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Energy requirements are highly variable among patients with liver disease [9] depending on body composition (fat vs. muscle), current

Table 4.5

Dietary Considerations for Adult Patients with End-Stage Liver Disease

Symptom

Nutrition recommendations

Cachexia

Encephalopathy

Ascites and edema

Hyponatremia

• Provide at least 120% of estimated energy expenditure

• Provide increased calories if malabsorption or malnutrition is present

• Offer small, frequent meals of calorie-dense foods

• Maximize medical therapy (e.g., lactulose, neomycin)

• Identify and treat cause(s) of acute bouts encephalopathy (e.g., variceal bleed, infection, electrolyte imbalance, sedatives, constipation, etc.)

• Supplement with zinc if deficiency is suspected

• Provide adequate calories to prevent catabolism of endogenous protein stores

• Limit sodium (restriction below 2 g/day may result in inadequate calorie and protein intake)

• Supplement protein if patient is undergoing frequent paracenteses

• If hyponatremia is due to excess fluid, restrict fluid to 1,000-1,500 ml/day

• If hyponatremia is due to sodium deficiency, supplement sodium cautiously

• Institute carbohydrate-controlled meal plan

• Treat with insulin or oral hypoglycemic agent as needed

• Provide frequent meals or snacks containing carbohydrate and protein

• Infuse intravenous dextrose if needed

• Restrict dietary fat; if diarrhea does not resolve or if restriction causes poor dietary intake, discontinue fat restriction

• Try medium-chain triglyceride supplementation

• Consider pancreatic insufficiency as a potential cause of steatorrhea

• Check fat-soluble vitamin levels and supplement if needed

• Maintain an appropriate weight

• Encourage intake of a well-balanced diet with a wide variety of food choices

• Provide enough protein to maintain muscle mass

• Provide 1,500 mg of calcium per day via diet and/or supplements

• Provide enough vitamin D via diet and/or supplementation (may need water-miscible form)

• Monitor for the development of steatorrhea and adjust the diet as needed to minimize nutrient losses

• Avoid alcohol

• Consider need for bone-rebuilding medications

Adapted with permission from Hasse J, Weseman B, Fuhrman MP, et al. Nutrition therapy for end-stage liver disease: a practical approach. Support Line 1997;19:8-15.

medical state, presence or absence of ascites and activity level. Measured energy expenditure of patients with cirrhosis has been shown in some studies to be similar to expenditure of controls [14, 31]. At least one study suggested that only a percentage (about one third) of patients with cirrhosis is hypermetabolic; others are normometabolic [32]. Other studies also reported no significant increase in REE, but found inverse relationships between energy expenditure and liver disease severity [33, 34]. Greco et al. [35], however, reported increased 24-h energy expenditure in ten male patients with Child B cirrhosis. Two studies reported that REE increased at 3 or 6 and 12 months after placement of a TIPS [15, 18]. The increase could have been due to an increase in lean body mass. Because of the variability of these findings, indirect calorimetry is recommended to determine caloric needs in patients in whom accurate caloric delivery is necessary [36]. In the absence of that technology, clinicians generally recommend 25

Hyperglycemia Hypoglycemia

Steatorrhea Osteopenia to 40 kcal/kg estimated dry weight depending on the current medical condition as well as the degree of liver and nutrition decompensation [13].

Fat is a preferred fuel in liver failure [14, 33, 37]. The preference for alternate fuels is due, in part, to alterations in insulin, glucagon, cortisol and epinephrine levels. Despite the preference toward fat as fuel, there is an impairment of triglyceride oxidation, and fat can deposit in the liver. Insulin resistance occurs frequently in patients with liver failure due to alcohol ingestion [2] and viral hepatitis. Insulin resistance impairs glucose uptake in the muscle cells; glycogen production is reduced resulting in reduced energy stores [2]. With severe liver impairment, storage of glycogen can be limited.

On the other hand, as many as two-thirds of individuals with cirrhosis have hyperglycemia. This can be caused by hyperinsulinism and insulin resistance in peripheral tissues [37]. Increased insulin production and reduced hepatic clearance or portosystemic shunting of insulin released from the liver can also contribute to insulin resistance [39]. An earlier section discussed insulin resistance as it relates to metabolic syndrome and NAFLD.

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