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Initial Management of Head Injury - sample

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Initial Management of Head Injury provides comprehensive guidance for non-neurosurgeons on managing patients with head trauma for better patient outcomes. Targeted at emergency physicians, paramedics, …

Initial Management of Head Injury provides comprehensive guidance for non-neurosurgeons on managing patients with head trauma for better patient outcomes. Targeted at emergency physicians, paramedics, general physicians, clinicians and intensivists who are part of trauma care teams, Initial Management of Head Injury gives the non-neurosurgeon all the information they need, enabling them to make accurate decisions for optimal initial care to save lives which may otherwise be lost or irretrievably impaired.

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  • 1. PART I Epidemiology 2 CHAPTER 1 Epidemiology of Acute Head Injury
  • 2. CHAPTER 1 Epidemiology of Acute Head Injury 3 Head Injury: The Magnitude of the Problem 3 Definition of Head Injury 3 Incidence of Head Injury 3 Classification of Head Injury 4 Causative Factors 4 Changing Patterns of Head Injury 5 Organisation of Head Injury Care 7 References
  • 3. EPIDEMIOLOGY OF ACUTE HEAD INJURY CHAPTER 1 3 Head Injury: The Magnitude of the Problem In 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 250000 of these patients require hospitalisation and approximately 52000 die. Long-term disability affects an estimated 70000–90000 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. Definition of Head Injury Head injury may be broadly defined 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 deficit, seizure) The scalp,skull and brain can be injured independently and only aproportionof patientswithaheadinjurysustainaconcomitant 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 Injury Epidemiological 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 difficult to obtain from routinely collected data from hospital admissions because of poor identification or categorisation of organ-specific 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 difficult to determine because most statistics are derived from specific 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 100000 population, similar to the average rate of three reports from Australia, but much higher than that reported for the US (103 per 100000) and India (160 per 100000).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 100000 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 Classification of Head Injury Head injury can be classified 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 classification, 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. 4 PART I EPIDEMIOLOGY Causative Factors In 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 traffic 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 traffic-related injuries. Head injury accounted for a significant 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, firearms have accounted for more head injury deaths than traffic accidents since 1990.36 Alcoholisanimportantcontributoryfactorinroadaccidents (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 Injury In 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 define injury severityisdiscussedinChapter4(NeurologiocalEvaluation) and Chapter 15 (Sports-Related Head Injury). International Classification of Diseases (ICD) Code31 This patho-anatomical classification 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 100000 population (hospitalised patients and deaths) 235 103 226 334 160 Mortality rate per 100000 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 Classification of Diseases (ICD-10)31 Injuries to the Head (S00–S09) S 0-0 Superficial injury of the head S 0-1 Open wound of the head S 0-2 Fractures of skull and facial bones S 0-3 Injuries of joints and ligaments of the head S 0-4 Injury of cranial nerves S 0-5 Injury of the eye and orbit S 0-6 Intracranial injury S 0-7 Crush injury of the head S 0-8 Traumatic amputation of part of head S 0-9 Other and unspecified injury of head Sub categorisation of S 0-6: Intracranial injury S 06-0 Concussion S 06-1 Traumatic cerebral oedema S 06-2 Diffuse brain injury S 06-3 Focal brain injury S 06-4 Epidural haemorrhage S 06-5 Traumatic subdural haemorrhage S 06-6 Traumatic subarachnoid haemorrhage S 06-7 Intracranial injury with prolonged coma S 06-8 Other intracranial injuries S 06-9 Intracranial injury unspecified
  • 5. EPIDEMIOLOGY OF ACUTE HEAD INJURY CHAPTER 1 5 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 traffic 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 traffic accidents (16%) and persons hit by objects (15%).38 In some parts of the US, the beneficial effect of a decline in motor vehicle-related head injury was undermined by a marked increase in firearm-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 significantly 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 significant 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 efficacy 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 identified.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, failuretoperformacranialCTscan,inadequatebloodgases and oxygen monitoring, inadequate fluid resuscitation, delayed respiratory resuscitation and delayed despatch to the operating room. In the operating room Failure to institute intracranial pressure(ICP)monitoring,inadequatefluidadministration 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 <100µg/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 firearms) • • • • • • • • •
  • 6. 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 financial and manpower resources. A study in Latin America showed that prehospital trauma care can be improved significantly 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 fluid 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 • • • • • • EMS, emergency medical service; ATLS, advanced trauma life support.
  • 7. EPIDEMIOLOGY OF ACUTE HEAD INJURY CHAPTER 1 7 References 1. 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. Traffic 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 Classification 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 Traffic 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 traffic 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.
  • 8. PART II Basic Principles 10 CHAPTER 2 Pathophysiology of Acute Non-Missile Head Injury 33 CHAPTER 3 Intracranial Pressure
  • 9. 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 Profile in Determining the Outcome of Head Injury 29 Summary 30 References
  • 10. PATHOPHYSIOLOGY OF ACUTE NON-MISSILE HEAD INJURY CHAPTER 2 11 INTRODUCTION The 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 influenced by events occuring after the initial injury. Phases of Acute Head Injury Acute 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, inflammatory 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 modified by reparative processes (Fig. 2.2).1 Biomechanics of Head Injury The 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 Injury A 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 and apoptosis) Macroscopic changes (focal or diffuse damage) Contusions, haematoma, brain swelling, brain shifts and herniations Microscopic changes Neurones, glia Axonal injury Changes in the microcirculation Capillary damage, hypoperfusion, oedema, hyperaemia, haemorrhage, ischaemia ▲ Figure 2.1 Spectrum of the pathophysiological changes after acute head injury
  • 11. 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, significant 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).
