Snapshot A 45-year-old man with a history of alcoholic cirrhosis is found on the sidewalk with altered mental status. He is brought in to the emergency room by the police. He has had multiple similar visits for intoxication. This time, however, he is noted to be markedly lethargic and jaundiced. On physical exam, he has pronounced asterixis, ascites, and other signs of liver disease such as telangiectasias and palmar erythema. Laboratory evaluation reveals negative serum alcohol levels but elevated ammonia and liver enzymes. A hepatic ultrasound shows a hyperechoic mass in his liver, which is concerning for malignancy in the setting of chronic cirrhosis and was thought to be the possible trigger for his episode of hepatic encephalopathy. Introduction Overview a reversible complication of liver failure characterized by altered mental status and asterixis often precipitated by acute stressors such as dehydration or infection Epidemiology incidence 30-40% of patients with cirrhosis risk factors alcohol use hepatitis Etiology acute triggers dehydration infection gastrointestinal bleed fluid and electrolyte abnormalities sedatives hepatocellular carcinoma transjugular intrahepatic portosystemic shunt (TIPS) Pathogenesis mechanism ↓ ammonia clearance due to liver dysfunction ammonia is normally metabolized in the liver to urea, which is easily excreted portosystemic shunts causing blood to bypass the liver ammonia is neurotoxic crosses blood-brain barrier and is converted to glutamine, which is an osmolyte and promotes swelling of brain cells this leads to cerebral edema alteres neurotransmitter function Associated conditions acute liver failure cirrhosis other complications of cirrhosis include portal hypertension, esophageal varices, and hepatocellular carcinoma Prognosis hepatic encephalopathy is reversible Classification Classification by underlying disease type A acute liver failure type B portosystemic bypass or shunting with preserved liver function type C cirrhosis Presentation Symptoms common symptoms mood changes slow to respond unsteadiness Physical exam inspection signs of liver disease jaundice ascites spider angiomata palmar erythema asterixis flapping tremor of wrists altered mental status coma/stupor in severe cases Imaging CT or MRI of the head indication rule out intracranial hemorrhage or mass as a cause of encephalopathy findings cerebral edema Studies Serum labs ↑ ammonia also check liver function panel blood urea nitrogen electrolytes Differential Other metabolic encephalopathies diabetic ketoacidosis distinguishing factor hyperglycemia with ketones in the blood and anion gap metabolic acidosis uremic encephalopathy distinguishing factor elevated urea and normal ammonia acute alcoholic intoxication distinguishing factor elevated blood alcohol level Treatment Nonoperative correct precipitating factor and electrolyte derangements lactulose mechanism gastrointestinal flora degrades lactulose into lactic acid and acetic acid, which results in the clearance of ammonia indication treatment and prevention rifaximin mechanism ↓ bacteria that produce ammonia indication treatment and prevention alongside lactulose Complications Persistent learning impairment