Nutrition in patients with liver disease

Published on 09/04/2015 by admin

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Chapter 45 NUTRITION IN PATIENTS WITH LIVER DISEASE

KEY POINTS

• Malnutrition is prevalent among patients with liver disease.
• Malnutrition is associated with higher risk of developing complications of cirrhosis.
• Malnutrition prior to transplant increases the risk of post-transplant complications such as infections and intensive care stay.
• The aetiologies of malnutrition in cirrhosis include low intake, malabsorption, medication effects, protein and salt dietary restriction, inattention to dietary intake in the hospital and possible increased requirements.
• Encourage increased oral intake, preferably in small frequent meals.
• Encephalopathy should be managed with medication while reserving protein restriction for difficult to control cases.
• Enteral feeding is feasible and as effective as parenteral nutrition (PN) in the immediate post-transplant period.
• Central obesity and insulin resistance are risk factors for the development of non-alcoholic steatohepatitis (NASH).
• Weight loss and increased physical activity improve insulin resistance and may be helpful in NASH.
• Antioxidants such as vitamin E may be helpful in NASH.
• NASH and progression to hepatic fibrosis are major complications of prolonged parenteral nutrition (PN) dependence in patients with short bowel syndrome.
• Recommendations to decrease parenteral nutrition-associated liver disease (PNALD) include avoiding overfeeding, cycling PN (12–16 hours rather than continuous) and limiting intravenous lipids to less than 1 g/kg/day.
• PNALD remains a serious complication of prolonged PN and is one of the indications for small bowel transplant in intestinal failure.

NUTRITIONAL ASSESSMENT IN CIRRHOSIS

Many of the commonly used parameters to assess nutrition are not as useful in advanced liver disease. Weight is complicated by ascites and oedema, which will mask the extent of lean and adipose tissue loss. Albumin and prealbumin levels may reflect decreased hepatic synthesis rather than malnutrition. Several techniques may be more useful in cirrhosis. Subjective global assessment (SGA) involves the assessment of several factors including weight loss during the previous 6 months, dietary intake, the presence of gastrointestinal symptoms and physical ailments that may limit intake and physical signs of malnutrition such as muscle wasting and peripheral oedema. This technique has been validated as a reliable technique for the assessment of nutritional status in cirrhosis and a useful predictor of outcome after liver transplant. Bioelectrical impedance (BIE) is a predictor of body cell mass and its validity has been confirmed in cirrhosis with and without ascites. Handgrip strength is a sensitive measurement of malnutrition and, compared with other measures (SGA and the prognostic nutritional index), is associated with the development of complications such as ascites, hepatic encephalopathy, hepatorenal syndrome and spontaneous bacterial peritonitis whereas SGA and prognostic nutritional index are not. Decreased handgrip strength prior to transplant is also associated with longer stay in the intensive care unit and more infection post transplant.

Protein–energy malnutrition

Protein–energy malnutrition (PEM) is a common problem in liver disease patients with significant loss of body cell mass and total body fat reported in all stages of liver diseases. Its prevalence increases with progression of liver disease with reported rates of 20% in patients with Child-Pugh A and 50%–60% in Child-Pugh C. The reported rate among patients awaiting liver transplant ranges between 18% and 100%. Although active alcoholism is a major risk factor for malnutrition, the prevalence may not be different among alcoholic and non-alcoholic aetiologies of liver cirrhosis.

Multiple factors may be involved in the development of PEM in advanced liver disease (Figure 45.1). Inadequate dietary intake has been described in up to 87% of patients. This may be caused by anorexia and dysgeusia, which may be related to zinc and vitamin A deficiencies. Commonly prescribed salt and protein dietary restrictions may also affect appetite. In addition, patients with large ascites may experience early satiety and abdominal pain, limiting food intake, and generalised weakness and encephalopathy may limit physical access to adequate intake. In the hospital, deficient intake is commonly iatrogenic. Malabsorption may be another factor contributing to PEM. Steatorrhoea has been reported in both cholestatic and non-cholestatic liver disease and may be caused by decreased intestinal bile salt pool, pancreatic insufficiency and bacterial overgrowth associated with impaired intestinal motility. The use of lactulose and neomycin in encephalopathy may exacerbate malabsorption. It has been suggested that increased nutritional requirement may exacerbate malnutrition in cirrhosis. However, studies comparing measured energy expenditure using indirect calorimetry and that calculated by Harris Benedict equations (Table 45.1) suggest the presence of large variability among patients with cirrhosis, with both hypermetabolism and hypometabolism equally observed in about one-third of patients (more than 20% discrepancy). Of significance, patients with increased energy expenditure experienced increased rates of morbidity and mortality. The mechanism of hypermetabolism in some cirrhotic patients may be related to infection, ascites and portal hypertension. Both the removal of ascites and the reduction of portal hypertension by transjugular intrahepatic portosystemic shunt (TIPS) have been associated with reduction of energy expenditure.

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FIGURE 45.1

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