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Acute liver failure (ALF) is a rare but life-threatening syndrome characterized by rapid onset of coagulopathy and encephalopathy in a patient without pre-existing liver disease. Acetaminophen toxicity is the leading cause in the United States, while viral hepatitis predominates in developing countries.
ALF results from massive hepatocellular necrosis or dysfunction impairing the liver's synthetic, metabolic, and detoxification functions. Loss of synthetic function produces coagulopathy (elevated PT/INR) and hypoalbuminemia. Accumulation of ammonia and other gut-derived toxins contributes to hepatic encephalopathy and cerebral edema. Hypoglycemia results from impaired gluconeogenesis.
Clinical reasoning requires identifying the underlying etiology — acetaminophen (NAC is antidote), Wilson's disease, autoimmune hepatitis, ischemic hepatitis, and Budd-Chiari syndrome each have targeted therapies. The King's College Criteria guide liver transplant listing. Serial assessment of encephalopathy grade, INR, creatinine, and bilirubin tracks trajectory. Differentiating ALF from acute-on-chronic liver failure is essential as management differs significantly.
Key imaging focus: Nodular liver surface, caudate hypertrophy, ascites, portal hypertension signs, varices