Hyperthermia, cerebral edema, and outcome in intracerebral hemorrhage: Too darn hot.

Fevers occur in over one-third of patients with intracerebral hemorrhage (ICH). Occurrence and duration of fevers have been associated with worse neurologic and functional outcomes. Fevers markedly increase cerebral metabolic rates and are thereby linked to a secondary injury cascade of increased intracranial pressure, cerebral edema, spreading ischemia, and triggered apoptosis.1–5