  • 12. Inertial Injury Contre 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 fluid (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 floor 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 fissure.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. PATHOPHYSIOLOGY OF ACUTE NON-MISSILE HEAD INJURY CHAPTER 2 13 ▲ 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 floor 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
  • 13. 14 PART II BASIC PRINCIPLES ▲ Figure 2.8 Effects of compression. Forces of compression can lead to significant 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 Injury Focal Injuries CEREBRAL CONTUSIONS Contusionsmayresultfromfocalimpactordiffuseacceleration– deceleration forces. Stress waves propagating from the area of impactmaydeformbraintissuedirectlyunderneath.Whensuch 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 haemorrhageadmixedwithareasof non-haemorrhagicnecrosis 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 Loading This 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 floor). Such forces occur over a longer duration (>200 msec) compared with impact forces and usually lead to significant 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
  • 14. PATHOPHYSIOLOGY OF ACUTE NON-MISSILE HEAD INJURY CHAPTER 2 15 ▲ 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 first 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
  • 15. 16 PART II BASIC PRINCIPLES 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 LACERATIONS Cerebral 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 Damage The 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 INJURY In 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 sufficiently 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.Insomeinstances,atraumaticICHmaydevelopwithin a cerebral contusion. Blood flow 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 CONTUSIONS A 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 coalescenceof smallhaemorrhagesordelayedhaemorrhage 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 first 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 first 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
  • 16. PATHOPHYSIOLOGY OF ACUTE NON-MISSILE HEAD INJURY CHAPTER 2 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 INJURY The 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 defined 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
  • 17. Evolution of Primary Brain Injury Damage to Parenchymal Cells The 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. Excitotoxiccascade Inthisscenario,mechanicaldeformation of the neuronal cell membrane results in depolarisation, major ionic fluxes and the release of excitatory amino acids, such as glutamate. There is an efflux of intracellular potassium and an influx of extracellular sodium and calcium. The entry of sodium and calcium is accompanied by water. The excess potassium in the extracellular space is takenupbyastrocytes,whichswell.21,26 Theinfluxofcalcium 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, finally, cell death through both necrotic and apoptotic processes (Fig. 2.12).21,26 Inflammatory cell responses Trauma-induced cytokine release and leucocyte accumulation in the injured brain 18 PART II BASIC PRINCIPLES 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 sodium chloride and water into the cell Efflux of intracellular potassium into the extracellular space Activation of proteases (calpains), lipases Destruction of cellular cytoskeleton Delayed cell deathCellular 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
  • 18. PATHOPHYSIOLOGY OF ACUTE NON-MISSILE HEAD INJURY CHAPTER 2 19 tissuesuggestthatinflammationmaycontributetotraumatic 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 inflammation dominated by macrophage infiltration, 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 neuroinflammatory 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 first 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 reflect 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 Cells Partially 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 acceleratetheadversecascadesof changesandresultincelldeath. 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 Oedema Accumulation 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 Therapy As 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 beneficial at the time of printing. Clearly, a proven ‘neuroprotective’ therapy would be a major breakthrough in head injury management.36 Damage to the Cerebral Vasculature Damage to the cerebral microvasculature may lead to: (i) narrowing and distortion of the capillary lumen by swelling of capillaryendothelialcells,extrinsiccompressionof 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 fluid 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 flow 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).
  • 19. 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 significant global reduction in cerebral blood flow during the early postinjury period (especially in the first 6–8 hours) after severe head injury. There may also be focal reductions in blood flow 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 reductionsinperfusion,contributingtothecommonoccurrence of ischaemic cell change in patients after severe head injury.17 Brain Swelling and Increased Intracranial Pressure Extracellular 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 Autoregulation Autoregulation is the capacity of the cerebral microvasculature to adjust cerebral blood flow 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 AUTOREGULATION The cerebral perfusion pressure (CPP) is the net force driving arterial blood into the cranial cavity: CPP=MAP–ICP where MAP is mean arterial blood pressure and ICP is intracranial pressure. In the uninjured brain, pressure autoregulation maintains a constant cerebral blood flow (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 AUTOREGULATION Normally, 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 significant 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 REACTIVITY Arteriolar 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 andadecreaseinCBF(potentialforischaemia).Inmostpatients with severe head injury, CO2 reactivity is temporarily disturbed, but returns to normal within 24 hours. The vulnerability to hypocapnia is especially significant 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. Ischaemia Vascular injury and ischaemia may also follow stretching and distortion of brain vessels as a result of mechanical 20 PART II BASIC PRINCIPLES
  • 20. 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 Injury Traumatic Intracranial Haematomas EXTRADURAL HAEMATOMA Extradural 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 confined 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 Lesions Intradural 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 patientswhoarecomatose.57 Associatedlesionsmaysignificantly influence the clinical picture and outcome. Posterior Fossa EDH Extradural 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 confluence of sinuses. PATHOPHYSIOLOGY OF ACUTE NON-MISSILE HEAD INJURY CHAPTER 2 21 SUBDURAL HAEMATOMA Subdural haematomas are classified 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 Haematoma Acute 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-
  • 21. 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 significant 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 SDH Subacute SDH becomes symptomatic between 48 hours and 2 weeks after injury. These lesions are usually not accompanied by significant associated injury. The haematoma undergoes degradation and is usually a mixture of semisolid and fluid blood at the time of presentation. Chronic SDH Chronic 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 fluid into the haematoma by osmotic mechanisms may also play a role in enlargement of the lesion. Subdural hygroma This 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 fluid from injured vessels in the meninges or in the underlying parenchyma may also play a role.61,62 The fluid in a subdural hygroma is usually clear and xanthrochromic, although at times it may be blood stained. INTRACEREBRAL HAEMATOMAS A typical traumatic ICH is a well-defined, homogeneous collection of blood within the brain parenchyma in contrast with a cerebral contusion,which is an ill-defined,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 22 PART II BASIC PRINCIPLES ▲ 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 significant mass effect.
  • 22. 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). PATHOPHYSIOLOGY OF ACUTE NON-MISSILE HEAD INJURY CHAPTER 2 23 Traumatic Basal Ganglia Haematomas Intracerebral 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 HAEMORRHAGE Post-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 HAEMORRHAGE Traumatic 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 fissures 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 superficial vessels. HAEMATOMAS IN THE CEREBELLUM AND BRAIN STEM Traumatic 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 HAEMATOMAS Intraparenchymal 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 HAEMATOMA Two 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).
