ASSESSMENT OF HEAD INJURIES
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1 Br.J. Anaesth. (976), 48, 76 ASSESSMENT OF HEAD INJURIES G. TEASDALE Most of the 00,000 patients admitted to hospital every year in Britain following head injury prove to have mild injuries, 75% being discharged within 48 h. Anaesthetists are involved in the management of only the more severely injured patients, in particular those with brain damage and depressed consciousness. BRAIN DAMAGE AFTER HEAD INJURY Brain damage may be primary or may manifest as a secondary delayed event. Either may affect the brain locally or diffusely. Primary impact damage This results mainly from acceleration/deceleration forces transmitted to the brain as a whole. Macroscopically, the most prominent features are the presence of contusions of the cerebral cortex, either underlying the site of impact (coup) or on the undersurfaces of the frontal lobes and the tips of the temporal lobes as a result of contra-coup impact. Of greater neurological significance are the microscopic lesions which affect nerve fibres in the sub-cortical white matter, in the long tracts in the brain stem and in the reticular activating system. These lesions are almost invariably present in many parts of the brain in severely injured patients. The concept of a primary injury limited to, or mainly within, the brain stem has been largely dismissed (Mitchell and Adams, 973). The severity of initial unconsciousness and neurological deficit reflects the extent of impact damage. Injuries resulting in prolonged unconsciousness differ from mild concussive injuries only in quantity, rather than kind. Secondary damage Processes such as haemorrhage, oedema and infection can interfere with recovery from initial damage or may develop in injuries which initially were not severe. Extradural haemorrhage in adults is almost always a complication of skull fracture. The classic lucid interval between injury and development of clinical GRAHAM TEASDALE, M.B., B.S., M.R.C.P., F.R.C.S.(EDIN.), University Department of Neurosurgery, Institute of Neurological Sciences, Southern General Hospital, Glasgow G5 4TF. features occurs in only a minority of patients (Jamieson and Yelland, 968). Subdural and intracerebral haematomas are usually complications of significant immediate impact damage and supervene upon impairment of consciousness from the time of injury. Oedema is found in the white matter adjacent to contusions and haematomas. Diffuse oedema, with swelling of both hemispheres, is a rare event and has a predilection for children, often after initially apparently trivial injuries. Brain abscess or meningitis complicates compound depressed skull fractures, or fractures of the base involving the paranasal sinuses. Clinically evident cerebrospinal fluid leak is not a prerequisite. Brain shift and increased intracranial pressure are consequences of many of the processes occurring after head injury. Shift and herniation result in local compression of the brain against the dural partitions within the intracranial cavity; in particular the cerebral peduncle, oculomotor nerve and temporal lobe may be compressed against the edge of the tentorium cerebelli. Ischaemic brain damage, in a pattern suggesting global reduction in cerebral blood flow, is found in up to 60% of fatal head injuries (Jennett et al., 973; Adams, 975). In addition to impaired cerebral perfusion from increased intracranial pressure, systemic hypotension may be a major cause of ischaemia in certain patients. The twin aims in patient management are to ensure favourable circumstances for the recovery from primary brain damage and to anticipate secondary complications, the so-called second accident. Ideally, the latter should be prevented, but it is usually more feasible to minimize secondary damage by the early recognition and treatment of complications. DIAGNOSIS OF HEAD INJURY Sometimes a clear story is not available when a patient is admitted in coma. Scalp trauma increases the possibility of head injury, but sometimes the primary condition may have been a cerebrovascular accident, an epileptic fit, or the ingestion of alcohol or drugs. The story should be pieced together as well as possible from all sources of information ambulance men,
