Results from lack of delivery of oxygen to the brain because of extreme hypotension or respiratory failure. Most common causes are myocardial infarction (MI), cardiac arrest, shock, asphyxiation, paralysis of respiration, and carbon monoxide or cyanide poisoning. In some circumstances, hypoxemia may predominate. Carbon monoxide and cyanide poisoning are termed histotoxic hypoxemia because they cause a direct impairment of the respiratory chain.
Mild degrees of pure hypoxemia (e.g., at 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 permanent cerebral damage usually results. 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 hypoxemia and hypoxia-ischemia is important, because 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 durations 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. The prognosis is better for pts with intact brainstem function, as indicated by normal pupillary light responses, intact oculocephalic (doll’s eyes), 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 low likelihood of a favorable outcome is suggested by the absence of a pupillary light reflex or an extensor or absent motor response to pain on day 3 following the injury. Bilateral absence of the cortical somatosensory evoked potentials (SSEP) also conveys a poor prognosis, as does a very elevated serum level (>33 µg/L) of the biochemical marker neuron-specific enolase (NSE) within the first 3 days. The presence of a burst-suppression pattern of myoclonic status epilepticus on EEG or a nonreactive EEG is associated with a low likelihood of good functional outcome. Administration of mild hypothermia after cardiac arrest may change the time points when these clinical and electrophysiologic predictors become reliable in identifying pts with a very low likelihood of clinically meaningful recovery. Current approaches to prognostication after cardiac arrest encourage the use of a multimodal approach that includes these diagnostic tests, along with CT or MRI neuroimaging, in conjunction with clinical neurological assessment.
Long-term consequences include persistent coma or vegetative state, dementia, visual agnosia, parkinsonism, choreoathetosis, ataxia, myoclonus, seizures, and an amnestic state. Delayed postanoxic encephalopathy is an uncommon phenomenon in which pts appear to make an initial recovery following an insult and then have a relapse with a progressive course often characterized by widespread demyelination on imaging studies.