  • 23. PROGRESSION OF INTRACRANIAL HAEMORRHAGIC LESIONS AND DEVELOPMENT OF NEW HAEMORRHAGE Acute 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 Injury In 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 Scans 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.80,81 Mechanisms responsible for delayed haemorrhage in patients with acute head injury include the following.82–87 Delayedruptureofbloodvesselspartiallydamagedduring 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 final 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 patientsandafterevacuationof largetraumaticintracranial haematoma.83 Acute SDH in the posterior fossa may enlarge during the first 4 days after injury, especially when it is associated with parenchymal cerebellar injury.93 Delayedenlargementofcerebralcontusions Mostcerebral contusions increase in size or appear as new lesions during the first 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 first 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 defined 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 INJURY Coagulation consists of conversion of fibrinogen to fibrin by a cascade of enzymatic changes initiated by tissue and/or vascular injury.The strands of fibrin trap blood cells (platelets) to form a clot.Coagulationitself,aswellasplateletactivity,releasesaseries of inflammatory 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, fibrinolysis and a depletion of clotting factors locally in the brain. The consumption of coagulation factors is reflected by changes in coagulation parameters: elevation of prothrombin time (PT), activated partial thromboplastin time (APTT), decreased serum levels of fibrinogen and increased serum levels of fibrin 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 24 PART II BASIC PRINCIPLES
  • 24. 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 fluid 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 inflammatory changes Blood coagulation can result in an excessive release of inflammatory 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 Swelling Brain 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 OEDEMA The two principal types of traumatic brain oedema are cytotoxic oedema (intracellular oedema) and vasogenic oedema. Cytotoxic (Intracellular) Oedema Cytotoxic 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 five times their normal size. Hence, glial swelling is considered the main contributor to cytotoxic oedema.98,99 Vasogenic Oedema Vasogenic oedema is the accumulation of fluid 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 fluid 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. PATHOPHYSIOLOGY OF ACUTE NON-MISSILE HEAD INJURY CHAPTER 2 25 Interstitial oedema due to obstructive hydrocephalus An obstruction to CSF outflow results in the accumulation of water in the extrcellular space in the periventricular region. Hydrostatic oedema Hydrostatic 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 first 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 SWELLING Brain 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
  • 25. 26 PART II BASIC PRINCIPLES 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 Herniations Focal 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 Insults Secondary 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 Causes Secondary brain damage due to extracranial causes is mostly preventable (see Table 2.1). HYPOXIA AND HYPOTENSION Hypoxia (PaO2 <65 mm Hg, O2 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. ANAEMIA Anaemia (haematocrit less than 30%) reduces the oxygen- carrying capacity of the blood and can contribute to ischaemic brain injury.116 HYPERPYREXIA Each 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 HYPERGLYCAEMIA The 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 SEIZURES Seizures 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 flow with the risk of increased ICP. Table 2.1 Types of secondary brain insults Extracranial insults Intracranial insults Hypoxia (PaO2 <60 mm Hg, O2 saturation <90%, apnoea or cyanosis before admission) Hypotension (SBP <90 mm Hg for adults) Hypocapnia, hypercapnia Acute anaemia (haematocrit <30%) Hyperpyrexia (temperature >38°C) Hyponatraemia (serum sodium <130 mmol/L) Hypoglycaemia, hyperglycaemia Sepsis Increased intracranial pressure, brain shifts and herniations Intracranial haematoma• Cerebral contusion• Brain swelling• Hydrocephalus• Traumatic vasospasm Seizures Intracranial infection Meningitis• Brain abscess• SBP, systolic blood pressure.
  • 26. PATHOPHYSIOLOGY OF ACUTE NON-MISSILE HEAD INJURY CHAPTER 2 27 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 Department Hypoxia 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 patients Hypotension 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 patients Late 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 worse Hypotension developed only during treatment in the ICU in 16.3% of patients 109, 113 107 patients with severe head injury Early postinjury phase Hypotension in 24% of patients Mortality 65% in hypotensive patients Even brief episodes of hypotension are associated with poor outcome 114 81 patients with severe head injury Early and late postinjury phase (first 24 hours after injury) Secondary insults occur mostly in the first 24 hours after injury Hypotension is associated with increased mortality Hypoxia is associated with a longer stay in the ICU 115 ICU, intensive care unit. Ischaemic Brain Damage Following Acute Head Injury Ischaemic 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 flow can occur within the first 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 DAMAGE The 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 microthrombosis Hypoxia, hypotension Increased ICP Intracranial haematoma (EDH, SDH, ICH)• Cerebral contusion• Brain swelling• Anaemia Increased metabolic demands (seizures, hyperthermia) ‘Ischaemic penumbra’ around cerebral contusions Hemispheric 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.
  • 27. 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 flow. 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 flow. 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 flow 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 significant ischaemic insults risk adverse outcomes similar to those with severe head injury.128 FOCAL ISCHAEMIC LESIONS Focal ischaemic lesions include: (i) an ischaemic zone around cerebralcontusionsorandICH;(ii)ischaemiainthehemisphere underlying an acute SDH (Fig. 2.15); (iii) arterial vascular territory ischaemia; (iv) venous infarction; and (v) watershed ischaemia. Arterial Vascular Territory Ischaemia Posteriorcerebralarteryterritory Thisisthemostcommon 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. 28 PART II BASIC PRINCIPLES Venous Infarction Fractures (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 Ischaemia Severe 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 Injury Intrinsic 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 Profile in Determining the Outcome of Head Injury Genetic factors may also play a role in the outcome of head injury. The apolipoprotein E (ApoE) genotype has been demonstrated to influence 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 deficiency 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 findings, are taken into account.21,74
  • 28. PATHOPHYSIOLOGY OF ACUTE NON-MISSILE HEAD INJURY CHAPTER 2 29 SUMMARY The 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 profile in influencing the course of these complex, interacting processes.
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  • 32. CHAPTER 3 Intracranial Pressure 34 Introduction 34 Definition of Increased ICP 34 Significance 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
  • 33. INTRODUCTION Increased 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. Definition of Increased ICP Normal mean ICP is 0–10 mmHg or 0–13.5 cmH2 O 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 levelsabove30mmHgareconsideredtobeseverelyincreased.1–5 The threshold for ICP treatment may vary in individual patients with severe head injury and this aspect will be discussed later. Significance Pathophysiology of Increased ICP in Acute Head Injury The intracranial contents are comprised of brain (70%), blood (15%) and cerebrospinal fluid (CSF; 15%). The contribution of extracellular fluid 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. 34 PART II BASIC PRINCIPLES Table 3.1 Causes of increased intracranial pressure in acute head injury Brain swelling Space-occupying lesions Increased CSF volume (obstruction to CSF outflow) 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 fluid.