2 762 BRITISH JOURNAL OF ANAESTHESIA police and relatives. However, 0% of patients with traumatic intracranial lesions are initially diagnosed as having had a cerebrovascular accident (Galbraith, 976). If there is scalp trauma and skull x-rays disclose a fracture, it is probable that a head injury has been the primary event and that the hemiplegia signifies an intracranial haematoma. Where alcohol is a complicating factor, blood concentrations may be useful; those below 200mg/00ml are rarely the cause of impairment of consciousness in patients with head injuries (Galbraith et al., 976). Biochemical analysis should exclude metabolic reasons for unconsciousness. ASSESSMENT OF IMPAIRED BRAIN FUNCTION Clinical monitoring of conscious level and focal neurological features is the foundation of the management of these patients. In patients treated electively by artificial ventilation, the clinical features usually relied upon to judge progress are lost. It is better to avoid, at least in the first h after injury, the use of drugs and procedures which may make it difficult to assess the patient's clinical state. Assessment of conscious level In spite of the importance of assessing impaired consciousness most existings systems have defects. Some depend upon specific anatomical-clinical correlations, which do not exist in practice. Some describe coma by a series of arbitrary steps, when in reality there are no clear watersheds in the continuous spectrum of responsiveness exhibited by patients. Few have been tested for the consistency with which they can be applied by different observers. As the management of severely injured patients depends upon observations made by junior medical and by nursing staff, to be of practical value a system must be simple and based upon clearly denned criteria. The Glasgow Coma Scale (Teasdale and Jennett, 974) was developed taking account of these considerations. Three separate aspects of the patient's responsiveness are evaluated: the stimulus required to induce eye opening; the best verbal response; and the best motor response. Each is described according to a well-defined series of responses which indicate increasing degrees of dysfunction. Eye opening. Spontaneous opening indicates that arousal mechanisms in the brain stem are active. It does not necessarily imply awareness. If spontaneous opening is not present verbal command is followed by painful stimulation, applied by pressure on the fingertips. Once the patient has been roused as fully as possible, speech and motor performance are assessed. Verbal response. Orientation requires the patient to know who he is, where he is and the date. Conversational exchange short of this is termed confused. Inappropriate words refer to intelligible articulation used in an exclamatory, random way. Moaning and groaning constitute incomprehensible sounds. While the presence of speech indicates a high degree of integration in the nervous system, speechlessness may, of course, be the result of reasons other than impaired consciousness such as dysphasia. Best motor response. To reflect the functional state of the brain as a whole, the best or highest response from any limb is recorded. Differences between the response of the two sides indicate focal brain damage. Obeying commands is judged from the response to instructions such as to lift the arm, or protrude the tongue. Reflex grasp responses occur in unconscious patients and asking a patient to squeeze the examiner's fingers is not a reliable test. Painful stimulation is applied in a standard way, fingertip pressure being used initially to induce a response, followed by pressure over the supraorbital notch to test for localization. Flexion responses may vary between normal rapid withdrawal and abnormal slow dystonic movements in which the limbs assume stereotyped postures. Experienced observers may distinguish the various types but generally this separation cannot be made consistently. Extension responses of the upper or lower limbs are clearly abnormal. The use of three separate responses avoids the need to make arbitrary distinctions between consciousness and different levels of coma, and does not entail assumptions of specific underlying anatomical lesions. The reliability of the scale in the hands of a wide range of observers has been confirmed (Teasdale, Knill-Jones and Jennett, 974). In our experience the introduction of the scale has greatly enhanced the value of routine observations (Teasdale, 975). A chart on which the responses are recorded provides a visual profile of the patient's progress which can be rapidly assessed (fig. ) (Teasdale, Galbraith and Clarke, 975). Many institutions in America and Europe have adopted the scale and found it an improvement on previous methods. Assessment of focal neurological signs Assessment is directed first to determine whether there is evidence of a lesion on one side of the brain, and second towards detecting evidence of
