Acute liver failure (ALF), also known as fulminant hepatitis, is the final common pathway of severe hepatocyte injury, regardless of cause, and remains one of the most enigmatic and frightening conditions in all of medicine. Defined by the onset of altered mental status (hepatic encephalopathy) and coagulopathy (prolonged prothrombin time) occurring within 8 weeks of initial symptoms, ALF is estimated to affect 2000 individuals annually in the United States, only 200-300 of whom receive liver transplants. The rapidity of the course of ALF often catches clinicians off guard. The ALF syndrome is characterized by the unique clinical features of cerebral edema and shock with poor tissue oxygenation, shared by all causes. Over 50% of ALF cases in the United States are now due to drug hepatotoxicity, either acetaminophen-related or caused by idiosyncratic drug reactions. The very high mortality observed in past decades has improved because of better intensive care, the advent of transplantation, and an increase in the number of acetaminophen cases that carry a good prognosis. However, hepatic transplantation is often inappropriate or unavailable. Even at transplant centers, only 29% of patients receive a liver graft, and 38% survive without transplantation. The mainstay of ALF management remains skilled intensive care focused on the specific problems of these patients. Liver support machines have not yet come of age. Because a large proportion of patients never receive a liver graft, renewed efforts to understand ALF itself make sense, with the goal of preserving remaining hepatocytes or regenerating the failing liver.
|Original language||English (US)|
|Number of pages||10|
|Journal||Clinical Perspectives in Gastroenterology|
|State||Published - Jan 1 2001|
ASJC Scopus subject areas