• Emmet B Keeffe.
• División de Gastroenterología y Hepatología, Departmento de Medicina, Stanford University School of Medicine, Stanford, CA, USA. ekeeffe@stanford.edu
• Rev Gastroenterol Mex. 2005 Jan 1; 70 (1): 56-62.

AbstractAcute liver failure, also called fulminant hepatic failure, is characterized by sudden hepatic synthetic dysfunction associated with coagulopathy and hepatic encephalopathy. Acute liver failure has most recently been defined based on the timing from onset of jaundice to encephalopathy as follows: 1) hyperacute (1-7 days); 2) acute (8-28 days), and 3) subacute (29-60 days). Rapid onset of encephalopathy in hyperacute liver failure is paradoxically associated with highest rate of spontaneous recovery, and subacute liver failure is associated with worst prognosis. The etiology of liver failure is established by history, serologic assays, and exclusion of alternative causes. Acute liver failure is most frequently caused by drug hepatotoxicity, including acetaminophen toxicity and idiosyncratic drug reactions, with viral hepatitis playing a lesser role in recent surveys. A substantial number of cases have an indeterminate etiology. Major complications of acute liver failure that require active intervention include metabolic disorders, coagulopathy, cerebral edema, renal failure, and infection. The focus of management of acute liver failure is comprehensive supportive care in an intensive care unit and assessment of the need for liver transplantation.

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