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37 HYPOXIC-ISCHEMIC ENCEPHALOPATHY

37 HYPOXIC-ISCHEMIC ENCEPHALOPATHY
Harrison’s Manual of Medicine

37

HYPOXIC-ISCHEMIC ENCEPHALOPATHY

Clinical Manifestations
Bibliography

Results from lack of delivery of oxygen to the brain because of hypotension or respiratory failure. Most common causes are MI, cardiac arrest, shock, asphyxiation, paralysis of respiration, and carbon monoxide or cyanide poisoning. In some circumstances, hypoxia may predominate. Carbon monoxide and cyanide poisoning are termed histotoxic hypoxia since they cause a direct impairment of the respiratory chain.
Clinical Manifestations
Mild degrees of pure hypoxia (e.g., high altitude) cause impaired judgment, inattentiveness, motor incoordination, and, at times, euphoria. However, with hypoxia-ischemia, such as occurs with circulatory arrest, consciousness is lost within seconds. If circulation is restored within 3–5 min, full recovery may occur, but with longer periods of hypoxia-ischemia some degree of permanent cerebral damage is the rule. Except in extreme cases, it may be difficult to judge the precise degree of hypoxia-ischemia, and some pts make a relatively full recovery even after 8–10 min of global ischemia. The distinction between pure hypoxia and hypoxia-ischemia is important, since a PaO2 as low as 2.7 kPa (20 mmHg) can be well tolerated if it develops gradually and normal blood pressure is maintained, but short periods of very low or absent cerebral circulation may result in permanent impairment.
Clinical examination at different time points after an insult (especially cardiac arrest) helps to assess prognosis (Fig. 37-1). The prognosis is better for pts with intact brainstem function, as indicated by normal pupillary light responses, intact oculocephalic (doll’s eyes) reflexes, and oculovestibular (caloric) and corneal reflexes. Absence of these reflexes and the presence of persistently dilated pupils that do not react to light are grave prognostic signs. A uniformly dismal prognosis is conveyed by the absence of pupillary light reflex or absence of a motor response to pain on day 3 following the injury. Bilateral absence of the cortical somatosensory evoked response (Chap. 181) also conveys a poor prognosis. Long-term consequences include persistent coma or vegetative state, dementia, visual agnosia, parkinsonism, choreoathetosis, ataxia, myoclonus, seizures, and an amnestic state.

FIGURE 37-1. Clinical examination at day 1 provides useful prognostic information in hypoxic-ischemic encephalopathy. Numbers in parentheses represent 95% confidence intervals. Recov, recovery; veg, vegetative; sev, severe; mod, moderate; spont eye movt, spontaneous eye movement; rov conj, roving conjugate. (From DE Levy et al: Predicting outcome for hypoxic- ischemic coma. JAMA 253:1420, 1985.)

TREATMENT
Initial treatment is directed at restoring normal cardiorespiratory function. This includes securing a clear airway, ensuring adequate oxygenation and ventilation, and restoring cerebral perfusion, whether by cardiopulmonary resuscitation, fluids, pressors, or cardiac pacing. Hypothermia and neuroprotective agents have not yet been shown to have clinical value. Severe carbon monoxide intoxication may be treated with hyperbaric oxygen. Anticonvulsants are not usually given prophylactically but may be used to control seizures. Posthypoxic myoclonus can be controlled with clonazepam (1.5–10 mg/d) or sodium valproate (300–1200 mg/d) in divided doses. Myoclonic status epilepticus after a hypoxic-ischemic insult portends a universally poor prognosis.

Bibliography

For a more detailed discussion, see Hemphill JC, Beal MF, Gress DR, Critical Care Neurology, Chap 376, p. 2491, in HPIM-15.

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