Toxic encephalopathy with hyperammonaemia during high-dose salicylate therapy.
High-dose, long-term aspirin therapy easily overloads the patient's individual capacity to metabolize salicylates and may lead to complex metabolic disturbances including fulminant hepatic failure, hyperammonemia and toxic metabolic encephalopathy. In the two cases presented there was a severe outbreak of hepatotoxic encephalopathy despite the fact that the dosage of salicylates did not exceed that generally recommended for children with rheumatic diseases. The justification of high-dose salicylate therapy is discussed, taking into account the fact that children with juvenile rheumatoid arthritis and allied conditions may have increased susceptibility to liver damage from drugs. EEG abnormalities in these two cases corresponded to those described in other metabolic encephalopathies including Reye's syndrome. The quality of the EEG changes gives prognostic signs, but is of restricted value in establishing the etiology without the anamnestic data of salicylate ingestion. Active therapeutic measures including exchange transfusions are needed to prevent irreversible metabolic and pressure changes in the brain.
D000293:Adolescent; D000641:Ammonia / Q000097:blood*; D056486:Chemical and Drug Induced Liver Injury / Q000209:etiology*; D002648:Child; D004569:Electroencephalography; D005260:Female; D006501:Hepatic Encephalopathy / Q000139:chemically induced*; D006801:Humans; D007592:Joint Diseases / Q000188:drug therapy; D008099:Liver / Q000187:drug effects*; D008297:Male; D012459:Salicylates / Q000008:administration & dosage / Q000009:adverse effects*
D012459:Salicylates; D000641:Ammonia