HEPATIC encephalopathy continues to present a serious complication in patients following portasystemic shunt. It results from multiple metabolic derangements in patients with chronic liver disease and hepatocellular damage and is related to a disturbance of ammonia metabolism. It has been extensively studied by Sherlock and associates,1 McDermott,2 Zuidema and associates,3 and others. Although other toxic substances have been implicated, the most commonly found metabolic product of protein metabolism that is indictable in its genesis is ammonia.
Our current concepts of management are oriented in attempts to limit exogenous sources of proteins and inhibition of bacterial decomposition in the colon with antibiotics. In addition, other methods of treatment of encephalopathy and ammonia intoxication have consisted of use of cation exchange resin, amino acid therapy with glutamic acid, and arginine, hemodialysis, isolated liver perfusion, total blood exchange and replacement, and finally colectomy or colon exclusion. In spite of vigorous