Hypoxic-Ischemic Encephalopathy

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 withlonger periods permanent cerebral damage is the rule. 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 PaO as 2

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. 21-1). The prognosis is better for pts

withintact brainstem function, as indicated by normal pupillary light responses,

intact oculocephalic (doll’s eyes) reflexes, and oculovestibular (caloric) and corneal reflexes (Chap. 17). 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 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.

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. Mild hypothermia (33_C),

initiated as early as possible and continued for 12–24 h, may improve outcome

in pts who remain comatose after cardiac arrest. Severe carbon

monoxide intoxication may be treated withh yperbaric 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.