Kwashiorkor

Kwashiorkor was first described in Ghana, in west Africa, in 1932 — the word is the

Ghanaian name for the condition. In addition to the wasting of muscle tissue, loss of intestinal mucosa and impaired immune responses seen in marasmus, children with kwashiorkor show a number of characteristic features which distinguish this disease:

  • Fluid retention and hence severe oedema, associated with a decreased concentration of plasma proteins. The puffiness of the limbs, due to the oedema, masks the severe wasting of arm and leg muscles.
  • Enlargement of the liver. This is due to the accumulation of abnormally large amounts of fat in the liver, to the extent that, instead of its normal reddish-brown colour, the liver is pale yellow when examined at post-mortem or during surgery. The metabolic basis for this fatty infiltration of the liver is not known. It is the enlargement of the liver that causes the paradoxical 'pot-bellied' appearance of children with kwashiorkor; together with the oedema, they appear, from a distance, to be plump, yet they are starving;
  • Characteristic changes in the texture and colour of the hair. This is most noticeable in African children; instead of tightly curled black hair, children with kwashiorkor have sparse, wispy hair, which is less curled than normal, and poorly pigmented — it is often reddish or even grey.
  • A sooty, sunburn-like skin rash.
  • A characteristic expression of deep misery.

8.5.1 Factors in the aetiology of kwashiorkor

The underlying cause of kwashiorkor is an inadequate intake of food, as is the case for marasmus. Kwashiorkor traditionally affects children aged between of 3 and 5 years. In many societies a child continues to suckle until about this age, when the next child is born. As a result, the toddler is abruptly weaned, frequently onto very unsuitable food. In some societies, children are weaned onto a dilute gruel made from whatever is the local cereal; in others the child may be fed on the water in which rice has been boiled — it may look like milk, but has little nutritional value. Sometimes the child is given little or no special treatment but has to compete with the rest of the family for its share from the stew-pot. A small child has little chance of getting an adequate meal under such conditions, especially if there is in any case not much food for the whole family.

There is no satisfactory explanation for the development of kwashiorkor rather than marasmus. At one time it was believed that it was due to a lack of protein, with a more or less adequate intake of energy. However, analysis of the diets of children suffering from kwashiorkor shows clearly that this is not so. Furthermore, children who are protein deficient have a slower rate of growth, and are therefore stunted (section 9.1.2.1); as shown in Figure 8.5, children with kwashiorkor are less stunted that those with marasmus. Finally, many of the signs of kwashiorkor, and especially the oedema, begin to improve early in treatment, when the child is still receiving a low-protein diet (section 8.5.2).

Very commonly, an infection precipitates kwashiorkor in children whose nutritional status is inadequate, even if they are not yet showing signs of malnutrition. Indeed, paediatricians in developing countries expect an outbreak of kwashiorkor a few months after an outbreak of measles.

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84.5

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w marasmus marasmic kwashiorkor kwashiorkor

Figure 8.5 Stunting of growth in kwashiorkor, marasmus and marasmic kwashiorkor.

The most likely precipitating factor is that, superimposed on general food deficiency, there is a deficiency of the antioxidant nutrients such as zinc, copper, carotene and vitamins C and E (section 7.4.3). As discussed in section 7.4.2.2, the respiratory burst in response to infection leads to the production of oxygen and halogen radicals as part of the cytotoxic action of stimulated macrophages. The added oxidant stress of an infection may well trigger the sequence of events that leads to the development of kwashiorkor.

8.5.2 rehabilitation of malnourished children

The intestinal tract of the malnourished patient is in a very poor state. This means that the child is not able to deal at all adequately with a rich diet, or a large amount of food. Rather, treatment begins with small frequent feeding of liquids — a dilute sugar solution for the first few days, followed by diluted milk, and then full-strength milk. This may be achieved by use of a nasogastric tube, so that the dilute solution can be provided at a slow and constant rate throughout the day and night. Where such luxuries are not available, the malnourished infant is fed from a teaspoon, a few drops at a time, more or less continually.

Once the patient has begun to develop a more normal intestinal mucosa (when the diarrhoea ceases), ordinary foods can gradually be introduced. Recovery is normally rapid in children, and they soon begin to grow at a normal rate.

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Responses

  • Sointu Salo
    Which of the following is not characteristic of children with kwashiorkor ?
    7 years ago

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