Hepatic Encephalopathy, from Diagnosis to Treatment in 2016

Hepatic encephalopathy (HE) is defined as neurological or neuropsychological manifestations associated with acute or chronic liver failure, and/or with portosystemic shunts. Pathophysiology of HE is still mostly unknown but many factors seem to be involved, including hyperammonaemia, systemic inflammation and blood- brain barrier permeability abnormalities. It is difficult to ascertain the diagnosis of HE, which is based on combining elements with a suggestive context. Indeed, clinical signs are not specific and complementary explorations, including ammonaemia and electroencephalogram should be mandatory if there is any doubt. Brain MRI with spectroscopy could be relevant in this setting. The onset of HE requires seeking a precipitating factor, in particular infection, gastro- intestinal bleeding, drug intake or electrolyte disorders. Specific treatments of HE are mostly non-absorbable disaccharides and rifaximine. Recently, treatments, which decrease ammonaemia, have been suggested in this indication, and seem to be effective. When HE is due to an interventional portosystemic shunt, its obstruction or calibration has to be discussed. Thus, HE in cirrhosis is now curable and hepatic transplant is not the only treatment in case of isolated neurological manifestations.