Hepatic encephalopathy: Nomenclature, pathogenesis, therapy

Abstract

The hepatic encephalopathy (HE) is a reversible metabolic syndrome that can appear due to acute liver failure, chronic liver failure or portosystemic shunt. The problem is that several neurotoxic compounds that are absorbed from the gut are not detoxicated by the liver and can reach the central nervous system. The cytotoxic effect on the astrocytes is a major point of the cerebral pathogenesis, which leads to the swelling of the astrocytes causing the development of brain oedema. The pathogenesis and the aetiology are not completely understood due to the complexity. In recent years, several theories have been developed about the pathomechanism. These focuses on the main actors: ammonia, gamma-aminobutyric acid, benzodiazepines and false neurotransmitter. New approaches to pathogenesis have also changed the treatment approaches. Concerning the treatment, there are several changes made especially in the dietary aspects. The exact molecular mechanism of how ammonia contributes to astrocyte swelling and so to brain oedema is not fully explained.