Reye syndrome (acute encephalopathy syndrome)

General: Etiology unknown, although some relation to ingestion of aspirin with fe 737d34h brile illnesses, especially varicella and influenza, have been reported; both sexes; onset 6 months to 10 years; acute metabolic encephalopathy largely affecting children and adolescents; pathogenesis is controversial, although there is new evidence for a generalized defect in intramitochondrial enzyme processing resulting in lowered ratio of adenosine triphosphate to adenosine diphosphate.

Ocular: Cortical blindness; dilated pupils with absent or sluggish reaction to light; papilledema.

Clinical: Respiratory infections with recovery between 3 and 21 days; vomiting after recovery from infection; dyspnea; hypotonia; coma; convulsions; fever; flexion of elbows and hands.

Brown AK, et al. Aspirin and Reye syndrome. J Pediatr 1983; 102:157-l58.

Glasgow JF, Moore R. Current concepts in Reye's syndrome. Br J Hosp Med 1993; 50:599-604.

Hoekelman RA. Take two aspirin and call me in the morning: salicylate use and Reye's syndrome. Am J Dis Child 1982; 136:973-974.

Massey JY, et al. Ocular manifestations of Reye syndrome. Arch Ophthalmol

Reye RDK, Morgan G. Baral J. Encephalopathy and fatty degeneration of the viscera: a disease entity in childhood. Lancet 1963; 2:749.

van Coster RN, et al. Adult Reye's syndrome: a review with new evidence for a generalized defect in intramitochondrial enzyme processing. Neurology 1991; 41:1815-l821.