Gastrointestinal haemorrhage may occur due to decreased synthesis of vitamin K-dependent clotting factors. Lactic acidosis can occur as a result of impaired hepatic uptake or metabolism of lactate or increased lactate production secondary to tissue hypoxia. Severe cases progress to fulminant hepatic failure which is characterised by development of encephalopathy. Potential complications of fulminant hepatic failure include cerebral oedema and raised intracranial pressure, and intractable hypotentension. All agents that may be contributing to hepatotoxicity should be immediately discontinued.
Care is primarily supportive.
Patients developing fulminant hepatic failure require intensive supportive management of acute complications including encephalopathy, coagulopathy, electrolyte and acid-base disturbances, renal failure, sepsis and cerebral oedema. Administration of intravenous n-acetyl cysteine is indicated in acute hepatic failure from acetaminophen poisoning. In patients who do not develop encephalopathy, complete recovery is the rule. Serum transaminases, INR, bilirubin, renal function and fluid balance should be carefully monitored until clinical improvement is noted. Development of fulminant hepatic failure is associated with extremely high acute mortality, even with aggressive intensive medical care.