Hypoxic-ischemic brain injury and prognosis after cardiac arrest.

PURPOSE OF REVIEW

: Cardiac death is the leading cause of death in the United States, and patients who have out-of-hospital cardiac arrest have only a 1% to 10% survival rate, despite improvements in advanced life support. The neurologic sequelae of hypoxic-ischemic brain injury after cardiac arrest vary from subtle cognitive impairment to coma, persistent vegetative state, and brain death. Neurologists are commonly asked to prognosticate neurologic outcome after cardiac arrest.

RECENT FINDINGS

: In 2002, two randomized controlled trials demonstrated that therapeutic hypothermia (32°C to 34°C [89.6°F to 93.2°F]) increases the odds of improved neurologic outcome and reduces the risk of death compared with normothermia when applied for the initial 12 to 24 hours after ventricular fibrillation or tachycardia cardiac arrest. Considerable research continues into neurologic prognostication after hypoxic-ischemic brain injury, especially with the advent of therapeutic hypothermia and its effects on the clinical examination, neurophysiologic studies, and serum biomarkers of brain injury. Recent reports indicate that poor motor response 72 hours after cardiac arrest, absent cortical responses on median nerve somatosensory-evoked potentials, and elevated neuron-specific enolase may not necessarily indicate poor prognosis in patients treated with therapeutic hypothermia compared with historical populations not treated with hypothermia, perhaps because of sedation and neuromuscular blockade.

SUMMARY

: Neurologic prognostication after cardiac arrest remains challenging because of the sedation and neuromuscular blocking agents given to patients who undergo therapeutic hypothermia. A multimodal algorithmic approach (clinical, electrophysiologic, and possibly serum biomarker testing) is suggested for cardiac arrest patients treated with hypothermia, but further research is needed to determine more accurate prognostic predictors.