Acute hepatic necrosis and fulminant hepatic failure

Abstract

Fulminant hepatic failure is defined as severe, acute impairment of hepatic function culminating in hepatic encephalopathy, the encephalopathy being the result of hepatocellular failure and supervening within three weeks of the onset of symptoms. This definition excludes the hepatic encephalopathy of hepatic cirrhosis and of chronic hepatitis, which produces a slightly different clinical picture, but fulminant hepatic failure as defined here may of course occur as a superimposed phenomenon in patients with these conditions. Likewise excluded is encephalopathy caused by sedatives in patients with viral hepatitis or by a direct cerebral action of certain halogenated hydrocarbons in subjects whose livers are already damaged by these compounds. The clinical features of a typical attack of fulminant hepatic failure are progressive jaundice of acute onset, shrinkage of the liver, factor hepaticus, and hepatic coma. Characteristic biochemical changes are increased prothrombin time, elevated serum transaminase activity, and raised blood ammonia concentration. This review discusses pathogenesis, etiology, clinical manifestations, prognosis and treatment.