Introduction Neuropsychiatric complications are known to occur in patients with advanced cirrhosis and hemorrhage from gastroesophageal varices. This clinical picture is associated with elevated blood ammonia levels. McDermott,1 Mann,2 and Levine3 also demonstrated blood hyperammonemia following portacaval anastomosis in humans and dogs. These observations have focused attention on the pathophysiology of hepatic coma, and the possible role of ammonia toxicity has been noted by Young et al.4 and Welch, Pender, and Kiley.5 Patients with cirrhosis show a prompt rise in portal blood ammonia when protein substances or blood is digested within the gastrointestinal tract.4,5 The normal liver easily detoxifies portal blood ammonia, but the liver whose function is impaired by disease or bypassed by portal systemic shunts is unable to metabolize this product of protein breakdown. Consequently, systemic blood ammonia reaches toxic levels, and neuropsychiatric phenomena occur secondary to central nervous system effects. Ammonia