelines for the management of severe head injury. J Neurotrauma 2000;17:449–627.

129. Teasdale GM, Graham DI. Craniocerebral trauma: protection and retrieval of the neuronal population after injury. Neurosurgery 1998;43:723–37.

130. Lee Y, Aono M, Laskowitz D, et al. Apolipoprotein E protects against oxidative stress in mixed neuronal–glial cell cultures by reducing glutamate toxicity. Neurochem Int 2004;44:107–118.

CHAPTER 3

Intracranial Pressure 34 Introduction

34 Defi nition of Increased ICP

34 Signifi cance 34 Pathophysiology of Increased ICP in Acute Head Injury 35 Relationship between intracranial volume and ICP

35 Incidence of Increased ICP 35 Patients with Severe Head Injury (Glasgow Coma Scale ≤ 8) 36 Patients with Moderate and Mild Head Injury 36 Elevation of ICP After Evacuation of Intracranial Mass Lesions 36 Delayed Increase of ICP

36 Harmful Effects of Increased ICP 36 Reduced Cerebral Perfusion and Cerebral Ischaemia 38 Brain Shifts and Brain Stem Compression

41 Monitoring ICP 41 Reasons for ICP Monitoring

44 Interpreting ICP Data 44 Thresholds for Therapy 44 Correlation Between Clinical Signs and Recorded ICP 44 Trends of ICP and CPP 44 Intracranial Compliance 44 Accuracy of ICP Measurement 44 Insensitivity of ICP Monitoring 44 Intracranial Pressure Waves

45 Summary

46 References

INTRODUCTIONIncreased intracranial pressure (ICP) is the main cause

of death in patients after severe head injury and the

main cause of deterioration of patients who sustain

moderate and mild head injury. Diverse pathological

processes resulting from head injury can contribute to

an increase in the volume of the intracranial contents.

Rational management of acute head injury mandates

an understanding of the complex relationship between

intracranial volume and ICP, as well as the deleterious

consequences of increased ICP. Because monitoring

of ICP has become a standard of care in patients with

severe head injury and in some with moderate injury, this

chapter also deals with important issues of indications

for ICP monitoring, monitoring methodology and

interpretation of ICP data.

Defi nition of Increased ICPNormal mean ICP is 0–10 mm Hg or 0–13.5 cmH

2O in adults

in the recumbent posture. Physiological elevations of ICP

may occur during coughing, straining and in the head-down

position.

A sustained mean ICP of 20 mm Hg or more is considered

to be increased. Intracranial pressure levels between 20 and

30 mm Hg are considered to be moderately increased, whereas

levels above 30 mm Hg are considered to be severely increased.1–5

The threshold for ICP treatment may vary in individual patients

with severe head injury and this aspect will be discussed later.

Signifi cancePathophysiology of Increased ICP in Acute Head InjuryThe intracranial contents are comprised of brain (70%), blood

(15%) and cerebrospinal fl uid (CSF; 15%). The contribution of

extracellular fl uid in the brain tissue to intracranial volume is

minimal in the uninjured brain. Increased ICP may result from

an increase in the volume of one or more of these components

or the addition of a new volume, such as an intracranial

haematoma.

The causes of increased ICP in the head-injured patient are

listed in Table 3.1.


Table 3.1 Causes of increased intracranial pressure in acute head injury

Brain swelling Space-occupying lesions

Increased CSF volume (obstruction to CSF outfl ow)

Increase in blood volume

1. Arteriolar dilatation

Hypoxia, hypercapnia•

Severe hypertension•

Loss of vasomotor tone (vascular injury)•

Seizures•

Hyperpyrexia•

Pain (e.g. with endotracheal suction)•

Inappropriate anaesthetic agents•

2. Venous dilatation

Posture (head low position)•

Valsalva manoeuvres (coughing, straining)•

Circumferential neck compression (tight cervical collar, • endotracheal tube ties)

Venous obstruction by brain swelling or brain shift•

Brain oedema

1. Cytotoxic oedema

Evolving primary injury•

Ischaemic–hypoxic secondary insults (hypotension, • hypoxia, hypocapnia, hyperpyrexia, seizures, cerebral vasospasm)

2. Osmotic oedema

Hyponatraemia•

3. Vasogenic oedema (e.g. oedema in the peripheral zone in cerebral contusions)

1. Intracranial haematoma

Extradural•

Subdural•

Intracerebral•

2. Cerebral contusion

1. Hydrocephalus (e.g. with a posterior fossa or intraventricular haematoma)

2. Obstruction of the contralateral ventricle by a mid-line shift

3. Entrapment of the temporal horn of the lateral ventricle

CSF, cerebrospinal fl uid.

INTRACRANIAL PRESSURE CHAPTER 3 35

The factors that may increase ICP vary with the phase of

injury. Systemic hypotension, hypoxia or hypercarbia are

most common immediately after injury, during resuscitation,

transport and initial stabilisation in the intensive care unit

(ICU). Cytotoxic oedema may develop within the fi rst 24

hours,6,7 whereas systemic hyperpyrexia may develop after

24–48 hours. Most intracranial haematomas develop during

the fi rst 48 hours (although cerebral contusions may enlarge

over a longer period). Intracranial hypertension not associated

with intracranial haematoma is most often due to brain

swelling, which may increase during the 48–72 hours after

injury. Pericontusional oedema may worsen from the 2nd day

onwards.

Acute head injury is heterogeneous and dynamic; hence,

more than one factor may be responsible for increased ICP

at any given time and the predominant factor responsible for

increased ICP may change with time.2,8

Relationship between intracranial volume and ICPIn the uninjured brain, the intracranial compartment is able to

accommodate modest, gradual increases in intracranial volume

(up to 50–100 mL), without a concomitant increase in ICP.

The increase in volume is balanced by a near equal decrease

in volume of one or more of the other normal constituents

(the Monro–Kellie–Burrows doctrine).9,10 The buffering

mechanisms include displacement of CSF from the intracranial

space into the spinal subarachnoid space and displacement of

venous blood via the venous sinuses into the extracranial venous

system. The viscoelastic properties of the brain may also allow

some degree of tissue compression. Once this buffering capacity

is exhausted, any further increase in intracranial volume results

in increased ICP. The relationship is exponential. In the initial

stages, increases in volume result in a modest increase of ICP,

after which small increases in volume lead to increasingly larger

increases in ICP (Fig. 3.1a). If the volume increase is rapid (as in

a very rapidly expanding haematoma), ICP will increase from

the outset because there will be insuffi cient time for volume

compensation to operate. The relationship between pressure

and volume in the intracranial compartment can be expressed

in terms of compliance. As the capacity to compensate

for increased volume is exhausted, the compliance of the

intracranial compartment is reduced.

The effect of reduced compliance after acute head injury,

perhaps due to a change in the viscoelastic properties of the

injured brain, is refl ected in the pressure–volume curve, which

is steeper and shifted to the left compared with the uninjured

brain (Fig. 3.1b) so that ICP begins to rise after a smaller

increment of volume; the rise in ICP is steeper and the ‘break

point’ beyond which the ICP rises exponentially occurs sooner.

That is, the therapeutic window for ICP control is narrowed.2,11

If intracranial buffering capacity (compliance) is reduced,

further increases in intracranial volume due to secondary

insults (such as hypercarbia due to inadequate ventilation,

hypoxia, hypotension, coughing, straining or tight neck ties)

can precipitate sudden, severe increases in ICP. For example,

hypoxia in the presence of moderate brain swelling or brain

contusions may cause a critical fall in compliance and a marked

rise in ICP.

Incidence of Increased ICPThe incidence of raised ICP is related to the severity of the head

injury.

Patients with Severe Head Injury (Glasgow Coma Scale ≤ 8)Nearly 50% of patients with severe head injury have moderately elevated ICP some time after injury and 10% have severely raised levels of ICP on admission to hospital.

(a)

90

80

70

60

50

40

30

20

10

ICP

(mm

Hg

)

D

B

A

Volume of intracranial contents

Break point

C

(b) Injured brain

Uninjured brain 90

80

70

60

50

40

30

20

10

ICP

(mm

Hg

)

D

B

A

Volume of intracranial contents

Break point

C

Break point

▲ Figure 3.1 (a) The intracranial volume–pressure relationship for the uninjured brain. A diagram of the volume–pressure relationship in the intracranial compartment. Initially, intracranial pressure (ICP) remains within normal limits due to volume compensation (Segment A–B). Further increases in intracranial volume initially result in a gradual increase in ICP until a critical volume is reached (Point C), after which even small increases in volume result in signifi cant increases in ICP (Segment C–D). (b) The volume–pressure relationship after injury. The pressure–volume curve becomes steeper and shifted to the left (i.e. ICP begins to rise with a smaller intracranial volume, the rise in ICP is steeper and the ‘break point’, beyond which there is an exponential rise in ICP, occurs with a smaller intracranial volume compared with uninjured brain).


Increased ICP is an important cause of secondary brain

damage, accounting for approximately 50% of mortality,

and is an important contributor to morbidity.12 ICP may be

elevated in 55%–63% of patients with severe head injury who

have abnormal computed tomography (CT) scans and in

approximately 13% of those with normal CT scans. In those

with normal CT scans, there is a higher risk of increased ICP in

patients with any two of following features: (i) age > 40 years;

(ii) unilateral or bilateral motor posturing; or (iii) systolic

blood pressure (SBP) < 90 mm Hg.13

It is estimated that 10%–15% of patients with severe

head injury will develop medically and surgically untreatable

intracranial hypertension, with a reported mortality ranging

between 84% and 100%.12–14 In some, this was a manifestation

of severe, irreversible brain injury.12,15 Marshall has observed

that with active initial care of acute head injury, patients with

overwhelmingly severe brain injury who would have previously

succumbed in the initial stages may survive, only to die later

from intractable intracranial hypertension.16 Even moderately

increased levels of ICP have been shown to be associated with

a worse prognosis in patients with mass lesions or diffuse brain

injury.8,17

Patients with Moderate and Mild Head InjuryLess than 3% of patients with mild head injury (Glasgow

Coma Scale (GCS) 14–15) and approximately 10%–20% of

patients with moderate head injury (GCS 9–13) deteriorate

to coma during the course of their injury. The main cause of

deterioration is increased ICP.1,18 Approximately one-third

of patients with moderate head injury who do not recover to

GCS 14 or 15 at 12 hours are found to have progression of CT

scan abnormalities.18 Early identifi cation of these patients is of

considerable importance.

Elevation of ICP After Evacuation of Intracranial Mass LesionsBrain swelling may occur after evacuation of an intracranial

mass lesion. This is most common after of an acute subdural

haematoma (SDH) and may be predicted by evidence of severe

primary injury (e.g. initial low GCS, CT evidence of brain

swelling and marked midline shift).

In one study, two-thirds of patients developed intracranial

hypertension after evacuation of intracranial mass lesions and,

in one-third, ICP was refractory to treatment. Approximately

85% of patients with a non-evacuated mass lesion also showed

an increase in ICP.19

Delayed Increase of ICPA delayed increase in ICP may indicate a new intracranial mass lesion, an increase in the size of an existing lesion or development of brain swelling. A single episode of neurological deterioration due to increased ICP has been shown to increase mortality by more than fi vefold.20 Delayed enlargement of haemorrhagic lesions occurs in approximately 50% of patients

with moderate and severe head injury. Most such patients demonstrate elevations of ICP. Patients with parenchymal contusions in the frontal and temporal lobes and those who had evidence of a coagulopathy have been found to be most likely to show progression of lesions.21 Approximately one in six patients with diffuse injury only on the initial CT scan have been shown to develop evolving changes in subsequent scans. These patients had a worse outcome.22

Delayed increases in ICP in patients with severe head injury have practical implications with respect to the timing of discontinuation of ICP monitoring in patients who appear to be stable and the withdrawal of sedation/analgesia. Such increases in ICP may occur after removal of monitoring devices and after return of the patient to the general ward from the ICU. Souter et al. observed delayed increases in ICP (after 48 hours) in nine of 35 patients with severe head injury who did not show an initial increase in ICP.23 When ICP increases, extracranial causes must always be considered immediately. Once excluded, a delayed rise in ICP in a ventilated patient is an indication for a CT scan.1,4,24

Harmful Effects of Increased ICPRaised ICP has two potentially harmful effects: (i) reduced cerebral perfusion with cerebral ischaemia; and (ii) brain shifts with herniation and brain stem compression.

Reduced Cerebral Perfusion and Cerebral IschaemiaThe cerebral perfusion pressure (CPP) is the net force driving blood into the intracranial compartment. It is the difference between the mean arterial blood pressure (MAP) and the mean ICP. In a healthy adult with an MAP in the range 90–100 mm Hg and mean ICP < 10 mm Hg, the CPP is > 80 mm Hg (Fig. 3.2). The levels of ICP and MAP are the primary determinants of cerebral perfusion: an increase in ICP or a reduction of MAP reduces CPP.

OTHER FACTORS CONTROLLING CEREBRAL PERFUSION

State of Autoregulation of the Cerebral VasculatureCerebral blood fl ow (CBF) varies directly with CPP and inversely with cerebral vascular resistance (CVR):

CBF = CPP

CVRCerebral vascular resistance is mainly determined by the

calibre of cerebral arterioles. Cerebral vascular resistance increases with arteriolar constriction and vice versa. Cerebral arterioles have the capacity to change their calibre with changes in CPP in order to maintain constant CBF, a phenomenon known as pressure autoregulation.

In the uninjured brain, pressure autoregulation maintains

a constant CBF through a physiological range of CPP, usually


50–150 mm Hg. When CPP falls below the autoregulatory

range, the CBF becomes passively and directly dependent on

MAP and cerebral ischaemia will occur (Fig. 3.3a).3

Acute head injury can impair autoregulation to varying

degrees. The lower threshold for pressure autoregulation (the

‘break point’) may be ‘reset’ above 50 mm Hg, increasing the

risk of cerebral ischaemia with hypotension or increased ICP

(Fig. 3.3b).25–29

▲ Figure 3.3 Pressure autoregulation in the uninjured brain. Between the cerebral perfusion pressure (CPP) range 50–150 mm Hg, a relatively constant cerebral blood fl ow (CBF) is maintained by alteration of vessel calibre. Below a CPP of 50 mm Hg, CBF can no longer be maintained by vasodilatation. The CBF becomes pressure passive and cerebral ischaemia ensues. (b) Disturbed autoregulation in acute head injury. Impaired autoregulation after acute head injury results in the lower limit of autoregulation being ‘reset’ at a higher level. Cerebral ischaemia may ensue at CPP below this level.

Therefore, it is important to maintain the MAP above

90 mm Hg prior to ICP monitoring, assuming that patients

have increased ICP. Maintaining SBP at the lower range of

normal (i.e. merely avoiding hypotension), may still result in an

inadequate CPP in some patients (Fig. 3.4). Cerebral ischaemia is

a stimulus for cerebral vasodilatation, which, in turn, increases

ICP. The increased ICP may contribute to further cerebral

ischaemia, thus establishing a vicious cycle (Fig. 3.5).30 Conversely,

prolonged elevations of MAP beyond the physiological range, in

the setting of impaired autoregulation and changes in capillary

permeability, may increase brain swelling and increase ICP.31–34

▲ Figure 3.2 Determinants of cerebral perfusion pressure. Cerebral perfusion pressure=mean arterial pressure–intracranial pressure.

▲ Figure 3.4 Effect of a low normal mean arterial blood pressure (MAP) in patients with severe head injury. A low normal MAP in patients with increased intracranial pressure (ICP) and disturbed autoregulation leads to an inadequate cerebral perfusion pressure (CPP) and cerebral ischaemia.


Regional Heterogeneity of Autoregulation, Perfusion and MetabolismIntracerebral microdialysis and perfusion CT studies have

demonstrated differences in autoregulation, perfusion and

metabolic requirements in different regions of the injured brain

at any given time and that these parameters change during the

course of the injury.29,35–39 Measures of the balance between global

oxygen supply and demand, such as jugular venous oximetry

and brain parenchymal oxygen monitoring, or measures of

cellular metabolism, such as cerebral microdialysis, may provide

additional information in this regard.40–43 These techniques are

largely restricted to specialised units and protocols for their use

have not been tested. In the usual absence of such guidance,

the recommendation to maintain CPP > 60 mm Hg should be

followed, even though the true optimal CPP may vary between

patients, in different brain regions and over time.32

OPTIMAL LEVELS OF ICP, MAP AND CPP

CPP = MAP

ICP

Both the CPP and ICP should be maintained at optimal

levels. Measures used to control ICP may compromise cerebral

perfusion. Osmotherapy and metabolic suppressants can cause

hypotension and aggressive hyperventilation can cause cerebral

ischaemia from cerebral vasoconstriction. Conversely, overly

aggressive measures to increase cerebral perfusion, such as

induced arterial hypertension, or overperfusion may increase

ICP. Hence, the balance between CPP and ICP should be

monitored constantly.

Early management of increased ICP prevents ischaemic

brain damage and may facilitate later control of ICP. Once

ischaemic brain damage is established, the deleterious effects

of ischaemic brain swelling may not be reversed by subsequent

attempts to control ICP.

Recent investigations and Guidelines1,26,44–48 have emphasised

that:

1. Intracranial pressure levels should be maintained below

20 mm Hg. But an ICP < 25 mm Hg may be acceptable if

CPP levels are adequate and there is no evidence of brain

stem compression. Treatment of small increases in ICP

by careful adjustment of therapy may prevent signifi cant

increases in ICP subsequently.

2. A CPP level > 60 mm Hg should be maintained in

adults because CPP levels of 50 mm Hg or lower may be

associated with critical reductions in brain tissue oxygen

levels, increased morbidity and mortality.

3. Mean arterial pressure should be maintained at or above

90 mm Hg (for adults) prior to ICP monitoring.

4. Extraordinary measures to maintain CPP at levels higher

than 70 mm Hg, such as the use of induced hypertension

and intravascular volume expansion, are no longer

recommended routinely in view of an increased risk of

acute respiratory distress syndrome and, perhaps, increased

brain swelling.

5. Even when optimal levels of CPP are maintained, failure

to control increased ICP would still result in an adverse

outcome.

Hence, a balanced approach to ICP control is advisable.

Therapy is directed at maintaining ICP < 20 mm Hg as well as

maintaining CPP > 60 mm Hg. It must be borne in mind that

patients with bifrontal and temporal fossa lesions can develop

brain stem compression even at ICP levels < 20 mm Hg. An

increase in ICP in the posterior fossa may not be detected by

monitoring ICP in the supratentorial compartment.

Brain Shifts and Brain Stem CompressionExpanding focal lesions produce pressure gradients that result

in shifts (herniations) of brain tissue within and between

the intracranial compartments. The types of brain shifts and

herniations include:

1. midline shift

2. subfalcine herniation

3. transtentorial herniation (lateral transtentorial herniation

and central transtentorial herniation)

4. tonsillar herniation

MIDLINE SHIFTA laterally placed supratentorial lesion can lead to compression

and displacement of the lateral and third ventricles and the

septum pellucidum across the midline (Figs 3.6, 3.7a). A signifi cant

midline shift may lead to impaired consciousness by:

1. compressing the diencephalic structures (thalamus,

hypothalamus)

2. ischaemia (by stretching of the deep perforating arteries to

the diencephalon at the base of the brain)

3. occluding the third ventricle and obstructing the opposite

lateral ventricle, which dilates and contributes further to

an increase in intracranial volume (this ominous sign is

readily visualised on a CT scan)

▲ Figure 3.5 Vasodilatory cascade. A decrease in cerebral perfusion pressure (CPP) results in cerebral vasodilatation and an increased cerebral blood volume, leading to an increase in the intracranial pressure (ICP), which, in turn, leads to a further reduction in CPP, establishing a vicious cycle.


superior cerebellar arteries, resulting in an ipsilateral

dilated pupil (third nerve palsy)

3. compression and downward herniation of the brain

stem, resulting in further deterioration of the level of

consciousness and compression of the ipsilateral cerebral

peduncle with a contralateral hemiparesis

4. compression of the posterior cerebral artery leading to

ischaemia/infarction of the calcarine (occipital) cortex

(Fig. 3.8)

SUBFALCINE HERNIATIONThe cingulate gyrus herniates beneath the free edge of the falx

cerebri (Figs 3.6, 3.7a), occasionally compressing the anterior

cerebral arteries against the free edge of the falx and resulting

in distal ischaemia (Fig. 3.7b).

TRANSTENTORIAL HERNIATION

Lateral Transtentorial (Uncal) HerniationAn expanding, laterally placed supratentorial lesion leads to

herniation of the medial temporal lobe (uncus and sometimes

the para-hippocampal gyrus) into the tentorial hiatus (shown

in Figs 3.8, 3.9). The consequences of this are:

1. compression and obliteration of the perimesencephalic

cisterns, a reliable indicator of increased ICP in a CT scan

(Fig 3.9)

2. compression of the ipsilateral third nerve against the

tentorial edge or between the posterior cerebral and

ba

▲ Figure 3.6 Transtentorial herniation. Brain shifts and herniations that occur secondary to a supratentorial expanding lesion (an extradural haematoma): subfalcine herniation of the cingulate gyrus (small open arrow) and midline shift of the lateral ventricles and septum pellucidum (large black arrow). There is obstruction of the foramen of Monro and dilatation of the opposite lateral ventricle. There is herniation of the uncus (small black arrow) with compression of the ipsilateral cerebral peduncle (black arrowheads), as well as downward herniation of the brain stem (large open arrow).

▲ Figure 3.7 (a) Computed tomography (CT) scan showing a large extradural haematoma (EDH) with signifi cant midline shift (white arrow). (b) A CT scan 2 days after evacuation of the EDH showing anterior cerebral artery territory ischaemia (right more than left) secondary to subfalcine herniation (white arrows).

▲ Figure 3.8 Changes at the tentorial hiatus during transtentorial herniation. The uncus and parahippocampal gyrus have herniated into the tentorial hiatus (large black arrow), with obliteration of the perimesencephalic cistern and compression of the ipsilateral third nerve (open arrow), ipsilateral cerebral peduncle (black arrowheads) and the ipsilateral posterior cerebral artery (curved arrow).

Cushing Refl exBrain stem compression may be associated with a triad of signs

indicating impending brain stem failure: an increase in SBP,

bradycardia and an irregular respiratory effort (termed the

Cushing refl ex). However, the full triad of the Cushing refl ex

is seen in only approximately one-third of patients with life-

threatening increases of ICP.49

Further herniation of the uncus with compression and

rostrocaudal (or downward) shift of the brain stem leads to

a progressive disturbance of function of the diencephalon,

midbrain, pons and medulla. Disturbance of midbrain function

leads to unconsciousness, tachypnoea and impaired conjugate

eye deviation. Pontine disturbance may result in rapid, shallow

respiration, loss of refl ex adduction or abduction of eyes and

fi xed mid-position pupils. Pupils may become fi xed and dilated

owing to bilateral third nerve palsies. Motor responses change

from withdrawal (fl exor), to abnormal fl exor and extensor

responses. Further brain stem compression/ischaemia leads to

fl accidity (loss of motor response); disturbances to the medulla


oblongata may lead to hypertension and bradycardia followed

by respiratory irregularity, hypotension, respiratory arrest and

death.50

The distortion of the brain stem leads to stretching and

shearing of the deep perforating arteries that supply the

brain stem, resulting in brain stem ischaemia or brain stem

haemorrhages (Duret’s haemorrhages), typically located

centrally in the lower midbrain and pons.51

Occasionally, a tentorial herniation may produce a

side-to-side shift of the brain stem, which compresses the

cerebral peduncle of the opposite side against the free edge

of the tentorium, resulting in an ipsilateral hemiparesis (the

‘Kernohan’s Notch’ phenomenon). Similarly, there may be

greater distortion of the opposite third nerve, resulting in initial

dilatation of the pupil contralateral to the side of the lesion.

