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Fulminant liver failure is the onset of encephalopathy occurring within 8 weeks of the onset of jaundice in someone with hepatic injury and no prior history of liver disease.
Fulminant liver failure most commonly follows acute viral infection with hepatitis A, B, C, D, or E viruses.
Hepatoxins such as acetaminophen, isoniazid, halothane, valproic acid, or muschroom toxins can also cause FHF.
Reye's syndrome, occurring primarily in children, and acute fatty liver of pregnancy can mimic FHF.
Rare causes include Wilson's disease, hepatic ischemia, autoimmune hepatitis, and malignancy.
Pathophysiology involves severe, widespread hepatic necrosis, commonly resulting from acute viral infection.
The pathology of hepatic encephalopathy is unclear, but is frequently associated with hypoglycemia and cerebral edema.
Diagnosis is based on combination of hepatic encephalopathy and liver failure.
Biochemically, levels of transaminases and bilirubin are markedly elevated, as is prothrombin time.
As the causes of FHF is rarely treatable, treatment remains supportive. Meticulous care improves survival.
Lactulose can be used to treat hepatic encephalopathy.
Liver transplantation is the treatment of choice for people unlikely to recover spontaneously.
Most processes that result in widespread liver cell necrosis are transient, and regeneration and liver function recovery often occurs if patients do not die. Short term survival for people in coma is 20% without liver transplantation.
Hypoglycemia results from impaired gluconeoneogenesis and insulin degradation.
Other metabolic abnormalities include hyponatremia, hypokalemia, respiratory alkalosis, and metabolic acidosis.
Bleeding frequently occurs due to coagulopathy.
Cerebral edema is the leading cause of death.
Infection is another important cause of death, and can occur without fever or leukocytosis.
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