  • 34. 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 first 24 hours,6,7 whereas systemic hyperpyrexia may develop after 24–48 hours. Most intracranial haematomas develop during the first 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 ICP In 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 insufficient 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 reflected 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 ICP The 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(mmHg) D B A Volume of intracranial contents Break point C (b) Injured brain Uninjured brain90 80 70 60 50 40 30 20 10 ICP(mmHg) 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 significant 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).
  • 35. 36 PART II BASIC PRINCIPLES 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 Injury Less 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 identification of these patients is of considerable importance. Elevation of ICP After Evacuation of Intracranial Mass Lesions Brain 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 ICP A 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 fivefold.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 ICP Raised 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 Ischaemia The 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 Vasculature Cerebral blood flow (CBF) varies directly with CPP and inversely with cerebral vascular resistance (CVR): CBF = CPP CVR Cerebral 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
  • 36. INTRACRANIAL PRESSURE CHAPTER 3 37 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 flow (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.
  • 37. 38 PART II BASIC PRINCIPLES Regional Heterogeneity of Autoregulation, Perfusion and Metabolism Intracerebral 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 courseoftheinjury.29,35–39 Measuresofthebalancebetweenglobal 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 significant 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 acuterespiratorydistresssyndromeand,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 Compression Expanding 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 SHIFT A 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 significant 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.
  • 38. INTRACRANIAL PRESSURE CHAPTER 3 39 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 HERNIATION The 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) Herniation An 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 significant 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 Reflex Brain 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 reflex). However, the full triad of the Cushing reflex 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 reflex adduction or abduction of eyes and fixed mid-position pupils. Pupils may become fixed and dilated owing to bilateral third nerve palsies. Motor responses change from withdrawal (flexor), to abnormal flexor and extensor responses. Further brain stem compression/ischaemia leads to flaccidity (loss of motor response); disturbances to the medulla
  • 39. 40 PART II BASIC PRINCIPLES 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 Herniation Central 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 Fossa In view of their proximity to the tentorial hiatus, as well as the confined 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 Herniation Tonsillar herniation occurs as the final 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
  • 40. INTRACRANIAL PRESSURE CHAPTER 3 41 to deterioration of consciousness, flaccid 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 ICP Reasons for ICP Monitoring Monitoring 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.
  • 41. 42 PART II BASIC PRINCIPLES 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. Specific 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 PatientswithGCS≤8aftercardiopulmonaryresuscitation and with an abnormal scan An abnormal scan is defined 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 fibre optic ICP catheters, reported a 15.3% incidence of radiological evidence of bleeding in patients who had coagulopathy (defined as clinically apparent bleeding or abnormalities in prothrombin activity, partial thromboplastin time or platelet count). Due to this high frequency, the use of fibre optic ICP monitors was not recommended in patients who had coagulopathy.58 However, a recent study on the use of fibre optic intraparenchymal ICP monitoring showed that, in head-injured patients with borderline coagulopathy, defined 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 beneficial 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 difficult 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 fluid column of the catheter system. An intracranial pressure transduction via fibre 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
  • 42. INTRACRANIAL PRESSURE CHAPTER 3 43 • 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 significant enough to warrant surgical evacuation in only 0.5% of patients.1 Catheter-tip Transducer Systems These are easier to place and avoid the problems of blockage. The transducer is located at the tip of a flexible 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 flexible diaphragm that is deformed by pressure and located at the tip of a narrow fibre optic catheter. Changes in light intensity reflected off this diaphragm are interpreted in terms of pressure changes. There is a close correlation between ICP measured by the fibre 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.Thesilicondiaphragmofthetransducerissensitive 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 fluid-filled 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 efficacy 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 shouldbeconsultedforadvicebeforeanyspecificmeasures for ICP control (such as mannitol or hyperventilation) are
  • 43. undertaken in view of the potential for adverse effects associated with such measures. SUMMARY Monitoring 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 Data Monitoring systems should continuously record mean ICP, CPP and show ICP waves. Thresholds for Therapy A 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 ICP Clinical 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 CPP The 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 Compliance Intracranial pressure responses to stimuli, such as endotracheal tube suctioning, and marked spontaneous fluctuations in pressure (pressure waves) indicate reduced intracranial compliance and the need for extra vigilance. Accuracy of ICP Measurement The 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 findings and the findings in the CT scan. Insensitivity of ICP Monitoring In 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 reflected immediately at a monitoring site remote from the lesion.78,79 Rapid increases in volume of unilateral supratentorial mass lesions can result in significant 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 Waves Three 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 reflect respiratory excursions and are more frequent in patients with impaired intracranial compliance. They have less adverse significance than A waves (Fig. 3.14b). 44 PART II BASIC PRINCIPLES
  • 44. 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 significance. 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 significant 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. SUMMARY Raised 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. INTRACRANIAL PRESSURE CHAPTER 3 45 80 70 60 50 40 30 20 10 0 0 5 10 15 20 (a) 25 30 35 40 ICP(mmHg) Time (minutes) 70 60 50 40 30 20 10 0 0 5 (b) 10 15 20 25 30 35 Time (minutes) ICP(mmHg) 70 60 50 40 30 20 10 0 0 5 10 (c) 15 20 25 30 35 Time (minutes) ICP(mmHg) ▲ 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).
  • 45. 46 PART II BASIC PRINCIPLES References 1. 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, Gofinos 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. Langfitt 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 classification. 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, Gofinos JG, eds. Head injury, 4th edn. New York: McGraw-Hill, 2000:229–64. 27. Cold GE. Cerebral blood flow in acute head injury. The regulation of cerebral blood flow and metabolism during the acute phase of head injury, and its significance 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 flow: 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 fit all. Anaesth Analg 2004;99:1208–10. 40. Cruz J, Jaggi JL, Hoffstad OJ. Cerebral blood flow, vascular resistance, and oxygen metabolism in acute brain trauma: redefining 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: influence 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.