Hence, contralateral hemiparesis and ipsilateral pupillary

dilatation are not absolute signs of lateralisation of a space-

occupying lesion producing transtentorial herniation.52

Central Transtentorial HerniationCentral transtentorial herniation occurs with diffuse brain

swelling or bilateral lesions, especially those near the vertex.

Central herniation in patients with bifrontal contusions may

lead to sudden, catastrophic deterioration.53

There is symmetrical, downward (caudal) displacement of

cerebral hemispheres and basal ganglia, with compression and a

downward shift of the diencephalon (thalamus, hypothalamus).

The compression of the diencephalon ‘reticular formation’ leads

to impaired consciousness, restlessness, sighing respirations

and small, sluggishly reactive pupils. Compression of the dorsal

midbrain may result in failure of upward gaze and bilateral

ptosis.

Subsequently, there is compression and downward

(caudal) displacement of the entire brain stem towards the

foramen magnum. There is elongation of the brain stem

in the anteroposterior diameter, with stretching and later

haemorrhage from the perforating branches of the basilar

artery. Bilateral uncal herniation occurs, leading to obliteration

of the perimesencephalic cistern around the midbrain at the

tentorial hiatus (Figs 3.10, 3.11). As noted before, the displacement

and ischaemia of the brain stem leads to a rostrocaudal

disturbance of the brain stem that can progress very rapidly to

produce severe, irreversible brain stem ischaemia.54,55

▲ Figure 3.9 Computed tomography scan of a patient with a large acute subdural haematoma showing obliteration of the perimesencephalic cisterns (white arrowheads).

▲ Figure 3.10 Central herniation secondary to diffuse brain swelling. There is symmetrical downward movement of the cerebral hemispheres and basal ganglia that leads to compression and caudal (downward) displacement of the diencephalon (black arrows) and the brain stem through the tentorial hiatus towards the foramen magnum (large open arrow). There is bilateral uncal herniation (small open arrows) with obliteration of the perimesencephalic cistern.

Brain Stem Compression due to Lesions in the Temporal FossaIn view of their proximity to the tentorial hiatus, as well as the

confi ned nature of the temporal fossa, enlargement of lesions

in the temporal fossa can lead to early impingement of the

uncus on the midbrain because the temporal lobe can only be

displaced in a medial and posterior direction—directly towards

the tentorial hiatus.56,57 Hence, lesions in the temporal fossa are

more likely to produce brain stem compression earlier in their

clinical course, even when the lesion volume is 15–20 mL and

at levels of ICP far lower compared with other supratentorial

lesions (Fig. 3.12).57

Tonsillar HerniationTonsillar herniation occurs as the fi nal stage of attempted

accommodation of a supratentorial mass lesion or at an earlier

stage with posterior fossa space-occupying lesions (Fig. 3.13) and

is characterised by the following.

Herniation of the cerebellar tonsils through the foramen magnum into the spinal subarachnoid space


to deterioration of consciousness, fl accid quadriplegia

(bilateral compression of the corticospinal tracts), irregular

and slow respiration and bradycardia.

Vasomotor and respiratory centre paralysis This may

lead to sudden apnoea, cardiovascular collapse and death.

With tonsillar herniation due to a posterior fossa mass

lesion, patients may remain conscious until the later stages of

haematoma evolution, when they may deteriorate rapidly to

unconsciousness and develop respiratory irregularity, followed

by apnoea and death. Hence, surgical evacuation of posterior

fossa haematomas with mass effect must be performed with

extreme urgency.

Monitoring ICPReasons for ICP MonitoringMonitoring ICP is an invaluable guide in managing head-

injured patients for the following reasons.

It determines CPP The current guidelines recommend

management of severe head injury based on maintenance

of optimal levels of CPP and ICP.1 However, CPP can only

be determined by continuous monitoring of ICP and

MAP.

Insensitivity of clinical and CT indicators of increased ICP Clinical parameters may not be available in a

sedated, ventilated patient (who may also be on muscle

relaxants) and are, in any case, are relatively insensitive

indicators of increased ICP. Computed tomography

▲ Figure 3.11 CT Scan showing diffuse brain swelling with obliteration of perimesencephalic cisterns (white arrow).

▲ Figure 3.12 Uncal herniation secondary to an extradural haematoma in the temporal fossa. The temporal lobe is displaced in a medial and posterior direction, directly towards the tentorial hiatus with early impingement of the uncus on the midbrain (black arrow). The brain stem may be compressed against the opposite edge of the tentorium—the ‘Kernohan’s Notch’ phenomenon (open arrow).

This leads to obliteration of the cisterna magna and

compression of the herniated tonsil against the spinal dura,

resulting in severe occipital headaches and neck stiffness

(without Kernig’s sign).

Compression and distortion of the medulla oblongata Disturbance of medullary function may lead

▲ Figure 3.13 Tonsillar herniation secondary to an expanding lesion in the posterior fossa. There is herniation of the cerebellar tonsil into the foramen magnum, obliterating the cisterna magna (open arrow). There is compression of the fourth ventricle with hydrocephalus, and of the pons and medulla oblongata (black arrow). Reverse tentorial herniation may compress the midbrain.


scanning is a valuable indicator, but patients with a normal

CT scan can still develop increased ICP and CT does not

provide information on ICP trends. Repeat CT scanning

involves transport of critically ill patients, a potentially

hazardous exercise.

Assesses response to treatment Monitoring ICP detects

the response of ICP to therapy, as well as the duration

of such responses. Specifi c therapies for the control of

ICP may, themselves, have adverse consequences, such

as compromise of CPP or paradoxical increases in ICP.

Monitoring ICP detects these effects and allows the

appropriate tailoring of therapies.

Detects delayed rises in ICP and the need for repeat CT

Monitoring ICP is helpful in the early detection of delayed

intracranial haematomas and in monitoring non-operated

mass lesions.

Indications for ICP monitoring include the following.1–4,13

Patients with GCS ≤ 8 after cardiopulmonary resuscitation and with an abnormal scan An abnormal scan is

defi ned as one showing a haematoma, cerebral contusion,

oedema or compressed basal cisterns. Monitoring ICP

is not appropriate in a patient with an overwhelmingly

severe brain injury who is unlikely to survive.

Patients with GCS ≤ 8 after resuscitation and a normal CT scan and 2 or more of the following features:

• age > 40 years

• SBP < 90 mm Hg after resuscitation

• unilateral or bilateral motor posturing

The ICP may be elevated in approximately 60% of such

patients.

After surgical evacuation of a haematoma When brain

swelling is observed during surgical evacuation of an acute

SDH, cerebral contusions or intracerebral haematoma, or

whenever postoperative brain swelling is considered likely

to develop.

Patients with moderate and mild head injury requiring prolonged sedation In patients with moderate and

mild head injury who have an abnormal CT scan and

the potential for deterioration, ICP monitoring may be

advisable if neurological evaluation is not be possible for

a prolonged period (e.g. a long surgical procedure under

general anaesthesia or ventilation with sedation and muscle

relaxants for management of extracranial injuries).

Contraindications for ICP monitoring include the following.

Coagulopathy Coagulopathy can increase the risk of

iatrogenic haemorrhage during ICP catheter insertion.

A study involving the use of a fi bre optic ICP catheters,

reported a 15.3% incidence of radiological evidence of

bleeding in patients who had coagulopathy (defi ned

as clinically apparent bleeding or abnormalities in

prothrombin activity, partial thromboplastin time or

platelet count). Due to this high frequency, the use of fi bre

optic ICP monitors was not recommended in patients who

had coagulopathy.58 However, a recent study on the use of

fi bre optic intraparenchymal ICP monitoring showed that,

in head-injured patients with borderline coagulopathy,

defi ned as International Normalized Ratio (INR) ≤ 1.6),

haemorrhagic complications after ICP monitor placement

were infrequent and the use of fresh frozen plasma to

‘normalize’ INR below this threshold was not benefi cial

and delayed monitor placement.59

Extensive scalp wounds These may increase the risk of

infection.

METHODOLOGY

Intraventricular Catheter (External Ventricular Drain or EVD)A catheter placed in the frontal horn of the lateral ventricle

(usually the non-dominant or right side) and connected to

an external strain gauge transducer is the most accurate and

cheapest method of monitoring ICP. It also allows CSF drainage

for control of ICP (see Fig. 11.1, Chapter 11, Neurosurgical

Techniques). An intraventricular catheter can be checked for

zero drift in vivo. This is the preferred method for monitoring

ICP.1

The drawbacks of the intraventricular catheter are as

follows.

1. Ventricular catheter placement requires skill and may

prove particularly diffi cult in patients with compressed

lateral ventricles.

2. The transducer level must be repositioned with any change

of head position.

3. Catheter blockage and failure of recording. When the

ventricle becomes slit-like or the catheter becomes

embedded in the brain parenchyma. Failure of recording

can also occur as a result of air bubbles or debris trapped

in the fl uid column of the catheter system. An intracranial

pressure transduction via fi bre optic or strain gauge devices

placed in the ventricular catheter may help to overcome

the loss of the pressure record under these circumstances.

4. Infection. The major complication with the use of external

ventricular drains is CSF infection. Various studies have

reported an incidence of ventriculostomy related CSF

infection ranging from 2.2% to 10.4% (Alleyne CH et al

2000, Holloway KL et al 1996, Paraore CG et al 1994).60,61,62

Current evidence63,64,65,66,67 suggests that EVD-associated

CSF infections are often acquired by the introduction of

bacteria at the time of insertion of the ventricular catheter

rather than by subsequent retrograde colonisation.

The following precautions are recommended:

• Catheter insertion should be performed with

full sterile precautions and in an operating

theatre whenever possible


• a strict protocol should be followed to prevent

infection during and after the procedure. This

includes:

• shampooing, hair clipping and full skin

prep

• tunneling the ventricular catheter a few

cms from the burrhole

• a closed drainage system

• dressing change every few days

• no routine CSF cultures, but only if

infection suspected

• avoid manipulation of the catheter

• Antibiotics may be useful to cover the insertion.

Prolonged antibiotic prophylaxis is not

advised

• A single external ventricular drain should

be used as long as clinically indicated, and

changed only to treat CSF infection or for

catheter malfunction. Elective replacement of

a ventricular catheter can increase the risk of

infection.

5. Haemorrhage. A review of published reports of monitoring

with all ICP devices (involving over 200 patients) showed

a 1.4% incidence of haematomas. Such haematomas were

signifi cant enough to warrant surgical evacuation in only

0.5% of patients.1

Catheter-tip Transducer SystemsThese are easier to place and avoid the problems of blockage.

The transducer is located at the tip of a fl exible 2 mm catheter

(see Fig. 11.2, Chapter 11, Neurosurgical Techniques). The

ICP is commonly monitored in the intraparenchymal space

(valid measurements may be obtained in the subdural space,

but extradural measurements are considered unreliable). One

of the principal drawbacks of catheter-tip transducers is the

inability to check calibration in vivo. Once these systems are

zeroed relative to atmospheric pressure during pre-insertion

calibration, their pressure output is dependent on the zero drift

of the sensor.

Zero or baseline drift can occur with catheter-tip ICP

monitoring devices. With zero drift, the ICP recorded may be

higher (positive drift) or lower (negative drift) than the true

ICP. This inaccuracy cannot be ascertained as the system cannot

be recalibrated in vivo. Therefore, the long-term accuracy of

catheter-tip devices depends on their zero drift characteristics.68

A zero drift should be suspected if the pressure recording is

discordant with clinical and radiological parameters and the

catheter should be replaced if monitoring is still needed.

Disadvantages of catheter-tip transducer systems compared

with an EVD include:

1. high cost

2. inability to calibrate in vivo

3. potential for zero drift, especially after 5 days

4. risk of damage and failure of recording (some types of

catheters are fragile and may be damaged during nursing

procedures or patient transport)

5. CSF drainage is not possible for the control of ICP

The most widely used catheter-tip transducer systems are

described below.

Fibre optic catheter-tip transducer (Camino type) The

ICP is measured by a fl exible diaphragm that is deformed

by pressure and located at the tip of a narrow fi bre optic

catheter. Changes in light intensity refl ected off this

diaphragm are interpreted in terms of pressure changes.

There is a close correlation between ICP measured by

the fi bre optic catheter-tip transducer and the direct

intraventricular method.69 Zero drift associated with these

devices has been reported to average 3.2 mm Hg/day.54

There are also reports of Camino probe failure owing

to technical complications (e.g. cable kinking, probe

dislocation), with failure rates of 10%–25%.68

Microchip transducer (Codman type) The Codman

transducer is a micro miniature strain gauge transducer

within a titanium housing side-mounted at the tip of a

catheter. The silicon diaphragm of the transducer is sensitive

to pressure changes. The accuracy of this system compares

well with direct intraventricular ICP measurements.70,71

Spiegelberg ICP monitoring system (Spiegelberg KG, Hamburg, Germany) This consists of a fl uid-fi lled

catheter–transducer system, with an air pouch balloon

situated at the tip and transduced by an external strain

gauge transducer. The system incorporates the facility for

regular automatic zeroing in situ. It is also less expensive

than other catheter-tip devices.72,73 The Spiegelberg ICP

monitoring system has been shown to record less zero

drift than other catheter-tip ICP devices.74 It is available

in versions for epidural, subdural, intraparenchymal and

intraventricular sites. The intraventricular catheter is a

double-lumen catheter that allows access to the CSF space

for drainage. To date, the Spiegelberg system has not been

widely used and its long-term effi cacy and robustness has

not been evaluated fully.68

The clinical circumstances and cost-effectiveness should

be consideration when selecting the optimal monitoring

methodology. In most patients, the intraventricular catheter

is the preferred methodology for reasons outlined already,

however, an intraparenchymal device may be preferred in

patients with slit-like ventricles. When ICP monitoring is

considered for patients with mild and moderate head injury,

a subdural device, such as a Microchip transducer, may be

preferred because it is less invasive.75

In situations where monitoring of ICP is not possible

owing to lack of facilities or expertise, a neurosurgeon

should be consulted for advice before any specifi c measures

for ICP control (such as mannitol or hyperventilation) are

undertaken in view of the potential for adverse effects

associated with such measures.

SUMMARYMonitoring ICP is an adjunct to the management of patients

with severe head injury by ventilation, with concurrent CPP

monitoring and ready access to a CT scan, and should only

rarely be undertaken in other circumstances and then only

with neurosurgical guidance and as part of a well-developed

protocol of management.

The techniques of insertion of a ventricular catheter and an

intraparenchymal ICP transducer are described in Chapter 11,

Neurosurgical Techniques.

Interpreting ICP DataMonitoring systems should continuously record mean ICP,

CPP and show ICP waves.

Thresholds for TherapyA sustained increase in ICP of > 20 mm Hg (in adults)

lasting more than 5 minutes in the absence of any correctable

extraneous factors is generally considered the treatment

threshold. The CPP levels should be maintained above 60 mm

Hg. Sustained ICP levels > 40 mm Hg will severely compromise

CPP and result in a poor outcome, unless controlled rapidly.4,76

In deciding the appropriate treatment threshold for ICP, the

available clinical and CT evidence should be considered. An

ICP slightly higher than the guideline treatment threshold (e.g.

25 mm Hg) may be acceptable if the CPP is adequate and there

are no signs of brain stem compression.

Lesions in the temporal fossa and deep inferior frontal

lobes can develop brain stem compression even at ICP levels of

approximately 15 mm Hg.56

Correlation Between Clinical Signs and Recorded ICPClinical signs of brain stem compression/herniation do not

always correlate with the level of recorded ICP, nor does the level

of ICP reliably indicate the degree of midline shift evident in a CT

scan.77 Clinical evidence of brain stem compression/herniation

demands urgent treatment, irrespective of the level of ICP.

Trends of ICP and CPPThe duration of any rise in ICP or fall in CPP should be noted.

Most monitoring systems provide direct digital readouts of ICP

and CPP (when MAP is monitored simultaneously) and record

the trends of these measurements.

Intracranial ComplianceIntracranial pressure responses to stimuli, such as endotracheal

tube suctioning, and marked spontaneous fl uctuations in

pressure (pressure waves) indicate reduced intracranial

compliance and the need for extra vigilance.

Accuracy of ICP MeasurementThe ICP measurements may be inaccurate as a result of:

1. zero drift

2. artefacts in the ICP recording due to technical defects in

the monitor

3. damping of a recording from a ventricular catheter due to

blockage or leakage of the catheter

Failure to recognise such errors can lead to inappropriate or

inadequate treatment. It is important to avoid uncritical

dependence on ICP data alone, but rather to relate ICP

data to clinical fi ndings and the fi ndings in the CT scan.

Insensitivity of ICP MonitoringIn certain instances, the ICP trends may not indicate the

development of an evolving intracranial haematoma.

1. The absolute level of ICP may be misleading with lesions

in the temporal fossa, such as temporal lobe contusions,

where lateral tentorial herniation can occur at levels of ICP

of 15–20 mm Hg.57

2. Elevations in ICP secondary to an expanding mass

lesion may not be distributed equally throughout the

brain. Pressure gradients can develop within the brain

parenchyma, with brain tissue pressures being higher near

the lesion. This may not be refl ected immediately at a

monitoring site remote from the lesion.78,79 Rapid increases

in volume of unilateral supratentorial mass lesions can

result in signifi cant interhemispheric pressure gradients

lasting 1–2 hours, after which the pressures may become

equalised.80

3. Mass lesions in the posterior fossa may expand and increase

pressure in the posterior fossa. Upward herniation of the

cerebellum may block the tentorial hiatus and pressure

transmission so that supratentorial pressure may not be

elevated and not detected by an ICP monitor placed in the

supratentorial compartment.81

Intracranial Pressure WavesThree types of ICP waves forms were described by Lundberg.82

A waves (plateau waves) are of greatest clinical interest in

head injury monitoring. A waves rise from a normal or

slightly raised baseline ICP to levels of approximately

50 mm Hg or even higher. They may last 5–20 minutes

and then fall abruptly. They indicate a markedly reduced

intracranial compliance and are considered to be due to

cerebral vasodilatation in response to reduced CPP (Fig.

3.14a).

B waves are rhythmic oscillations of ICP, rising sharply

to 10–20 mm Hg and then falling abruptly. They occur

at a frequency of 0.5–2 waves/minute. B waves refl ect

respiratory excursions and are more frequent in patients

with impaired intracranial compliance. They have less

adverse signifi cance than A waves (Fig. 3.14b).


C waves are small rhythmic oscillations of 20 mm Hg

occurring at a frequency of 4–8 /minute. They correspond

to arterial Traube–Hering waves and are of doubtful

clinical signifi cance. Although they may be more frequent

in some patients who have compromised intracranial

compliance, C waves may fail to appear in others who have

a signifi cant reduction of intracranial compliance, but

may occasionally be seen in patients with normal ICP and

normal compliance (Fig. 3.14c).

In practice, treatment is based on the level and duration of any

rise in ICP rather than the wave form.

SUMMARYRaised ICP after head injury may reduce cerebral

perfusion, leading to cerebral ischaemia, and be associated

with brain shifts, herniation and brain stem compression.

Cerebral perfusion is governed by the relationship

between mean arterial blood pressure and ICP, as well

as changes in the cerebral microcirculation, especially

the capacity for autoregulation. When intracranial

compliance is reduced, any addition to intracranial

volume, by an expanding mass lesion, brain swelling or

increased blood volume due to hypoventilation, may

lead to catastrophic deterioration in an otherwise stable

patient. Less than 10% of patients with severe head injury

who show signs of transtentorial herniation make a

functional recovery, underscoring the need for extreme

vigilance and early diagnosis of patients at risk for brain

stem herniation so that treatment can be initiated prior to

the actual process of brain stem compromise.


80

70

60

50

40

30

20

10

00 5 10 15 20

(a)

25 30 35 40

ICP

(mm

Hg

)

Time (minutes)

70

60

50

40

30

20

10

0

0 5

(b)

10 15 20 25 30 35Time (minutes)

ICP

(mm

Hg

)

70

60

50

40

30

20

10

00 5 10

(c)

15 20 25 30 35

Time (minutes)

ICP

(mm

Hg

)

▲ Figure 3.14. Intracranial pressure (ICP) wave forms. (a) A waves, characterised by a steep rise of pressure (ramp) to 50–80 mm Hg or higher for 5–20 minutes (arrow), followed by an abrupt fall; (b) B waves are pressure pulses of 10–20 mm Hg that occur at a frequency of 0.5–2 waves/minute (arrows); and (c) C waves, small rhythmic oscillations of 20 mm Hg occurring at a frequency of 4–8 /minute (arrows).


References1. Bullock MR, Chesnut RM, Clifton GL, et al.

Guidelines for the management of severe head injury. J Neurotrauma 2000;17:449–627.

2. Reilly P. Management of intracranial pressure and cerebral perfusion. In: Reilly P, Bullock R, eds. Head injury. London: Chapman & Hall, 1997:387–407.

3. Lang EW, Chesnut RM. Intracranial pressure: monitoring and management. Neurosurg Clin North Am 1994;5:573–605.

4. Feldman Z, Narayan RK. Intracranial pressure monitoring: techniques and pitfalls. In: Cooper PR, Gofi nos JG, eds. Head injury, 4th edn. New York: McGraw-Hill, 2000:265–92.

5. Johnston IH, Johnston JA, Jennet B. Intracranial pressure changes following head injury. Lancet 1970;ii:433–6.

6. Marmarou A. Pathophysiology of traumatic brain edema: current concepts. Acta Neurochir Suppl 2003;86:7–10.

7. Unterberg AW, Stover J, Kress B, et al. Edema and brain trauma. Neuroscience 2004;129:1019–27.

8. Maas AIR, Dearden M, Servadei F, et al. Current recommendations for neurotrauma. Current Opin Crit Care 2000;6:281–92.

9. Monro A. Observations on the structure and functions of the nervous system. Edinburgh: Creech and Johnson. 1823.

10. Kellie G. An account of the appearances observed in the dissection of two of three individuals presumed to have perished in the storm of the 3rd and whose bodies were discovered in the vicinity of Leith on the morning of 4th November 1824. Trans Med Chirurg Soc Edin 1824;1:84–169.

11. Miller JD. Volume and pressure in the craniospinal axis. Clin Neurosurg 1975;22;76–105.

12. Miller JD, Butterworth JF, Gudeman SK, et al. Further experience with management of severe head injury. J Neurosurg 1981;54:289–99.

13. Narayan RK, Kishore PR, Becker DP, et al. Intracranial pressure: to monitor or not to monitor? A review of our experience with severe head injury. J Neurosurg 1982;56:650–9.

14. Langfi tt TW, Genarelli TA. Can outcome from head injury be improved? J Neurosurg 1982;56:19–25.

15. Marmarou A, Anderson RL, Ward JD, et al. Impact of ICP instability and hypotension on outcome of patients with severe head trauma. J Neurosurg 1991;75:S59–66.

16. Marshall LF. Head injury: recent, present, future. Neurosurgery 2000;47:546–61.

17. Becker DP, Miller JD, Ward JD, et al. The outcome from severe head injury with early diagnosis and intensive management. J Neurosurg 1977;47(4):491–502.

18. Stein SC, Ross SE. Moderate head injury: a guide to initial management. J Neurosurg 1992;76:562–4.

19. Poca MA, Sahuquillo J, Biguena M, et al. Incidence of intracranial hypertension after severe head injury: a prospective study using the Traumatic Coma Data Bank classifi cation. Acta Neurochir Suppl (Wien) 1998;71:27–30.

20. Ananda A, Morris GF, Juul N, et al. The frequency, antecedent events, and causal relationships of neurologic worsening following severe head injury. Executive Committee of the International Selfotel Trial. Acta Neurochir Suppl (Wien) 1999;73:99–102.

21. Oertel M, Kelly DF, McArthur D, et al. Progressive hemorrhage after head trauma: predictors and consequences of the evolving injury. J Neurosurg 2002 ;96:109–16.

