Clinical manifestations of protein-energy malnutrition range from mild growth retardation and weight loss to a number of distinct clinical syndromes. In the developing world, children manifest marasmus and kwashiorkor. In industrialized nations, clinical manifestations of secondary protein-energy malnutrition are affected by the patient's nutritional status prior to illness, illness resulting in the protein and energy deficiency, and degree of the deficiency.
Progressive wasting that begins with weight loss and proceeds to more severe cachexia typically develops in most patients with marasmus-like secondary protein-energy malnutrition. In the most severe form of this disorder, most body fat stores disappear and muscle mass decreases, most noticeably in the temporalis and interosseous muscles. Laboratory studies may be unremarkable-serum albumin, for example, may be normal or slightly decreased, rarely decreasing to less than 2.8 g/dL (28 g/L) . In contrast, owing to its rapidity of onset, kwashiorkor -like secondary proteinenergy malnutrition may develop in patients with normal subcutaneous fat and muscle mass or, if the patient is obese, even in patients with excess fat and muscle. The serum protein level, however, typically declines and the serum albumin is often less than 2.8 g/dL (28 g/L) . Dependent edema, ascites, or anasarca may develop. As with primary protein-energy malnutrition, combinations of the marasmus-like and kwashiorkor-like syndromes can occur simultaneously, typically in patients with progressive chronic disease in whom a superimposed acute illness develops.
- What is the difference between "kwashiorkor" and "marasmus"?
- What is the best treatment of severe protein-energy malnutrition?