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Nutrition in Children


The liver plays a central role in energy and nutrient metabolism. Malnutrition is highly prevalent among patients with chronic liver disease and leads to increased morbidity and mortality rates. The main goals of providing nutritional support to these patients are multiple: to prevent further liver injury and promote liver regeneration, to slow the overall deterioration of the patient, to minimize the risk of infection, and to prevent macro and micro nutrient deficiencies and, thereby, maximize growth potential.


Energy: Patients with compensated cirrhosis do not appear to need modification of their energy intakes. Optimal nutritional therapy involves maintaining high caloric intake while preventing specific nutrient deficiencies

Protein: Patients with cirrhosis have been shown to have high protein requirements to maintain positive nitrogen balance. Recommended protein intake for cirrhotics is 1.0 – 1.5g protein/kg/day. Increased protein requirement is due to both a defect in meal-induced protein synthesis and increased protein degradation during feeding as well as fasting.

Carbohydrate: Both complex and simple carbohydrates are not restricted unless patient has insulin resistance or diabetes. For those patients, 50% – 60% of calories from carbohydrates (mainly complex carbohydrates); intake should be consistent from day to day and at each meal and snack.

Fat: Medium-chain triglyceride oil is well absorbed in patients with cholestasis; however, long-chain triglycerides should not be decreased to less than 10% of total energy intake, to prevent deficiencies in essential fatty acids. Polyunsaturated fatty acid (PUFA) deficiency is common in cirrhosis, especially alcoholic cirrhosis, because PUFA synthesis from essential fatty acid precursors occurs in the liver. PUFA deficiency is an independent predictive factor of mortality in alcoholic cirrhosis.

Fluid: If ascites is accompanied by low serum sodium levels (< 128mEq/L) restrict fluids to 1200 to 1500ml/day in severe cases (<125mEq/L) restrict fluids to 1000 to 1200ml/day.




  • Deficiencies in water-soluble vitamins (B and C) are common in alcoholic cirrhosis in particular but also occur in nonalcoholic liver disease.
  • The risks of Wernicke’s encephalopathy and Korsakoff’s dementia are well described in alcoholic and hepatitis C-related patients deficient in thiamine.
  • Fat-soluble vitamin deficiencies occur more commonly in the cholestatic liver syndromes.
  • Vitamin A (retinol) deficiency has been described in cirrhosis and is considered a risk factor for development of cancer, including hepatocellular carcinoma.
  • Vitamin E, an antioxidant, is reduced in cholestasis and alcoholic liver disease.


  • The presence of advanced chronic liver disease leads to water-electrolyte imbalances clinically characterized by ascites and peripheral edema.
  • Sodium retention plays a key role in the pathophysiology of ascites and edema formation in chronic liver disease. Dietary sodium restriction, with accurate fluid monitoring, is needed to maintain homeostasis.
  • Potassium supplementation is often required to correct the hypokalemia due to losses from diarrhea, use of diuretics, or hyperaldosteronism.
  • Low levels of trace elements such as selenium and zinc have been described in patients with chronic alcoholism is attributed to decreased intake and absorption and diuretic-induced increased urinary excretion.
  • Supplementation with zinc has been shown to improve glucose disposal in cirrhotic patients, and deficiency may contribute to the impaired glucose tolerance and diabetes commonly observed.
  • Magnesium deficiency occurs in alcoholic liver disease, and muscle magnesium is an independent predictor of muscle strength. This is probably related to the reduced content of sodium-potassium pumps in skeletal muscle that accompanies magnesium deficiency.