Hepatic Encephalopathy: Are NH4 Levels and Protein Restriction Obsolete?

Hepatic encephalopathy is a major complication of acute and chronic liver disease. This neuropsychiatric syndrome presents clinically with abnormalities in mental status and neuromotor function. Symptoms exist on a spectrum ranging from subtle deficits in attentiveness to severe confusion and even coma. The pathogenesis of this disease is not fully understood, but the accumulation of gut-derived neurotoxins in the setting of hepatic insufficiency remains central to current investigations. Over 5.5 million people in the United States have been diagnosed with cirrhosis.1 Of this population, 30–45% of patients develop overt hepatic encephalopathy during the course of their disease.2 This debilitating condition can negatively impact quality of life for patients and their families.1 Furthermore, admissions for hepatic encephalopathy commonly result in prolonged hospital stays and a costly burden on our health care system.2 Hepatic encephalopathy is usually classified into three groups differentiated by the absence or presence of liver disease: encephalopathy due to acute liver failure (Type A), portosystemic shunting without associated liver disease (Type B), and cirrhosis with portal hypertension (Type C).3 Further subdivisions distin-