Protein-energy malnutrition (PEM) can refer to either acute or chronic malnutrition. Because children between 6 months and 5 years of age (especially at the time of weaning) are among the most acutely affected by malnutrition, assessment of this age group by physical measurement is usually done to determine PEM prevalence in a population. In general, acute malnutrition results in wasting and is assessed by an index of weight-for-height (WFH); however, edema of the extremities may also be associated with acute malnutrition, in which case a clinical assessment is necessary. Chronic malnutrition produces stunting and typically results in a diminished height-for-age index.
The prevalence of moderate to severe acute malnutrition in a random sample of children less than 5 years of age is generally a reliable indicator of this condition in a population. Because weight is more sensitive to sudden changes in food availability than height, nutritional assessments during emergencies focus on measuring WFH. Also, WFH is a more appropriate measurement foregoing monitoring of the effec-tiveness of feeding programs. As a screening measurement, the mid-upper-arm-circumference (MUAC) method may also be used to assess acute malnutrition.
PEM is a problem in many developing countries, even under normal conditions. Severe PEM is usually precipitated by low food intake associated with infection. Displaced people are particularly vulnerable to PEM. PEM has three forms, which are described below.
The most frequent form of PEM, also know as marasmus which occurs in cases of prolonged food shortage, is a severe wasting away of body fat and muscle. Affected children become very thin, may have an "old person" face, and loose folds of skin. They may appear, however, relatively active and alert. Marasmus can be confused with dehydration; very often children suffer both. Dehydrated children appear sicker, have a very rapid pulse, usually have a fever, and are usually very thirsty.
Kwashiorkor is seen most commonly in areas where the staple food is mainly carbohydrate, such as tubers and roots like cassava. Many factors other than protein defi-ciency, however, precipitate this disease. The main sign of kwashiorkor is edema, a swelling that usually starts at the lower extremities and extends in more advanced cases to the arms and face. Edema must be present for the diagnosis of kwashiorkor, but edema can also occur in other diseases. Where gross edema occurs, the child may look "fat" and be regarded by the parents as well fed. To check for edema, press the area on the back of the foot; edema is indicated if the dent remains after you remove your finger (often called pitting edema). Associated signs of kwashiorkor, which do not always occur, include hair changes (color becomes lighter, curly hair becomes straight, hair comes out easily with a gentle pull) and skin changes (dark skin may become lighter in places, skin may peel off, especially on the legs, and ulcerations may occur). Children with kwashiorkor are usually apathetic, miserable, and withdrawn, and often refuse to eat. Profound anemia is a common complication of kwashiorkor.
(3) Marasmic Kwashiorkor
Marasmic kwashiorkor is a mixed form of PEM, with edema occurring in children who are marasmic, and who may or may not have other associated signs of kwashiorkor. Mixed forms will often be seen.
In addition to PEM, micronutrient deficiencies play a key role in nutrition-related morbidity and mortality. Following are common micronutrient deficiencies.
The most common deficiency syndrome in displaced populations is caused by a lack of vitamin A. Vitamin A deficiency is also known as xerophthalmia. It can cause night blindness in early stages and permanent eye dam-age and blindness in later stages. Famine-affected and displaced populations often have low levels of dietary vitamin A intake before experiencing famine or displace-ment, and therefore may have very low vitamin A reserves. Furthermore, the typical rations provided in large-scale relief efforts lack vitamin A, putting these populations at high risk. In addition, some diarrheal dis-eases rapidly deplete vitamin A stores. Depleted vitamin A stores need to be adequately replenished during recovery from these diseases to prevent the disease from becoming worse. Vitamin A is stored in the liver, so daily doses are not necessary; after initial treatment, supplemental doses can be as much as 3 months apart.
Although scurvy rarely occurs in stable populations in developing countries, many outbreaks have occurred in displaced and famine-affected populations, primarily because of inadequate vitamin C in rations. Scurvy is marked by spongy gums, loosening of the teeth, and a bleeding into the skin and mucous membranes. Fortification of foods with vitamin C is problematic because vitamin C cannot be stored in the body. The best solution is to provide vitamin C through a variety of fresh foods, either by including them in the general ration or by promoting access to local markets. In addition, local cultivation of foods containing vitamin C foods should be encouraged. Patients with clinical scurvy should be treated with 250 mg of oral vitamin C two times a week for 3 weeks.
Pellagra is caused by a severe deficiency of biologically available niacin in the diet. This disease is endemic where people eat a maize-based diet with little protein-rich food. Pellagra is characterized by dermatitis, gastrointestinal disorders, and central nervous system problems. Treatment of maize flour with lime (which converts niacin into a biologically available form of niacin) and the inclusion of beans, peanuts (ground nuts), or fortified cereals in daily rations increases the total intake of available niacin and will prevent the development of pellagra.
Anemia is caused by a lack of hemoglobin and indicates a lack of iron in the diet. Diets that are lacking in vitamin C or are high in fiber reduce iron absorption. The condition is marked by a lack of energy. Severe anemia in a dis-placed population can be a major cause of mortality for young children and pregnant women. Treatment for ane-mia includes a daily administration of iron/foliate tablets and vitamin C. Supplementary feeding of high-risk groups with corn-soya milk (CSM) will also help reduce the like-lihood of anemia (100 g of CSM contains 18 g of iron).
Beriberi is caused by an inability to assimilate thiamine. It occurs where people have to exist on a starchy staple food such as cassava or polished white rice. Beriberi is characterized by inflammatory or degenerative changes of the nerves, digestive system, and heart. Sources of thiamine include dried peas and beans and whole-grain cereals. One major problem is that thiamine is destroyed during cooking.