3 ASSESSMENT OF HEAD INJURIES 763 NAri/IE RECORD No. C 0 M A S C A L E Eyes open Best verbal response Best motor response Spontaneously To speech To pain None Orientated Confused Inappropriate Incomprehensible None Obey commands Localise pain Flexion to pain INSTITUTE OF NEUROLOGICAL SCIENCES. GLASGOW OBSERVATION CHART 26 OCT n «. -#. _ 27 OCT A, V -». a 28 OCT V - «.. *, V V 29 OCT i \,» 30 OCT J f- _ I-- improvement or deterioration. In the presence of impaired consciousness, classical neurological signs are difficult to elicit and the findings may be at variance with conventional teaching. Detailed accounts of the examination of unconscious patients are given by Fisher (969) and Plum and Posner (972). The detection of lateralizing features and their evolution is more important than niceties of localization. Signs of supratentorial damage Hemianopia may be detected by the absence of blinking when a patient is threatened from one side. This distinction is often somewhat unreliable and subjective. Unilateral facial weakness is indicated by a cheek blowing out during respiration or by lack of contraction in response to a painful stimulus. Deviation of the eyes towards the affected side of the brain occurs with frontal lesions. During an epileptic fit, on the contrary, the eyes are deviated away from the side of the irritative focus. Unilateral pontine lesions also cause contralateral conjugate eye deviation. Hemiparesis. When trying to detect focal weakness, the emphasis is upon the function of the worst side. Paucity of spontaneous movement on one side may provide the first clue. If both arms are held upright and then released, hypotonia and paresis are shown by the more rapid collapse of the affected limb. Reflex asymmetry alone is rarely helpful. Asymmetrical response to painful stimulation is a useful test, as when a patient preferentially localizes stimulation Extension to pain - - None FIG.. Chart illustrating use of Glasgow Coma Scale. (Reproduced by kind permission of the Journal of the Royal College of Physicians.) V» - - DATE TIME Eyes closed by swelling =r C Endotracheal tube or tracheostomy = T Usually record the best arm response with one side. With more severe brain lesions, and abnormal flexion or extension posturing, asymmetry may still be detected, for example abnormal flexion on one side and extension on the other. A posture of flexion in the upper limbs with extension in the lower is often termed "decorticate", while "decerebrate" posturing refers to internal rotation and extension of the arms. In neither case does the anatomical assumption underlying the term justify its use and many patients fluctuate between the two postures, either in response to varying stimulation at the same examination or at different times after injury. Signs of brain stem damage Examination of the size and reactivity of the pupils reflects the integrity of the upper brain stem. With an expanding supratentorial lesion, hypothalamic dysfunction may initially produce small pupils. With herniation and involvement of one side of the midbrain and third nerve, the pupil on the same side as the mass becomes dilated and non-reactive. Light shone in that eye gives consensual constriction of the opposite pupil, distinguishing a third nerve lesion from an optic nerve injury. The pathways subserving eye movements traverse both the mid-brain and the pons (fig. 2). If the patient is too drowsy to carry out voluntary eye movements, vestibulo-ocular reflexes can be utilized. The doll's eyes phenomenon is a response to rapid rotation of the
