Two important manifestations of chronic liver disease, ascites and portal-systemic encephalopathy, can be effectively treated with dietary modifications. The prime dietary objective in the treatment of ascites is sodium restriction. Some authorities have recommended restriction of dietary sodium intake to as little as 10-20 mmol/day for patients with symptomatic, large-volume ascites. However, it is almost impossible to design a palatable diet or provide sufficient protein to maintain nitrogen balance with such stringent restrictions, and therefore these will not be satisfactory for long-term use. Well-motivated patients can often be maintained on a 40 mmol sodium diet (equivalent to about 1 g of sodium or 2.5 g of sodium chloride).

The treatment of portal-systemic encephalopathy includes dietary protein restriction. Management will obviously need to be individualized for patients with fulminant hepatic failure or stage IV coma, but patients with chronic liver disease and mild to moderate encephalopathy should usually have dietary protein intake restricted to 0.5-0.8 g/kg body weight. Even more rigorous restriction may be necessary to control encephalopathy in the short term, but is difficult to maintain for prolonged periods because of limited patient compliance and negative nitrogen balance. It is believed that vegetable protein may be less ammoniagenic than meat, but part of this may relate to decreased efficiency of absorption of vegetable protein. Disproportionately high levels of aromatic amino acids are found in plasma of patients with decompensated cirrhosis. Hence, nutritional supplements rich in branched-chain amino acids have been advocated; however, unequivocal evidence for their efficacy is lacking.

Patients with advanced cirrhosis often have hepatic glycogen depletion. During fasting, glucagon and catecholamines will be released to maintain blood glucose levels. In the absence of hepatic glycogen stores, this requires gluconeogenesis, and the substrate is provided to a significant extent from muscle catabolism. Utilization of the amino acids for gluconeogenesis will lead to ammonia production. It is not known whether dietary manipulations designed to provide a continuous supply of glucose, and therefore to reduce gluconeogenesis, would improve the hyperammonemia in these individuals. Cholestatic liver diseases, including primary biliary cirrhosis (PBC), secondary biliary cirrhosis, sclerosing cholangitis and biliary atresia, may be accompanied by malabsorption of fat-soluble vitamins. Vitamin K deficiency can be easily confirmed with the demonstration of a prolonged prothrombin time that corrects with administration of parenteral vitamin K. Assays for vitamins D, A and E are generally available only in specialized laboratories. If confirmatory tests are not available and if there are strong clinical grounds for suspecting a deficiency state, appropriate replacement therapy should be initiated. Table 8 lists a number of hereditary liver diseases for which appropriate therapy includes specific dietary interventions.