In acute starvation, the nervous system sustains itself first on glucose derived from alanine, then on ketone bodies from the breakdown of fats. This process continues until fat is depleted, and then catabolism returns to visceral proteins. Death results from cardiac muscle resorption and eventual cardiac failure. In chronic PEM, the nervous system adapts poorly, and a retarded rate of brain growth, hypomyelination, and slowed conduction velocities of peripheral nerves results.
Chronic PEM has traditionally been a disease of the Third World, particularly Africa and Asia. In industrialized countries, it is seen in young children in poverty, the elderly, alcoholics, or in children born to malnourished mothers. PEM also occurs in hospitalized elderly, particularly those suffering from sepsis, burns, or other serious illnesses that preclude a normal diet. Up to 27 percent of hospitalized elderly develop PEM during their hospital stay, with an associated increased risk of mental status changes, depression, and prolonged length of stay. [7 In patients with third-degree burns, up to 500 g of muscle may be lost in a day, and death from malnutrition may occur in 2 to 3 weeks.
Traditionally, PEM has been viewed as either a primary protein deficiency (kwashiorkor), or an energy deficiency (marasmus). Kwashiorkor occurs in children older than 18 months and is often associated with diarrheal illnesses or other infectious diseases. Owing to the severe protein deficiency, circulating serum proteins are inadequate to maintain normal oncotic pressure, leading to marked peripheral edema. Marasmus occurs in children younger than 1 year of age and is not accompanied by edema. PEM may cause mental changes, including apathy and irritability, muscle wasting, generalized weakness, hypotonia, hyporeflexia, and gait impairment. Following a return to a normal diet, an acute encephalopathy has been described in some patients with PEM marked by rigidity, tremors, asterixis, and mental confusion.y , y Infectious diseases may precipitate kwashiorkor in a patient with borderline malnutrition. PEM needs to be distinguished from other wasting conditions and edematous states such as thiamine deficiency, HIV infection, and the cachexia of malignancy.
The patient's nutritional status should be assessed by a careful dietary history. Energy malnutrition is defined as a 10 percent loss of ideal body weight. M Protein malnutrition requires assessment of serum proteins, including albumin, prealbumin, and total lymphocyte count. Because asterixis may be seen in some patients recovering from kwashiorkor and mistaken for hepatic encephalopathy, measurement of serum ammonia is often helpful to exclude this diagnosis.
Nutritious food and vitamin supplements generally lead to a complete recovery. Whether PEM results in long-term growth retardation and delayed intellectual development is controversial. y This condition is best prevented by education of affected family members on proper nutrition. In the United States, hospitalized elderly are perhaps at the greatest risk for PEM, and nutritional assessments of all patients at risk should be undertaken at admission to prevent serious malnutrition and to reduce the incidence of morbidity and mortality.
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