Chronic hepatic encephalopathy

A review is presented of chronic hepatic encephalopathy, particularly its treatment. The exact cerebral toxin or group of toxins in hepatic encephalopathy is uncertain. However, major candidate toxins include ammonia, the amino acid methionine, short chain fatty acids and beta hydroxylated biogenic amines, and the encephalopathy probably results from the interaction of several of these toxins. Gastrointestinal hemorrhage, excessive dietary protein, azotemia, anesthesia, surgery, infections, constipation and the use of diuretics, sedatives, tranquilizers or analgesics are the precipitating factors for promoting hepatic encephalopathy. As established therapy, dietary protein restriction, gut cleansing and bowel sterilization are usually effective. The relatively nonabsorbable antibiotic neomycin is commonly given orally or by rectum for bowel sterilization. However, because of the potential risk of long term administration of neomycin, the synthetic disaccharide lactulose has been widely used recently in chronic hepatic encephalopathy. Increased gut motility due to a distended gas filled colon and lowering of stool pH into an acid range are thought to be major actions of lactulose. This agent, which is usually given orally but can be given by enema, appears to be more effective than neomycin from a multi center double blind study. The use of L dopa for displacement of the false neurochemical transmitters, colonic exclusion for removal of almost all the intestinal bacteria or the administration of ketoanalogue of essential amino acids which combine with labile nitrogen have all not yet provided conclusive evidence that these agents are beneficial. Patients who received portacaval shunt have more severe and more frequent encephalopathy than non shunted patients. (Tanikawa - Kurume)