22. Servadei F, Murray GD, Penny K, et al. The value of the ‘worst’ computed tomographic scan in clinical studies of moderate and severe head injury. European Brain Injury Consortium. Neurosurgery 2000;46:70–5.

23. Souter MJ, Andrews PJD, Pereirinha MR, et al. Delayed intracranial hypertension: relationship to leukocyte count. Crit Care Med 1999;27(1):177–81.

24. Unterberg A, Kiening K, Schmiedek P, et al. Long-term observations of intracranial pressure after severe head injury: The phenomenon of secondary rise of intracranial pressure. Neurosurgery 1993;32:17–24.

25. Dunn LT. Raised intracranial pressure. J Neurol Neurosurg Psychiatry 2002;73:i23–7.

26. Chesnut RM. Medical management of intracranial pressure. In: Cooper PR, Gofi nos JG, eds. Head injury, 4th edn. New York: McGraw-Hill, 2000:229–64.

27. Cold GE. Cerebral blood fl ow in acute head injury. The regulation of cerebral blood fl ow and metabolism during the acute phase of head injury, and its signifi cance for therapy. Acta Neurochir Suppl (Wien) 1990;49:1–64.

28. Lee JH, Kelly DF, Oertel M, et al. Carbon dioxide reactivity, pressure autoregulation, and metabolic suppression reactivity after head injury: a transcranial Doppler study. J Neurosurg 2001;95:222–32.

29. Steiner LA, Coles JP, Johnston AJ, et al. Assessment of cerebrovascular autoregulation in head-injured patients: a validation study. Stroke 2003;34:2404–9.

30. Rosner MJ, Daughton S. Cerebral perfusion pressure management in head injury. J Trauma 1990;30:933–41.

31. Contant CF, Valadka AB, Gopinath SP, et al. Adult respiratory distress syndrome: a complication of induced hypertension after severe injury. J Neurosurg 2001;95:560–8.

32. Czosnyka M, Pickard JD. Monitoring and interpretation of intracranial pressure. J Neurol Neurosurg Psychiatry 2004;75:813–21.

33. Steiner LA, Czosnyka M, Piechnik SK, et al. Continuous monitoring of cerebrovascular pressure reactivity allows determination of optimal cerebral perfusion pressure in patients with traumatic brain injury. Crit Care Med 2002;30:733–8.

34. Vespa PM. Perfusing the brain after traumatic brain injury: what clinical index should we follow? Crit Care Med 2004;32:1621–3.

35. Doppenberg EM, Zauner A, Bullock R, et al. Correlations between brain tissue oxygen tension, carbon dioxide tension, pH, and cerebral blood fl ow: a better way of monitoring the severely injured brain. Surg Neurol 1998;49:650–4.

36. Goodman JC, Valadka AB, Gopinath SP, et al. Extracellular lactate and glucose alterations in the brain after head injury measured by microdialysis. Crit Care Med 1999;27:2063–4.

37. Stahl N, Mellergard P, Hallstrom A, et al. Intracerebral microdialysis and bedside biochemical analysis in patients with fatal traumatic brain lesions. Acta Anaesthesiol Scand 2001;45:977–85.

38. Coles JP, Fryer TD, Smielewski P, et al. Incidence and mechanisms of cerebral ischemia in early clinical head injury. J Cereb Blood Flow Metab 2004;24:202–11.

39. Warner DS, Borel CO. Treatment of traumatic brain injury: one size does not fi t all. Anaesth Analg 2004;99:1208–10.

40. Cruz J, Jaggi JL, Hoffstad OJ. Cerebral blood fl ow, vascular resistance, and oxygen metabolism in acute brain trauma: redefi ning the role of cerebral perfusion pressure? Crit Care Med 1995;23:1412–17.

41. Reinert M, Barth A, Rothen HU, et al. Effects of cerebral perfusion pressure and increased fraction of inspired oxygen on brain tissue oxygen, lactate and glucose in patients with severe head injury. Acta Neurochir (Wien) 2003;145:341–9.

42. Menzel M, Soukup J, Henze D, et al. Brain tissue oxygen monitoring for assessment of autoregulation: preliminary results suggest a new hypothesis. J Neurosurg Anesthesiol 2003;15:33–41.

43. Vespa P, McArthur D, Glenn T, et al. Persistently reduced levels of extracellular glucose early after traumatic brain injury correlate with poor outcome at six months: a micro-dialysis study. J Cereb Blood Flow Metab 2003;23:865–77.

44. Juul N, Morris GF, Marshall SB, et al. Intracranial hypertension and cerebral perfusion pressure: infl uence on neurological deterioration and outcome in severe head injury. The Executive Committee of the International Selfotel Trial. J Neurosurg 2000;92(1):1–6.

45. Robertson CS. Management of cerebral perfusion pressure after traumatic brain injury. Anaesthesiology 2001;95:1513–17.

46. Robertson CS, Valadka AB, Hannay HJ, et al. Prevention of secondary ischemic insults after severe head injury. Crit Care Med 1999;27(10):2086–95.

47. Chesnut RM. Management of brain and spine injuries. Crit Care Clin 2004;20:25–42.

48. Brain Trauma Foundation. Update notice. Guidelines for the management of severe traumatic brain injury: cerebral perfusion pressure. The Brain Trauma Foundation, 2003: http://www2.braintrauma.org/guidelines/ [Accessed 5 August 2004].

49. Greenberg MS. Head trauma. In: Handbook of neurosurgery. Lakeland, FL: Greenberg Graphics, 1997:571–600.


50. Marmarou A, Beaumont A. Physiology of cerebrospinal fl uid and intracranial pressure. In: Winn HR, ed. Youman’s neurologiocal surgery. Philadelphia: WB Saunders, 2003:175–94.

51. Britt PM, Heiserman JE. Imaging evaluation. In: Cooper PR, Gofi nos JG, eds. Head injury, 4th edn. New York: McGraw-Hill, 2000:63–131.

52. Liau LM, Bergsneider M, Becker DP. Pathology and pathophysiology of head injury. In: Youmans JR, ed. Neurological surgery, 4th edn, Vol. 3. Philadelphia: WB Saunders, 1996:1549–94.

53. Statham PF, Johnston RA, Macpherson P. Delayed deterioration in patients with traumatic frontal contusions. J Neurol Neurosurg Psychiatry 1989;52:351–4.

54. Ropper AH. Syndrome of transtentorial herniation: is vertical displacement necessary? J Neurol Neurosurg Psychiatry 1993;56:932–5.

55. Aldrich MS, Bassetti C. Consciousness and coma. In: Crocard A, Haywrad R, Hoff JT, eds. Neurosurgery. The scientifi c basis of practice, Vol. 1, 3rd edn. London: Blackwell Science, 2000:181–91.

56. Chesnut RM, Marshall LF. Treatment of abnormal intracranial pressure. Neurosurg Clin North Am 1991;2(2):267–84.

57. Marshall LF, Cotton JM, Bowers-Marshall S, et al. Pupillary abnormalities: elevated intracranial pressure and mass location. In: Miller JD, Teasdale GM, Rowan JO et al., eds. Intracranial pressure VI. Berlin: Springer-Verlag, 1986;656–60.

58. Martínez-Mañas RM, Santamarta D, de Campos JM, et al. Camino® intracranial pressure monitor: prospective study of accuracy and complications. J Neurol Neurosurg Psychiatry 2000;69:82–6.

59. Davis JW, Davis IC, Bennink LD, et al. Placement of intracranial pressure monitors: are ‘normal’ coagulation parameters necessary? J Trauma Injury Infect Crit Care 2004;57(6):1173–7.

60. Alleyne CH, Hassan M, Zabramski, JM. The effi cacy and cost of prophylactic and

periprocedural antibiotics in patients with external ventricular drains. Neurosurgery 2000;47:1124–9.

61. Holloway KL, Barnes T, Choi S, et al. Ventriculostomy infections: the effects of monitoring duration and catheter exchange in 584 patients. J Neurosurg 1996;85:419–26.

62. Paramore CG, Turner DA. Relative risks of ventriculostomy infection and morbidity. Acta Neurochir (Wien) 1994;127:79–84.

63. Lo CH, Spelman D, Bailey M et al. External ventricular drain infections are independent of drain duration: an argument against elective revision. J Neurosurg 2007;106(3):378–83.

64. Wong GK, Poon WS, Wai S et al. Failure of regular external ventricular drain exchange to reduce cerebrospinal fl uid infection: result of a randomised controlled trial. J Neurol Neurosurg Psychiatry. 2002;73(6):759–61.

65. Poon WS, Ng S, Wai S. CSF antibiotic prophylaxis for neurosurgical patients with ventriculostomy: a randomized study. Acta Neurochir Suppl (Wien) 1998;71:146–8.

66. Dasic D, Hanna SJ, Bojanic S et al. External ventricular drain infection: the effect of a strict protocol on infection rates and a review of the literature. Brit J Neurosurg 2006;20:296.

67. Korinek A–M, Reina M, Boch AL et al. Prevention of external ventricular drain – related ventriculitis . Acta Neurochirurgica 2005;147:39–46.

68. Piper I, Barnes A, Smith D, et al. The Camino intracranial pressure sensor: is it optimal technology? An internal audit with a review of current intracranial pressure monitoring technologies. Neurosurgery 2001;49:1158–65.

69. Shapiro S, Bowman R, Callahan J, et al. The fi beroptic intraparenchymal cerebral pressure monitor in 244 patients. Surg Neurol. 1996;45(3):278-82.

70. Bavetta S, Norris JS, Wyatt M, et al. Prospective study of zero drift in fi breopticpressure monitors used in clinical practice. J Neurosurg 1997;86:927–30.

71. Gopinath SP, Robertson CS, Constant CF, et al. Clinical evaluation of a miniature strain-gauge transducer for monitoring intracranial pressure. Neurosurgery 1995;36(6):1137–41.

72. Lang J, Beck J, Zimmermann M, et al. Clinical

evaluation of intraparenchymal Spiegelberg

pressure sensor. Neurosurgery 2003;52:1455–9.

73. Maas AI, Dearden M, Teasdale GM, et al.

EBIC-guidelines for management of severe

head injury in adults. European Brain

Injury Consortium. Acta Neurochir (Wien)

1997;139:286–94.

74. Czosnyka M, Czosnyka Z, Pickard JD.

Laboratory testing of the Spiegelberg brain

pressure monitor: a technical report. J Neurol

Neurosurg Psychiatry 1997;63:732–5.

75. Gopez JJ, Meagher RJ, Narayan RK. When and

how should I monitor intracranial pressure. In:

Valadka AB, Andrews BT, eds. Neurotrauma:

evidence-based answers to common questions.

New York: Thieme, 2005:53–7.

76. Bullock MR, Chesnut R, Ghajar J, et al Surgical

management of traumatic brain injury.

Neurosurgery 2006;58(Suppl. S2):1–61.

77. Marshall LF, Barba D, Toole B, et al. The

oval pupil and relationship to intracranial

hypertension. J Neurosurg 1983;58:566–8.

78. Chambers IR, Kane PJ, Signorini DF, et al.

Bilateral ICP monitoring. Its importance in

detecting the severity of secondary insults.

Acta Neurochir 1998;71(Suppl.):42–3.

79. Mindermann Th, Gratzl O, Interhemispheric

pressure gradients in severe head trauma in

humans. Acta Neurochir 1998;71(Suppl.):

56–65.

80. Gambardella G, Davila D, Staropoli C, et al.

Bilateral intraparenchymal pressure in patients

with unilateral supratentorial mass lesions.

In: Avezaat CJ, van Eijendhoven JM, Maas AR,

Tans JJ, eds. Intracranial pressure VIII. Berlin:

Springer-Verlag, 1993:82–4.

81. Rosenwasser RH, Kleiner LI, Krzeminski

JP. Intracranial pressure monitoring in

the posterior fossa. A preliminary report.

J Neurosurg 1989;71:503–5.

82. Lundberg N. Continuous recording and

control of ventricular fl uid pressure in

neurosurgical practice. Acta Psychiatr Neurol

Scand 1960;36(Suppl. 149):1–193.

PART III

Evaluation and Diagnosis50 CHAPTER 4 Neurological Evaluation

62 CHAPTER 5 Radiological Evaluation

CHAPTER 4

Neurological Evaluation 51 Introduction

51 Protocol for Neurological Evaluation 51 History of the Initial Injury 52 Neurological Examination

57 Assessment of the Severity of Brain Injury

57 Clinical Features of an Intracranial Haematoma

58 Clinical Monitoring

58 Diagnosis of Brain Death 60 Criteria for the Diagnosis of Brain Death

60 Summary

61 References

INTRODUCTIONAn early, accurate neurological evaluation in the

immediate postinjury period is the basis for initial

clinical decisions and for comparison during subsequent

examinations. The widespread availability of computed

tomography (CT) scans has contributed tremendously to

identifi cation of intracranial pathology after head injury,

but does not supplant the need for careful neurological

evaluation.

The neurological examination of the patient determines management decisions at each phase of assessment:

1. in the prehospital phase

• initial triage decisions

• need for intubation/ventilation

• rapidity of initial transfer and nature of receiving hospital

2. in the emergency department

• triage decisions

• need for intubation/ventilation

• urgency of initial CT scan

3. later phase

• detection of secondary complications

• assessment of the effectiveness of therapy

• assessment of the need for surgery for lesions causing increases in intracranial pressure (ICP)

• whether to continue intensive care

Computed tomography evaluation of head injury has its limitations:

1. it does not demonstrate certain important pathological changes, such as axonal injury or early ischaemic damage

2. it only provides a ‘snap shot’ of macroscopic pathology at a given moment in the course of the injury; the CT scan is unable to capture the dynamic changes that occur with progression of acute head injury

Hence, the importance of an adequate neurological examination.

After head injury, evaluation of neurological function may be confounded by several factors related to injury and treatment, including hypoxia and hypotension, sedation and muscle relaxants, endotracheal intubation, alcohol or drug intoxication, postictal states and hypothermia. The presence of these factors should be recorded and the components of neurological evaluation unaffected by them should be given extra emphasis. Where the confounding effects of such factors can be remedied, neurological evaluation should be recorded before and after their correction.

Finally, simple as it may seem, neurological evaluation

should be accurately and legibly recorded on a time-based chart

and maintained continuously through all phases of care.

Protocol for Neurological EvaluationIn patients with severe head injury, the extent of the initial

neurological examination is often governed by the need

for immediate cardiopulmonary resuscitation. When such

resuscitative measures are urgently required, a rapid assessment

of the level of consciousness and pupils would suffi ce (Algorithm

4.1). Neurological fi ndings should be recorded where possible

prior to administration of sedation, muscle relaxants and

endotracheal intubation. Where immediate resuscitation is

not required in the emergency setting, an effi cient neurological

examination should include an evaluation of mental status,

Glasgow Coma Scale (GCS), pupillary size and responsiveness,

and motor strength and symmetry. An awake, stable patient

can undergo a relatively complete neurological examination,

especially in the later stages of the injury.

NEUROLOGICAL EVALUATION CHAPTER 4 51

History of the Initial InjuryA detailed history should be obtained from the emergency

medical personnel who admit the patient, eyewitnesses or

family members. A patient who is orientated will be able to

provide important details.

The following aspects should be recorded.

Nature of the injury The injury mechanism may give

an indication of the severity and likely pattern of injury

(e.g. an estimate of the height of a fall (a fall from a

▲ Algorithm 4.1 Neurological evaluation in the patient with acute head injury

52 PART III EVALUATION AND DIAGNOSIS

height > 3 metres can cause signifi cant primary brain

damage), the estimated speed of a vehicle (or vehicles),

whether the victim wore a seat belt or a protective

helmet, whether the victim was ejected from a moving

vehicle or was trapped for some time and needed diffi cult

extrication.)

Time of injury The time of injury should be recorded as

accurately as possible (e.g. preferably ‘at approximately

2.30 pm today’ rather than ‘ this afternoon’) and events

thereafter referred to that time.

Neurological state of the patient immediately after injury and thereafter Whether there was loss of consciousness

after the injury and its duration (the defi nition of ‘cerebral

concussion’ and evaluation of the concussed patient has

been discussed in detail in Chapter 15, Sports-Related Head

Injury), changes in the level of consciousness from the time

of the injury until admission, focal defi cits (such as limb

weakness) and the occurrence and description of seizures.

The records of emergency medical services EMS who admit

the patient (neurological signs, vital signs, sedation, fl uid

administration and other initial manoeuvres performed)

should be documented.

History of alcohol or drug abuse This is relevant in

interpreting the level of consciousness and risk of

complications, such as alcohol withdrawal.

Last Meal An obvious consideration if the patient needs to

be intubated or undergo emergency surgery.

Present and past illnesses This includes a record of all

current medication.

Neurological ExaminationImportant assessments include the level of consciousness (by

GCS), the state of the pupils, localising signs (hemiparesis/

hemiplegia, monoparesis/monoplegia, paraparesis/paraplegia,

aphasia/dysphasia), signs of brain stem compromise, cranial

nerve defi cits and signs of a spinal cord injury.

ASSESSMENT OF LEVEL OF CONSCIOUSNESSConsciousness is defi ned as a state of awareness of self and

the surrounding environment with the ability to respond to

changes in the environment. Consciousness requires intact

functioning of both cerebral cortices (for awareness) and the

reticular activating system of the brain stem (for arousal).

Therefore, any alteration in the level of consciousness refl ects

either a disturbance of function of the brain stem reticular

activating system or a global disturbance of function of both

cerebral cortices.

Assessment of the level of the consciousness is the most

important component of the neurological assessment.

Glasgow Coma ScaleThe GCS has been in use almost universally for nearly 30 years

(see Table 4.1), during which time it has demonstrated ease of

Table 4.1. The Glasgow Coma Scale

Assessment Score

1. Eye openingSpontaneousTo speechTo painNone

4321

2. Verbal responseOrientatedConfusedInappropriate wordsIncomprehensible soundsNone

54321

3. Motor responseObeying commandsLocalising to painFlexing to painAbnormal fl exionExtension to painNone

654321

Total 15

application and good inter/intra-observer reproducibility across

observers with varying degrees of experience.1,2 It is determined

by objective clinical recording of eye opening, verbal response

and motor response.

The Glasgow Coma Scale and the Glasgow Coma ScoreThe Glasgow Coma Scale assesses three components of the state

of consciousness: (i) eye opening (a measure of ‘awakeness or

arousal’); (ii) verbal response (a measure of ‘awareness’, an

index of cortical function); and (iii) motor response (quality

of motor response). Each response is given a score according

to increasing degrees of impairment. Teasdale and Murray3

emphasised that the summed Glasgow Coma Score obtained

by adding scores for the three responses is an artifi cial index.

Although the Glasgow Coma Score is used to categorise

patients, it contains less information than separate descriptions

of the three responses. Teasdale and Murray3 stressed that it is

the Glasgow Coma Scale, not the Glasgow Coma Score, that

should provide the basis for the monitoring and exchange of

information about individual patients. They also observed that

errors can be introduced by using only the total Glasgow Coma

Score, because a single combined total Glasgow Coma Score can

be made up in different ways.3 Hence, the individual scores

for these responses should be recorded separately.

For children under 5 years of age, a Paediatric Coma Scale

should be used (see Chapter 14, Head Injury in Children).

Guidelines for the Accurate Assessment of the GCS

1. Assessment of verbal response:

• Verbal Score 5: orientated in time, place and

person and able to give appropriate answers to

questions


▲ Figure 4.1 Motor responses.

a

b

c

d

e

• Verbal Score 4 (confused): able to talk in sent-ences or phrases, but is not orientated; speech lacks proper sense or may be inappropriate

• Verbal Score of 3: can only utter a few inappropriate words

• Verbal Score of 2: can only make incoherent sounds (groaning, indistinct mumbling)

• Verbal Score of 1: no verbal response

A drowsy patient may be orientated. An alert patient may be confused.

2. Points of application of pain stimuli:

• supraorbital notch: pressure with the ball of thumb, avoided if there is orbital trauma

• retromandibular region: pressure with the tip of the index fi nger

• nail bed: blunt pressure with a pencil

• manubrium sternum: pressure with the knuckles, avoided if there is thoracic injury

• pectoralis major: muscle squeezed between thumb and fi ngers

In the assessment of eye opening to pain, stimulation at the surpaorbital notch or retromandibular region should be avoided because the eyes may close in response to stimulation of these areas.4

3. Motor response in limbs

• upper limbs should be in a neutral position during application of painful stimuli (Fig. 4.1a)

• the best motor response in any of the four limbs is recorded

• localising response: during application of pain at the supraorbital notch or at the retromandibular region, the hand is brought above the chin or the patient tries to fend off the hand of the examiner; when nail bed pressure is applied on one hand, a localising response is identifi ed in the opposite arm if the latter moves across the midline attempting to reach the point of painful stimulation (Fig. 4.1b)

• fl exor response: during application of pain at the supraorbital notch or at the retromandibular region, the elbow is fl exed without bringing the hand above the chin and no attempt is made to fend off the hand of the examiner applying the painful stimulus; a motor response is also judged to be fl exor if, on painful stimulus to the nail bed, the arm bends at the elbow and pulls away from the stimulus (withdrawal) with the arm usually abducted away from the trunk (Fig. 4.1c)

• abnormal fl exor response: there is abnormal fl exion of the arm and extension of the leg;

there is a slow fl exion of the arm at the elbow and wrist, with fi sting of the fi ngers over the thumb; the arm is adducted, the leg is extended and rotated internally, with plantar fl exion of the foot (Fig. 4.1d); the features of adduction of the arm and fl exion at the wrist differentiate abnormal fl exion from the normal fl exor (or withdrawal) response

• extensor response: the arm is extended

abnormally (internally rotated at the shoulder,

extended at the elbow, the wrist pronated,

fl exed and the arm adducted); the neck may

assume a position of abnormal extension and

the teeth may become clenched; the leg is

extended and rotated internally, with plantar

fl exion of the foot (Fig. 4.1e).

An abnormal fl exor response has been regarded as indicating

an injury above the level of the mid brain (i.e. in the diencephalic

region around the third ventricle) and an extensor response

as indicating a more caudal injury involving the brain stem.5

However, there is evidence to suggest that these responses may

also result from severe injuries involving the cortex or cerebral

hemispheres.6

Factors confounding interpretation of the GCS

EFFECTS OF SEDATION/MUSCLE RELAXANTS, ENDOTRACHEAL INTUBATIONIn current practice, a signifi cant proportion of patients with

severe head injury receives sedation/analgesia and muscle

relaxants for endotracheal intubation (during the prehospital


phase or shortly after admission to hospital). The European

Brain Injury Consortium Study demonstrated that all three

responses in the GCS could not be assessed in 39% of head-

injured patients in the prehospital phase and in 23% of patients

after their initial admission to hospital.7

Although the effects of muscle relaxants persist in the

intubated patient, none of the components of the GCS can be

assessed and the GCS may be erroneously recorded as 3/15.3

Even after the effects of muscle relaxants have waned, intubation

prevents assessment of the verbal response and sedation impairs

eye opening.

The type of sedative/muscle relaxant, the doses

administered and the time of administration should be

recorded so that allowance can be made for their effects

on the GCS.

The verbal score for intubated patients should not be

recorded as ‘1’; instead a non-numerical designation, such

as VT, should be used.

When verbal response and eye opening cannot be

scored because of intubation and sedation, the motor

response may still provide valuable prognostic information,

especially in the severely injured patient.3

INTOXICATIONThe median blood alcohol concentration compatible with

a normal GCS was found to be 115 mg/100 mL. High blood

alcohol concentrations (> 240 mg/100 mL) are associated with

a two- to three-point reduction in the GCS. The depressant

effects of alcohol in patients after trauma have also been

demonstrated to be highly variable.8 Hence, where alcohol

intoxication is suspected, the blood alcohol concentration

should be determined where possible, before assuming

that intoxication is infl uencing assessment of the GCS.

