Hepatic Encephalopathy in Liver Cirrhosis

Abstract

Hepatic encephalopathy (HE) is the most severe and often fatal complication of liver cirrhosis. Intestine-derived neurotoxic substances, such as ammonia, are believed to be the cause of HE. As the results from hepatocellular dysfunction or portosystemic shunt associated with liver cirrhosis, those toxins, which should be detoxified in the liver, flow into the systemic circulation and perturb the brain function. The symptoms of HE include consciousness disorders that range from mild disorders, such as minimal hepatic encephalopathy, to severe disorders that result in deep coma. HE associated with liver cirrhosis develops when some additional triggers overlie liver failure or portosystemic shunt, such as constipation, a high-protein diet, and gastrointestinal bleeding, which are the therapeutic targets of medical treatment. Synthetic disaccharides and rifaximin are used to suppress intestinal ammonia production, and BCAA and zinc are used to support ammonia detoxification in the liver or muscle.