A. Failure of blood flow (cardiac arrest) or reduced oxygenation to the brain (respiratory failure, carbon monoxide, or cyanide poisoning) for 4 to 5 minutes’ duration results in brain damage.

B. Anoxia resulting from isolated respiratory arrest is better tolerated than when the primary event is a cardiac arrest.

II. PROGNOSIS. Many factors determine the prognosis after anoxic brain insult. These include the cause of the anoxic/ischemic insult, effective time to reestablish circulation (arrest time [AT], cardiopulmonary resuscitation [CPR] time), level of consciousness, age of patient, and neurologic signs present at 24 to 72 hours.

A. Favorable prognostic indicators include the following:

1. Retained consciousness during the anoxic/ischemic insult.

2. Primary respiratory failure carries a better prognosis than primary cardiac arrest.

3. Recovery of multiple brainstem responses within 48 hours of arrest (pupillary, corneal, and oculovestibular).

4. Return of purposeful motor movements within 24 hours (localization of pain).

5. Younger age (children may do well even beyond this time period).

6. Hypothermia (e.g., cold water drowning).

B. Poor prognostic indicators in patients with persistent coma after 72 hours include the following:

1. The absence of pupillary responses at 24 hours or loss of pupillary reflexes at 72 hours.

2. No motor response or extensor-only response to pain at 72 hours.

3. Presence of diffuse cerebral edema on computed tomography (CT) scan with loss of gray-white differentiation.

4. Certain abnormal electroencephalogram (EEG) patterns, including burst suppression, α-coma, and low-voltage unreactive delta activity. Myoclonic status epilepticus has a very poor prognosis even with treatment.

5. Absence of bilateral N20 somatosensory response within 1 to 3 days after CPR.

6. Elevated levels of serum neuron specific enolase >33 µg/L at days one to three days post-CPR.

A. Cardiac arrest from any cause.

B. Respiratory failure from any cause.

C. Poisoning (carbon monoxide, cyanide, others).

IV. PATHOPHYSIOLOGY. Following these injuries, excess glutamate release results in activation of the excitotoxic cascade, calcium influx into neurons, and cell death.

A. History.

1. Cardiac arrest.

2. Respiratory failure.

3. Drowning.

4. Toxic drug exposure/intoxication.

B. Examination: Patients are comatose usually without focal neurologic deficits. Rarely soft neurologic signs have been documented.

C. Imaging and laboratory studies.

1. CT or MRI scans to rule out structural lesions and brain herniation and demonstrate evidence of ischemic encephalopathy (cortical ribbon on diffusion MRI and loss of gray-white differentiation on CT).

2. Blood glucose and liver function tests, including ammonia, blood urea nitrogen, and creatinine, should be obtained to rule out metabolic encephalopathy. Toxicologic screen should be obtained when the cause of coma is unknown. An immediate EEG if nonconvulsive status epilepticus is suspected.