4 764 BRITISH JOURNAL OF ANAESTHESIA CALORIC RESPONSES Nystagmus < lf^c=h MR III Tonic Conjugate LRVI Semicircular Canal FIG. 2. Neural pathways involved in eye movements. The oculomotor (III), abducent (VI) and vestibular (VIII) nuclei are connected by the medial longitudinal bundle (solid line) and the reticular formation (dashed line). MR = medial rectus; LR = lateral rectus. patient's head. It should be elicited only if there is no suspicion of cervical spine injury. Rotation of the head induces currents in the semicircular canals and, by a reflex mechanism, results in movement of the eyes away from the direction in which the head is turned. Movements may be impaired either because the patient's consciousness is only slightly impaired, when reflexes are suppressed, or as a manifestation of brain stem depression. The caloric response distinguishes between these two states. Cold water, prepared by placing ice cubes in a bowl of tap water, is introduced into the external ear from a 20-ml syringe. Providing brain stem function is not severely depressed, this provokes eye movements after a delay of s (fig. 3). Nystagmus is observed if the reticular activating system is functioning. Sustained ocular deviation may be conjugate where both eyes move towards the irrigated side, or may be dysconjugate. The latter indicates either a lesion of the third nerve or of the medial longitudinal bundle within the brain stem. Complete absence of eye movement signals a severe degree of brain stem dysfunction. However, there are occasional exceptions to this (Rosenberg, Sharpe and Hoyt, 975) and drug effects complicate the response. A vital part of the initial assessment of any patient is to determine his ability to maintain his airway and respiration. Before further assessment or diagnostic procedures can be carried out, it is essential to secure a free airway, either by positioning the patient or by intubation. Tonic Dysconjugate Absent FIG. 3. Categories of vestibulo-ocular reflex disturbances found in patients with impaired consciousness. Abnormal breathing patterns are common but have proved disappointing localizing features in acute situations (North and Jennett, 974). In an individual patient the pattern often fluctuates over short periods, and may reflect primary respiratory pathology rather than intracranial events. However, gross and persistently irregular respiration, in association with hypercapnia, is evidence of brain stem dysfunction and points to a medullary lesion. Measurement of intracranial pressure after head injury Measuring intracranial pressure (ICP) allows more precise management of patients with head injury (Johnston and Jennett, 973). The success or failure of regimens to decrease pressure can be determined. Measurement of pressure by itself is not a reliable guide to prognosis, but the combination of abnormal limb postures with high intracranial pressure from the start carries a poor prognosis (Becker et al., 975). Intracranial pressure is often normal in patients with severe diffuse primary brain injury, cerebral oedema is not present (as so often thought), and osmotic and steroid therapy are irrational. Although increased ICP is such a common feature of secondary complications, elevation of pressure rarely seems to occur in advance of clinical deterioration, the latter probably initially being a manifestation of brain shift rather than an abnormality of the absolute value of ICP. Advance warning of brain tightness and ICP increase might be provided by determining the amount of reserve still remaining in the compensating system. This can be achieved by observing the change in pressure resulting from adding or withdrawing ml fluid to the cranial
5 ASSESSMENT OF HEAD INJURIES 765 cavity through a ventricular catheter (Miller and Pickard, 974). Expertise in measuring ICP is largely confined to neurosurgical units, yet in Britain most head injuries are admitted primarily to general or accident surgical wards and transferred only when clinical evidence has raised a suspicion of secondary intracranial complications (Jennett, 975). Definitive management at that stage can often be determined on clinical criteria. In Glasgow we find ICP monitoring to be of most value in patients harbouring intradural lesions, in whom the necessity for surgery is not evident on clinical grounds. Demonstration of normal ICP saves these patients operations, while high pressure or a "tight brain" favours surgery. With the increasing use of the EMI scan changing the pattern of head injury care, such lesions may be disclosed more frequently and ICP measurements may play a much larger role in patient management. If it has been found necessary to paralyse and ventilate a patient with head injuries, ICP measurement is an extremely useful form of monitoring. RADIOLOGICAL