  • 46. INTRACRANIAL PRESSURE CHAPTER 3 47 50. Marmarou A, Beaumont A. Physiology of cerebrospinal fluid 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, Gofinos 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 scientific 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 efficacy 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 fluid 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 fiberoptic 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 fibreopticpressure 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 fluid pressure in neurosurgical practice. Acta Psychiatr Neurol Scand 1960;36(Suppl. 149):1–193.
  • 47. PART III Evaluation and Diagnosis 50 CHAPTER 4 Neurological Evaluation 62 CHAPTER 5 Radiological Evaluation
  • 48. 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
  • 49. INTRODUCTION An 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 identification 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 • rapidityof initialtransferandnatureof 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 canberemedied,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 Evaluation In 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 suffice (Algorithm 4.1). Neurological findings 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 efficient 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 Injury A 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
  • 50. 52 PART III EVALUATION AND DIAGNOSIS height >3 metres can cause significant 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 difficult 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 definition 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 deficits (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, fluid 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 Examination Important 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 deficits and signs of a spinal cord injury. ASSESSMENT OF LEVEL OF CONSCIOUSNESS Consciousness is defined 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 reflects 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 Scale The 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 opening Spontaneous To speech To pain None 4 3 2 1 2. Verbal response Orientated Confused Inappropriate words Incomprehensible sounds None 5 4 3 2 1 3. Motor response Obeying commands Localising to pain Flexing to pain Abnormal flexion Extension to pain None 6 5 4 3 2 1 Total 15 applicationandgoodinter/intra-observerreproducibilityacross 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 Score The 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 artificial 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
  • 51. NEUROLOGICAL EVALUATION CHAPTER 4 53 ▲ 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 finger • 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 fingers 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 identified in the opposite arm if the latter moves across the midline attempting to reach the point of painful stimulation (Fig. 4.1b) • flexor response: during application of pain at the supraorbital notch or at the retromandibular region,the elbow is flexed 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 flexor 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 flexor response: there is abnormal flexion of the arm and extension of the leg; there is a slow flexion of the arm at the elbow and wrist, with fisting of the fingers over the thumb; the arm is adducted,the leg is extended and rotated internally, with plantar flexion of the foot (Fig. 4.1d); the features of adduction of the arm and flexion at the wrist differentiate abnormal flexion from the normal flexor (or withdrawal) response • extensor response: the arm is extended abnormally (internally rotated at the shoulder, extended at the elbow, the wrist pronated, flexed 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 flexion of the foot (Fig. 4.1e). An abnormal flexor response has been regarded as indicating aninjuryabovethelevelof themidbrain(i.e.inthediencephalic 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 INTUBATION In current practice, a significant proportion of patients with severe head injury receives sedation/analgesia and muscle relaxants for endotracheal intubation (during the prehospital
  • 52. 54 PART III EVALUATION AND DIAGNOSIS 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 INTOXICATION The 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 influencing assessment of the GCS. HYPOXIA, HYPOTENSION AND HYPOTHERMIA Inviewof theeffectsof hypoxia,hypotensionandhypothermiaon neuronalfunction,theGCSrecordedimmediatelyafteradmission to the emergency department may not be a true reflection 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 GCS The following drawbacks associated with the use of GCS need to be recognised. ERRORS WITH RESPECT TO ACCURACY OF GCS RECORDING Despite 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 EVALUATION In their original description of the GCS, Jennett and Teasdale specified that for the purpose of head injury classification, 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 influences, 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 reflect 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 first 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 definitive treatment of a head injury has been significantly 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 five brain stem reflexes to the GCS: 1. fronto-orbicular reflex (elicited by a light tap on the glabella) 2. vertical oculo-vestibular reflex (elicited by rotating the head fully in the vertical plane, if a cervical spine injury has been excluded) 3. pupillary reflex 4. horizontal oculo-vestibular reflex (elicited by rotating the head fully in the horizontal plane, if a cervical spine injury has been excluded) 5. oculocardiac reflex The five reflexes are lost in descending order during rostral– caudal deterioration. The disappearance of the oculocardiac reflex coincides with brain death.11 INSENSITIVITY TO IMPAIRMENTS IN MENTAL FUNCTION The 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 significant amnesia, have a higher risk of harbouring a significant 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 SIGNS Lateralising neurological signs, especially in the form of limb weakness, are not considered because only the best motor response is recorded.
  • 53. NEUROLOGICAL EVALUATION CHAPTER 4 55 A HIGH GLASGOW COMA SCORE DOES NOT ELIMINATE THE RISK OF SERIOUS BRAIN INJURY In 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 FUNCTION The 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 Scale In 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 Characterisedbymotorrestlessness,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 Amnesia Post-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 defined 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 difficult 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 Size Pupillary 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 significant.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 Light Pupillary reactivity is assessed for both direct and consensual light reflex. 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 developedsubsequently.Inlaterstagesof headinjury,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 pupil A 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 reflex. 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.
  • 54. 56 PART III EVALUATION AND DIAGNOSIS 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 herniation Direct trauma to the third nerve Optic nerve injury Injury to the iris Both pupils dilated, non- reactive Brain stem failure Brain stem compression/ischaemia due to space-occupying lesion or diffuse swelling Primary brain stem injury Severe hypotension Postepileptic state Administration of anticholinergic drugs (atropine) Barbiturates • • Oval pupil Early stages of brain stem compression due to a space-occupying lesion Pin-point, fixed pupils Pontine lesion Normal-sized fixed pupils Mid brain lesion Unilateral, normal-sized fixed pupil Injury to the iris In some instances of optic nerve injury Bilateral dilated, non-reactive pupils Bilateral 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 fixed pupils may also occur with barbiturates used in coma-inducing doses. Normal-Sized Fixed Pupils Normal-sized fixed pupils may result from a mid brain lesion. A unilateral fixed pupil that is of normal size may also occur after injury to the iris or in some instances of optic nerve injury. The Oval Pupil An oval-shaped, eccentric pupil may indicate the early stages of brain stem herniation.21 FOCAL NEUROLOGICAL SIGNS Lateralised Limb Weakness Lateralised 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 compressionoftheunderlyingmotorcortexorcompression 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 reflexes are of little significance in the early stages after injury. However, absent reflexes in a paretic limb may indicate a peripheral nerve lesion, such as a brachial plexus injury. Speech defects and hemi-anopic field 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 MOVEMENTS The presence of spontaneous roving eye movements or ability to fix 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 reflexes.
