Abstract

Hepatic encephalopathy (HE) is a precondition for the diagnosis of acute liver failure and a frequent complication of cirrhosis. Three types of HE are differentiated: type A in patients with acute liver failure; type B in patients with portosystemic shunts in the absence of liver dysfunction; and type C in patients with cirrhosis. HE symptoms are nonspecific; patients present with an alteration of cognition and sometimes consciousness accompanied by altered motor function. Patients with types B and C may have extrapyramidal and cerebellar disturbances in addition to pyramidal signs. Minimal HE is diagnosed when a patient without clinical signs of cerebral dysfunction has abnormalities on neuropsychologic or neurophysiologic testing. Hyperammonemia and the effects of inflammatory cytokines are considered to play a key role in the development of HE. In severe forms of acute liver failure, HE is accompanied by severe brain edema. Therapy of HE aims to reduce plasma ammonia and proinflammatory cytokine levels. When medical treatment is insufficient, liver transplantation becomes necessary. In contrast to HE, pancreatic encephalopathy is less well defined; the pathophysiology is uncertain and thus treatment remains symptomatic.

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