Encephalopathy Treatment

Encephalopathy Treatment

TREATMENT OF PRECIPITATING CAUSES It is important to recognize that hepatic encephalopathy, acute and chronic, is reversible and that a precipitating cause rather than worsening of hepatocellular function can be identified in the majority of patients. In one classic study, over 80 percent of 100 cases were attributable to such factors as gastrointestinal bleeding, increased protein intake, hypokalemic alkalosis, infection, and constipation (all of which increase arterial ammonia levels), or to hypoxia and the use of sedatives and tranquilizers (show table 3) [3]. Patients with advanced cirrhosis may be particularly sensitive to benzodiazepines because of an increased concentration of benzodiazepine receptor ligands in the brain (see Treatments based upon the GABA hypothesis" below).
Treatment of precipitating events is typically associated with a prompt and permanent improvement of hepatic encephalopathy. As a result, every attempt should be made to identify such precipitating events while instituting therapy with the specific agents described below
TREATMENTS BASED UPON THE AMMONIA HYPOTHESIS The gastrointestinal tract is the primary source of ammonia, which enters the circulation via the portal vein. Ammonia is produced by enterocytes from glutamine and by colonic bacterial catabolism of nitrogenous sources such as ingested protein and secreted urea. The intact liver clears almost all of the portal vein ammonia, converting it into glutamine and preventing entry into the systemic circulation. Elevations of ammonia are detected in 60 to 80 percent of patients with hepatic encephalopathy and therapy aimed at reduction of the circulating ammonia level usually results in resolution of the encephalopathy. (See "Pathogenesis of hepatic encephalopathy"). Treatment is aimed at either reducing or inhibiting intestinal ammonia production or increasing the removal of ammonia.