Anemia is common in young children. It has many causes but nutritional deficiencies, i.e., inadequate nutrient intakes and anemia secondary to disease processes, explain much childhood anemia. Acceptable hemoglobin levels in children are lower on average than in adults. The World Health Organization (WHO) accepted lower limit of normal hemoglobin is 110gl-1 for children 1-6 years old and 120gl-1 for those over 6 years. Infants are born with relatively high hemoglobin levels which, whilst appropriate for the low oxygen tensions of intrau-terine life, are unnecessary for postnatal life. The bone marrow therefore becomes quiescent and hemoglobin levels fall. Although erythropoeisis increases again after about 2 months of postnatal life, hemoglobin levels remain lower than in adults for most of childhood perhaps partly because ery-thropoeisis cannot keep up with the rapid expansion of the blood compartment as body size increases.
Nutritional anemia is most commonly due to iron deficiency. Table 3 outlines some causes of iron deficiency. Iron absorption from foods other than breast milk is never very efficient although deficiency increases the proportion of iron absorbed from the
Table 3 Some causes of iron deficiency in children Categorization of problem Causative condition
Too little iron ingested
Too much iron lost from body
Failure to absorb
Failure to utilize
Diet poor in meats, dark green leaves, iron-fortified cereals Anorexia and low iron intakes Hemorrhage from any cause if severe or chronic Insidious intestinal blood loss, e.g., cows' milk protein intolerance Crohn's disease
Vegetarian diets where no heme iron in diet Low fruit and vegetable intake so ferric iron not reduced in stomach by dietary vitamin C Lack of gastric acid: achlorhydria Pyrexia reducing absorption Malabsorption involving jejunum and upper ileum, e.g., celiac syndrome Deficiency of other essential nutrients for formation of hemoglobin, e.g., vitamin A, riboflavin Chronic inflammatory conditions After blood loss In rapid catch up growth jejunum. Absorption of iron in heme from meat is more efficient than as inorganic ferrous or ferric iron. Thus, vegetarian diets present increased risk of iron deficiency. However, most diets, even in affluent westernized countries, are marginal in the amount of iron in relation to population needs. All children are at risk of developing iron deficiency with minor disturbances in dietary quality, iron absorption and metabolism, or with blood loss. Iron absorption takes place in the jejunum and upper ileum so conditions such as gluten-sensitive enteropathy (celiac syndrome), where the brunt of intestinal damage is in the jejunum and upper ileum, may present as severe iron deficiency. Reduced iron absorption during pyrexial illness contributes to iron deficiency in children who suffer frequent infections.
Anemia is not easy to recognize clinically since pallor is a very nonspecific sign. Koilonychia (spoon-shaped nails) although fairly specific is not obvious in the small finger nails of children. Iron deficiency affects mentality and behavior making children irritable, uncooperative and anorexic, or tired and apathetic. Severe iron deficiency is associated with pica or desire for abnormal foods particularly those with metallic earthy tastes such as clay and coal.
Hypochromic, microcytic anemia is the end point of iron deficiency when stores have been exhausted, tissue iron levels are falling, and there is insufficient iron to meet the needs of red cell production. If severe, iron deficiency anemia (IDA) causes breath-lessness, tiredness, poor appetite, and failure to thrive. Anemia develops slowly so there is physiological adaptation to the developing anemia and hemoglobin levels may be very low (<40 gl-1) before symptoms are noticed. Oral iron therapy allows gradual return to normal physiology and is safer than blood transfusion even when hemoglobin levels are very low.
Worldwide, iron deficiency is possibly the commonest nutritional deficiency. Studies show that IDA is associated with poor outcomes in growth and intellectual capacity. The evidence that impaired growth and intellectual development can also result from iron deficiency without anemia is less definite and remains an area of research.
Circulating iron-binding factors such as transfer-rin are reduced in children with protein energy malnutrition. Normally, iron circulating in plasma and tissues is bound to proteins such as transferrin. When these proteins are reduced in quantity, iron in the tissues may be inadequately 'bound.' Unbound tissue iron encourages free radical damage in tissues and cells, counteracting immunological resistance and facilitating overwhelming infection. Iron supplements should not be given to malnourished children until they are showing signs of recovery by which time they will need the iron for catch up growth.
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