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.