Hepatitis B virus is sometimes responsible for fulminant hepatitis, and up to 50% of cases of fulminant hepatitis B involve hepatitis D virus coinfection. Fulminant hepatitis with hepatitis A virus is rare but may be more likely in people with preexisting liver disorders. Occasionally, hepatitis E virus causes fulminant hepatitis. The role of hepatitis C virus remains uncertain.
Alcoholic hepatitis may cause fulminant liver failure, but most patients have a long history of heavy drinking and so probably have underlying chronic liver disease.
Drugs (especially acetaminophen) are the most common cause of fulminant hepatitis in the US.
Symptoms of fulminant hepatitis develop and become severe very quickly. Patients rapidly deteriorate because portosystemic encephalopathy develops, progressing to coma and cerebral edema over a period of several days to several weeks. Coagulopathy commonly results from liver failure or disseminated intravascular coagulation, and functional renal failure (hepatorenal syndrome) may develop.
Increasing prothrombin time (PT) or international normalized ratio (INR), portosystemic encephalopathy, and particularly renal failure are ominous.
Fulminant hepatitis should be suspected if
Laboratory tests to confirm the diagnosis of fulminant hepatitis include liver tests (eg, aminotransferases, alkaline phosphatase) and other tests to evaluate liver function (prothrombin time/international normalized ratio [PT/INR], bilirubin, albumin).
Laboratory tests for acute hepatitis A, B, and C viruses, as well as some other viruses (eg, cytomegalovirus, Epstein-Barr virus, herpes simplex virus), are done to determine whether a virus is the cause.
The serum acetaminophen level should be measured in all patients if acetaminophen toxicity is suspected.
Meticulous medical care, usually in an intensive care unit, and aggressive treatment of complications improve the outcome of patients with fulminant hepatitis.
If fulminant hepatitis results from hepatitis B, treatment with oral nucleoside or nucleotide analogs can increase the likelihood of survival.
N-Acetylcysteine is an antidote for acetaminophen poisoning. This drug is most effective if given within 8 hours of acetaminophen ingestion but may still have a role in chronic acetaminophen toxicity.
However, emergency liver transplantation provides the best hope for survival. Survival in adults is uncommon without transplantation; children tend to do better.
Patients who survive usually recover fully.
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