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GULU UNIVERSITY MEDICAL JOURNAL

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Gulu University Medical Journal (GUMJ) 2009/2010 Vol 5.<br />

Malnutrition: A main cause of children’s death!<br />

Luigi Greco, M.Sc. (MCH), M.D., D.C.H., PhD (Hon)<br />

Department of Pediatrics, University of Naples Federico II and European Laboratory for Food Induced Disease<br />

Valentina Fiorito, M.D. Department of Pediatrics, University of Naples Federico II<br />

Malnutrition is one of the greatest public health<br />

problems facing the world today because of the number<br />

of children affected and the long-term consequences.<br />

The World Health Organization (WHO) estimates<br />

that malnutrition contributes to 53% of child mortality<br />

worldwide (1-2). There is a strong association between<br />

malnutrition and mortality in developing countries<br />

because even mild degrees of malnutrition double the<br />

risk of mortality for other diseases such as respiratory<br />

tract infection, diarrhoea, pneumonia, malaria and<br />

measles (3-4) (Figure 1).<br />

Table I shows how WHO defines a patient’s nutritional<br />

status.<br />

Mild Acute Malnutrition benefits of health counselling<br />

and community mobilization.<br />

Moderate Acute Malnutrition is still manageable<br />

in community setting but needs a specific program:<br />

Supplementary Feeding Program (SFP). This program<br />

is based on Supplementary Feeding Centres (SFC) that<br />

monitor every week the patient and provide antibiotics,<br />

antihelminthics, vitamin A and high energy fortified<br />

supplementary food like Ready–to-Use Therapeutic<br />

Food (RUFT).<br />

Severely malnourished children and infants less then<br />

6 months old with specific features (Wt < 4Kg, Wt/<br />

Length< 85% and not able to suckle/not fed on<br />

breast-milk, mother died or mother has no or little<br />

milk or presence of oedema) have to be admitted in<br />

a Therapeutic Feeding Centre (TFC). In this centre<br />

they are managed, according to a specific Therapeutic<br />

Feeding Program (TFP).<br />

Almost all severely malnourished children have<br />

infections, impaired liver and intestinal function, and<br />

problems related to imbalance of electrolytes when<br />

first admitted to hospital. Because of these problems,<br />

they are unable to tolerate the usual amounts of dietary<br />

protein, fat and sodium. It is important, therefore, that<br />

children begin feeding on a diet that is low in these<br />

nutrients, and high in carbohydrate.<br />

To this purpose UNICEF and WHO prepared two<br />

formula diets based on the Modified Cow’s Milk F75<br />

(starter 75 KCal/100 ml) and F100 (follow up 100<br />

KCal/100ml).<br />

These milks are given, in proportion of the body<br />

weight, at 3 hourly intervals. F75 has a moderate<br />

protein and energy content and is given in the early<br />

phase of severe malnutrition, F100 has a higher energy<br />

and protein content and is useful for maintenance. The<br />

milks have to be given frequently and in small amounts<br />

to avoid overloading the intestine, liver and kidneys.<br />

Children unable to drink are fed by plastic syringes<br />

and nasogastric tube. The theoretical daily supply of<br />

energy is 140 to 200 Calories/kg body weight. But<br />

this amount is very difficult to administer to any single<br />

child. Night feeds are generally not available.<br />

Table II shows the composition of the two milk feeds:<br />

F75 starter, to be given for the first few days and F100<br />

for follow up. From the table is clear that the feeds<br />

are based on skimmed milk with added sugar and<br />

vegetable oil.<br />

The mineral mix with potassium, magnesium and<br />

other essential minerals must be added to the diet. The<br />

potassium deficit, present in all malnourished children,<br />

adversely affects cardiac function and gastric emptying.<br />

Magnesium is essential for potassium to enter cells and<br />

be retained. The mineral mix does not contain iron as<br />

this is withheld during the initial phase.<br />

Unfortunately about 95.4% of African children have<br />

the C/C- 13910 genotype of the lactase-Y-phlorizin-<br />

hydrolase gene that causes adult-type hypolactasia (vs<br />

14.5% of Finnish children). The decline of the lactase<br />

activity in African children occurred earlier than<br />

Finnish children, as 30% of the children already had<br />

low levels of lactase (< 10 U/g protein) at the age of<br />

five years (9).<br />

Gulu University Medical Students’ Association (GUMSA) Passion for life 13

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