Clinical Manifestations and Pathology

In the earliest stages of PEM, the child simply appears smaller than he or she should be for that age. If the condition deteriorates further, however, clinical symptoms will begin to emerge. Although the mix is likely to be complex, for ease of description the symptoms are still best portrayed as those char-acterstics of either kwashiorkor or marasmus.

The edema that defines all cases of kwashiorkor varies. It can be mild and localized on the extremities and sacrum or more severe and general. Although muscle wasting is discernible, subcutaneous fat is usually retained, and consequently the child takes on a bloated appearance, known as the "sugar baby" look in the West Indies. There also tends to be some growth retardation in head length and circumference.

More often than not there are skin changes, including ulcerating areas, open and healed sores, scabies, and a condition known as "flaky-paint dermatosis," in which removal of the flakes reveals lighter patches of skin. When kwashiorkor persists, the hair begins to be affected; it loses its luster, and dark hair becomes lighter. Curly hair straightens, and eventually the hair becomes brittle and falls out, leaving bare areas of scalp clearly visible.

Upon examination, the liver and spleen frequently are found to be enlarged, and a range of other symptoms have been documented. Among the more common are anemia and vitamin A deficiency, with some vision impairment, a range of micro-nutrient deficiencies, plus tendencies to hypothermia, higher bilirubin, hyponatremia, hypoglycemia, and very low plasma albumin.

Behavioral changes are quite marked. Vomiting and diarrhea become persistent; without resolution, anorexia usually sets in. As the child's strength wanes, motor skills regress, and eventually he or she becomes almost totally apathetic to external stimuli. It is as if the burden of life has become too great to bear. Because of this withdrawal, treatment is difficult outside of a clinical setting where the child can be fed intravenously.

The overt symptoms of classical marasmus are far fewer and less medically unusual. There is extreme wasting of both muscles and subcutaneous tissues, and stunting is quite marked. Because the victim is so emaciated, the head appears abnormally large, especially the eyes. The skin tends to be dry and patchy, but dermatosis is not seen, nor are there any significant hair changes. Anorexia is uncommon, and, in fact, the appetite is usually good, which helps to simplify therapy. As in kwashiorkor, there is likely to be hypothermia and a tendency to hypoglycemia. Dehydration is a problem as marasmus worsens, and behavior changes from being fretful and highly irritable to a semicomatose state that immediately precedes death.

With severe PEM, mortality is high - over 20 percent. It is seldom, however, that starvation is the final cause of death; rather it is one or more of the infections that brought on the condition, and these usually run their fatal course in just a few days. Although there is some debate among authorities, the onset of hypothermia and hypoglycemia probably signals the need for immediate treatment.

For those children who have suffered mild-to-moderate PEM or who have recovered from one of the clinical syndromes, the question of long-term effects remains. The available evidence does support a relationship between chronic PEM and some permanent stunting, but this by itself cannot be considered a serious impairment to performance later in life. Indeed, stunting can be viewed as an adaptation to food shortages that conserves energy supplies. Nevertheless, there is one possible impact on skeletal development that does have serious repercussions. In areas where chronic PEM is prevalent, there also appears to be a high incidence of cephalo-pelvic disproportion among women, a condition that leads to birth difficulties, notably miscarriages, stillbirths, and heightened maternal mortality. The theory is that PEM somehow interferes with calcium metabolism, thereby producing incomplete pelvic development, but this has yet to be proven conclusively. Although the data are even less adequate, there is also some suggestion that later-aged cardiovascular, liver, and pancreas diseases might somehow be connected with childhood PEM.

The issue that has stimulated the most interest and controversy, however, is the effect of PEM on the brain. A considerable amount of research has shown that subnormal mental and psychomotor functioning tends to follow PEM, and during the 1960s and 1970s it was common for direct causal connections to be made. Some investigators even hypothesized that severe attacks of PEM resulted in permanent mental disabilities. But once again important reassessments have been forthcoming. The earlier tests generally failed to control for the learning environment of their subjects, and thus to sort out all the other factors that might be contributing to poor performance, such as reduced mother-child interaction and a lack of stimulating surroundings upon which the child could act in order to learn. This illustrates yet another dimension of the "total deprivation" that surrounds PEM. Currently, the prevailing view is that neither mild-to-moderate nor acute clinical PEM seems to be associated with long-term intellectual and psychological disabilities, assuming, of course, that the necessary social interventions are made. The matter of permanent injury caused by chronic PEM, notably of the marasmic variety during the first year of life, however, remains unresolved. There may very well be irreversible brain damage in the more serious of these cases, as is strongly suggested by research on laboratory animals.

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