HYPOXIA, HYPOTENSION AND HYPOTHERMIAIn view of the effects of hypoxia, hypotension and hypothermia on

neuronal function, the GCS recorded immediately after admission

to the emergency department may not be a true refl ection of

the severity of the head injury. Therefore, the GCS should be

recorded before and after correction of hypoxia, hypotension and

hypothermia (pre- and post-resuscitation GCS).

Limitations of the GCSThe following drawbacks associated with the use of GCS need

to be recognised.

ERRORS WITH RESPECT TO ACCURACY OF GCS RECORDINGDespite versatility and ease of use, errors may occur with

GCS scoring. In one study, there was a disparity between the

GCS quoted by referring physicians and the actual GCS in

49% of patients referred with acute head injury.9 Teasdale

et al., in a recent review, observed that many physicians making

neurosurgical referrals were not fully conversant with the use of

the GCS.3 To achieve high levels of consistency in the application

of the GCS, all medical and nursing staff involved in the care of

head-injured patients should be trained and regularly updated

in the use of the scale.

TIMING OF THE INITIAL GCS EVALUATIONIn their original description of the GCS, Jennett and Teasdale specifi ed that for the purpose of head injury classifi cation, the initial Glasgow Coma Score should be assigned 6 hours after head injury has been sustained.1 This time interval allowed for the diagnosis and management of other injuries (especially transient infl uences, such as hypotension, hypoxia and alcohol intoxication) that may have affected neurological function . A GCS assessment performed too early in the course of the injury may also refl ect the generalised depression of the neurological status that follows the initial injury, which may not necessarily correlate with the severity of the head injury or with outcome.10 In practice, neurological observations should begin at the fi rst opportunity, as discussed in the section on prehospital care, and be continued regulary thereafter.

With current improvements in prehospital care, as well as advances in diagnostic and treatment modalities, the time interval between injury and defi nitive treatment of a head injury has been signifi cantly reduced. The impact of early postinjury assessment of GCS (which may overestimate of the extent of brain damage) has to be borne in mind when management decisions (such as endotracheal intubation, initial triage) are made on the basis of the initial Glasgow Coma Score.

The GCS does not consider the state of the pupils or other indicators of brain stem dysfunction.

The Glasgow–Liege Scale was developed to overcome this limitation. This scale adds the assessment of fi ve brain stem refl exes to the GCS:

1. fronto-orbicular refl ex (elicited by a light tap on the glabella)

2. vertical oculo-vestibular refl ex (elicited by rotating the head fully in the vertical plane, if a cervical spine injury has been excluded)

3. pupillary refl ex

4. horizontal oculo-vestibular refl ex (elicited by rotating the head fully in the horizontal plane, if a cervical spine injury has been excluded)

5. oculocardiac refl ex

The fi ve refl exes are lost in descending order during rostral–caudal deterioration. The disappearance of the oculocardiac refl ex coincides with brain death.11

INSENSITIVITY TO IMPAIRMENTS IN MENTAL FUNCTIONThe GCS is a global assessment of the level of consciousness and does not comprehensively assess the mental state. Patients with ‘normal GCS’ who have subtle changes in mental function, such as lethargy or signifi cant amnesia, have a higher risk of harbouring a signifi cant intracranial haematoma.12–14 Attention to such subtle changes of mental function is helpful in selecting patients with mild head injury for CT scanning.

THE GCS DOES NOT CONSIDER FOCAL NEUROLOGICAL SIGNSLateralising neurological signs, especially in the form of limb weakness, are not considered because only the best motor response is recorded.


A HIGH GLASGOW COMA SCORE DOES NOT ELIMINATE THE RISK OF SERIOUS BRAIN INJURYIn a study of patients with minor head injury, 17% of those

requiring craniotomy for acute traumatic intracranial

hematoma had an initial Glasgow Coma Score of 15.15

RELATIVE INSENSITIVITY TO SUBTLE DETERIORATIONS IN NEUROLOGICAL FUNCTIONThe GCS is a qualitative assessment and does not assess the

vigour or strength of a response. Subtle, early changes in the

neurological state may not be detected by the GCS (e.g. a

patient opening eyes readily to a command may have the same

GCS for eye opening as another who needs the command to be

shouted aloud several times to elicit the same response. These

qualitative differences are important to note in serial

assessments of patients, because subtle deterioration

may go unnoticed.

The AVPU ScaleIn emergency situations, especially during initial resuscitation,

a rapid assessment of the level of consciousness may be made

using the AVPU scale. (A – Alert; V – Verbal stimulus response;

P – Pain stimulus response; U – Unresponsive).

Other terminology that has been used to describe

disturbances of consciousness include the following:16

Confusion Characterised by disorientation and an impaired

ability to perceive, as well as respond (impaired ability for

clear thinking).

Delirium Characterised by motor restlessness, disorientation,

transient hallucinations and sometimes delusions.

Obtundation Impaired level of alertness, with some degree

of psychomotor retardation.

Stupor Conscious, but exhibits little or no spontaneous

activity.

Coma Unrousable and unresponsive to external stimuli

(there is no spontaneous eye opening, no verbal response

and an inability to obey commands). The Glasgow Coma

Score is 8 or less in comatose patients.

Post-traumatic AmnesiaPost-traumatic amnesia (PTA) is a period of confusion and

memory loss immediately following an acute head injury that

is characterised by loss of the ability to register ongoing events.

The duration of the PTA is defi ned as the time elapsed between

the accident and the return of continuous memory. It is an

important index of the severity of the injury, especially because

the duration of loss of consciousness after an injury may, at

times, be diffi cult to determine. A patient with a concussive

injury will not be able to recollect the immediate circumstances

of the injury (retrograde amnesia) and may be disorientated in

place, time and person.17

The PTA may be estimated retrospectively, but is more

accurately measured prospectively by regular repeated

testing with standardised questionnaires, such as the

Galveston Orientation and Amnesia Test (GOAT).18

Cerebral concussion and its grading will be discussed in

Chapter 15, Sports-Related Head Injury. Cerebral concussion

and PTA can be used as indices of the severity of the injury.

Kushner proposed that patients who sustain a period of loss of

consciousness longer than 30 minutes or have PTA exceeding

24 hours could not be considered as having sustained a mild

head injury.19

EXAMINATION OF PUPILS

Pupillary SizePupillary size is measured in millimetres and any asymmetry

in size between the two sides recorded. The pupil is considered

dilated if its size is > 4 mm. An asymmetry of > 1 mm between

the two pupils is signifi cant. Pupillary dilatation is an important

indicator of a mass lesion producing brain stem compression

(usually ipsilateral to the dilated pupil). The greater the

asymmetry in size, the more likely the presence of a mass

lesion.

Pupillary Reactivity to LightPupillary reactivity is assessed for both direct and consensual

light refl ex. The reactivity is recorded as being brisk, sluggish

or non-reactive.

It is important to determine whether any pupillary

abnormality was present from the moment of injury or

developed subsequently. In later stages of head injury, periorbital

haemorrhage may preclude pupillary assessment. As with the

GCS, it is important to record the examination of pupils before

and after cardiopulmonary resuscitation. Pupillary size and

reaction may be affected by drugs, such as opiates and fentanyl,

and ocular injuries.

Interpretation of pupillary abnormalities seen in acute head

injury is indicated in Table 4.2.

Unilateral dilated, non-reactive pupilA unilateral dilated, non-reactive pupil is an important

indicator of third nerve compression due to brain stem

herniation, especially if the pupil had been of normal size and

reactive earlier. A unilateral dilated, non-reactive pupil due to

a direct injury of the third nerve (efferent pupillary defect) or

the optic nerve (afferent pupillary defect) may be caused by a

traction injury of the nerve or following a fracture of the base

of the skull (in these instances, the pupillary abnormality is

often evident soon after the injury). The presence of ocular/

orbital injury should always be recorded during assessment of

the pupils.

Pupillary dilatation due to a third nerve lesion may be

differentiated from an optic nerve/ocular injury by the

consensual light refl ex. In case of a third nerve palsy, when the

light is shone on the eye with the dilated pupil, the opposite

pupil constricts. In optic nerve/ocular injury, there is no

reaction in the opposite pupil. In addition, a dilated pupil due

to a third nerve lesion may be accompanied by ptosis and a

divergent squint.


Table 4.2. Range of pupillary abnormalities seen in acute head injury

Pupillary abnormality Underlying pathology

One pupil dilated and non-reactive

Third nerve compression due to uncal herniationDirect trauma to the third nerveOptic nerve injuryInjury to the iris

Both pupils dilated, non-reactive

Brain stem failureBrain stem compression/ischaemia due to space-occupying lesion or diffuse swellingPrimary brain stem injury

Severe hypotensionPostepileptic stateAdministration of anticholinergic drugs (atropine)Barbiturates

••

Oval pupil Early stages of brain stem compression due to a space-occupying lesion

Pin-point, fi xed pupils Pontine lesion

Normal-sized fi xed pupils Mid brain lesion

Unilateral, normal-sized fi xed pupil

Injury to the irisIn some instances of optic nerve injury

Bilateral dilated, non-reactive pupilsBilateral dilated, non-reactive pupils usually indicate severe

primary brain stem damage where they are evident immediately

after injury and irreversible upper brain stem damage from

brain stem compression when evident in later stages of the

injury. It is important to remember that both pupils may

be dilated and unreactive during a postepileptic state or

owing to inadequate cerebral perfusion.20 Bilateral dilated,

unreactive pupils may also be a result of the administration

of atropine. Hence, atropine should not be administered to

a patient with acute head injury for examination of the optic

fundi. Bilateral fi xed pupils may also occur with barbiturates

used in coma-inducing doses.

Normal-Sized Fixed PupilsNormal-sized fi xed pupils may result from a mid brain lesion.

A unilateral fi xed pupil that is of normal size may also occur

after injury to the iris or in some instances of optic nerve

injury.

The Oval PupilAn oval-shaped, eccentric pupil may indicate the early stages of

brain stem herniation.21

FOCAL NEUROLOGICAL SIGNS

Lateralised Limb WeaknessLateralised limb weakness may be demonstrated with ease in

the patient who obeys commands. In less-responsive patients,

diminished spontaneous movement, the need for increased,

direct painful stimulation to elicit movement or asymmetric

motor posturing may indicate lateralised limb weakness.

1. Hemiparesis or monoparesis immediately after injury,

indicates primary damage.

2. Hemiparesis developing in the later stages of injury

often indicates a contralateral mass lesion causing direct

compression of the underlying motor cortex or compression

of the ipsilateral cerebral peduncle by uncal herniation.

Hemiparesis may be ipsilateral to the mass lesion when

the opposite cerebral peduncle is compressed against the

tentorial edge (‘Kernohan’s Notch’ phenomenon).

3. Flaccid paraparesis/paraplegia may indicate: (i) spinal cord

injury (low cervical, thoracic); or (ii) damage to both leg

areas in the parasagittal motor cortices (e.g. by a depressed

fracture over the vertex).

4. Flaccid quadriparesis/quadriplegia may indicate: (i) a

high cervical spinal cord injury (often associated with

bradycardia, increased skin temperature and loss of

sensation in the limbs, loss of sweating in the affected limbs

and priapism); or (ii) damage to the pons or medulla.

Plantar responses may be extensor with severe head injury.

Tendon refl exes are of little signifi cance in the early stages after

injury. However, absent refl exes in a paretic limb may indicate a

peripheral nerve lesion, such as a brachial plexus injury. Speech

defects and hemi-anopic fi eld defects can only be detected in

cooperative patients, but a dysphasia should not be mistaken

for confusion.

SIGNS OF BRAIN STEM IMPAIRMENT

Ocular Signs

EYE MOVEMENTSThe presence of spontaneous roving eye movements or ability

to fi x on a target and follow usually indicates preservation of

brain stem function. Brain stem impairment may result in

disturbances of conjugate eye movements, such as in forced

downward deviation or lateral deviation of both eyes and may

result in a divergent squint.

More severe disturbances of brain stem function result in

loss of oculocephalic and oculovestibular refl exes.


Oculocephalic refl ex (doll’s eyes manoeuvre) Prior

to performing this test, a cervical spine injury must be

excluded. The head is rotated to the full extent in horizontal

and vertical planes. Loss of oculocephalic refl ex is indicated

by absence of conjugate movement of the eyes in the

direction opposite to head turning. The oculocephalic

refl ex tests the integrity of the pontine gaze centres.

Oculovestibular refl ex This refl ex should not be performed

in patients who have evidence of a middle cranial fossa

fracture. The external auditory canal is slowly irrigated

with approximately 20 mL ice-cold water. A positive

response is indicated by deviation of eyes towards the side

of stimulation.

Motor signs An extensor response to pain is a sign of severe

brain stem injury.

Abnormalities of Vital Signs

Respiration Abnormalities of respiration include

tachypnoea, irregular and shallow respiration and

Cheyne–Stokes respiration (shallow breathing alternating

with deep breathing).

Pulse rate Bradycardia is a sign of severe brain stem

compromise.

Blood pressure Systolic hypertension occurs with severely

increased intracranial pressure (the Cushing refl ex).

Subsequent systolic hypotension is a terminal sign of brain

stem failure. Although neurogenic hypotension has been

reported to occur in a small subset of patients with severe

head injury,22 in general, hypotension after acute head injury

is usually caused by hypovolaemia due to blood loss.

Signs of a severe brain stem disturbance shortly after injury are

most likely due to primary brain stem damage. Such patients

are almost invariably unconscious from the time of injury.

Signs of brain stem disturbance manifesting in later stages are

usually due to brain stem compression.

CRANIAL NERVE SIGNSThe cranial nerves that are most often injured are the olfactory,

optic, oculomotor, abducens, facial and vestibulocochlear

nerves.

SKULL AND SCALPEvaluation of acute head injury also involves examination of

the cranium, with attention to following:

1. scalp haematoma, open wounds of the scalp (including

examination for depressed fracture and foreign bodies),

evidence of cerebrospinal fl uid (CSF) or brain tissue at the

wound site

2. clinical evidence of depressed fracture (by palpation)

3. evidence of basal fracture (periorbital ecchymosis, blood or

CSF from nostrils or ears, haemotympanum, retromastoid

ecchymosis)

4. ocular and fundoscopic examination (where possible)

5. otoscopic examination for haemotympanum

In case of assault, injuries should be accurately drawn, with

measurements, or photographed where possible.

Assessment of the Severity of Brain InjuryA clinical assessment of the severity of brain injury may be

made using the following criteria.

1. history

• mechanism of injury

• duration and depth of loss of consciousness

2. examination

• a Glasgow Coma Score of 8 or less (after

resuscitation) indicates a severe head injury

provided the level of consciousness is

not compromised by factors others than

brain injury, such as hypotension, hypoxia,

sedation, intoxication, hypothermia or a

postepileptic state. Hence, the level of

consciousness in the very early stages after

injury (e.g. at < 6 hours postinjury) may not

be a true refl ection of injury severity.

• clinical evidence of brain stem dysfunction may

be indicated by an extensor response to pain,

ocular or pupillary changes and respiratory

abnormalities

• evidence of diencephalic dysfunction, such as

the presence of an abnormal fl exor response to

pain or features of sympathetic hyperactivity,

such as hypertension, tachycardia and central

sweating (involving the face and trunk)

Stein23 stratifi ed brain injury severity by Glasgow Coma Score

at presentation, duration of loss of consciousness, PTA and the

presence of focal neurological defi cit (Table 4.3).

Clinical Features of an Intracranial HaematomaThe following features may indicate an evolving intracranial

haematoma:24

1. a sustained deterioration in the level of consciousness (a

decrease of 1 GCS point in the verbal or motor response or

2 GCS points in the eye opening)

2. subtle changes in mental state, such as slowing of

responsiveness to commands, increased irritability or

agitation, and persistent confusion

Table 4.3. Head injury severity scale22

Injury category Glasgow Coma Score

Minimal GCS 15, no loss of consciousness or amnesia

Mild GCS 14orGCS 15, with amnesia, brief loss of consciousness (< 5 minutes) or impaired alertness and memory

Moderate GCS 9–13orLoss of consciousness > 5 minutesorPresence of a focal neurological defi cit

Severe GCS 5–8

Critical GCS 3–4

3. failure of improvement of impaired consciousness (static

neurological state)

4. severe or increasing headaches, repeated vomiting

5. bradycardia, systolic hypertension

6. development of localising signs, such as pupillary asymmetry

and/or dilatation, limb paresis, facial asymmetry

7. a seizure without full recovery

The most reliable clinical indicator of an intracranial

haematoma is deterioration of the level of consciousness.

Pupillary dilatation (ipsilateral to the lesion) and contralateral

hemiparesis (manifesting as an arm drift in the early stages)

are recognised as defi nitive localising features of a mass lesion.

However, localising features may be absent in a large proportion

of patients who develop signifi cant intracranial haematoma.25,26

Conversely, lateralising features may be evident in many patients

with diffuse brain injury who do not have mass lesions.27

At times, hemiparesis and pupillary dilatation may be ‘false

localising signs’. The hemiparesis may be ipsilateral to the lesion

(‘Kernohan’s Notch’ phenomenon) due to compression of the

contralateral cerebral peduncle against the tentorial edge. The

pupil contralateral to a mass lesion may be the fi rst to dilate if

the opposite third nerve becomes stretched to a greater degree

during brain stem herniation. False localising signs on motor

examination can also result from occult injury to the limbs, the

spinal cord or nerve roots.

Bradycardia and systolic hypertension are usually only

evident in the late stages of intracranial hypertension and the

diagnosis of a mass lesion should not await these changes.

PATIENTS WHO ‘TALK AND DIE’ (OR ‘TALK AND DETERIORATE’)A subset of patients capable of talking at sometime after

injury may deteriorate over a very short period and some

may die. Such deterioration has been clearly shown to be due

to secondary effects of the injury, in particular evolution of

contusion, intracranial haematoma and brain swelling. Nearly

80% of patients in this ‘talk and die’ category of patients have

intracranial haematomas.28,29 The National Traumatic Coma

Data Bank reported that 10% of patients who presented with

severe head injury were able to talk during the immediate

postinjury period and, of these, 35% were orientated.30 Such

deterioration has been described to occur between 15 minutes

and 3 days after the injury (with a mean of 3 hours). Over

50% of such patients died, despite surgical evacuation of the

intracranial haematoma responsible for the deterioration.31

These fi ndings indicate that a good outcome is only possible in

patients who ‘talk and deteriorate’ if emergency measures are

taken to evacuate mass lesions before irreversible brain stem

compression occurs.

Therefore, early diagnosis of operable intracranial lesions by

CT scanning, prior to clinical deterioration, is an important

aspect of management of patients with head injuries of all

grades of severity.

Clinical MonitoringPatients with acute head injury should have neurological and

vital function assessments recorded at half-hourly intervals

initially on a Neurological Observation Chart (Fig. 4.2). In

patients with moderate and severe head injury, the duration of

subsequent monitoring is dictated by the degree of neurological

recovery. Patients with mild head injury who are admitted to

hospital are usually monitored for at least 8–12 hours. With

improvement of neurological function, the frequency of

observations may be reduced.

Diagnosis of Brain DeathBrain death has been defi ned as ‘… irreversible cessation of all functions of the entire brain, including the brain stem’.32 Death should be regarded a process rather than an event and brain death is the step that defi nes death of the person. It is now recognised that brain stem death is the essential step in the sequence of events that defi nes brain death. Some cells of the cerebral cortex or basal ganglia may survive temporarily after brain stem death, but they cannot sustain the function of the brain as a whole.33 Cardiac function may continue after the brain stem death of a patient who is on a life-support system. Traumatic brain injury is one of the common causes of brain death in patients on life support. It is therefore important that medical personnel entrusted with the care of patients with acute head injury are conversant with the criteria for accurate, unequivocal identifi cation of brain stem death.

The diagnosis of brain death is important for several reasons:

1. futile treatment may cease and scarce resources be made available for other patients

2. organ donation is possible

The UK criteria specify that two doctors should be involved

in tests to confi rm brain death: one a consultant, the other

a senior registrar or consultant. The tests must confi rm

brain death on two separate occasions. An EEG study is


▲ Figure 4.2 Neurological observation chart.


BRAIN DEATH IN ADULTSUnited Kingdom Brain Death Criteria33

1. Four preconditions

• Patient on a ventilator (i.e. no spontaneous

respiratory effort)

• In deep coma

• Coma due to irreversible structural brain

damagea

• Exclusion of reversible factors

- CNS depressant or neuromuscular

blocking drugs

- Primary hypothermia (body temp-

erature < 35°C during testing)

- Metabolic or endocrine abnormalities

2. Five tests

• No pupillary response to light

• No tracheal, gag or cough refl ex

• No response to facial and peripheral painb

• No caloric vestibulo-ocular refl exc

• No respiratory effort after achieving a

PaCO2 of 50 mm Hg for 10 min or mored

BRAIN DEATH IN CHILDRENe

• Diagnosis of brain death should not be

made in the fi rst 7 days of life

• From 7 days until 2 months of age, in

addition to criteria for adults, two

isoelectric EEG records 48 hours apart are

recommended

• Children 2–12 months old, in addition to

criteria for adults, two isoelectric EEG

records 24 hours apart are recommended

• Children > 1 year of age, diagnosis is

according to adult criteria with up to

12 hours observation, no EEG

confi rmation

a Where irreversibility of brain damage is uncertain,

suffi cient time should be allowed for confi rmation.

b Automatic movements of limbs may be observed in

brain-dead patients as a result of activity of spinal

refl exes. These must be distinguished from genuine limb

movements in response to pain.

c Caloric vestibulo-ocular refl ex: the external auditory

canal is irrigated with at least 20 mL ice-cold water. The

eyes deviate towards the side of irrigation if the refl exes

are intact.

d To prevent hypoxia during disconnection from the

ventilator, pre-oxygenation is achieved with 100%

oxygen for 10 minutes before disconnection. During

disconnection, oxygen is delivered at 6 L/min via a

catheter in the trachea.

e Based on the US Task Force for Determination of Brain

Death in Children34 and the UK Conference of Medical

Royal Colleges.35

SUMMARYNeurological evaluation is essential for the initial triage

of the head-injured patient, yet numerous factors

may compromise its usefulness during the immediate

postinjury period. Notwithstanding the signifi cant

contribution made by CT scanning in the delineation of

intracranial pathology, the fi ndings on the CT scan need

to always be correlated with the neurological status of

the head-injured patient. Severely injured patients often

undergo endotracheal intubation early in the postinjury

period, after administration of sedation, analgesia and

muscle relaxants, preventing adequate assessment of

neurological function thereafter. Hence, prehospital

care providers and emergency department personnel

need to be competent in performing an accurate

neurological evaluation expeditiously, prior to intubation.

Neurological evaluation also remains invaluable in

identifying patients with mild head injury who are at risk

of intracranial complications. Although the GCS remains

the most important method of neurological assessment

of the head-injured patient, drawbacks related to its use

need to be recognised. Current advances in primary care

have also resulted in some patients with overwhelmingly

severe brain injury and no prospect of survival being

admitted to hospital. Early neurological evaluation

plays a role in the identifi cation of such patients. Serial

neurological evaluations may detect the progression of

an intracranial haematoma and determine treatment.

Neurological evaluation is essential in the diagnosis of

brain death.


not required.33 In addition, it may be advisable to wait for

6 hours between the brain death examinations in adults to

confi rm the diagnosis, although exceptions to this practice

may clearly exist.

Criteria for the Diagnosis of Brain Death

References1. Jennett B, Teasdale GM. Assessment of Coma

and impaired consciousness: a practical scale. Lancet 1974;2:81–4.

2. Bullock RM, Chesnut RM, Clifton GL, et al. Guidelines for the management of severe head injury. J Neurotrauma 2000;17:449–627.

3. Teasdale GM, Murray R. Revisiting the Glagow Coma Scale and Coma Score. Intensive Care Med 2000;26:153–64.

4. Simpson DA. Clinical examination and grading. In. Reilly P, ed. Head injury. London: Chapman & Hall, 1997:145–65.

5. Denny-Brown D. Selected writings of Sir Charles Sherrington. Oxford: Oxford University Press, 1979.

6. Greenberg RP, Stable DM, Becker DP. Non-invasive localization of brain stem lesions in the cat with multimodal evoked potentials: correlation with human head injury data. J Neurosurg 1981;54:740–50.