ASSESSMENT Skull x-rays Lateral, antero-posterior and Towne's view films should always be obtained. Patients are rarely too uncooperative to allow for adequate radiology. A fracture signals the need for extra alertness about the development of a secondary haematoma. In the event of an extradural clot, the fracture site provides an excellent guide to location. Depressed fractures beneath scalp lacerations may be undetected clinically but require debridement in order to prevent infection. Intracranial air or fluid levels inside the paranasal sinuses indicate basal skull fractures and the need for antibiotic prophylaxis. If the pineal gland is calcified, its position indicates whether or not there is shift of the cerebral midline. Angiography and EMI scan Both investigations afford reliable identification of intracranial space-occupying lesions, but their use is limited to circumstances in which clinical grounds raise the possibility of a haematoma. In many of these patients general anaesthesia is required. This restricts the application of the EMI scan, the role of which in routine assessment of head injury has still to be determined. Echo-encephalography Standard echo-encephalography often gives misleading results in patients with intracranial haematomas" (Talalla and Morin, 97). Computerized models may be more reliable, but Brisman, Buchanan and Rosegay (974) found that only 8% of midline shifts were correctly detected by technicians using an automated midliner, and Klinger and colleagues (975) concluded that their use in head injury is unwarranted. ASSESSMENT OF EXTRACRANIAL COMPLICATIONS In the unconscious patient it is tempting to concentrate upon the injury to the head. Spinal, chest and abdominal injuries and complications should always be sought. Hypotension and hypoxia from these may be more significant in the production of depressed consciousness and eventual morbidity than the clinically more obvious head injury. ASSESSMENT OF OUTCOME AND PROGNOSIS In patients who recover, the duration of posttraumatic amnesia affords a good index of the severity of brain damage, but can only be measured retrospectively. Because of the discrepancies in terms used to describe the outcome to patients after severe brain damage, Jennett and Bond (975) have outlined a simple five-point scale (table I). In many patients, their outcome on this scale can be predicted from their clinical features in the first few days after injury (Jennett et al., 976; Teasdale and Jennett, 976). Code D PVS SD MD GR TABLE I. Glasgow outcome scale Assessment Dead Persistent vegetative state Severe disability Moderate disability Good recovery Description Awake but non-sentient Conscious but dependent Independent but disabled May have non-disabling sequelae CONCLUSION ASSESSMENT OF AN APPROPRIATE COURSE OF MANAGEMENT Patients with head injuries whose consciousness is impaired can be assigned to one of three categories on the basis of serial assessments of their state. The evidence of witnesses and ambulance personnel makes this possible even at the time of the first examination in hospital. () Patients whose condition is improving. Progressive improvement in consciousness indicates recovery from primary damage, and only supportive care and continuing observation are required.
6 766 BRITISH JOURNAL OF ANAESTHESIA (2) Patients whose condition is stable. It is likely that these patients also have only primary damage, but of greater severity. While management is similar to the first group, they are more liable to develop secondary complications and observation needs to be especially acute. (3) Patients who are deteriorating. It is in this group that secondary brain damage resulting from intracranial haematoma is most likely, but precipitate exploratory surgery should be avoided (Garfield, 972). Alternative mechanisms, such as airway obstruction, an epileptic fit, metabolic imbalance and impaired cerebral perfusion from extracranial complications, should first be sought. Deterioration resulting from an intracranial lesion is never so rapid that neurosurgical advice cannot be obtained, at least by telephone, and the condition of a patient suffering solely from a head injury rarely precludes transfer to a specialist unit. Patients with expanding supratentorial lesions display an orderly progression of increasing clinical features, with impairment of consciousness and hemisphere signs