Liver Transplantation for Fulminant Hepatic Failure

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 encephalopathy.1,2 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 non-specific supportive medical measures. Plasma or whole blood exchange and charcoal hemoperfusion therapy have been tried with some success.3,4 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 of these obstacles had been partly eliminated in the last few years. The one-year survival after liver transplantation has improved to over 70% with cyclosporine-steroid therapy, and more donors have become available due to an increasing public awareness of the need. When a complete summary of a 19-year experience was brought up-to-date to May 1982,5 there had been only one attempt at the treatment of fulminant hepatic failure by transplantation, the recipient being a youth with fulminant B-virus hepatitis (OT 87). Numerous other candidates had been referred either to the University of Colorado (through 1980) or to the University of Pittsburgh. However, almost all of these patients died while a search was being conducted for an appropriate donor. A very few recovered. During the last three years, durther attempts have been made to treat patients with fulminant hepatic failure, and now with some success. We report here eight attempts at hepatic replacement under these dire circumstances during the last 36 months. The causes of massive hepatic necrosis were variable, ranging from drug intoxication to viral hepatitis. Although the perioperative mortality has been high, primarily because of irreversible brain injury and severe systemic complications, four of these eight patients have recovered fully. In this article, we will consider three issues. First will be the appropriate bare bones evaluation and preoperative management that are designed to allow a decision to be made about the potential reversibility of the acute hepatic disease. The second will consider the special technical and other perioperative problems that may be important. Third, we will report our results.