7. Murray GD, Teasdale GM, Braakman R, et al. The European Brain Injury Consortium survey of head injuries. Acta Neurochir (Wien) 1999;141:223–36.

8. Brickley MR, Shepherd JP. The relationship between alcohol intoxication, injury severity and Glasgow Coma Score in assault patients. Injury 1995;26:311–14.

9. Crossman J, Bankes M, Bhan A, et al. The Glasgow Coma Score: reliable evidence? Injury 1998;29:435–7.

10. Marion DW, Carlier PM. Problems with initial Glasgow Coma Scale assessment caused by prehospital treatment of patients with head injuries: results of a national survey. J Trauma 1994;36:89–95.

11. Born JD. The Glasgow–Liege Scale. Acta Neurochir 1988;91:1–11.

12. Mendelow AD, Campbell DA, Jeffrey RR, et al. Admission after mild head injury; Benefi ts and costs. BMJ 1982;285:1530–2.

13. Mendelow AD, Teadsale GM, Jennett B, et al. Risks of intracranial haematoma in head injured adults. BMJ 1983;287:1173–6.

14. Stein SC, Ross SE. The value of computed tomographic scans in patients with low risk head injuries. Neurosurgery 1990;26:638–40.

15. Miller JD, Murray LS, Teasdale GM. Development of a traumatic intracranial hematoma after a ‘minor’ head injury. Neurosurgery 1990;27:669–73.

16. Bates D. The management of medical coma. J Neurol Neurosurg Psychiatry 1993;56:589–98.

17. Goldstein FC, Levin HS. Postconcussion syndrome and neurobehavioral disorders. In: Barrow DL, ed. Head injury. Park Ridge, IL: American Association of Neurological Surgeons, 1992:133–48.

18. Levin HS, O’Donnell VM, Grossman RG. The Galveston Orientation and Amnesia Test. A practical scale to assess cognition after head injury. J Nerv Ment Dis 1979;167:675–84.

19. Kushner D. Mild traumatic brain injury: toward understanding manifestations and treatment. Arch Intern Med 1998;158:1617–24.

20. Narayan RK. Emergency room management of the head injured patient. In: Gudeman SK, ed. Textbook of head injury. Philadelphia: WB Saunders, 1989:Chapter 2.

21. Marshall LF, Barba D, Toole B, et al. The oval pupil: clinical signifi cance and relationship to intracranial hypertension. J Neurosurg 1983;58:566–8.

22. Chesnut RM. Evaluation and management of severe closed head injury. In: Tindall GT, Cooper PR, Barrow DL, eds. Current practise of neurosurgery. Baltimore: Williams & Wilkins, 1995:1401–24.

23. Stein S. Classifi cation of head injury. In: Narayan RK, Wilberger JE, Povlishock JT, eds. Neurotrauma. New York: McGraw-Hill, 1996:31–41.

24. Kay A, Teasdale GM. Head injury in the United Kingdom. World J Surg 2001;25:1210–20.

25. Kluge D. Cranial trephination for diagnosis

and therapy of closed injuries of the head. Am

J Surg 1960;99:707–12.

26. Rand BO, Ward AA, White LE. The use

of the twist drill to evaluate head trauma.

J Neurosurg 1966;25:410–15.

27. Wilberger JE. Emergency care and evaluation.

In. Cooper PR, ed. Head injury. Baltimore:

Williams & Wilkins, 1993:27–41.

28. Reilly PL, Adams RH, Graham DI, et al.

Patients with head injury who talk and die.

Lancet 1975;ii:375–7.

29. Lobato RD, Rivas JJ, Gomez PA, et al. Head

injured patients who talk and deteriorate

into coma: analysis of 212 cases studied

with computed tomography. J Neurosurg

1991;75:256–61.

30. Marshall LF, Toole BM, Bowers SA. The

National Traumatic Coma Data Bank. Part II.

Patients who talk and deteriorate: implications

for treatment. J Neurosurg 1985;59:285–8.

31. Rockswold GL, Leonard PR, Nagib MG.

Analysis of management of 33 patients who

‘talked and deteriorated’. Neurosurgery

1987;21:51–5.

32. President’s Commission for the study of

ethical problems in medicine and biochemical

and behavioral research. Defi ning death:

medical, legal and ethical issues in the

determination of death. Washington, DC: US

Government Printing Offi ce, 1981.

33. Jennett WB. Outcome after severe head

injury. In: Reilly P, ed. Head injury. London:

Chapman & Hall, 1997:439–61.

34. Task Force for the Determination of

Brain Death in Children. Guidelines for

determination of brain death in children. Arch

Neurol 1987;44:587–8.

35. Conference of Medical Royal Colleges and

their faculties in the UK. Report of the

Working Party on organ transplantation in

neonates. London: Department of Health and

Social Security, 1988.


CHAPTER 5

Radiological Evaluation 63 Introduction

63 Radiology in the Emergency Department 63 X-Rays of the Skull 65 X-Rays of the Cervical Spine

67 Cranial CT Scan 67 Indications 68 Technical Aspects 69 Computed Tomography Diagnosis of Different Pathological Entities 82 Computed Tomography Indicators of Injury Severity

83 Serial CT Scanning 83 Delayed Progression of Lesions and the Development of New Lesions: Implications for Radiological Evaluation 83 Recommendations for a Repeat CT Scan

85 Limitations of CT Scanning 85 Limitations in Sensitivity for some Macroscopic Lesions 85 Artefacts 85 Lesions at the Vertex 85 Computed Tomography Performed too Early

85 Imaging Evaluation of the Cervical Spine in the Head-Injured Patient 85 Computed Tomography Scan of the Cervical Spine 86 Magnetic Resonance Imaging of the Cervical Spine 87 Dynamic X-Rays of the Cervical Spine

87 Evaluation of the Thoracolumbar Spine

87 Summary

88 References

RADIOLOGICAL EVALUATION CHAPTER 5 63

INTRODUCTIONRadiological evaluation is essential in the management

of all patients with moderate and severe head injury

and in selected patients with mild head injury. Clinical

evaluation may be inadequate in many patients with

acute head injury (e.g. patients who are on sedation

or artifi cial ventilation, those who are obtunded and

uncooperative and in very young children). In addition,

patients who appear intact on neurological examination

may yet harbour potentially lethal intracranial pathology

and early imaging is vital in identifying such patients

prior to deterioration. In current practice, the emphasis is

on pre-emptive investigation to detect potentially harmful

intracranial pathology prior to the onset of neurological

deterioration.

The goals of radiological evaluation in acute head injury are:

1. to detect intracranial lesions that (i) require urgent

surgical evacuation because of the potential for increased

intracranial pressure and brain stem compression; and

(ii) may cause delayed complications (e.g. contusions or

traumatic cerebrospinal fl uid (CSF) fi stulae)

2. assess head injury severity: radiological (and clinical)

parameters allow stratifi cation of head-injured patients by

injury severity

3. detect associated injuries, such as spinal injury and injuries

of the thorax and abdomen

Note: Radiological investigations should only be

undertaken after initial cardiopulmonary resuscitation and

stabilisation of the patient.

Radiology in the Emergency DepartmentX-Rays of the SkullA computed tomography (CT) scan is the appropriate initial

investigation for patients with acute head injury (for all those

with moderate or severe head injury and selected patients with

mild head injury). With the wide availability of CT scanning,

the need for plain X-rays of the skull in the evaluation of the

patient with acute head injury has been brought into question.

A recent, extensive meta-analysis of the role of plain X-rays

in triage of patients with minor head injury concluded that

demonstration of a skull fracture increases the risk of signifi cant

intracranial haemorrhage by only fi vefold,1 instead of the 40-

fold risk indicated by the study of Mendelow et al.2 It was also

demonstrated that the prevalence of intracranial haemorrhage

in patients with mild head injury presenting at an emergency

department was in the order of 0.10 (range 0.03–0.18), higher

than the previously reported value of 0.003.2 It was therefore

concluded that intracranial haemorrhage may be missed

in patients with minor head injury who are selected for CT

scanning based on demonstration of a fracture on a skull X-ray.

It is also important to remember that inexperienced clinicians

may miss approximately 10% of skull fractures on plain X-rays.3

Plain X-rays of the skull are clearly not indicated in patients

who already fulfi l the criteria for neurosurgical referral or in

whom a CT scan is indicated by clinical criteria.4,5

Although the limitations of the role of skull X-rays are

recognised, several guidelines for the management of acute

head injury have identifi ed a role for plain X-rays of the skull

in the triage of patients with minor head injury, especially

in situations where logistical diffi culties or cost prevent

CT scans being performing on all patients with Glasgow

Coma Scale (GCS) 15/15, in whom a CT is not indicated

by clinical criteria. The demonstration of a skull fracture in

such patients would be considered an indication for a CT

scan.5,6 In addition, diagnosis of a skull fracture may point to

the site of an extradural haematoma in a rapidly deteriorating

patient and evidence of signifi cant pneumocephalus in a

skull X-ray may require consideration prior to air transport

of a patient. These advantages are important in evaluation of

head-injured patients in remote locations where head-injured

patients need to be transported over long distances for a CT

scan.6

INDICATIONS FOR SKULL X-RAYS IN PATIENTS WITH GCS 15/15 5,6

1. mechanism of injury with potential for brain injury (e.g.

hit by a moving vehicle, assault with a heavy blunt weapon,

fall of > 3 metres onto a hard surface)

2. loss of consciousness or amnesia after injury

3. scalp injury in the form of: (i) full-thickness scalp

laceration; or (ii) boggy scalp haematoma

4. visible or palpable skull deformity suggesting a depressed

fracture

5. suspected penetrating injury

6. clinical evidence of a skull base fracture

7. lack of certainty of the severity of injury (intoxication,

epilepsy)

8. persisting headaches

9. focal neurological defi cit


IMAGING PROTOCOL FOR SKULL X-RAYSAnteroposterior (AP) and lateral views of the skull are

performed (a Townes view may be added if an occipital bone

fracture is suspected). The lateral view should be performed

with the patient supine and with the X-ray beam parallel to the

fl oor. This will ensure a non-rotated fi lm, so that fl uid levels

due to bleeding into the paranasal sinuses from a basal fracture

and intracranial air may be visualised.4 If a depressed fracture is

suspected, a view tangential to the point of impact is helpful in

diagnosis.6 Non-rotated fi lms must be obtained and the upper

cervical spine must be included in the lateral view. Care should

be taken with respect to the quality of the X-rays. Indeed, it has

been reported that approximately 25% of routine skull X-rays

for evaluation of head-injured patients are of poor quality.7

DIAGNOSIS OF SKULL FRACTURES BY SKULL X-RAYS

Linear Skull FracturesLinear fractures should be differentiated from vascular grooves.

Fractures are thinner and more lucent (appear black) than

vascular grooves, do not cross skull suture lines and involve

both tables of the skull and the diploe. Vascular grooves are

found in specifi c locations (such as the middle meningeal artery

and vein), are lined by thin margins of sclerotic bone and are

less lucent (appear grey rather than black). Vascular markings

also have corticated branching paths that cross sutures lines

(Fig. 5.1).

Linear fractures increase the risk of:

Extradural haematoma Fractures crossing vascular

grooves (especially the middle meningeal artery and vein)

and dural venous sinuses increase the risk of extradural

haematoma (EDH).

Dural tear and CSF fi stula Fractures that extend to the

frontal sinuses may result in a dural fi stula if they involve

the posterior wall of the sinus. Linear skull vault fractures

that extend to the skull base carry a risk of CSF fi stulae

if they extend to the paranasal sinuses or the middle ear.

A dural fi stula may sometimes be indicated by air seen in

the subdural and subarachnoid spaces, in the ventricles or

in the brain substance (pneumocephalus).

Damage to structures at the skull base Fractures that

extend to the skull base also risk damage to cranial nerves

or blood vessels in the skull base (especially the internal

carotid artery).

Diastatic FracturesDiastatic fractures result from disruption of suture lines.

A diagnosis may be made when the suture gap is > 2 mm.

Most diastatic fractures involve the Lambdoid suture and are

demonstrated by a Townes view.

Depressed FracturesA depressed fracture of the skull should be suspected if an area

of reduced density lies adjacent to an area of increased density

due to superimposition of the depressed bone on the adjacent

normal bone. Depressed fractures are best demonstrated by

viewing both AP and lateral views (Fig. 5.2a). If the standard views

are inadequate, a tangential view of is often helpful (Fig. 5.2b).

▲ Figure 5.1 Linear skull fracture. Plain X-rays showing a linear skull fracture (arrow) which appears thinner and more lucent (appears blacker) than a vascular groove and is not in a location where vascular grooves are usually found.

▲ Figure 5.2 Depressed fracture. (a) An anteroposterior view of the skull showing a depressed fracture (large white arrow) visualised as an area of increased density in the vault of the skull due to rotation and superimposition of the depressed fragment (the inner and outer tables of the depressed fragment are visible). There is an adjacent area of reduced density or lucency (small white arrow).

a


X-Rays of the Cervical SpineA comprehensive radiological evaluation of the cervical spine

is mandatory in all patients who are unconscious or who are

obtunded after acute head injury and in any patients with clinical

signs suggestive of a cervical spine injury. The consequences

of missing a cervical spine injury can be devastating. Lapses

are commonly due to failure to suspect an injury to the

cervical spine, inadequate radiological evaluation or incorrect

interpretation of radiological studies.8

Patients who are admitted unconscious after acute head

injury are often intubated, sedated and on muscle relaxants; in

such patients, radiological evaluation remains the only method

of excluding a cervical spine injury. Clinical evaluation may

also be unreliable in patients with less severe head injury owing

to confusion, intoxication or inability to cooperate in a reliable

examination as a result of pain. Full spinal immobilisation

must be maintained until complete radiological examination

of the vertebral column can be performed safely and the

results interpreted by a competent clinician. Cardiopulmonary

resuscitation must be completed and immediate life-

threatening injury excluded before a comprehensive

radiological evaluation of the spine is undertaken.

The standard fi lms for radiographic evaluation of cervical

spine injury include a three-view series:

Lateral X-ray of the cervical spine This view should reveal

the entire cervical spine from the base of the occiput to

the upper border of the fi rst thoracic vertebra because

approximately 30% of injuries occur at the C7–T1 level

(Fig. 5.4a, b). Caudal traction of the arms with the patient’s

head and pelvis stabilised (where this is not otherwise

contraindicated) is helpful to demonstrate the C7/T1

interspace. This manoeuvre should not be performed if

the cervical spine views already performed show a fracture

or subluxation. Alternatively, a Swimmer’s view may be

performed to view the lower cervical spine. A lateral X-ray

of the cervical spine alone is insuffi cient to exclude

cervical spine injury.

Anteroposterior view (revealing the spinous processes of C2–T1 vertebra) This view demonstrates vertical

alignment of the spinous and articular process and any

abnormalities in joint and disc spaces.

Open mouth odontoid view This view should reveal the

lateral masses of the fi rst cervical vertebra and the entire

odontoid process to assess the integrity of the atlanto-

occipital and atlanto-axial joints, as well as the odontoid

process. Open mouth views may not be possible in patients

who are intubated, ventilated and immobilised in a cervical

collar.

The criteria for the radiographic evaluation of the cervical spine

are summarised in Table 5.1.

Radiographic fi ndings in injuries of the cervical spine are

summarised in Table 5.2.

Basal FracturesSkull X-rays are relatively insensitive in detecting basal skull

fractures. There may be indirect evidence of a basal fracture in

the form of a linear vault fracture extending to the skull base

or the presence of air-fl uid levels in maxillary or sphenoid

air sinuses or demonstration of air in the intracranial space

(Fig. 5.3). Sinus (Caldwell) views may be helpful in identifying

some basal fractures.

▲ Figure 5.3 Basal fracture with pneumocephalus. Skull X-ray showing a signifi cant collection of air (pneumocephalus) in the intracranial compartment, with an air-fl uid level (white arrowheads).

▲ Figure 5.2 Depressed fracture. (b) Tangential view of the skull showing a depressed fracture (white arrow).

b


b

c d

a

Table 5.1 Criteria for radiographic evaluation of the cervical spine9–11

Atlas and axis Distance from the occiput to the atlas should not exceed 5 mmOpen-mouth view: the odontoid peg is examined for fractures and malalignment in relation to the lateral masses of the atlas (Fig. 5.5b)

The ADI in adults should be < 3 mm (< 5 mm in a child)

••

•

Alignment (C3–C7)

Anterior and posterior longitudinal lines and posterior facet margins should trace out smooth lordotic curves from T1 to the base of the skull (Fig. 5.4c)

The spinolaminar line should be a smooth curve, except at C2, where there can be a posterior displacement of up to 2 mm (Fig. 5.4c)

Normally the spinous processes are nearly equidistant but tend to converge to a point behind the neck (a simple loss of the cervical lordosis may be due to muscular spasm, age, previous injury, radiographic positioning or a hard collar)

•

•

•

Vertebral bodies (C3–C7)

Heights of the anterior and posterior aspects of each vertebral body from C3 to T1 should be the sameVertebral bodies should have a smooth cuboidal contourThe cortical surface should be inspected for steps, breaks or abnormal angulationsOverlapping of bone at the cortical margins suggests fracture or dislocationChanges in the internal trabecular pattern, lucencies and increases in density indicate a possible overlap of bone fragmentsAlignment (using spinal lines)

•••••

•

Joint spaces (C3–C7)

The joint spaces should be similar and the articulating surfaces should be parallel to one another•

ADI, atlas–dens interval.

a

b

▲ Figure 5.4 Plain X-rays of Cervical Spine. (a) An optimal lateral view showing C7/T1 interspace (arrow) clearly; (b) A suboptimal lateral view, the lower cervical spine is obscured by the shoulder (arrow); (c) A lateral view showing the lines for assessment of spinal alignment, namely the anterior and posterior cervical lines and the spinolaminar line (white lines). (d) A lateral view showing a subluxation at the C6/C7 level (white arrow).

▲ Figure 5.5 Lateral views of the C1/C2 region. (a) Normal relationships between the atlas and axis. (b) A fracture through the base of the odontoid process with separation of the odontoid from the body of the axis (white arrow) is shown.


Table 5.2 Radiographic fi ndings in injuries of the cervical spine10,11

Injuries of the upper cervical spine

Retropharyngeal swellingWidening of the interlateral mass distance (with displacement of the fractured lateral mass)Transverse ligament insuffi ciency suspected if the ADI is > 3 mm in an adult (>/5 mm in a child)Intermass widening is greater than 6.9 mmOdontoid fracturesa

•••••

Injuries of the lower cervical spine

Facet subluxationRotation of facet surfaces ( the ‘bow tie’ sign in the lateral view)b

Unilateral facet dislocation associated with approximately 25% subluxationBilateral facet dislocations commonly with associated cord injury and a subluxation of approximately 50%; there may be fanning of spinous processes, narrowing of disc–disc space and soft tissue swelling but no rotation (Fig. 5.4d)

Bony injuryc

Compression fractureBurst fractureTear-drop fracture

Changes in alignmentWidening of the interspinous spaces (divergence or ‘fanning’)Break in the contour of the anterior and posterior longitudinal lines, posterior facet margins or the spinolaminar lineTranslation of one cervical vertebral body on the other more than 3.5 mm or angulation greater than 11° indicates disruption of the posterior longitudinal ligament

•••

•••

••

•

aOdontoid fractures are divided into Types I, II and III. Type I fractures involve fracture of the odontoid above the waist; Type II fractures are at the junction of the odontoid process with the vertebral body of the axis; and Type III fractures extend into the body of C2.

bUnifacetal dislocation. If unifacetal dislocation is suspected, oblique views should be taken.

cVertebral body injury. A disparity of greater than 2 mm in the heights of the anterior and posterior margins of a vertebral body suggests a compression fracture. A disparity > 25% occurs with tears involving the posterior longitudinal ligament and posterior ligamental complexes, a sign of mechanical instability. In extension injuries or fl exion–rotation and compression injuries of the spine, there may be separation of a triangular chip of bone from the inferior margin of the vertebral body (tear-drop fracture).

ADI, atlas–dens interval.

In summary, the radiographic features suggestive of cervical

instability in the lower cervical spine are as follows:10,11

1. subluxation of the vertebra above on the vertebra below

(25% with unilateral facet dislocation, 50% with bilateral

facet dislocation)

2. facet joint overriding, facet joint widening

3. interspinous fanning (indicates a possible tear in the

posterior ligamental complex)

4. > 25% compression of the vertebral body, > 10° angulations

between vertebral bodies

5. burst fractures with disruption of the posterior column

6. > 3.5 mm anterior vertebral body translation

7. tear-drop fracture, hyperextension fracture, hyperextension

fracture–dislocation

Cranial CT ScanThe CT scan is the best imaging modality for accurate

delineation of macroscopic lesions in the brain and the cranium

in the patient with acute head injury. The current generations

of CT scanners are able to provide high-resolution images in

a rapid acquisition time, increasing the accuracy of diagnosis

and reducing the risks to critically injured patients during the

period of examination.

Computed tomography scanning is increasingly available

in Level 2 Care Centres and District General Hospitals,

where services of a Neuroradiologist or a Neurosurgeon

may not be available. It is therefore essential for those

entrusted with the initial management of the head-injured

patient in such situations to have suffi cient expertise in

the accurate interpretation of CT fi ndings. This knowledge

is indispensable for making important initial management

decisions on-site, as well as providing accurate information

to a Neurosurgeon who may undertake the subsequent

management.

IndicationsIndications for an emergency CT scan (i.e. as soon as

feasible) are:

1. severe head injury (GCS ≤ 8) and moderate head injury

(GCS 9–13)

2. deteriorating level of consciousness or increasing focal

neurological signs (especially pupillary asymmetry

and hemiparesis)

Note: Patients with a Glasgow Coma Score of 13 are

considered under the category of moderate head injury.

Indications for an urgent CT scan (i.e. within 4 hours)

are:

1. GCS 14, especially if the GCS does not improve after

approximately 4 hours of observation


2. GCS score of 15, with the following features:

• severe or increasing headaches

• persistent vomiting

• a focal neurological defi cit

• irritability or altered behaviour

• a seizure without recovery

• plain X-ray showing a vault fracture or

evidence of a basal fracture

Where CT scanning is readily available, a more liberal policy

may be adopted for CT scans in patients with mild head injury,

whereas a more selective policy may be required where CT

facilities are not available or have limited availability on-site.

Indications for CT scans in patients with mild head injury will

be discussed further in Chapter 13, Management of Mild Head

Injury.

Technical Aspects

COMPUTED TOMOGRAPHY PROTOCOLA standard scout lateral view is performed. Axial sections are

made parallel to the orbitomeatal line (approximately 15-

20° caudal to the infra-orbitomeatal line), extending from

the foramen magnum to the vertex, avoiding irradiation of

the orbits. Section thickness is 5 mm for the posterior fossa

(foramen magnum to pituitary fossa) and 10 mm (less with

more modern scanners) for the supratentorial region12 (Fig.

5.6). In patients with faciomaxillary injury, the lowest axial CT

sections can include the upper facial skeleton.

