Reye's syndrome is a fatal biphasic disorder characterized by a preceding viral illness, prolonged vomiting preceding encephalopathy, and liver dysfunction onset. Clinical manifestations include delirium, fever, convulsions, vomiting, respiratory collapse, stupor, seizures, or coma, typically following an earlier viral infection. Encephalopathy rapidly progresses from lethargy to coma within 24 to 48 hours. The primary etiology of Reye's syndrome involves universal mitochondrial injury and triglyceride accumulations. High concentrations of ammonia contribute to encephalopathy and anicteric hepatitis, accompanied by a threefold increase in liver enzymes. Mitochondrial permeability transition induction is a frequent pathophysiological mechanism. Reye's syndrome carries a high mortality rate, and treatment involves symptomatic management, including intensive care to correct metabolic abnormalities (hypotension, hypoglycemia, acidosis), seizure control, and monitoring intracranial hypertension due to cerebral edema. Agents to decrease serum ammonia concentrations, such as neomycin sulfate or lactulose, are commonly used, along with anti-emetics like ondansetron to inhibit vomiting and prevent potential aspiration.