The diagnosis of SAM is obvious in its most severe forms. In mild to moderate forms, the usual approach is to compare the body weight for a given height against standard tables; other helpful parameters are fat stores, muscle mass, and levels of certain serum proteins. With a loss of fat, measured skinfold thickness (which includes skin and subcutaneous tissue) is reduced. If the somatic protein compartment is catabolized, the resultant reduction in muscle mass is reflected by reduced circumference of the midarm. Measurement of serum proteins (albumin, transferrin, and others) provides an estimate of the adequacy of the visceral protein compartment. Recent studies suggest a role for the gut microbiome in the pathogenesis of SAM. There is a substantial difference in the microbial flora of children with SAM when compared with the gut microbiome of normal children. It seems that the alterations in the microbiome are not merely the consequences of SAM but play a role in their causation.
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Fig. 8.17 Childhoodmalnutrition.(A)Marasmus.Notethelossofmusclemassandsubcutaneousfat;theheadappearstobetoolargefortheemaciatedbody.(B)Kwashiorkor.Theinfantshowsgeneralizededema,seenasascitesandpuffinessoftheface,hands,andlegs.(A, From Clinic Barak, Reisebericht Kenya.)
Marasmus develops when the diet is severely lacking in calories (
Fig. 8.17A ). A marasmic child suffers growth retardation and loss of muscle mass as a result of catabolism and depletion of the somatic protein compartment. This seems to be an adaptive response that provides the body with amino acids as a source of energy. Of interest, the visceral protein compartment, which presumably is more critical for survival, is depleted only marginally, so serum albumin levels are either normal or only slightly reduced.
In addition to muscle proteins, subcutaneous fat is also mobilized and used as fuel. Leptin (discussed later under “Obesity”) production is low, which may stimulate the hypothalamic-pituitary-adrenal axis to produce the high levels of cortisol that contribute to lipolysis. With such losses of muscle and subcutaneous fat, the extremities are emaciated; by comparison, the head appears too large for the body. Anemia and manifestations of multivitamin deficiencies are present, and there is evidence of immune deficiency, particularly of T-cell–mediated immunity. Hence, concurrent infections are usually present, which impose an additional stress on an already weakened body.
Kwashiorkor occurs when protein deprivation is relatively greater than the reduction in total calories (
Fig.
8.17B ). This is the most common form of SAM seen in African children who have been weaned too early and subsequently fed, almost exclusively, a carbohydrate diet (the name kwashiorkor, from the Ga language in Ghana, describes the illness in a baby that appears after the arrival of another child). The prevalence of kwashiorkor also is high in impoverished countries of Southeast Asia. Less severe forms may occur worldwide in persons with chronic diarrheal states, in which protein is not absorbed, or in those with chronic protein loss (e.g., protein-losing enteropathies, the nephrotic syndrome, or the aftermath of extensive burns). Rare cases of kwashiorkor resulting from fad diets or replacement of milk by rice-based beverages have been reported in the United States.
In kwashiorkor, unlike in marasmus, marked protein deprivation is associated with severe loss of the visceral protein compartment, and the resultant hypoalbuminemia gives rise to generalized or dependent edema (
Fig. 8.17 ). The weight of children with severe kwashiorkor typically is 60% to 80% of normal. However, the true loss of weight is masked by the increased fluid retention (edema). In further contrast with marasmus, there is relative sparing of subcutaneous fat and muscle mass. The modest loss of these compartments may also be masked by edema.