The majority of patients with fulminant hepatitis B negative for hepatitis B e antigen are infected with a mutant virus that is unable to produce the e antigen. In Japan, about 50% of patients with fulminant non-A, non-B hepatitis are infected with hepatitis C virus but this virus does not appear to cause acute liver failure in the United States or United Kingdom. Cerebral edema is still a major cause of death and the insertion of an intracranial pressure monitoring device is currently the only method available to establish the diagnosis of intracranial hypertension and to monitor the response to therapy. The influence of cerebral blood flow on intracranial pressure remains to be determined. WhereasN-acetylcysteine improves outcome in patients with acetaminophen-induced fulminant hepatic failure, and may do so by enhancing tissue oxygen transport, steroids and insulin-glucagon therapy are of no benefit. Artificial liver support systems are being developed but have yet to prove their benefit in clinical use.