The scanning time is 1–5 minutes with most CT scanners

and shorter with helical CT scanners.4 The estimated dose

radiation in a CT scan of the brain is approximately 2.0 mSv

(equivalent to 1 years background radiation). By comparison,

the dose radiation for three skull fi lms is 0.14 mSv.5

WINDOW WIDTHS AND WINDOW LEVELSImages may be viewed at different ‘settings’, as determined by

window widths and window levels, in order to demonstrate

different pathological processes.13

1. ‘bone’ windows (window width 2000–4000, window level

500) demonstrate skull fractures (Fig. 5.7a)

2. ‘brain’ windows (window width 80, window level 40)

demonstrate intrinsic pathology and most extracerebral

lesions (Fig. 5.7b)

3. ‘intermediate’ windows (window width 150, window

level 60) are very helpful for the demonstration of small

extracerebral lesions adjacent to the cranium (which may

be obscured by the high density of the cranium in ‘brain’

windows; Fig. 5.7c)

▲ Figure 5.6 Digital Lateral Scout View. A Digital Lateral Scout View showing the plane and thickness of computed tomography (CT) Scan sections for cranial CT (5 mm for the Posterior Fossa and 10 mm for the Supratentorial region). The upper cervical spine is also visualised in a lateral view.

a

▲ Figure 5.7 Window settings for cranial computed tomography (CT) scan. (a) The ‘bone’ window setting, which can delineate fractures, (b) the ‘brain’ window setting, which enables visualisation of changes in brain parenchyma and extra-axial lesions, but may not clearly delineate a small extra-axial haematoma (white arrowhead) and (c) the intermediate window setting which clearly demonstrates the small extra-axial haematoma (white arrowhead).

b

c


Table 5.3 Computed tomography densities of normal and pathological elements14

Normal elements Pathological elements

Normal brain (40–50 HU)Isodense (considered the benchmark for comparison of the densities of other structures)

•Haemorrhage

Hyper-acute haemorrhage (fresh, unclotted blood): IsodenseClotted blood: Hyperdense (60–100 HU)Resolving haematoma: Hyperdensity progressively diminishes; isodense to brain in approximately 2–4 weeksBrain oedema: Hypodense

•••

•

Cranial bone (1000 HU)Extremely hyperdense •

CSF is of low density (0 HU)Hypodense •

Air in paranasal air sinuses (–1000 HU)Extremely hypodense •

Intracranial air: Extremely hypodense (–1000 HU)

CSF, cerebrospinal fl uid; HU, Hounsefi eld units.

COMPUTED TOMOGRAPHY DENSITIES OF DIFFERENT ELEMENTSDensities of different intracranial structures and pathologies determine the degree of linear X-ray absorption (or attenuation) within a selected imaging volume of tissue. The linear X-ray absorption of different structures (CT density) is measured in Hounsefi eld units (HU). The CT density of normal brain (40–50 HU) is considered to be the benchmark for comparison with densities of other structures. The CT densities of normal elements of the cranium and pathological elements in acute head injury are given in Table 5.3.

PARTIAL VOLUME AVERAGINGThe image picture elements that constitute a slice in the CT scan are termed pixels, with each pixel representing a unit volume of tissue within the slice. If material with a high attenuation coeffi cient (such as cranial bone) is partially included in a pixel, the entire pixel would be ‘bright’ and may give the appearance of blood. This is termed a partial volume averaging artefact.14 Such artefacts are common in CT slices performed near the skull base, where parts of the bony petrous ridge or the bony fl oor of the anterior cranial fossa may be included in a pixel to resemble haemorrhage.

Computed Tomography Diagnosis of Different Pathological EntitiesA systematic, comprehensive approach is needed for proper evaluation by CT scanning. Table 5.4 outlines a protocol for CT evaluation.

EXTRACRANIAL PATHOLOGY

Scalp HaematomaOn a CT scan, a scalp haematoma usually has a crescent-shaped appearance with unrestricted extension in the subgaleal plane (Fig. 5.8). A scalp haematoma indicates the site of an impact injury to the cranium. It may be associated with lesions immediately beneath the area of impact (such as skull fracture, EDH, direct or coup contusion) or lesions directly opposite the area of impact, such as contre coup contusions.

Table 5.4 Protocol for evaluation of acute head injury by computed tomography scanning

Preliminary checklist Check

Name, registration number of patientDate and time of CT scanRight–left orientation in the CT scan fi lm

•••

Extracranial pathology Scalp haematoma Skull fracture

Linear fracturesDiastatic fracturesComminuted fracturesDepressed fracturesPenetrating trauma

•••••

Intracranial pathology Focal lesions

Traumatic space-occupying lesions (EDH, AcSDH, cerebral contusion, ICH)Focal ischaemic lesions

Diffuse pathologyMass effectMidline shiftState of perimesencephalic cisternsDiffuse axonal injuryTraumatic subarachnoid haemorrhageDiffuse brain swellingIntracranial air

•

•

•••••••

EDH, extradural haematoma; AcSDH, acute subdural haematoma; ICH, intracerebral haematoma.

Skull FracturesThe CT scan fi ndings in skull fractures are listed in Table 5.5.

Fractures are best seen with the ‘bone’ window settings.

Fracture Types

Linear fractures A linear fracture is evident on a CT scan as

a well-defi ned, linear translucency in the bone. Often there

is evidence of a scalp haematoma adjacent to a skull vault

fracture, indicating the impact site (Fig. 5.9).

▲ Figure 5.11 Skull base fracture. (a) Axial computed tomography (CT) scan showing multiple air–fl uid levels (white arrowheads) in the paranasal air sinuses (indirect evidence of basal fractures). (b) An axial CT showing a fracture extending across the central skull base involving the body of sphenoid bone, extending to the apex of the petrous pyramid (black arrowheads), which resulted in damage to the internal carotid artery.

a b

▲ Figure 5.9 Linear skull fracture. Axial computed tomography scan with ‘bone’ window settings showing a linear skull fracture (white arrowhead) as a well-defi ned linear translucency in the bone beneath a scalp haematoma, which extends diffusely.

▲ Figure 5.10 Depressed fracture. Axial computed tomography scan with ‘bone’ window settings showing a fragment of bone driven below the level of the surrounding cranium (white arrow); (b) the outer table fractured to a greater extent than the inner table fragment (white arrow), in another section of the scan.

a b

▲ Figure 5.8 Scalp haematoma with an extradural haematoma (EDH). The axial computed tomography scan shows a subgaleal haematoma (white arrowhead), with an underlying EDH. Note the marked midline shift and contralateral ventricular enlargement.

Depressed fractures Computed tomography is ideal for

the diagnosis of depressed fractures. A fragment (or

fragments) of bone can be seen driven below the level

of the surrounding cranium. Typically, the inner table is

fractured more widely than the outer table (Fig. 5.10).

Basal fractures Basal fractures are best demonstrated by

thin-section CT (2–3 mm cuts) under ‘bone’ window

settings taken at right angles to the line of fracture.

• An axial CT scan may show indirect evidence of a

basal fracture in the form of multiple air–fl uid levels

in the paranasal sinuses. Less commonly, an axial CT

scan may show a fracture line across the skull base

(Fig. 5.11a, b). Fractures in the frontal sinuses are best

shown in axial sections (Fig. 5.12).

• Direct coronal sections are best for demonstrating

fractures of the anterior fossa fl oor (cribriform plate,

ethmoids, planum sphenoidale) and of the middle

cranial fossae (sphenoid, petrous bone; Fig. 5.13a, b).

Craniofacial fractures Axial and coronal CT with

bone window settings and three-dimensional (3D)

reconstructions demonstrate fractures in the orbits,

zygoma, maxilla and mandible (Fig. 5.14). Three-dimensional

CT reconstructions can also provide information about

the facial nerve canal, carotid canal and otic capsule.15


Table 5.5 Computed tomography scan fi ndings in skull fractures

Fracture type CT scan appearance Other comments

Linear fractures Affect both inner and outer tablesMargins not scleroticIn scout CT fi lms, linear fractures may be seen as

sharply defi ned, straight or curvilinear lucencies in the cranial bone (which may angulate sharply in their course)

CT may be less sensitive than plain X-rays for detecting some linear skull fractures

A linear fracture may be missed if the fracture line runs parallel to the axial section of the scan

Differentiating fractures from vascular grooves and sutures:

Vascular grooves have sclerosed margins and constant position and orientationVascular grooves are bilateral, symmetrical and involve only the inner table Sutures are usually < 2 mm wide in adults

•

•

•

Depressed fractures Localised, wedge-shaped fragment or fragments of bone driven below the surrounding cranium to a depth equivalent to or more than the thickness of the cranium

Typically, inner table fractured more than outer table

Depressed fragments may appear hyperdenseDepressed fragments may remain attached to

margins of defect or may be driven inwardsDamage from fracture fragments may lead to a

contusion or an intracerebral haematoma in the underlying brain

Depressed fractures over vertex may be missed if scans do not include the vertex (a coronal CT or a lateral X-ray can be helpful in detecting a depressed fracture over the vertex)

Depressed fractures involving posterior walls of the frontal sinus can result in a dural fi stula (air may be seen in the subdural or subarachnoid space and fl uid in the sinus)

Depressed fractures overlying venous sinuses may lead to sinus thrombosis/occlusion

Basal fractures High-defi nition, biplanar (axial+coronal), thin section CT is best for defi nition of basal skull fractures

Fractures best shown if they are perpendicular to the plane of the CT

Fractures parallel to the plane of the CT scan can be missed

CT best for:Delineating bone defects in frontal sinuses, cribriform plate, ethmoids and middle cranial fossa that may result in dural fi stulaeDemonstrating fractures involving optic canal, body of sphenoid, petrous pyramid

Pneumocephalus indicates a dural fi stula (small amounts of intracranial air may occur with penetrating injuries)

•

•

Fluid level in sphenoid sinus is indirect evidence of a basal fracture provided there is no associated maxillofacial fracture

Undisplaced fractures of the frontal sinus may be missed if fracture lines are very thin

Maxillofacial fractures High-defi nition, biplanar (axial+coronal), thin section CT with 3D reconstructions best for defi ning fractures involving the naso-orbital complex, zygoma, maxilla, mandible and complex Le Fort fractures

CT, computed tomography; 3D, three-dimensional.

• intracerebral haematoma (ICH)

• haematomas in the cerebellum and brain stem

• delayed traumatic ICH

3. focal ischaemic lesions

The CT scan features of cerebral contusions and traumatic ICH are summarised in Table 5.6.

INTRACRANIAL PATHOLOGYFocal pathology:

1. cerebral contusions and lacerations

2. traumatic intracranial haematomas

• extradural haematoma

• subdural haematoma (SDH)



Table 5.6 Computed tomography scan features of traumatic space-occupying lesions

Lesion Typical CT features Associated lesions Other important features

EDH Biconvex, hyperdense, extracerebral lesion

Does not cross the suture linesMay cross falx or tentorium

Skull fracture in 66%–95%Associated intracranial lesions

in 30%–50% of adults (mostly cerebral contusions, intracerebral haemorrhage followed by AcSDH, diffuse swelling; risk of associated lesions higher in comatose patients)

Approximately 20% associated with an underlying AcSDH

May be missed if CT is done too early after injury

Scans with intermediate window settings helpful in identifying small EDH

Ongoing haemorrhage may result in the ‘swirl sign’

Lesion may be crescentic in a few

AcSDH (presents within 48 hours)

Crescent shaped (concavoconvex), hyperdense lesion

Wide extent (in contrast with EDH, which is more confi ned)

Conforms to cortical surfaceDoes not cross falx, may cross

suture lines

AcSDH may be adjacent to a cerebral contusion (‘burst lobe’) or cerebral contusions may be found at sites remote from AcSDH

Unilateral hemisphere swelling (midline shift exceeding haematoma thickness by > 5 mm)

Diffuse axonal injury

May be iso- or hypodense in anaemic patients and those with haemodilution

Subacute SDH (presents between 48 hours and 2 weeks)

Typically an extracerebral, isodense lesion

– May be missed because of isodensitya

Chronic SDH (presents after 2 weeks)

Usually a low-density lesionOften biconvex shaped

– May sometimes appear as a mixed-density lesion (due to fresh bleeding or haematomas in different stages of evolution within the subdural space)

Cerebral contusion Lesion of heterogenous density (‘salt and pepper’ appearance)

Typically located at the cortical surface

Irregular, ill-defi ned edgePeripheral ring of hypodensity

develops in later stagesOften multiple

AcSDH may be adjacent to a contusion (‘burst lobe’)

May be associated with AcSDH, EDH at other locations

Size and extent may be underestimated on initial CT

Multiple contusions may be missed

Delayed increase of mass effect

Traumatic ICH Uniformly hyperdense lesionLocated within brain tissueWell-defi ned edgeRounded or irregular shapePeripheral ring of hypodensity

develops in later stages

May occur in an area of cerebral contusion

May manifest several days after injury even when initial CT is negative

Risk of delayed enlargementPoor prognosis when located

in basal ganglia

EDH, extradural haematoma; AcSDH, acute subdural haematoma; SDH, subdural haematoma; ICH, intracerebral haematoma; tSAH, traumatic subarachnoid haemorrhage; CT, computed tomography.

aThe following features are useful in the diagnosis of an isodense SDH: displacement of grey–white junction from the cranium; contrast enhancement of the inner membrane; and midline shift±dilatation of the opposite lateral ventricle.

Cerebral ContusionsThe CT appearance of a cerebral contusion mirrors the

pathological changes:

1. An ill-defi ned, central area of heterogenous density,

consisting of hyperdense areas corresponding to areas

of haemorrhage interspersed with hypodense areas

corresponding to areas of necrotic brain and oedematous,

swollen brain (the characteristic ‘salt and pepper’

appearance).

2. Pericontusional zone of hypodensity, where the brain

parenchyma may be less severely damaged and where there

is vasoparalysis, vasogenic oedema and perhaps some


▲ Figure 5.14 A three-dimensional computed tomography scan showing fractures involving the superior and inferior orbital margins and the zygoma (black arrowheads).

▲ Figure 5.13 Direct coronal thin-section computed tomography (CT) scans with ‘bone’ window settings. (a) Normal anatomy of the anterior cranial fossa, showing the cribriform plate, crista galli and ethmoidal sinuses. (b) A direct coronal CT scan showing extensive comminution of the right ethmoids (white arrowhead) and roof of the right orbit, with a free fragment of bone in the orbital cavity.

a b

a

▲ Figure 5.15 Computed tomography (CT) features of cerebral contusion. (a) A CT scan demonstrating the typical pathological changes in a cerebral contusion: location at the cortical surface and involvement of grey matter at the crests of the gyri. There is a central area of haemorrhage (large black arrow) admixed with areas of low density (small black arrow) representing non-haemorrhagic necrosis or partly damaged, oedematous brain and a zone of pericontusional oedema (white arrows). (b) Frontobasal contusion. The frontobasal contusion (white arrow) may be easily mistaken for the irregular anterior cranial fossa fl oor.

b

▲ Figure 5.12 Frontal sinus fracture. Axial thin-section computed tomography (CT) scan with ‘bone’ window settings showing fractures involving the anterior wall (white arrow), as well as the posterior wall (white arrowhead), of the right frontal sinus. The fracture fragment on the posterior wall of the sinus is rotated, increasing the risk of a dural tear and cerebrospinal fl uid fi stula.

degree of ischaemia. Hypodensity usually appears after

8 hours and reaches a peak at around 3–5 days (Fig. 5.15a).

Most contusions are located in relation to the basal surfaces of

the frontal and temporal lobes. Therefore, small contusions in

these areas may be missed as a result of partial volume averaging

or by artefacts from the adjacent bone, or they may be mistaken

for the bony skull base (Fig. 5.15b).

▲ Figure 5.16 Cerebral laceration (burst lobe). Computed tomography scan showing a cerebral laceration in the left temporal lobe (white arrow) with an overlying complicated acute subdural haematoma (black arrowhead).

In some cerebral contusions, the haemorrhagic component

is insignifi cant and the lesion appears uniformly hypodense as

a ‘bland’ contusion.

The mechanisms responsible for contusions usually

result in multiple lesions. This is important to bear in mind

when a solitary contusion is visualised on an early CT

scan.

Evolution of Contusions on CT ScanningThe extent of contusional injury may be underestimated in the

CT scans performed during the early postinjury period (< 24

hours) because:

1. the haemorrhagic component of the contusion may consist

of unclotted blood, which is isodense

2. the haemorrhagic component of the contusion may consist

of multiple small areas of haemorrhage, which may be

below the power of resolution of the CT scan

3. pericontusional oedema (low density) has not yet

developed

With time, a contusion becomes more apparent owing to

development of the pericontusional zone of oedema (at

approximately 8 hours) and the hyperdensity of clotted blood

(at approximately 24–48 hours). The mass effect of a contusion

peaks at 3–5 days after injury.16

After 3–4 days, the clotted blood within the contusions

begins to degrade, so that by the end of the fi rst week the

central area of the contusion gradually become isodense and,

eventually, hypodense.17

In some instances, delayed haemorrhage can occur within a

contusion, resulting in an increase in the size of the haemorrhagic

component or development of a discrete ICH within the

contusion. Delayed haemorrhage and pericontusional swelling

can lead to a delayed increase of the mass effect (see Fig. 2.13b, c).

Although an increase in the mass effect usually occurs within

3–5 days of injury, delayed haemorrhage has been reported up

to 7–10 days and even, rarely, 3 weeks after an injury.16

After the fi rst week, there is usually a gradual reduction in the

mass effect of a contusion as pericontusional swelling subsides

and the haemorrhagic component undergoes liquefaction and

absorption.

Cerebral LacerationsCerebral lacerations may be direct or indirect. Direct lacerations

occur with penetrating wounds, including penetration by

depressed skull fractures. Indirect lacerations occur most

commonly in the inferior frontal lobes and temporal poles.

The pia-arachnoid on the surface of the involved area in

the cerebral cortex is disrupted. There may be a mixture of

laceration, underlying haematoma and adjacent acute subdural

haematoma termed a ‘burst’ frontal or temporal lobe. (Fig.

5.16). An acute subdural haematoma (AcSDH) associated with

cerebral laceration or contusion is termed a ‘complicated

SDH’.18 It is often not possible, nor is it important, to make the

distinction between a contusion and an indirect laceration.

EXTRADURAL HAEMATOMAThe typical CT scan features of an EDH are:

1. appears as a sharply localised, biconvex (lentiform shape),

hyperdense, extracerebral lesion, often associated with a

skull fracture; a small proportion of EDH may be crescent

shaped (Fig. 5.17a, b)

2. often underlies scalp haematoma (site of direct impact)

3. usually does not cross the suture lines, but may cross

attachments of dural folds, such as the falx or tentorium

Active bleeding may be indicated by hypodense areas owing to

unclotted blood of ongoing haemorrhage; this feature is termed

the ‘swirl sign’ (Fig. 5.17c).19 Approximately 20% of EDH are

associated with an underlying AcSDH. In such circumstances,

the appearances of the EDH may be atypical. Some EDH are

associated with a contralateral AcSDH.16

An EDH may be missed on a CT scan if:

The CT scan is performed very early after injury If CT scans are performed very early after injury (e.g. < 2 hours), an EDH in the early stages of development may be isodense or a small EDH may be obscured by the proximity to hyperdense bone. Scans with intermediate or ‘blood’ windows are helpful in the latter situation.

There is distortion by bone artefacts Distortion may occur, for example, in the case of an EDH in the temporal fossa or in the posterior fossa (Fig. 5.18).

The EDH is over the vertex The EDH lying in the axial plane of the scan may not be seen in the CT scan unless


▲ Figure 5.19 Posterior fossa extradural haematoma (EDH). A non-contrast axial computed tomography scan showing a large EDH in the posterior fossa, with a mass effect on the fourth ventricle and early hydrocephalus.

sections are continued to the vertex. An EDH located at the vertex has ill-defi ned margins.

Posterior Fossa EDHApproximately 3%–13% of EDH are located in the posterior

fossa. An EDH is the most common traumatic lesion in the

posterior fossa and is most often seen during the 2nd and 3rd

decades20 (Fig. 5.19). The impact is usually over the occipital

region and causes a fracture crossing the transverse, sigmoid or

confl uence of sinuses. A high index of suspicion is warranted in

such circumstances.

Posterior fossa EDH may be overlooked on the CT scan if:

1. the haematoma is unclotted (isodense)

2. the CT sections are not performed low enough in the

posterior fossa

3. the CT scanner has a poor capacity for resolution

4. artefacts from adjacent bone or movement artefacts in

children and uncooperative adults obscure the clot.

▲ Figure 5.17 Extradural haematoma (EDH). (a) A non-contrast axial computed tomography scan showing the typical appearance of a biconvex, well-localised extra-axial lesion, with evidence of impact in the form of a scalp haematoma (white arrow). (b) The ‘bone’ window setting shows a skull fracture adjacent to the EDH (white arrow). (c) An EDH with the ‘swirl sign’, namely low density within the haematoma as a result of unclotted blood (black arrowhead).

c

b

a

▲ Figure 5.18 Effects of bone artefacts. A non-contrast axial computed tomography scan showing an extradural haematoma in the right temporal fossa (white arrow), nearly masked by bone artefacts.


Delayed Enlargement of EDHApproximately one-quarter of EDH have been reported to

enlarge in the postinjury period and approximately 8% appear

in follow-up CT scans after an initially negative CT study.16,21

Caution needs to be exercised when a small EDH is visualised on

a CT scan in the very early postinjury period. Such ‘innocuous-

looking’ EDH sometimes enlarge without producing signifi cant

warning symptoms or signs and deterioration can be sudden.

Computed tomography scans performed at admission should

be carefully evaluated with intermediate window settings (width

150 HU; level 40 HU) to detect thin and/or isodense EDH,

especially in patients who have had signifi cant impact injury.

Patients in whom a very early postinjury period shows a small

EDH should undergo a repeat CT scan, ideally within 36 hours,

if their neurological state does not improve satisfactorily.22

ACUTE SDHAn AcSDH is symptomatic within 48 hours of the injury.23

Typical CT scan features of AcSDH include:

1. a crescent shaped, hyperdense, extracerebral lesion

conforming to the cortical surface

2. often spread over a wide area (in contrast with the EDH,

which is usually more confi ned)

3. may cross suture lines but does not cross the falx or the

tentorium

However, an AcSDH may extend medial to the falx in the

interhemispheric fi ssure (parafalcine SDH) or along the

tentorium (peritentorial SDH; Fig. 5.20a, b).

Most AcSDH are located over the cerebral convexity.

‘Complicated SDH’ are located adjacent to cortical contusions

and lacerations (‘burst lobe’; shown in Fig. 5.16).

An acute subdural hematoma may appear isodense in an

anaemic patient (haemoglobin < 10 g/dL,), in the presence of

coagulopathy or if there is an associated tear in the arachnoid

leading to admixture of blood and CSF.16

Computed Tomography Lesions Often Associated with AcSDH

Severe unilateral hemisphere swelling Diffuse low density

(ischaemia and swelling) that extends throughout the

ipsilateral hemisphere with loss of contrast between

grey and white matter and loss of the CSF spaces in the

sulci. The hemisphere has a structureless, bland (ground

glass) appearance. Unilateral hemisphere swelling may be

identifi ed on the CT scan when the midline shift exceeds

haematoma thickness by > 5 mm (Fig. 5.20b).24 Evaluation of

the mass effect of an AcSDH on a CT scan should involve

measurement of the thickness of the SDH as well as the

degree of associated midline shift. These parameters have

been shown to be inversely correlated with outcome.24

Cerebral contusions

Diffuse axonal injury

▲ Figure 5.20 Acute subdural haematoma (AcSDH). (a) Typical computed tomography appearance of AcSDH (black arrow) as a crescentic, extra-axial lesion, with relatively unrestricted extension over a wide area. (b) An SDH with unilateral hemisphere swelling. There is low density swelling of the hemisphere underlying the SDH with loss of contrast between the grey and white matter resulting in a structureless, bland (ground glass) appearance and a signifi cant mass effect.

a

b


SUBACUTE SDHSubacute SDH becomes symptomatic between 48 hours and

2 weeks after injury.23 On CT scan, subacute SDH appears

isodense or hypodense to the surrounding brain.

An isodense SDH may be suspected when there is a midline

shift on a CT scan without an identifi able mass lesion.

