Encephalopathy, Postanoxic

After successful prehospital cardiac resuscitation: 59–65% of pts remain comatose.

0–5% of successful resuscitations result in chronic vegetative state.

Worsening of neurologic status; blindness most common residuum.

Postpone surgery in all but emergency situations.

Do what is necessary to treat precipitating cause and to decrease sequelae (e.g., treat elevated ICP).

Repeat of events that initially caused encephalopathy (e.g., arrhythmias leading to cardiac arrest)

Hypotension, hypercapnia, hypoxia, and sepsis that can exacerbate encephalopathy

Brain injury resulting from prolonged period of insufficient cerebral oxygenation.

Clinical picture ranges from mild confusion to brain death.

Chances for acceptable neurologic recovery: 1% with continued coma after 24 h and lack of two of the following reflexes: Pupillary, corneal, and oculovestibular.

Absence of brainstem function 72 h after event associated with irreversible coma.

Therapeutic hypothermia (especially after cardiac arrest with initial VFIB or VTach) improves neurologic outcome.

Good prognosis seen in 50% of pts awakening within 24 h of insult.

Seizures occur in 25% of pts.

Anoxic damage may have been sustained by other organs (e.g., MI, shock liver, acute renal failure, stress ulcers, ARDS).

DI is poor prognostic sign.

Caused by inadequate O ₂ delivery to CNS due to inadequate cardiac output, resp dysfunction, severe anemia, and/or increased ICP

Most often secondary to primary cardiac (MI or arrhythmia) or pulm (asthma, pulm embolism) event

May also be result of CO poisoning, suffocation, and cyanide poisoning