Nutrition and Hepatic Encephalopathy

Abstract

Hepatic encephalopathy (HE) is a severe neuropsychiatric complication occurring both in acute and chronic liver failure. Among patients with cirrhosis, HE is most frequent in patients with advanced liver disease. The restriction of protein intake has long been considered useful in the treatment of such a complication, despite the risk of a worsening in nutritional status. Protein-calorie malnutrition (PCM) is in fact widely recognized to be a frequent finding in cirrhotic patients and to adversely affect the patients’ outcome.

Previous data have shown that protein restriction may increase muscle catabolism and, as a consequence, the release of amino acids, with an elevation in serum ammonia concentration and worsening of HE. The muscle tissue may also play a role in ammonia detoxification, suggesting that protein restriction, by inducing protein malnutrition, may be a contributor of HE instead of an aid in the treatment of this complication. European nutritional guidelines have suggested higher protein requirements in cirrhotic patients and the presence of HE has not been considered a reason to decrease the protein content in the diet. In light of these data, together with the evidence of the safety of a normal protein diet even during acute episodes of HE, much attention has been given to nutritional support in these patients. Multiple meals to shorten the fasting periods have been shown to improve nitrogen economy. When the patient is unable to obtain an adequate nutrient intake, oral supplementation may be used and, if needed, enteral tube feeding or parenteral nutrition is recommended. To improve protein tolerance, vegetable protein-based diets or oral branched-chain amino acid supplementation have been proposed. Branched-chain amino acids have been shown to exert a beneficial effect as they stimulate protein synthesis, secretion of hepatocyte growth factor, and inhibit proteolysis.