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Assessment & Emergency Measures
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The diagnostic workup of the comatose patient must proceed concomitantly with management Supportive therapy for respiration or blood pressure is initiated; in hypothermia, all vital signs may be absent and all such patients should be rewarmed before the prognosis is assessed The patient can be positioned on one side with the neck partly extended, dentures removed, and secretions cleared by suction; if necessary, the patency of the airways is maintained with an oropharyngeal airway Blood is drawn for serum glucose, electrolyte, and calcium levels; arterial blood gases; liver and renal function tests; and toxicologic studies as indicated Dextrose 50% (25 g), naloxone (04 12 mg), and thiamine (50 mg) are given intravenously Further details are then obtained from attendants of the patient s medical history, the circumstances surrounding the onset of coma, and the time course of subsequent events Abrupt onset of coma suggests subarachnoid hemorrhage, brainstem stroke, or intracerebral hemorrhage, whereas a slower onset and progression occur with other structural or mass lesions A metabolic cause is likely with a preceding intoxicated state or agitated delirium On examination, attention is paid to the behavioral response to painful stimuli, the pupils and their response to light, the position of the eyes and their movement in response to passive movement of the head and ice-water caloric stimulation, and the respiratory pattern
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A Response to Painful Stimuli
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Purposive limb withdrawal from painful stimuli implies that sensory pathways from and motor pathways to the stimulated limb are functionally intact Unilateral absence of responses despite application of stimuli to both sides of the body in turn implies a corticospinal lesion; bilateral absence of responsiveness suggests brainstem involvement, bilateral pyramidal tract lesions, or psychogenic unresponsiveness Inappropriate responses may also occur Decorticate posturing may occur with lesions of the internal capsule and rostral cerebral peduncle, decerebrate posturing with dysfunction or destruction of the midbrain and rostral pons, and decerebrate postur-
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Diseases causing coma may lead to respiratory abnormalities Cheyne-Stokes respiration may occur with bihemispheric or diencephalic disease or in metabolic disorders Central neurogenic hyperventilation occurs with lesions of the brainstem tegmentum; apneustic breathing (in which there are prominent end-inspiratory pauses) suggests damage at the pontine level (eg, due to basilar artery occlusion); and atactic breathing (a completely irregular pattern of breathing with deep and shallow breaths occurring randomly) is associated with lesions of the lower pontine tegmentum and medulla
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responses, the development of spontaneous eye movements (roving, conjugate, or better), and extensor, flexor, or withdrawal responses to pain at this early stage imply a relatively good prognosis Treatment of metabolic encephalopathy is of the underlying disturbance and is considered in other chapters If the cause of the encephalopathy is obscure, all drugs except essential ones may have to be withdrawn in case they are responsible for the altered mental status
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Stevens RD et al Approach to the comatose patient Crit Care Med 2006 Jan;34(1):31 41 [PMID: 16374153] Wijdicks EF et al Practice parameter: prediction of outcome in comatose survivors after cardiopulmonary resuscitation (an evidence-based review): report of the Quality Standards Subcommittee of the American Academy of Neurology Neurology 2006 Jul 25;67(2):203 10 [PMID: 16864809]
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1 Stupor & Coma Due to Structural Lesions
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Supratentorial mass lesions tend to affect brain function in an orderly way There may initially be signs of hemispheric dysfunction, such as hemiparesis As coma develops and deepens, cerebral function becomes progressively disturbed, producing a predictable progression of neurologic signs that suggest rostrocaudal deterioration Thus, as a supratentorial mass lesion begins to impair the diencephalon, the patient becomes drowsy, then stuporous, and finally comatose There may be Cheyne-Stokes respiration; small but reactive pupils; doll s-head eye responses with side-to-side head movements but sometimes an impairment of reflex upward gaze with brisk flexion of the head; tonic ipsilateral deviation of the eyes in response to vestibular stimulation with cold water; and initially a positive response to pain but subsequently only decorticate posturing With further progression, midbrain failure occurs Motor dysfunction progresses from decorticate to bilateral decerebrate posturing in response to painful stimuli; Cheyne-Stokes respiration is gradually replaced by sustained central hyperventilation; the pupils become middle-sized and fixed; and the oculocephalic and oculovestibular reflex responses become impaired, perverted, or lost As the pons and then the medulla fail, the pupils remain unresponsive; oculovestibular responses are unobtainable; respiration is rapid and shallow; and painful stimuli may lead only to flexor responses in the legs Finally, respiration becomes irregular and stops, the pupils often then dilating widely In contrast, a subtentorial (ie, brainstem) lesion may lead to an early, sometimes abrupt disturbance of consciousness without any orderly rostrocaudal progression of neurologic signs Compressive lesions of the brainstem, especially cerebellar hemorrhage, may be clinically indistinguishable from intraparenchymal processes A structural lesion is suspected if the findings suggest focality In such circumstances, a CT scan should be performed before, or instead of, a lumbar puncture in order to avoid any risk of cerebral herniation Further management is of the causal lesion and is considered separately under the individual disorders
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