Malnourished children are more susceptible to infection, especially sepsis, pneumonia, and gastroenteritis. Hypoglycemia is common after periods of severe fasting but may also be a sign of sepsis. Hypothermia may signify infection or, with bradycardia, may signify a decreased metabolic rate to conserve energy. Bradycardia and poor cardiac output predispose the malnourished child to heart failure, which is exacerbated by acute fluid or solute loads. Micronutrient deficiencies also can complicate malnutrition. Vitamin A and zinc deficiencies are common in the developing world and are an important cause of altered immune response and increased morbidity and mortality. Depending on the age at onset and the duration of the malnutrition, malnourished children may have permanent growth stunting (from malnutrition in utero, infancy, or adolescence) and delayed development (from malnutrition in infancy or adolescence). Environmental (social) deprivation may interact with the effects of the malnutrition to impair further development and cognitive function.
Micronutrients include vitamins and trace elements. In industrialized societies, frank clinical deficiencies are unusual in healthy children, but they can and do occur in certain high-risk circumstances. Risk factors include diets that are consistently limited in variety, especially with the exclusion of entire food groups, malabsorption syndromes, and conditions causing high physiologic requirements. Various common etiologies of vitamin and nutrient deficiency states are highlighted in Table 31-1, and characteristics of vitamin deficiencies are outlined in Table 31-2. Treatment is noted in Table 31-3.
Water-soluble vitamins are not stored in the body except for vitamin B12; intake therefore alters tissue levels. Absorption from the diet is usually high, and the compounds exchange readily between intracellular and extracellular fluids; excretion is via the urine. Water-soluble vitamins typically function as coenzymes in energy, protein, amino acid, and nucleic acid metabolism; as cosubstrates in enzymatic reactions; and as structural components.
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The principal forms of vitamin C are ascorbic acid and the oxidized form, dehydroascorbic acid. Ascorbic acid accelerateshydroxylation reactions in many biosynthetic reactions, including hydroxylation of proline in the formation of collagen. Theneeds of full-term infants for ascorbic acid and dehydroascorbicacid are calculated by estimating the availability in human milk.
A deficiency of ascorbic acid results in the clinical manifestations of scurvy. Infantile scurvy is manifested by irritability, bone tenderness with swelling, and pseudoparalysis of the legs. The disease may occur if infants are fed unsupplemented cow’s milk in the first year of life or if the diet is devoid of fruits
Vegans (strict) Protein, vitamins B12, D, riboflavin, iron
Breastfed infant Vitamins K, D
Bulimia, anorexia nervosa Electrolytes, other deficiencies
Parenteral alimentation Essential fatty acids, trace elements
Alcoholism Calories, vitamin B1, B6, folate
Malabsorption syndromes Vitamins A, D, E, K, zinc, essential fatty acids
Cholestasis Vitamins E, D, K, A, zinc, essential fatty acids
Sulfonamides Folate Phenytoin, phenobarbital Vitamins D, K, folate Mineral oil Vitamins A, D, E, K Antibiotics Vitamin K Isoniazid Vitamin B6 Antacids Iron, phosphate, calcium Digitalis Magnesium, calcium Penicillamine Vitamin B6
Transcobalamin II or intrinsic Vitamin B12 factor deficiency Other digestive enzyme Carbohydrate, fat, protein deficiencies Menkes kinky hair syndrome Copper