  • 55. NEUROLOGICAL EVALUATION CHAPTER 4 57 Oculocephalic reflex (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 reflex is indicated by absence of conjugate movement of the eyes in the direction opposite to head turning. The oculocephalic reflex tests the integrity of the pontine gaze centres. Oculovestibular reflex This reflex 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 reflex). 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 headinjury,22 ingeneral,hypotensionafteracuteheadinjury 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 SIGNS The cranial nerves that are most often injured are the olfactory, optic, oculomotor, abducens, facial and vestibulocochlear nerves. SKULL AND SCALP Evaluation 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 fluid (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 Injury A 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 reflection 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 flexor response to pain or features of sympathetic hyperactivity, such as hypertension, tachycardia and central sweating (involving the face and trunk) Stein23 stratified brain injury severity by Glasgow Coma Score at presentation, duration of loss of consciousness, PTA and the presence of focal neurological deficit (Table 4.3). Clinical Features of an Intracranial Haematoma The 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
  • 56. Table 4.3. Head injury severity scale22 Injury category Glasgow Coma Score Minimal GCS 15, no loss of consciousness or amnesia Mild GCS 14 or GCS 15, with amnesia, brief loss of consciousness (<5 minutes) or impaired alertness and memory Moderate GCS 9–13 or Loss of consciousness >5 minutes or Presence of a focal neurological deficit 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. developmentoflocalisingsigns,suchaspupillaryasymmetry 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 definitive localising features of a mass lesion. However,localising features may be absent in a large proportion of patients who develop significant 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 first 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 findings 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 Monitoring Patients 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 Death Brain death has been defined 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 defines death of the person. It is now recognised that brain stem death is the essential step in the sequence of events that defines 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 identification 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 confirm brain death: one a consultant, the other a senior registrar or consultant. The tests must confirm brain death on two separate occasions. An EEG study is 58 PART III EVALUATION AND DIAGNOSIS
  • 57. ▲ Figure 4.2 Neurological observation chart. NEUROLOGICAL EVALUATION CHAPTER 4 59
  • 58. BRAIN DEATH IN ADULTS United 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 reflex • No response to facial and peripheral painb • No caloric vestibulo-ocular reflexc • 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 first 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 confirmation a Where irreversibility of brain damage is uncertain, sufficient time should be allowed for confirmation. b Automatic movements of limbs may be observed in brain-dead patients as a result of activity of spinal reflexes. These must be distinguished from genuine limb movements in response to pain. c Caloric vestibulo-ocular reflex: the external auditory canal is irrigated with at least 20 mL ice-cold water. The eyes deviate towards the side of irrigation if the reflexes 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 SUMMARY Neurological 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 significant contribution made by CT scanning in the delineation of intracranial pathology, the findings 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 identification 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. 60 PART III EVALUATION AND DIAGNOSIS not required.33 In addition, it may be advisable to wait for 6 hours between the brain death examinations in adults to confirm the diagnosis, although exceptions to this practice may clearly exist. Criteria for the Diagnosis of Brain Death
  • 59. References 1. 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; Benefits 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 significance 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. Classification 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. Defining death: medical, legal and ethical issues in the determination of death. Washington, DC: US Government Printing Office, 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. NEUROLOGICAL EVALUATION CHAPTER 4 61
  • 60. 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
  • 61. RADIOLOGICAL EVALUATION CHAPTER 5 63 INTRODUCTION Radiological 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 artificial 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 fluid (CSF) fistulae) 2. assess head injury severity: radiological (and clinical) parameters allow stratification 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 Department X-Rays of the Skull A 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 significant intracranial haemorrhage by only fivefold,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 fulfil 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 identified a role for plain X-rays of the skull in the triage of patients with minor head injury, especially in situations where logistical difficulties 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 significant 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 15/155,6 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 deficit
  • 62. 64 PART III EVALUATION AND DIAGNOSIS IMAGING PROTOCOL FOR SKULL X-RAYS Anteroposterior (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 floor. This will ensure a non-rotated film, so that fluid 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 films 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 Fractures Linear 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 specific 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 fistula Fractures that extend to the frontal sinuses may result in a dural fistula if they involve the posterior wall of the sinus. Linear skull vault fractures that extend to the skull base carry a risk of CSF fistulae if they extend to the paranasal sinuses or the middle ear. A dural fistula 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 Fractures Diastatic 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 Fractures A 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
  • 63. RADIOLOGICAL EVALUATION CHAPTER 5 65 X-Rays of the Cervical Spine A comprehensive radiological evaluation of the cervical spine is mandatory in all patients who are unconscious or who are obtundedafteracuteheadinjuryandinanypatientswithclinical 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 films 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 first 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 insufficient 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 first 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 findings in injuries of the cervical spine are summarised in Table 5.2. Basal Fractures Skull 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-fluid 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 significant collection of air (pneumocephalus) in the intracranial compartment, with an air-fluid level (white arrowheads). ▲ Figure 5.2 Depressed fracture. (b) Tangential view of the skull showing a depressed fracture (white arrow). b
  • 64. 66 PART III EVALUATION AND DIAGNOSIS 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 mm Open-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 same Vertebral bodies should have a smooth cuboidal contour The cortical surface should be inspected for steps, breaks or abnormal angulations Overlapping of bone at the cortical margins suggests fracture or dislocation Changes in the internal trabecular pattern, lucencies and increases in density indicate a possible overlap of bone fragments Alignment (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.
