Introduction
Chronic liver disease (CLD) occupies a major portion in pediatric gastrointestinal diseases. Around two third pediatric populations with CLD awaiting liver transplantation are malnourished.1There is a to and fro interaction between CLD and malnutrition. Majority of children with CLD are often malnutrition, and malnutrition adversely affects the course of liver disease1. Nutritional deficiencies are frequently noted in children with CLD, particularly in cholestatic liver disease and onset is in infancy period2,3. It has been demonstrated in many studies that malnutrition is an independent risk factor for poor outcome of CLD, which lead to the emergence of many severe complications in patients with cirrhosis, such as ascites, hepatic encephalopathy and various infections4. An imbalance between nutritional intake and nutrient requirement can adversely affect and lead to metabolic abnormalities, physiological changes, reduces organ and tissue function, and loss of body mass5. Protein and energy intake may be inadequate because of multiple factors such as anorexia, early satiety (caused by impingement upon viscera by enlarged liver, spleen or ascites) recurrent infections. Malabsorption of dietary fat due to impaired bile flow is also observed in many children with CLD6,7. In addition, alteration in amino acid metabolism8, 9 and increased energy requirements due to disease process and many other factors10 may contribute to suboptimal energy and nitrogen balance. These nutritional imbalances are thought to be secondary to the interaction between factors such as reduced energy intake, lipid and fat-soluble vitamins malabsorption, increased energy expenditure, altered intermediate metabolism, hormonal dysregulation and chronic anemia related to hypersplenism and portal hypertension.11,12,13,14
Regarding laboratory parameters, which are markers of nutritional status, such albumin and prealbumin could be low because of low levels of synthesis, rather than because of poor nutritional status. So, their levels may not reflect true nutritional status.
Weight for height more useful as it assesses weight in relation to current stature. It might be more accurate as it can assess weather wasting, stunting or both have occurred and it is also age independent parameter to assess nutritional status in children. Other important parameter is body mass index (BMI), a very important index of nutritional status, may also be overvalued in patients with edema and ascites because fluid in form of ascites and edema will reflect as falsely extra body weight. Intelligent and analytical interpretation of nutritional data using these techniques in the presence of these complications is therefore required. Generally accepted methods for assessment of the clinical status and severity of disease in cirrhotic patients are the Child-Pugh-Turcotte classification15. The uses of anthropometric parameters that are not affected by the presence of ascites or peripheral edema are mid-arm muscle circumference (MAMC), mid-arm circumference (MAC), and triceps skin fold thickness (TSF). Subcutaneous fat is approximately (50%) of body fat stores, therefore measuring subcutaneous fat would reflect total body fat (TBF)16. Diagnosis of malnutrition is established by values of MAMC and/or TST17. By measuring TSF and MAC it enables arm muscle area (AMA) and arm fat area (AFA) to be calculated. AMA reflects calorie intake and muscle mass and is sensitive to changes in nutritional status18. Skinfold thickness is not useful in infants less than three months because of variations in fluid compartments.
Dual-energy X-ray absorptiometry (DEXA) is an indirect, low radiation exposure of bone mineral content or bone mineral density. It uses the same assumptions as the body compartment approach of assessment, that is, Soft tissue = bodyweight − skeletal mass and soft tissue = fat + water equivalent tissue.
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It also assumes soft tissue-overlying bone cannot be sampled and its composition has to be extrapolated from the composition of adjacent tissue. Bone mass, FFM and fat body mass (FBM) can be determined with a 2–3% precision in adults (5% in newborns). The comfort of use, very less radiation exposure and ability to obtain bone mineral content makes this method very useful19.The availability of report of DEXA is instant so no time spent in getting report.
Detailed nutritional status assessment should be done at the time of diagnosis of CLD by a trained dietician/nutritionist and subsequently while on nutritional rehabilitation20. Serial measurement of nutritional status can guide and confirm the effects of successful nutritional therapy. Till date there are scarcity of literature on nutritional assessment of children with CLD. We have prospectively evaluated the usefulness of various nutritional assessment techniques to find out magnitude and type of malnutrition present in children with CLD.We also correlated the anthropometric, biochemical and whole body DEXA scan parameters.
Discussion
We found that nearly half of the patients had chronic malnutrition, and in many of them it was compounded by superadded acute malnutrition. Under nutrition and stunting is explainable on the basis of primary disease process and reduced oral intake leading to inadequate calories. More than two third of children had low caloric intake, which may be due to various factors, i.e. chronic disease process leading to anorexia, easy satiety due to extrinsic compression of stomach by organomegaly and ascites. Muscle wasting was more prominent in younger age group (1-5 years) children indicating that this subset children is more vulnerable to morbidity and complications. As expected, children with ascites have more protein depleting parameters. This also indicates that there is more severe catabolic state in ascetic form of CLD patients. Both low serum albumin and total proteins values reflect poor synthetic functions of the liver in the majority of disease process is advanced.
The whole body DEXA scan reveals that total body fat was less affected as compared to muscle mass, because CLD patients have higher catabolic state that leads to protein utilization as energy source leading to protein depletion and sparing of fat. Only few children have low bone mineral density content might suggesting that Vitamin D3 metabolism is least affected in children with chronic liver disease.
Conclusion
Majority of children with CLD were malnourished. Children below 5 years were more affected compared to older children. Bone metabolism was less affected in children with CLD.Early detection of malnutrition and early specific and therapeutic nutritional intervention is the key point in the nutritional management of CLD.
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