Hepatic encephalopathy: pathophysiology and advances in therapy

Abstract

Hepatic encephalopathy is a major neuropsychiatric complication of cirrhosis. Hepatic encephalopathy can occur in patients with fulminant liver disease without evidence of portosystemic shunting. The syndromes are distinct in acute liver failure and cirrhosis. The pathogenesis of hepatic encephalopathy probably is multifactorial, although the predominant causative agent appears to be ammonia. Prevention and treatment of hepatic encephalopathy in cirrhotic patients continues to rely on ammonia lowering strategies which include assessment of dietary protein intake and the use of lactulose, neomycin, sodium benzoate and L-ornithine-aspartate. This review provides recent information on the classification of hepatic encephalopathy, current theories for pathophysiological basis and evaluates the available therapies.