  • 65. RADIOLOGICAL EVALUATION CHAPTER 5 67 Table 5.2 Radiographic findings in injuries of the cervical spine10,11 Injuries of the upper cervical spine Retropharyngeal swelling Widening of the interlateral mass distance (with displacement of the fractured lateral mass) Transverse ligament insufficiency suspected if the ADI is >3 mm in an adult (>/5 mm in a child) Intermass widening is greater than 6.9 mm Odontoid fracturesa • • • • • Injuries of the lower cervical spine Facet subluxation Rotation of facet surfaces ( the ‘bow tie’ sign in the lateral view)b Unilateral facet dislocation associated with approximately 25% subluxation Bilateral 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 fracture Burst fracture Tear-drop fracture Changes in alignment Widening of the interspinous spaces (divergence or ‘fanning’) Break in the contour of the anterior and posterior longitudinal lines, posterior facet margins or the spinolaminar line Translation 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 • • • • • • • • • a Odontoid 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. b Unifacetal dislocation. If unifacetal dislocation is suspected, oblique views should be taken. c Vertebral 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 flexion–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-dropfracture,hyperextensionfracture,hyperextension fracture–dislocation Cranial CT Scan The 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. Computedtomographyscanningisincreasinglyavailable 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 sufficient expertise in the accurate interpretation of CT findings. 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. Indications Indications 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
  • 66. 68 PART III EVALUATION AND DIAGNOSIS 2. GCS score of 15, with the following features: • severe or increasing headaches • persistent vomiting • a focal neurological deficit • 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 PROTOCOL A 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 films is 0.14 mSv.5 WINDOW WIDTHS AND WINDOW LEVELS Images 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
  • 67. RADIOLOGICAL EVALUATION CHAPTER 5 69 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): Isodense Clotted blood: Hyperdense (60–100 HU) Resolving haematoma: Hyperdensity progressively diminishes; isodense to brain in approximately 2–4 weeks Brain 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 fluid; HU, Hounsefield units. COMPUTED TOMOGRAPHY DENSITIES OF DIFFERENT ELEMENTS Densities of different intracranial structures and pathologies determinethedegreeof linearX-rayabsorption(orattenuation) within a selected imaging volume of tissue. The linear X-ray absorption of different structures (CT density) is measured in Hounsefield 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 AVERAGING The 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 coefficient (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 floor of the anterior cranial fossa may be included in a pixel to resemble haemorrhage. Computed Tomography Diagnosis of Different Pathological Entities A systematic, comprehensive approach is needed for proper evaluation by CT scanning. Table 5.4 outlines a protocol for CT evaluation. EXTRACRANIAL PATHOLOGY Scalp Haematoma On 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 patient Date and time of CT scan Right–left orientation in the CT scan film • • • Extracranial pathology Scalp haematoma Skull fracture Linear fractures Diastatic fractures Comminuted fractures Depressed fractures Penetrating trauma • • • • • Intracranial pathology Focal lesions Traumatic space-occupying lesions (EDH, AcSDH, cerebral contusion, ICH) Focal ischaemic lesions Diffuse pathology Mass effect Midline shift State of perimesencephalic cisterns Diffuse axonal injury Traumatic subarachnoid haemorrhage Diffuse brain swelling Intracranial air • • • • • • • • • EDH, extradural haematoma; AcSDH, acute subdural haematoma; ICH, intracerebral haematoma. Skull Fractures The CT scan findings 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-defined, 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).
  • 68. ▲ Figure 5.11 Skull base fracture. (a) Axial computed tomography (CT) scan showing multiple air–fluid 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-defined 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–fluid 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 floor (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,maxillaandmandible(Fig.5.14).Three-dimensional CT reconstructions can also provide information about the facial nerve canal, carotid canal and otic capsule.15 70 PART III EVALUATION AND DIAGNOSIS
  • 69. Table 5.5 Computed tomography scan findings in skull fractures Fracture type CT scan appearance Other comments Linear fractures Affect both inner and outer tables Margins not sclerotic In scout CT films, linear fractures may be seen as sharply defined, 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 orientation Vascular 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 hyperdense Depressed fragments may remain attached to margins of defect or may be driven inwards Damage 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 fistula (air may be seen in the subdural or subarachnoid space and fluid in the sinus) Depressed fractures overlying venous sinuses may lead to sinus thrombosis/ occlusion Basal fractures High-definition, biplanar (axial+coronal), thin section CT is best for definition 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 fistulae Demonstrating fractures involving optic canal, body of sphenoid, petrous pyramid Pneumocephalus indicates a dural fistula (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-definition, biplanar (axial+coronal), thin section CT with 3D reconstructions best for defining 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 PATHOLOGY Focal pathology: 1. cerebral contusions and lacerations 2. traumatic intracranial haematomas • extradural haematoma • subdural haematoma (SDH) RADIOLOGICAL EVALUATION CHAPTER 5 71
  • 70. 72 PART III EVALUATION AND DIAGNOSIS 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 lines May 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 confined) Conforms to cortical surface Does 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 lesion Often 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-defined edge Peripheral ring of hypodensity develops in later stages Often 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 lesion Located within brain tissue Well-defined edge Rounded or irregular shape Peripheral 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 enlargement Poor 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. a The 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 Contusions The CT appearance of a cerebral contusion mirrors the pathological changes: 1. An ill-defined, 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
  • 71. RADIOLOGICAL EVALUATION CHAPTER 5 73 ▲ 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 floor. 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 fluid fistula. 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).
  • 72. ▲ 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 insignificant 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 Scanning The 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 first week the central area of the contusion gradually become isodense and, eventually, hypodense.17 In some instances, delayed haemorrhage can occur within a contusion,resultinginanincreaseinthesizeofthehaemorrhagic 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 first 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 Lacerations Cerebral 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 HAEMATOMA The 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. Thereisdistortionbyboneartefacts 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 74 PART III EVALUATION AND DIAGNOSIS
  • 73. ▲ 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-defined margins. Posterior Fossa EDH Approximately 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 confluence 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. RADIOLOGICAL EVALUATION CHAPTER 5 75
  • 74. Delayed Enlargement of EDH Approximately 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 significant 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 significant 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 SDH An 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 confined) 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 fissure (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 identified 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 significant mass effect. a b 76 PART III EVALUATION AND DIAGNOSIS SUBACUTE SDH Subacute 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 identifiable 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
  • 75. 4. midline shift and dilatation of the opposite lateral ventricle 5. opacification of the superficial 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 SDH A 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 fluid 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 HYGROMA On 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 ICH An intracerebral haematoma is usually identified by the following CT scan features:16 1. a homogeneous, hyperdense, well-defined 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 difficult and may have little practical significance, 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 fluid–blood interface may appear as a result of the liquefaction of the brain parenchyma. The presence of such a fluid 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 fluid (white arrowhead). a c b RADIOLOGICAL EVALUATION CHAPTER 5 77
  • 76. FOCAL ISCHAEMIC LESIONS Areas of transient ischaemia and of infarction both appear as areas of low density on the CT scan. Focal Ischaemic Lesions Focal 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). Ischaemiainthehemisphereunderlyinganacutesubdural 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 Ischaemia With 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 Hemispheres The 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-defined (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 HAEMATOMAS Haematomas 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. 78 PART III EVALUATION AND DIAGNOSIS INTRACEREBRAL HAEMATOMA SECONDARY TO COAGULOPATHY This type of haematoma is increasing with the use of anticoagulants and is discussed in Chapter 16. TRAUMATIC CEREBELLAR HAEMATOMAS Intraparenchymal 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 HAEMORRHAGE Delayed 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 developwithinanareaof cerebralcontusion.Inaddition,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 identification of DTICH prior to clinical deterioration.
