Hepatic failure

Hepatic encephalopathy defines, and is the sine qua non for, fulminant hepatic failure. The pathogenesis is associated with widespread hepatic necrosis, commonly due to an acute viral infection or exposure to hepatotoxins. Common hepatotoxins that lead to fulminant liver failure include acetaminophen, isoniazid, halothane, valproic acid, mushroom toxin, and carbon tetrachloride. (59> Hepatic encephalopathy that accompanies acute fulminant liver failure differs from that associated with chronic hepatic impairment in two aspects: first, it is rarely due to a reversible factor, and, second, it is frequently associated with cerebral oedema, which might be reversible and a treatable factor. Therapy includes protein restriction and lactulose. Cerebral oedema is the leading cause of death in acute hepatic failure. It may respond to the administration of mannitol and measures to control agitation. (59) Other signs of hepatic failure include hypoglycaemia, gastrointestinal haemorrhage, and coagulopathy. For patients with acute hepatic failure who have significant hepatic encephalopathy, liver transplantation increases survival from 20 per cent to 80 per cent, making rapid and accurate diagnosis vital.

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