The following features may be helpful in making a diagnosis

of subacute SDH:16,25

1. displacement and effacement of the cortical sulci

2. abnormal separation of the grey–white junction from the

calvarial bone

3. effacement of the ipsilateral lateral ventricle

4. midline shift and dilatation of the opposite lateral

ventricle

5. opacifi cation of the superfi cial cortical veins and

enhancement of the medial membrane in the haematoma

after contrast administration (Fig. 5.21a)

Towards the end of the subacute phase of the SDH, the cellular

elements are lysed and the lesion may appear hypodense.16

CHRONIC SDHA chronic SDH becomes symptomatic more than 2 weeks

after injury.23 On CT scan, a chronic SDH usually appears as a

biconvex lesion, which is hypodense to the brain parenchyma.

There may be septations and fl uid levels within the lesion as

a result of haematomas at different stages of evolution within

the subdural space. At times, a chronic SDH may show a

haematocrit effect: the high-density cellular elements in the

haematoma layer posteriorly and low density serum forms the

supernatant. Where fresh haemorrhage has occurred, the lesion

may appear isodense or even hyperdense (Fig. 5.21b).

SUBDURAL HYGROMAOn CT scan, a subdural hygroma appears as a crescent-shaped

extra-axial lesion whose density is identical to that of the CSF

(Fig. 5.21c). Bilateral lesions may be present.

TRAUMATIC ICHAn intracerebral haematoma is usually identifi ed by the

following CT scan features:16

1. a homogeneous, hyperdense, well-defi ned lesion within

the brain tissue

2. the margin of the lesion may be rounded or irregular

3. a peripheral zone of low density (ischaemia and swelling)

that appears after approximately 8 hours and increases in

size gradually to peak by 3–5 days (Fig. 5.22a)

The differentiation between a traumatic ICH and a cerebral

contusion may be diffi cult and may have little practical

signifi cance, because an ICH may arise within an area of

contusion.4 The mass effect from a traumatic ICH may increase

during the postinjury period owing to further haemorrhage

and increased perilesional swelling. With time, the haematoma

becomes isodense and subsequently hypodense as a result of

lysis of haemoglobin. The mass effect usually diminishes by

approximately 1 week.16

An ICH may not be detected on a CT scan performed shortly

after a head injury. Solonuik et al.26 reported that approximately

20% of ICH after severe head injury are seen in the immediate

postinjury CT scan, with 35% detected at 24 hours and 80%

detected by 72 hours.

A fl uid–blood interface may appear as a result of the

liquefaction of the brain parenchyma. The presence of such

a fl uid level within the haematoma is associated with a worse

prognosis.4,27

▲ Figure 5.21 (a) Subacute subdural haematoma (SDH). The SDH is nearly isodense (black arrow). There is effacement of cortical sulci abnormal separation of the cortical surface, as well as the grey–white junction from the inner table of the skull (white arrowheads) (b) Chronic SDH. A non-contrast axial CT scan showing a crescentic, extra-axial lesion (large white arrow) with effacement of sulci in the hemisphere underlying the lesion. There is local mass effect as evidenced by effacement of sulci in hemisphere underlying the lesion. (c) Subdural hygroma. A non-contrast axial CT scan showing an extra-axial lesion of similar density to the cerebrospinal fl uid (white arrowhead).

a

c

b


FOCAL ISCHAEMIC LESIONSAreas of transient ischaemia and of infarction both appear as

areas of low density on the CT scan.

Focal Ischaemic LesionsFocal ischaemia may occur in the later stages of head injury and

in several forms:

Ischemic zone around cerebral contusions and intracerebral haematoma (Fig. 5.15a).

Ischaemia in the hemisphere underlying an acute subdural haematoma See AcSDH (Fig. 5.20b).

Arterial vascular territory ischaemia The most common

arterial vascular territory ischaemia involves the posterior

cerebral artery. During transtentorial herniation, the uncus

and parahippocampal gyrus may compress the posterior

cerebral artery against the tentorial edge, leading to an

ischaemic lesion in the occipital lobe. During subfalcine

herniation, the pericallosal branch of the anterior cerebral

artery may be compressed between the herniating cingulate

gyrus and the free edge of the falx cerebri, resulting in a

ischaemic lesion located along the medial aspects of the

frontal and parietal lobes (Fig. 3.7b).

Injury to major extracranial vessels may manifest as a focal

ischaemic lesion (e.g. traumatic dissection of the extracranial

internal carotid artery may manifest as an area of ischaemia

in the middle cerebral artery territory; Fig. 5.23a). Detection of

such a lesion is an indication for an angiographic study of the

extracranial vessels.

Watershed IschaemiaWith severe hypotension, ischaemic areas may be evident

in the junctional zones (watershed areas) between the major

intracranial vascular territories. Areas of low density are usually

seen in the frontal parafalcine region (at the watershed between

the anterior and middle cerebral artery territories) and in the

parietal convexity region (the watershed between the middle

and posterior cerebral artery territories; Fig. 5.23b).4

Diffuse Ischaemia of the Cerebral HemispheresThe small, multiple foci of ischaemic damage seen on

pathological examination to be diffusely distributed in the

brain parenchyma in very severe head injury are not evident on

CT scans; hence, a CT scan underestimates the severity of

ischaemic brain injury.

Diffuse ischaemic damage due to severe hypoxia,

hypotension or markedly increased intracranial pressure (ICP)

may manifest as diffuse swelling of both hemispheres, with

loss of contrast between grey and white matter, a loss of CSF

spaces in the sulci and compression of both lateral ventricles

and the third ventricle, resulting in both hemispheres having a

structureless, bland (‘ground glass’) appearance.

▲ Figure 5.22 (a) Intracerebral haematoma (ICH). An axial non-contrast computed tomography (CT) scan showing an ICH in the right frontal lobe, seen as a homogeneous, hyperdense, well-defi ned (usually rounded) lesion within the brain tissue (black arrow), with a peripheral zone of low density (white arrow). (b) Traumatic basal ganglia haemorrhage. An axial non-contrast CT scan showing an ICH in the head of the left caudate nucleus (white arrow).

a b

TRAUMATIC BASAL GANGLIA HAEMATOMASHaematomas in the thalamus and basal ganglia have been

reported in approximately 3% of patients with severe closed

head injury28 (see Fig. 5.22b). They are often associated with diffuse

axonal injury and are caused by shearing of deep penetrating

blood vessels, such as the anterior choroidal and lenticulostriate

arteries, by rotational acceleration.29 Basal ganglia ICH are

associated with a poor prognosis.


INTRACEREBRAL HAEMATOMA SECONDARY TO COAGULOPATHYThis type of haematoma is increasing with the use of

anticoagulants and is discussed in Chapter 16.

TRAUMATIC CEREBELLAR HAEMATOMASIntraparenchymal haematomas of the cerebellum may develop

within areas of cerebellar contusions or in areas that appear

normal on initial CT scans.30

DELAYED TRAUMATIC INTRACEREBRAL HAEMORRHAGEDelayed traumatic intracerebral haematoma (DTICH)

typically develops in a previously normal area of the brain, as

demonstrated by a CT scan.12,16,31 However, DTICH may also

develop within an area of cerebral contusion. In addition, known

ICH may undergo delayed enlargement.32 The mechanisms

predisposing to DTICH have been discussed in Chapter 2.

Delayed traumatic intracerebral haematoma is more

common in the elderly, chronic alcoholics, patients on

anticoagulation and following the evacuation of a large

intracranial haematoma. There may be no neurological

deterioration during the initial stages of development of

DTICH. Hence, repeat CT scanning plays an important role in

identifi cation of DTICH prior to clinical deterioration.

The degree of the mass effect is a guide to ICP and the risk of brain stem compression and distortion, and therefore helps to determine the need for and urgency of surgical evacuation of a mass lesion. As a general guideline, a post-traumatic lesion with a volume of 25–30 mL or more is considered to carry a signifi cant risk of brain stem compression. However, lesions in the temporal fossa and posterior fossa may be symptomatic at even smaller volumes (15–20 mL). Estimates of the dimensions and volume of an ICH are important in determining the initial management and for conveying CT scan fi ndings over a telephone to a neurosurgeon who may take over subsequent management.

A simple estimation of the volume of the mass lesion can be be conveyed by describing the dimensions of the lesion (e.g. an EDH may be described as being 6 cm in its longest extent, 2 cm maximal thickness and seen in fi ve 1 cm sections of the CT scan).

More accurate measurements of volume can be made as follows:

Direct measurement Direct measurements of volume made

using the software in the CT scanner are the most accurate,

although this may not always be possible.12

The ‘ellipsoid’ method 33 The volume of an intracranial

mass lesion can also be calculated following the steps

listed below that use dimensions of a mass lesion, which

can be determined directly from the CT scan (using the

centimetre scale on the scan console or the centimetre

scale printed in the scan.). The CT slice with the largest

area of haemorrhage is selected for the measurement of

dimensions (see Fig. 5.24a, b). (Note, the area of oedema

surrounding an intrinsic lesion should also be included in

the measurement.) When counting slices:

1. haemorrhage > 75% (by area) compared with

slice with the largest area of haemorrhage:

count as one slice

2. haemorrhage 25–75% (by area) compared with

slice with the largest area of haemorrhage:

count slice as 0.5 of a slice

3. haemorrhage < 25% (by area) compared with

slice with the largest area of haemorrhage: do

not count

Midline ShiftMidline shift is indicated by the position of the bodies of

the lateral ventricles and septum pellucidum. The septum

pellucidum lies on a line connecting the crista galli and the

internal occipital protuberance in a normally symmetrical

skull. The true midline may also be calculated in a method not

dependant on skull symmetry by halving the distance between

the inner tables of the skull along the plane of the septum

pellucidum. Midline shift is calculated by measuring the shift of

the septum pellucidum from the midline (Fig. 5.25a, b). A midline

shift of 5 mm or more is signifi cant. With considerable midline

shift, the ipsilateral lateral ventricle is compressed and the third

ventricle will become occluded, resulting in dilatation of the

opposite lateral ventricle. This is an ominous sign indicating

Venous InfarctionFractures (especially depressed fractures) overlying a major

venous sinus can lead to sinus thrombosis and venous

infarction. Venous infarcts typically appear as heterogeneous

lesions (patchy areas of haemorrhage surrounded by an area

of low density) that are located in the white matter in a non-

arterial distribution.4 With superior sagittal sinus thrombosis,

venous infarcts are usually seen in the parasagittal regions.

NON-FOCAL PATHOLOGY

Mass EffectThe mass effect is proportional to the volume of the intracranial lesion. The CT evidence of a mass effect depends on the lesion location.

Localised frontal lesions (such as contusions) Posterior displacement of the anterior horns of the lateral ventricles.

Temporal fossa lesions Medial displacement of the temporal horns.

Convexity SDH Compression of sulci of the ipsilateral hemisphere (Fig. 5.21a)

Posterior fossa lesions Compression and displacement of the fourth ventricle (Fig. 5.19)

The most important CT indicators of clinically signifi cant mass effect are:

1. midline shift (discussed later)

2. lesion size (volume)

3. position of the haematoma (lesions in the temporal fossa and in the posterior fossa exert a more signifi cant mass effect in view of the narrow confi nes of such spaces and their proximity to the brain stem)

▲ Figure 5.23 Ischaemic lesions. (a) Middle cerebral artery (MCA) territory infarction. An axial non-contrast computed tomography (CT) scan showing gyriform hyperdensity (due to petecheal haemorrhages) in the right MCA distribution (white arrowheads) indicating an infarct secondary to an internal carotid artery dissection. (b) Watershed ischaemia. An axial non-contrast CT scan showing low-density areas at the border zones between the anterior cerebral artery and MCA territories (white arrowhead) in a patient with severe head injury who developed a prolonged episode of hypotension.

a b


a b

▲ Figure 5.25 Measurement of a midline shift. Axial non-contrast computed tomography scans showing (a) landmarks for measurement of the midline shift, namely the crista galli (white arrow), the internal occipital protuberance (black arrow) and the septum pellucidum (white arrowhead)) and (b) a midline shift associated with a subdural haematoma, showing shift of the septum pellucidum away from the midline (the midline is drawn from the crista galli to the internal occipital protuberance).

a b

c

▲ Figure 5.26 Evaluation of the perimesencephalic cisterns (PMC). Axial computed tomography (CT) scans showing (a) patent PMC, approximately 2 mm wide (arrowheads), (b) compressed PMC, where the cisterns are slit like (arrowheads), and (c) obliteration of the PMC (arrowhead). There is also a signifi cant midline shift with dilatation of the opposite lateral ventricle (white arrow), an ominous sign.

▲ Figure 5.24 Calculation of the volume of (a) intra-axial and (b) extracerebral lesion on a computed tomography (CT) scan. AP, anteroposterior.

a

Volume of an extra-axial lesion = A B C

CT scan slice showing largest area of lesion selected

12

A = longest AP extent of lesion (in the CT scan slice showing the largest area of lesion)B = maximal thickness of lesion (in the same CT slice)C = no. 10 mm CT sections showing the lesion

(a)

B

A

b

imminent brain stem compression and the need for urgent

surgical evacuation of the space-occupying lesion.

Lesions in the temporal fossa or more posterior regions may

not show a midline shift, even in the presence of signifi cant local

mass effect. With bilateral lesions (e.g. bifrontal contusions),

there may be no midline shift, yet the intracranial volume may

be at a critical level.

State of the Perimesencephalic CisternsThe state of the perimesencephalic cisterns is an important CT

indicator of raised ICP due either to a focal lesion or to diffuse

brain swelling. In advanced raised ICP, the most medial part of

the temporal lobe (uncus) herniates into the tentorial hiatus,

compressing and distorting the brain stem. This crowding of

structures at the tentorial hiatus results in compression and

later obliteration of the CSF cisterns surrounding the midbrain,

the perimesencephalic cisterns. Initially, the laterally placed

ambient cisterns (lateral limbs) will be effaced, followed by the

posteriorly placed quadrigeminal cistern (posterior limb). The

perimesencephalic cisterns are considered: (i) patent if all three

limbs are open; (ii) compressed if one or two limbs are closed

or if all three limbs are slit like; and (iii) obliterated if all three

limbs are no longer visible (Fig. 5.26a–c).

Compression or obliteration of the perimesencephalic

cisterns has been associated with a threefold risk of increased

ICP and a two- to threefold increase of mortality.35

With subarachnoid haemorrhage (SAH), the peri-

mesencephalic cisterns may be diffi cult to visualise. In this

instance, compression or obliteration of the third ventricle is a

useful indicator of increased ICP.4

Diffuse Axonal InjuryAxonal injury per se is not visible on a CT scan. This may

account for a lack of correlation between the clinical

picture and CT scan fi ndings in a patient with moderate

or severe head injury. However, larger, haemorrhagic foci

of diffuse vascular injury (‘marker’ lesions) may be seen on

the CT scan as small (< 2 cm diameter), discrete, hyperdense

lesions in the corticomedullary junction, deep white matter,

cerebellum, corpus callosum (especially splenium), internal


▲ Figure 5.29 Diffuse brain swelling. An axial computed tomography (CT) scan showing featureless cerebral hemispheres with loss of grey–white differentiation, effacement of the lateral and third ventricles and the perimesencephalic cisterns.

a b

c

▲ Figure 5.27 Diffuse axonal injury (DAI). Axial non-contrast computed tomography (CT) scans showing haemorrhagic ‘marker’ lesions. (a) In the left basal ganglia region (black arrowhead). There is also haemorrhage in the right lateral ventricle (white arrows), which may be an indirect indicator of a DAI lesion in the corpus callosum (usually in the splenium). (b) In the deep white matter of the right temporal lobe (white arrow). (c) In the dorsal aspect of the midbrain (white arrowhead).

a b

▲ Figure 5.28 Traumatic subarachnoid haemorrhage (tSAH). Axial non-contrast computed tomography (CT) scans showing tSAH in (a) the left Sylvian fi ssure (arrowhead) , (b) the basal subarachnoid cisterns (arrowhead).

capsule and brain stem (typically in the dorsolateral aspect of the midbrain; Fig. 5.27a–c). The more extensive the axonal injury (and, hence, the severity of brain injury), the deeper the locations of the ‘marker’ lesions.

Intraventricular haemorrhage is often associated with

diffuse axonal injury (DAI). This may result from extension of a

haemorrhagic lesion in the corpus callosum or from a shearing

injury of the subependymal veins or the choroid plexus4

(Fig. 5.29b). Hence, intraventricular haemorrhage (in the absence

of a contusion or an ICH communicating with the ventricular

system) may be an indirect indicator of DAI.

Traumatic SAHComputed tomography evidence of subarachnoid haemorrhage

is found in 25%–53% of severely head-injured patients.35

Traumatic SAH (tSAH) is usually seen in cortical sulci

over the cerebral convexity (the most frequent location),

Sylvian fi ssures and the basal subarachnoid cisterns (Fig. 5.28a–b)

There may also be localised areas of SAH adjacent to cerebral

contusions. The presence of tSAH in the Sylvian fi ssure may

indicate temporal lobe contusion, even though the latter is

not visible on the initial CT scan.34 Traumatic SAH indicates a

potential for delayed ischaemic damage due to vasospasm. The

risk of mortality has been shown to increase by twofold in the

presence of tSAH, with blood in the basal cisterns carrying the

worst prognosis.35

A spontaneous SAH (e.g. due to a ruptured cerebral

aneurysm) may rarely be the precipitating factor in a head

injury. The anatomical location of the SAH in relation to

known locations of aneurysmal rupture should raise this

suspicion.

Diffuse Brain SwellingEarly diffuse brain swelling may appear on a CT scan as a

diffuse loss of distinction between the grey and white matter

and a ‘slit-like’ appearance of the lateral ventricles. There may

be effacement of the sulci over the cerebral cortex. With further

progression of swelling and increased ICP, the third ventricle

becomes compressed, followed by compression and later

obliteration of the perimesencephalic cisterns (Fig. 5.29). Diffuse

brain swelling may be more common in children. Early diffuse

brain swelling in children may be diffi cult to diagnose because

the ventricles may be slit like in normal children. However, when

there is compression or obliteration of the third ventricle and/

or effacement of the perimesencephalic cisterns, a diagnosis of

diffuse brain swelling may be made with greater confi dence.36

Intracranial Air (Pneumocephalus)Air can enter the intracranial space when a breach of the dura

mater (a dural fi stula) establishes a communication with

atmospheric air. This is usually caused by a basal fracture of

the skull that involves the paranasal sinuses (frontal, ethmoid

or sphenoid sinuses), the mastoid air cells or the middle ear.

The air can accumulate in the subdural space, subarachnoid

space, the ventricular system or, rarely, in the brain substance



a b

▲ Figure 5.30 Pneumocephalus. (a) Air in the subarachnoid space (white arrows) typically appears as small, localised collections in the cortical sulci. (b) An axial computed tomography scan showing a subdural collection of air (white arrows), which appears as an extra-axial collection of very low density, conforming to the inner surface of the skull and the surface of the brain. A sudural collection of air does not cross the falx.

(the latter is termed a ‘pneumatocele’). An overt CSF leak may

not always be evident in patients with a dural fi stula.4

Because it has a very low attenuation value, intracranial

air is easily detected. Air in the subarachnoid space is usually

loculated in small areas (Fig. 5.30a), whereas in the subdural space

air is seen as a confl uent collection capping the frontal poles,

conforming to the shape of the skull in its outer perimeter,

when the scan is performed with the patient supine (Fig. 5.30b).

Rarely, progressive accumulation of a large amount of air may

occur under tension, known as a tension pneumocephalus.

Tension pneumocephalus usually caps and compresses the

frontal lobes, fl attening the normally convex outer surface of

the frontal lobes, resulting in a ‘tented’ appearance.

Less commonly, air may also enter the intracranial space via

a compound depressed fracture with a dural tear. In the later

stages of injury, loculations of air may be found at the site of

a compound depressed fracture owing to an infection by gas-

producing organisms. Small bubbles of air may, at times, be

seen in the extradural space near a simple skull fracture

in an early CT scan; such a fi nding is not indicative of a

breach in the meninges.

The investigation of dural fi stulae and CSF leaks will be

discussed in Chapter 9.

Computed Tomography Indicators of Injury SeverityIn assessing injury severity, CT features always need to be

correlated with neurological fi ndings. There are limitations

to the sensitivity of CT in demonstrating certain pathological

changes after acute head injury. Allowing for these drawbacks,

the following CT fi ndings are useful indicators of injury

severity.

Obliteration of perimesencephalic cisterns This is a sign

of advanced raised ICP and points to an ominous outcome

unless the intracranial hypertension can be effectively

controlled.

Severe unilateral hemisphere swelling associated with AcSDH Midline shift exceeding haematoma thickness

by > 5 mm.

Bilateral and widespread contusions For example, con-

tusions involving frontal and temporal lobes of both sides.

Large ICH situated in the basal ganglia/capsular region.

Contusions or lacerations extending deep into the hemisphere These lesions may be associated with a

poor outcome owing to damage to eloquent areas deep in

the hemisphere.

Marker lesions of diffuse axonal injury Small

haemorrhagic lesions in the basal ganglia and thalamus or

the brain stem are an indicator of severe diffuse injury.

COMPUTED TOMOGRAPHY CLASSIFICATION OF DIFFUSE BRAIN INJURYMarshall et al.37 proposed a CT classifi cation of diffuse brain

injury, in which four grades of diffuse brain injury were

identifi ed on the basis of compressed or obliterated basal

cisterns, midline shift and the presence of intracranial mass

lesions. These authors demonstrated that outcome became

progressively worse from diffuse injury Type I through to diffuse

injury Type IV (Table 5.7).37 The fi ndings were later confi rmed

by several prospective Class I studies.25,38 A recent review

proposed that the predictive value of this classifi cation

system is enhanced by including the presence of tSAH,

intraventricular haemorrhage and specifying the type of

mass lesion (e.g. EDH versus intradural lesions).39

SIGNIFICANCE OF A NORMAL INITIAL CT SCAN IN PATIENTS WITH SEVERE HEAD INJURY (DIFFUSE INJURY TYPE I)The ICP is elevated in approximately 13% of patients with

severe head injury who have a normal CT scan. The risk of

increased ICP is higher in those aged > 40 years, those with

systolic blood pressure < 90 mm Hg and those with unilateral

or bilateral motor posturing).35,40 Approximately one-third of

patients with severe head injury and a normal initial CT scan

develop lesions in a subsequent CT scan.41

COMPUTED TOMOGRAPHY FEATURES OF POTENTIALLY LIFE-THREATENING INTRACRANIAL PATHOLOGY

The following CT scan features indicate a risk of brain stem

compression/herniation due to increased ICP, irrespective of

the clinical state of the patient.

Compressed or obliterated perimesencephalic cisterns.

Lesions ≥ 25 mL Lesions in the temporal fossa or lesions in

the posterior fossa of 15–20 mL, because these lesions can

directly distort the brain stem in view of their proximity

to it.

Lesions producing a midline shift ≥ 5 mm Especially if

associated with dilatation of the opposite lateral ventricle.

Bifrontal contusions or temporal lobe contusions These

lesions can result in sudden, catastrophic deterioration.

b

▲ Figure 5.31 Development of a delayed extradural haemorrhage (EDH). (a) Computed tomography (CT) scan showing a very small extradural haematoma (arrow); (b) A repeat CT scan 24 hours later shows delayed development of an EDH.

a


Table 5.7 Computed tomography classifi cation of head injury by the Traumatic Coma Data Bank35,37

Category Defi nition Incidence in severe head injury

Diffuse injury Type I (no visible pathology)

No visible intracranial pathology seen on the CT scan 7%–12%

Diffuse injury Type II Cisterns present with a midline shift of 0–5 mmNo high- or low-density lesions > 25 mL (may include bone fragments and foreign bodies)

23%–32%

Diffuse injury Type III (swelling)

Cisterns compressed or absent with a midline shift of 0–5 mmNo high- or low-density lesions > 25 mL (may include bone fragments and foreign bodies)

10%–20%

Diffuse injury Type IV (shift)

Midline shift > 5 mmNo high- or low-density lesions > 25 mL

2%–4%

Evacuated mass lesion Any lesion evacuated surgically 37%–48% (approximately)

Non-evacuated mass lesion High- or low-density lesions > 25 mL not surgically evacuated 4% (approximately)

Serial CT ScanningDelayed Progression of Lesions and the Development of New Lesions: Implications for Radiological EvaluationAcute Head Injury is a dynamic process. With the wide avail-

ability of CT scanners in general hospitals and improvements

in patient transport, CT scans are often obtained within

2–3 hours after injury.42 However, a single CT scan performed

very early in the course of an acute head injury may not

provide an insight into progressive changes during the course

of the injury, such as enlargement of existing haemorrhagic

mass lesions, development of new haemorrhagic mass lesions,

progression of oedema, development of a mass effect and raised

ICP (Fig. 5.31a, b; also see Fig. 2.13b, c).

