Fulminant hepatic failure is the clinical syndrome associated with acute massive necrosis of liver cells. It is characterized by the sudden onset of progressive jaundice, decrease in size of the liver, fetor hepaticus, and hepatic encephalopathy within eight weeks of acute illness. This syndrome carries a mortality rate of more than 80% when the patient develops grand IV hepatic en~ephalopathy.l*~ The depth of encephalopathy is important as an index of the severity of hepatic failure and in the assessment of the prognosis. Other systemic manifestations of fulminant hepatic failure include hypoglycemia, metabolic acidosis, respiratory failure, renal impairment, coagulopathy, and bacteremia. Fulminant hepatic failure is treated with nonspecific supportive medical measures. Plasma or whole blood exchange and charcoal hemoperfusion therapy have been tried with some s u c ~ e s s . ~ ~ ~ These treatments may prevent or correct some of the systemic complications of this syndrome and allow enough time for the liver to regenerate. However, when the liver cells are destroyed beyond the level of potential regeneration, all supportive measures are fruitless without liver replacement. For many years, there has been an interest in treating fulminant hepatic failure by liver transplantation. Until recently, this could not be achieved because of a generally low success rate (one-year survival rate of 33% with azathioprine-prednisone therapy) and a lack of organ donors at the appropriate time. Both
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