  • 77. 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 significant 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 findings 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 five 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’ method33 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 Shift Midline 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 significant. 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 Infarction Fractures (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 Effect The 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. Temporalfossalesions 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 significant 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 significant mass effect in view of the narrow confines 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 RADIOLOGICAL EVALUATION CHAPTER 5 79
  • 78. 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 significant 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 1 2 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 significant 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 Cisterns The 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 difficult to visualise. In this instance, compression or obliteration of the third ventricle is a useful indicator of increased ICP.4 Diffuse Axonal Injury Axonal 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 findings 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 80 PART III EVALUATION AND DIAGNOSIS
  • 79. ▲ 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 fissure (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 SAH Computedtomographyevidenceof subarachnoidhaemorrhage 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 fissures 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 fissure 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 Swelling Early 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 difficult 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 confidence.36 Intracranial Air (Pneumocephalus) Air can enter the intracranial space when a breach of the dura mater (a dural fistula) 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 RADIOLOGICAL EVALUATION CHAPTER 5 81
  • 80. 82 PART III EVALUATION AND DIAGNOSIS 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 fistula.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 confluent 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, flattening 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 finding is not indicative of a breach in the meninges. The investigation of dural fistulae and CSF leaks will be discussed in Chapter 9. Computed Tomography Indicators of Injury Severity In assessing injury severity, CT features always need to be correlated with neurological findings. There are limitations to the sensitivity of CT in demonstrating certain pathological changes after acute head injury. Allowing for these drawbacks, the following CT findings 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 INJURY Marshall et al.37 proposed a CT classification of diffuse brain injury, in which four grades of diffuse brain injury were identified 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 findings were later confirmed by several prospective Class I studies.25,38 A recent review proposed that the predictive value of this classification 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.
  • 81. 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 RADIOLOGICAL EVALUATION CHAPTER 5 83 Table 5.7 Computed tomography classification of head injury by the Traumatic Coma Data Bank35,37 Category Definition 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 mm No 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 mm No high- or low-density lesions >25 mL (may include bone fragments and foreign bodies) 10%–20% Diffuse injury Type IV (shift) Midline shift >5 mm No 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 Scanning Delayed Progression of Lesions and the Development of New Lesions: Implications for Radiological Evaluation Acute 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 developmentof delayedtraumaticICHin52%.Nearly80% 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 Scan The 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. Significant 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 SCANNING The timing of repeat CT scanning is determined by the initial injury severity, the timing and findings of the initial CT scan,
  • 82. Patients with moderate head injury (GCS 9–13) Patients with severe head injury (GCS 8 or less) Patients with diffuse injury Type I • Risk of evolving changes approximately 4% Recommendation • Repeat CT within 24 hours of admission Patients with diffuse injury Types 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 findings of an extensive study of repeat CT scanning by the European Brain Injury Consortium38 ). For details of the classification 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 deficits 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 Scan The 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 changeswereobservedintherepeatCTscanin18.4%of patients but only one in five of such patients required interventions based on the findings of the repeat CT scan. All patients with worsening CT findings 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 worseningontherepeatCTscan.47 Thesefindingsemphasisethe importance of clinical findings 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 thirdofthesuperiorsagittalsinus Delayedthrombosis of the sinus may be a consequence. 84 PART III EVALUATION AND DIAGNOSIS
  • 83. ▲ 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 fistula Bacterial meningitis may be a possible delayed complication in these patients. Limitations of CT scanning Limitations in Sensitivity for some Macroscopic Lesions Computed tomography is most useful for demonstrating haemorrhagic lesions and skull fractures. It is relatively insensitivetosmallnon-haemorrhagiclesions(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 definition of the scanner is suboptimal, some non-haemorrhagic and small haemorrhagic lesions may escape detection. ISODENSE HAEMORRHAGIC LESIONS Haemorrhagic 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 difficult. 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 Vertex Lesions at the vertex may be missed in axial sections. Computed Tomography Performed too Early Lesions 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 Patient Computed Tomography Scan of the Cervical Spine The scout film 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 /C2 region and the C6 –T2 region (Figs 5.33a, b, 5.34a, b, c). Plain X-rays may miss approximately 50% of injuries at the cervicothoracic junction.49 RADIOLOGICAL EVALUATION CHAPTER 5 85
  • 84. 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 identified 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 /C2 region A CT study of the C1 /C2 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 C1 /C2 region can be difficult in the unconscious, intubated patient on collar immobilisation. C7 /T1 region A CT scan evaluation of the C7 /T1 region is mandatory in all patients where this region is not satisfactorily demonstrated in a lateral X-ray. C3 /C7 region A CT scan of these levels is indicated if satisfactory plain films 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 identified.54 Magnetic Resonance Imaging of the Cervical Spine Magnetic 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). 86 PART III EVALUATION AND DIAGNOSIS 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.
  • 85. 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 Spine The use of dynamic fluoroscopic 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 flexion 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 Spine The 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 findings indicative of an injury to the thoracolumbar region The absence of any abnormality on plain X-rays of the thoracolumbar spine is sufficient for exclusion of an injury to the thoracolumbar spine. SUMMARY Cranial 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 findings 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 findings on the initial CT scan. Clearance of cervical spine injury is an important component of initial radiological evaluation. Tailoring radiological evaluation to patients stratified by risk remains the most effective method of identifying cervical spine injury. RADIOLOGICAL EVALUATION CHAPTER 5 87
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