Treatment of hepatic coma has evolved into a well-defined, if not always successful, regimen. The use of protein restriction, high carbohydrate diet, neomycin, and fluid and electrolyte replacement is standard therapy. 1-4 However, in those patients not responsive to this regimen, other approaches have been sought. These include hemodialysis, perfusion of the patient's blood through animal (porcine) liver, liver transplants, corticosteroids, urease immunization, and many others. Unfortunately most of these regimens have met with only limited success. More recently, total exchange blood transfusions have been added to this list. To date, no single toxic substance has been proven to be responsible for all cases of hepatic encephalopathy. Rather it is believed that a variety of nitrogenous compounds produced as metabolic by-products in the catabolism of proteins and amino acids are incompletely removed or detoxified by a previously diseased liver. These subsequently produce a suppression of cerebral function resulting ultimately in