Snapshot A 50-year-old man with cirrhosis is brought to the emergency room for altered mental status. He lives at home with his mother, who noted that he was slow in his responses and disoriented. He has a history of alcoholic cirrhosis, and for the past week he has not eaten much food. His last drink was a day ago. On physical exam, he is noted to be jaundiced with asterixis. His mucous membranes are dry and his capillary refill is delayed. An ultrasound of his abdomen shows ascites. Labs are significant for hyperkalemia and elevated ammonia to 200 μmol/L. He is started on lactulose and rifaximin and admitted to the inpatient unit for further management. Introduction 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 Associated conditions acute liver failure cirrhosis other complications of cirrhosis include portal hypertension, esophageal varices, and hepatocellular carcinoma 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) 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 Prognosis Hepatic encephalopathy is reversible