ABSTRACT
Nutritional factors play a major role both in the pathogenesis as well as management of hepatic encephalopathy (HE). Physicians treating patients with chronic liver disease often restrict the intake of dietary protein to prevent a rise in blood ammonia levels. The role of protein restriction in patients with chronic hepatic encephalopathy (CHE) has been questioned recently as the efficacy of protein withdrawal in patients with CHE has never been subjected to a controlled trial. Evidence suggests that protein intake plays only a limited role in precipitating encephalopathy. In fact, measures taken to suppress endogenous protein breakdown are more effective than dietary restrictions in reducing the load of amino acids on the decompensated liver. A protein intake of less than 40 g per day, as has been indicated, contributes to a negative nitrogen balance, which along with increased endogenous protein breakdown, worsens encephalopathy. A positive nitrogen balance may have positive effects on encephalopathy. Rather, depressed plasma branched-chain amino acid (BCAA) levels, implicated in the pathogenesis of HE, also supervene in cirrhosis only when malnutrition is present as well. Therefore, the emphasis in the nutritional management of patients with HE should not be on the reduction of protein intake. Instead, the goal should be to promote synthesis by making available ample amounts of amino acids, while instituting other measures to reverse the ongoing catabolism. Different protein sources have varying effects on HE and efforts should be made to identify the most tolerated protein source to prevent malnutrition and maintain these patients on a long-term basis.