Halothane Hepatitis

Halothane, first synthesized in 1951, may cause fatal and nonfatal hepatitis in one of 9000 recipients and fatal hepatitis in 1 of 40000 recipients. Female sex, age, intrahepatic hypoxia, repeated halothane exposure, obesity, alcohol, genetic predisposition and enzyme induction have been considered to be risk factors. The more common mild form may result from reductive biotransformation of halothane, possibly influenced by genetic factors or reduced liver oxygenation, whereas the rare fulminant form is most likely to be immune mediated. Halothane hepatotoxicity is idiosyncratic. Clinical Manifestations include fever, malaise, anorexia, nausea, vomiting, jaundice, skin rash, liver tenderness. Fulminant hepatitis is rarely seen. Eleveated serum transaminases, alkaline phosphatase and bilirubin and eosinophillia are also seen. Manifestations usually begin 4 days after exposure. Treatment includes supportive care. Liver transplantation may be needed in severe fulminant cases. Prognosis of those who develop jaundice is grave (with 14 –70% mortality). Other cases have much better prognosis. In order to prevent hepatotoxity, halothane exposures should be at least 6 months apart.