Fulminant hepatitis is a rare syndrome of massive necrosis of liver parenchyma and a decrease in liver size (acute yellow atrophy) that usually occurs after infection with certain hepatitis viruses, exposure to toxic agents, or drug-induced injury.
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. The role of hepatitis C virus remains uncertain.
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 PT or INR, portosystemic encephalopathy, and particularly renal failure are ominous.
Fulminant hepatitis should be suspected if patients are acutely ill with new-onset jaundice, rapid changes in mental status, or unexplained bleeding or if patients with known liver disease rapidly deteriorate.
Laboratory tests to confirm the diagnosis of fulminant hepatitis include liver function tests and PT/INR.
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.
Meticulous nursing care and aggressive treatment of complications improve the outcome.
If fulminant hepatitis results from hepatitis B, treatment with oral nucleoside or nucleotide analogs can increase the likelihood of survival.
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.