Serial CT scanning is an essential component of the

management of patients with head injury. Several investigations

have highlighted the incidence and implications of progressive

changes demonstrated by serial radiological evaluation. These

aspects have been discussed in Chapter 2 (Pathophysiology).

New haematomas and progression of existing haematomas A study of serial CT investigations in 48patients with cerebral contusions revealed the development of delayed traumatic ICH in 52%. Nearly 80% of such delayed ICH appeared within 12 hours.43 In another study of 412 patients with head injury, 37 developed new intracranial lesions, with surgical evacuation required in 22 of these patients.43

New mass lesions in patients with a diffuse injury on the initial CT scan A study of patients with moderate and severe head injury by the European Brain Injury Consortium demonstrated that in one of six patients whose initial CT scan showed evidence of a diffuse injury, subsequent CT scans showed evidence of deterioration, especially in the form of new mass lesions, and that this worsened prognosis.38

New mass lesions in patients with no abnormality on the initial CT scan The incidence of delayed lesions after a normal initial CT scan is low (4%–9%) in current studies of comatose patients when high-resolution CT scanners are used.38,44 (See also page 82).

Recommendations for a Repeat CT ScanThe principal aim of repeating CT scanning in acute head injury

is to detect the progression of mass lesions or the occurrence of

new mass lesions prior to clinical deterioration or an increase

in ICP. Signifi cant changes in post-traumatic haematomas

and the appearance of new haematomas can occur without

changes in the clinical status of the patient or, initially, without

changes in the ICP.42,45 Repeat CT scanning can also be useful

to show improvement in pathological changes. Lobato et al. demonstrated that a repeat CT scan (within 48 hours) is a better

prognostic indicator of outcome than the initial CT scan.44

THE TIMING OF REPEAT SCANNINGThe timing of repeat CT scanning is determined by the initial

injury severity, the timing and fi ndings of the initial CT scan,

Patients with moderate headinjury (GCS 9–13)Patients with severe headinjury (GCS 8 or less)

Patients with diffuse injuryType I

• Risk of evolving changes approximately 4%

Recommendation• Repeat CT within 24 hours of admission

Patients with diffuse injuryTypes II–IV

• Risk of evolving changes approximately 14%–20%

Recommendations• Repeat CT within 12 hours, if first CT scan is done < 3 hours after injury

• Repeat CT within 24 hours in all other situations

• A third CT scan may be indicated on the 3rd day after injury depending upon circumstances

Recommendation• Repeat CT if neurological state remains static

Patients with GCS 13/14

▲ Figure 5.32 Recommendations for an elective repeat computed tomography (CT) scan (based on fi ndings of an extensive study of repeat CT scanning by the European Brain Injury Consortium38). For details of the classifi cation of diffuse head injury (Types I–IV), please refer to Table 5.7.

changes in the clinical state during observations and the results

of ICP monitoring (Fig. 5.32).

Emergency Repeat CT Scan (as Soon as Permissible)An emergency repeat CT scan should be performed in patients

who develop neurological deterioration or sustained, refractory

increases in ICP.

Urgent Repeat CT Scan (Within 4 Hours)An urgent repeat CT scan should be performed in patients with

GCS 15 who develop severe or worsening headaches, repeated

vomiting, new neurological defi cits and seizure without

recovery.

In addition, urgent repeat scans should be performed in

patients with GCS 13/15 and 14/15, whose conscious level does

not improve after a period of observation.

Elective Repeat CT ScanThe intention of an elective repeat CT scan is to identify patients

at risk of increased ICP prior to deterioration.

However, not all changes demonstrated on repeat CT scans

lead to new intervention. A recent study of repeat CT scanning

of patients with severe blunt head injury found that progressive

changes were observed in the repeat CT scan in 18.4% of patients

but only one in fi ve of such patients required interventions

based on the fi ndings of the repeat CT scan. All patients

with worsening CT fi ndings who required intervention had

coagulopathy, hypotension, increased ICP or a marked decrease

in Glasgow Coma Score.46 Another review of 180 patients with

blunt head injury concluded that changes in Glasgow Coma

Score or cerebral perfusion pressure were correlated with

worsening on the repeat CT scan.47 These fi ndings emphasise the

importance of clinical fi ndings and physiological monitoring in

the selection of patients with severe blunt head injury for repeat

CT scans and in interpreting the results.

Complications may occur during transfer of a critically

ill patient for a repeat CT scan. Lee et al. reported a 16.9%

complication rate in the form of haemodynamic instability,

increased ICP, desaturation and agitation during follow-up

CT scanning of patients with acute head injury, especially in

patients with severe head injury.47

LESIONS THAT HAVE THE CAPACITY FOR DELAYED DETERIORATION

Lesions < 25 mL by volume Extradural haematomas are

more likely to enlarge in the early stages (24–48 hours),

whereas contusions may enlarge up until 7–10 days after

injury. Small contusions in the temporal lobe and small

bifrontal contusions can lead to sudden deterioration.

The potential for delayed progression is higher if the initial

CT scan is performed soon after injury.

Traumatic SAH Delayed ischaemic damage may result from

tSAH.

Depressed fractures overlying the middle and posterior third of the superior sagittal sinus Delayed thrombosis

of the sinus may be a consequence.


▲ Figure 5.33 Axial computed tomography scans of the C1/C2 region. (a) The odontoid process in normal alignment with the lateral masses of the axis. (b) A fractured odontoid process with loss of alignment with the lateral masses of the atlas and body of the axis.

a

b

Fractures of the anterior skull base or middle ear with risk of CSF fi stula Bacterial meningitis may be a possible

delayed complication in these patients.

Limitations of CT scanningLimitations in Sensitivity for some Macroscopic LesionsComputed tomography is most useful for demonstrating

haemorrhagic lesions and skull fractures. It is relatively

insensitive to small non-haemorrhagic lesions (DAI, contusions)

and very small areas of haemorrhage. The sensitivity of CT is

also determined by the quality of the scanner, with the new

spiral CT scanners achieving a high degree of sensitivity. When

the power of defi nition of the scanner is suboptimal, some

non-haemorrhagic and small haemorrhagic lesions may escape

detection.

ISODENSE HAEMORRHAGIC LESIONSHaemorrhagic lesions with unclotted blood and resolving

haematomas (after approximately 7 days) may be isodense to

brain and, hence, may not be easily visualised. In patients with

coagulopathy, the blood in haemorrhagic lesions may remain

unclotted, making detection diffi cult.

Artefacts

Beam-hardening artefacts The beam-hardening artefacts

from bone may obscure abnormalities in the adjacent

brain. This is especially relevant for contusions in the

inferior (orbital) surface of the frontal lobe, temporal fossa

and the posterior fossa and for EDH in the temporal fossa

and the posterior fossa (Fig 5.18).

Partial volume artefacts Discussed earlier in this chapter.

Movement artefacts Movement of an uncooperative

patient during scanning degrades the quality of a CT scan.

When there is a strong clinical suspicion of an intracranial

haematoma, a general anaesthetic may need to be

administered in order to obtain a good-quality CT scan.

Lesions at the VertexLesions at the vertex may be missed in axial sections.

Computed Tomography Performed too EarlyLesions in very early stages of evolution may be missed if the

CT scan is performed early after the injury (especially within

2 hours).

Imaging Evaluation of the Cervical Spine in the Head-Injured PatientComputed Tomography Scan of the Cervical SpineThe scout fi lm of the cranial CT Scan provides a lateral view

of the upper part of the cervical spine and may yield valuable

information about injury to the neck and cervical spine that

may not be visualised on the axial CT images.48 A CT scan

evaluation of the cervical spine may be performed after the

cranial CT scan. Computed tomography is most useful in

evaluating vulnerable regions that are not easily visualised on

plain X-rays. These regions include the occiput, C1/C

2 region

and the C6–T

2 region (Figs 5.33a, b, 5.34a, b, c). Plain X-rays may

miss approximately 50% of injuries at the cervicothoracic

junction.49


A high degree of sensitivity for the detection of cervical spine injury is achieved by modern-generation helical scanners. The standard scan protocol includes imaging the whole cervical spine (occiput to T2) in 2 mm axial slices with sagittal and coronal reformations. Such scanning is able to demonstrate, with reasonable accuracy, bony injury in the form of compression fractures, isolated fractures of the vertebral body and fractures of posterior elements, and provides indirect evidence of disc or ligamentous injury in the form of translation, angulation and rotational abnormalities, which are evident in sagittal and coronal reconstructions. An accurate picture of the relationships of any fractures to the spinal canal can also be obtained.50–52 The sensitivity is less with older-generation CT scanners, in which the CT slices are 3 mm or greater and where only sagittal reconstruction may be possible. Fractures orientated purely in the axial plane and subtle changes due to ligamentous injury may be missed in such studies.51,53

Although the CT scan is very sensitive in detecting osseous injury, some fractures may not be identifi ed easily (e.g. undisplaced fractures of the odontoid, especially Type II fractures). Soft tissue injury and spinal cord injury are not shown well on CT.54

GUIDELINES FOR CT EVALUATION OF THE CERVICAL SPINE

C1 /C

2 region A CT study of the C

1/C

2 region should be

performed in all patients with GCS < 8 after the cranial CT study is completed because there is a high risk of upper cervical spine injury in patients with GCS < 8. Obtaining a satisfactory open-mouth view of the C

1/C

2 region can be

diffi cult in the unconscious, intubated patient on collar immobilisation.

C7 /T

1 region A CT scan evaluation of the C

7/T

1 region

is mandatory in all patients where this region is not satisfactorily demonstrated in a lateral X-ray.

C3 /C

7 region A CT scan of these levels is indicated if

satisfactory plain fi lms of the cervical spine at these levels are not available.

Patients with a cervical spine fracture evident on plain radiology In patients with a cervical spine fracture at any level, a CT scan of the rest of the cervical spine is advisable because additional fractures not visualised on routine plain radiographs may be identifi ed.54

Magnetic Resonance Imaging of the Cervical SpineMagnetic resonance imaging (MRI) is not indicated for routine evaluation of the cervical spine after trauma. However, MRI should be considered when there is evidence or suspicion of the following:

Spinal cord injury Especially where plain radiography and CT do not show an abnormality. In such instances, a lesion in the spinal cord and cord compression due to extruded disc or haematoma may be demonstrated (Fig. 5.35).


b

c

a

▲ Figure 5.34 Computed tomography (CT) scans of the cervical spine. (a) An axial CT scan of the C6 vertebra with bone window settings showing fractures involving the lamina on the right side (white arrow) and the lateral mass on the left side (white arrowhead). (b) A burst fracture of the vertebral body (white arrows). (c) A burst fracture of the vertebral body (white arrow) demonstrated by a three-dimensional CT scan with sagittal reconstruction.

Injuries of ligaments, paraspinal soft tissues The MRI

is very sensitive for demonstration of ligamentous, soft

tissue injury.

Magnetic resonance imaging is insensitive in detecting some

fractures of the cervical spine. Hence, MRI evaluation alone

cannot exclude spinal bony injury.52

Dynamic X-Rays of the Cervical SpineThe use of dynamic fl uoroscopic screening of the cervical spine

remains controversial in view of the risks to the unprotected

spinal cord in the presence of an unstable cervical spine. Where

an MRI scan is not possible and a high index of suspicion

of a ligamentous injury with cervical spine instability exists

(despite initial plain X-rays and CT scan of the cervical spine),

lateral views of the cervical spine in fl exion and extension,

performed with adequate precautions by a trained and

competent clinician, may be useful in detecting cervical spine

subluxation.

▲ Figure 5.35 Magnetic resonance imaging (MRI) of cervical spine demonstrating spinal cord injury. A T2-weighted sagittal MRI scan showing oedema of the spinal cord at the C6 and C7 levels following a spinal cord injury.

Current recommendations for radiological clearance of

cervical spine injury are discussed in detail in Chapter 7.

Evaluation of the Thoracolumbar SpineThe thoracolumbar spine should be imaged:

1. in all unconscious patients

2. whenever there is clinical or radiological evidence of

cervical spine trauma

3. when there is a high-risk mechanism of injury or clinical

fi ndings indicative of an injury to the thoracolumbar

region

The absence of any abnormality on plain X-rays of the

thoracolumbar spine is suffi cient for exclusion of an injury to

the thoracolumbar spine.

SUMMARYCranial CT remains the most useful imaging modality

during initial evaluation of head injury. Despite its

obvious usefulness in enabling management decisions,

the cranial CT scan is insensitive to important changes

that occur at a microscopic level, such as DAI, changes in

brain parenchymal cells, haemodynamic changes in the

cerebral microcirculation and diffuse ischaemic damage.

In addition, a cranial CT can only provides a single ‘snap-

shot’ of the constantly evolving processes that characterise

acute head injury. Therefore, cranial CT needs to always

be interpreted in relation to clinical fi ndings and other

data, such as changes in ICP. A systematic approach to

the evaluation of the CT scans is essential for the accurate

interpretation of intracranial pathology and to avoid

missing lesions. The limitations of CT scanning due to

image distortion by artefacts, partial volume averaging

and reduced sensitivity for isodense lesions, as well as

the drawbacks of relying on CT scans performed very

early after injury, need to be recognised. The need for

repeat CT scanning should be dictated by clinical and

monitoring criteria, as well as the fi ndings on the initial

CT scan.

Clearance of cervical spine injury is an important

component of initial radiological evaluation. Tailoring

radiological evaluation to patients stratifi ed by risk

remains the most effective method of identifying cervical

spine injury.



References1. Hofman PAM, Nelemans P, Kemerink GJ,

et al.Value of radiological diagnosis of skull

fracture in the management of mild head

injury: meta-analysis. J Neurol Neurosurg

Psychiatry 2000;68:416–22.

2. Mendelow AD, Teasdale G, Jennett B, et al.

Risks of intracranial haematoma in head

injured adults. Br Med J Clin Res Edn

1983;287:1173–6.

3. Thillainayagam K, Macmillan R, Mendelow

AD, et al. How accurately are fractures of the

skull diagnosed in an accident and emergency

department. Injury 1987;18:319–21.

4. Teasdale E, Hadley DM. Imaging the injury. In:

Reilly P, Bullock RS, eds. Head injury. London:

Chapman & Hall, 1997:167–207.

5 Scottish Intercollegiate Guidelines Network.

Early management of patients with a head

injury sign, publication no. 46. Edinburgh:

Royal College of Physicians Edinburgh, 2000.

6. Royal Australian College of Surgeons.

Guidelines for the management of acute

neurotrauma in rural and remote locations.

Melbourne: The Royal Australian College of

Surgeons, 2000.

7. Rosenorn J, Duus B, Neilsen K, et al Diability

caused by minor head injury. Neurosurgery

1991;9: 221–8.

8. Brohi K, Wilson-Macdonald J. Evaluation

of unstable cervical spine injury: a 6-year

experience. J Trauma 2000;49:76–80.

9. White AA III, Punjabi MM. Update on the

evaluation of instability of the lower cervical

spine. Instr Course Lect 1987;36:513–20.

10. Driscoll PA, Ross R, Nicholson DA. A-B-C of

emergency radiology: cervical spine, I. BMJ

1993;307:785–9.

11. Patel RV, DeLong W, Vresilovic E. Evaluation

and treatment of spinal injuries in the

patient with polytrauma. Clin Orthop

2004;1(422):43–54.

12. Bullock MR, Chesnut R, Ghajar J, et al Surgical

management of traumatic brain injury.

Neurosurgery 2006;58(Suppl. S2):1–61.

13. Hughes M, Cohen WA. Radiographic

evaluation. In: Cooper PR, ed. Head injury,

Baltimore: Williams & Wilkins, 1993:65–89.

14. Britt PM, Heisermann JE. Imaging evaluation.

In: Cooper PR, Golofi nos JG, eds. Head injury.

New York: McGraw-Hill, 2000:63–132.

15. Katzen JT, Jarrahy R, Eby JB, et al.

Craniofacial and skull base trauma. J Trauma

2003;54:1026–34.

16. Gean AD. Concussion, contusion and

haematoma. In: Gean AD, ed. Imaging of

head trauma, 1st edn. New York: Raven Press,

1994:147–206.

17. Hesselink JR, Dowd CF, Healy ME, et al. MR imaging of brain contusions: a comparative study with CT. Am J Roentgenol 1988;150:1133–42.

18. Graham DI, Gennarelli TA. Trauma. In: Graham DI, Lantos PL, eds. Greenfi eld’s neuropathology, 61st edn. London: Arnold, 1997:197–262.

19. Zimmermann DR, Bilanuik LT. Computed tomographic staging of traumatic epidural bleeding. Radiology 1982;144:809–12.

20. Chiles BW, Cooper PR. Extra-axial hematomas. In: Loftus CM, ed. Neurosurgical emergencies. Chicago: AANS Publications, 1994:44–8.

21. Knuckey NW, Gelbard S, Epstein MH. The management of ‘asymptomatic’ epidural hematomas: a prospective study. J Neurosurg 1989;70:392–6.

22. Sullivan TP, Jarvik JG, Cohen WA. Follow-up of conservatively managed epidural hematomas: implications for timing of repeat CT. Am J Neuroradiol 1999;20(1):107–13.

23. Graham DI. Neuropathology of head injury. In: Narayan RK, Povlishock JT, eds. Neurotrauma. New York: McGraw-Hill, 1996:43–60.

24. Zumkeller M, Behrmann R, Heissler HE, et al. Computed tomographic criteria and survival rate for patients with acute subdural hematoma. Neurosurgery 1996;39(4):708–12.

25. Walder AD, Yeoman PB, Turnbull A. The abbreviated injury scale as a predictor of outcome of severe head injury. Intensive Care Med 1995;21:606–9.

26. Soloniuk D, Pitts LH, Lovely M, et al. Traumatic intracerebral hematomas: timing of appearance and indications for operative removal. J Trauma 1986;26(9):787–94.

27. Katayama Y, Tsubokawa T, Kinoshita K, et al . Intraparenchymal blood-fl uid levels in traumatic intracerebral haematomas. Neuroradiology 1992;34(5):381–3.

28. Colquhoun IR, Rawlinson J. The signifi cance of haematomas in the basal ganglia in closed head injury. Clin Radiol 1989;40:619–21.

29. Adams JH, Doyle D, Graham DI, et al. Deep intracerebral (basal ganglia) haematomas in fatal non-missile head injury in man. J Neurol Neurosurg Psychiatry 1986;9:1038–43.

30. d’Avella D, Servadei F, Scerrati M, et al. Traumatic intracerebellar hemorrhage: clinicoradiological analysis of 81 patients. Neurosurgery 2002;50:16–27.

31. Gentleman D, Nath F, Macpherson P.

Diagnosis and management of delayed traumatic haematomas. Br J Neurosurg 1989;3:367–72.

32. Fukamachi A, Nagaseki Y, Kohno K, et al. The incidence and developmental process of delayed traumatic intracerebral haematomas. Acta Neurochir (Wien) 1985;74:35–9.

33. Kothari R, Brott T, Broderick J, et al. The ABCs of measuring intracerebral hemorrhage volumes. Stroke 1996;27:1304–5.

34. Shigemori M, Tokutomi T, Hirohata M, et al. Clinical signifi cance of traumatic subarachnoid haemorrhage. Neurol Med Chir (Tokyo) 1990;30:336–40.

35. Bullock MR, Chesnut RM, Clifton GL, et al. Guidelines for the management of severe head injury. J Neurotrauma 2000;17:449–627.

36. Lang DA, Teasdale GM, Macpherson P, et al. Diffuse brain swelling after injury: more often malignant in adults than children? J Neurosurg 1994;80:675–80.

37. Marshall LF, Gautille T, Klauber MR, et al. The outcome of severe closed head injury. J Neurosurg 1991;75(Suppl.):S28–36.

38. Servadei F, Murray GD, Penny K, et al. The value of the ‘worst’ computed tomographic scan in clinical studies of moderate and severe head injury. Neurosurgery 2000;46:70–7.

39. Maas AIR, Hukkelhoven CWPM, Marshall LF, et al. Prediction of outcome in traumatic brain injury with computed tomographic characteristics: a comparison between the computed tomographic classifi cation and combinations of computed tomographic predictors. Neurosurgery 2005;57(6):1173–82.

40. Narayan RK, Kishore PRS, Becker DP, et al. Intracranial pressure: to monitor or not to monitor? J Neurosurg 1982;54:751–62.

41. Lobato RD, Sarabia L, Rivas JJ, et al. Normal CT scan in severe head injury. Prognostic and clinical implications. J Neurosurg 1986;65:784–9.

42. Servadei F, Nanni A, Nasi MT, et al. Evolving brain lesions in the fi rst 12 hours after head injury: analysis of 37 comatose patients. Neurosurgery 1995;37:899–907.

43. Yamaki T, Kirakawa K, Ueguchi T, et al. Chronological evaluation of acute traumatic intracerebral haematoma. Acta Neurochir (Wien) 1990;103:112–15.

44. Lobato RD, Gomez PA, Alday R, et al. Sequential computerized tomography changes and related fi nal outcome in severe head injury patients. Acta Neurochir 1997;139:385–91.

46. Sakai H, Takagi H, Ohtaka H, Tanabe T, Ohwada T, Yada K. Serial changes in acute extradural hematoma size and associated changes in level of consciousness and intracranial pressure. J Neurosurg 1988;68:566–70.

46. Kaups KL, Davis JW, Parks SN, et al. Routinely repeated computed tomography after blunt head trauma: does it benefi t patients? J Trauma Injury Infect Crit Care 2004;56:475–81.

47. Lee TT, Aldana PR, Kirton OC, et al. Follow-up computerized tomography (CT) scans in moderate and severe head injuries: correlation with Glasgow Coma Scores (GCS), and complication rate. Acta Neurochir (Wien) 1997;139:1042–7.

48. Emamian SA, Dubovsky EC, Vezina LG et al. CT scout fi lms: don’t forget to look! Pediatr Radiol 2004;3:535–9.

49. Annis JAD, Finlay DBL, Allen MH, et al. A review of cervical spine radiographs in casualty patients. Br J Radiol 1987;60:1059–61.


50. Anglen J, Metzler M, Bunn P, et al. Flexion and extension views are not cost-effective in a cervical spine clearance protocol for obtunded trauma patients. J Trauma Injury Infect Crit Care 2002;52:54–9.

51. Brohi K, Healy M, Fotheringham T, et al. Helical computed tomographic scanning for the evaluation of the cervical spine in

the unconscious, intubated trauma patient.

J Trauma Injury Infect Crit Care 2005;58:

897–901.

52. Crim JR, Moore K, Brodke D. Clearance of the

cervical spine in multitrauma patients: the role

of advanced imaging. Semin Ultrasound CT

MR 2001;22:283–305.

53. Ford P, Nolan J. Cervical spine injury and airway management. Curr Opin Aneasthesiol 2002;15:193–201.

54. Holmes JF, Mirvis SE, Panacek EA, et al. Variability in computed tomography and magnetic resonance imaging in patients with cervical spine injuries. J Trauma Injury Infect Crit Care 2002;53:524–30.

Initial Management of Head Injury - sample

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