preceding those of tentorial herniation and brain stem dysfunction. Changes in "vital" functions hardly ever presage deterioration in conscious level (Troupp, 975). The monitoring of impaired consciousness is the foundation upon which assessment of head-injured patients is based. ACKNOWLEDGEMENT I am happy to acknowledge the influence and advice of Professor Bryan Jennett, who stimulated and guided many of the studies from which evolved this approach to assessing head-injured patients. REFERENCES Adams, J. H. (975). The neuropathology of head injuries; in Handbook of Clinical Neurology (eds P. J. Vinken and G. W. Bruyn), vol. 23, p. 35. Amsterdam: North Holland Publishing Co. Becker, D. P., Vries, J. K., Young, H. F., and Ward, J. D. (975). Controlled cerebral perfusion pressure and ventilation in human mechanical brain injury: prevention of progressive brain swelling; in Intracranial Pressure II (eds N. Lundberg, U. Ponten and M. Brock), p Berlin: Springer-Verlag. Brisman, R., Buchanan, D. S., and Rosegay, H. (974). Reliability of technicians in computerised and standard A-mode midline echo-encephalography. J. Neurosurg,. 4, 736. Fisher, C. M. (969). The neurological examination of the comatose patient. Acta Neurolog. Scand., 45 (Suppl.), 36. Galbraith, S. (976). Misdiagnosis and delayed diagnosis in traumatic intracranial haematoma. Br. Med. J., (in press). Murray, W. R., Patel, A. R., and Knill-Jones, R. (976). The relationship between alcohol and head injury and its effect on the conscious level. Br. J. Surg., 63, 28. Garfield, J. (972). Emergency situations: deteriorating head injuries. Br. J. Hosp. Med., 8, 262. Jamieson, K. G. 3 and Yelland, J. D. N. (968). Extradural haematoma: report of 67 cases. J. Neurosurg., 29, 3. Jennett, B., and Bond, M. (975). Assessment of outcome after severe brain damage. A practical scale. Lancet,, 480. Teasdale, G., Braakman R., Minderhoud, J., and Knill-Jones, R. P. (976). Predicting outcome in individual patients with severe head injury. Lancet (in press). Jennett, W. B. (975). Who cares for head injuries? Br. Med.J., 3,267. Graham, D. I., Adams, J. H., and Johnston, I. H. (973). Ischaemic brain damage after fatal blunt head injury; in Cerebral Vascular Diseases, Eighth Conference (eds F. H. McDowell and R. W. Brennan), p. 63. New York: Grune and Stratton. Johnston, I. H., and Jennett, B. (973). The place of continuous intracranial pressure monitoring in neurosurgical practice. Acta Neurochir. (Wien), 29, 53. Klinger, M., Kazner, E., Grummej T. H., Amtenbrink, V., Graef, G., Hartmann, K. H., Hopman, H., Meese, W., and Vogel, B. (975). Clinical experience with automatic mid-line echo-encephalography: co-operative study of three neurosurgical clinics. J. Neurolog. Neurosurg. Psychiatry, 38, 272. Miller, J. D., and Pickard, J. (974). Intracranial volume/ pressure studies in patients with head injury. Injury, 5, 265. Mitchell, D. E., and Adams, J. H. (973). Primary focal impact damage to the brain stem in blunt head injuries. Does it exist? Lancet, 2, 25. North, J. B., and Jennett, S. (974). Abnormal breathing patterns associated with acute brain damage. Arch. Neurol., 3, 338. Plum, F., and Posner, J. B. (972). The Diagnosis of Stupor and Coma, 2nd edn. Philadelphia: F. A. Davis. Rosenberg, M., Sharpe, J., and Hoyt, W. F. (975). Absent vestibulo-ocular reflexes and acute supratentorial lesions. J. Neurolog. Neurosurg. Psychiatry, 38, 6. Talalla, A., and Morin, M. A. (97). Acute traumatic subdural haematoma: a review of one hundred consecutive cases. J. Trauma, H, 77. Teasdale, G. (975). Acute impairment of brain function. I: Assessing "conscious level". Nurs. Times, 7, 94. Galbraith, S., and Clarke, K. (975). Acute impairment of brain function. II: Observation record chart. Nurs. Times, 7, 972. Jennett, B. (974). Assessment of coma and impaired consciousness: a practical scale. Lancet, 2, 8. (976). Assessment and prognosis of coma after severe head injury. Acta Neurochir., (in press). Knill-Jones, R., and Jennett, B. (974). Assessing and recording "conscious level". J. Neurolog. Neurosurg. Psychiatry, 37, 286. Troupp, H. (975). Neurological problems in trauma: deployment of resources; in Intensive Care: Proceedings of the 8th Pfizer International Symposium (eds W. F. Walker and D. E. M. Taylor), p. 99. Edinburgh, London, New York: Churchill Livingstone.
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