Fulminant Hepatitis

Fulminant hepatitis represents massive hepatocyte necrosis resulting in acute liver failure within 8 weeks of symptom onset in a patient without pre-existing liver disease. The pathological process involves overwhelming hepatocellular destruction that exceeds the liver's regenerative capacity, caused by viral hepatitis (hepatitis B most common worldwide, hepatitis A in endemic areas), drug-induced liver injury (acetaminophen toxicity is the leading cause in developed countries), autoimmune hepatitis, Wilson disease, or ischemic hepatitis. Hepatocyte death releases intracellular contents including transaminases (AST, ALT often greater than 10,000 U/L), while loss of synthetic function produces coagulopathy (rising INR), hypoalbuminemia, and hypoglycemia. Hepatic encephalopathy results from impaired ammonia clearance, leading to astrocyte swelling (through glutamine accumulation) and cerebral edema with risk of uncal herniation. The nurse monitors coagulation studies, ammonia levels, blood glucose (every 1-2 hours), neurological status (hepatic encephalopathy grade), fluid and electrolyte balance, administers lactulose and rifaximin for encephalopathy, manages N-acetylcysteine infusion for acetaminophen toxicity, and coordinates evaluation for emergent liver transplantation.