Nutritional Anemias



Nutritional Anemias


Paul L. Martin



The important nutritional anemias result from dietary deficiencies of iron, folic acid, or vitamin B12. Deficiencies of other nutrients such as vitamins B6 and E may be associated with anemia, but they are unusual in pediatric practice (Table 289.1).


IRON DEFICIENCY ANEMIA

Iron deficiency anemia is defined as anemia caused by inadequate availability of iron to sustain bone marrow erythropoiesis. Anemia caused by iron deficiency is the most common hematologic disease of infancy and childhood. The body of the newborn infant contains 0.3 to 0.5 g of iron; the body of an adult contains up to 5 g. To make up the 4.5-g difference, an average net increase of 0.5 mg of iron must be absorbed each day during the first 15 years of life. In addition to this requirement for growth, a small amount of iron is necessary to balance normal losses, estimated at 0.5 to 1 mg/day. To maintain a positive iron balance during childhood, 0.8 to 1.5 mg of iron must be absorbed each day from the diet. Because less than 10% of dietary iron is absorbed from the average mixed diet, 8 to 15 mg of iron daily is necessary for optimal nutrition. During the first years of life, when relatively small quantities of iron-rich food are ingested, it is difficult to attain these amounts. An infant’s diet should include iron-fortified foods, such as cereals or iron-supplemented formulas, by 6 months of age.


Pathophysiology

Most of a newborn’s iron is contained in the circulating hemoglobin. As the high hemoglobin concentration of the newborn decreases during the first 2 to 3 months of life, iron is reclaimed and stored. These stores are usually sufficient for the first 6 to 9 months of life. In low-birth-weight infants or in those with perinatal blood loss, the transplacental iron may be depleted earlier.

Although abundant, iron’s relative insolubility makes its bioavailability extremely low. Most environmental iron exists as insoluble salts. Gastric acidity assists conversion to absorbable forms, but the efficiency of this process is limited. Any medication that affects the gastric pH, such as histamine2 blockers and acid pump blockers, impedes this process, and impaired iron absorption can result. Heme is the most readily absorbed form of iron. Uptake occurs independently of gastric pH. Heme iron is derived primarily from animal tissue. The relative absence of meat from much of the world’s diet is one of the leading causes of iron deficiency anemia.

Other environmental factors that share iron’s absorption machinery can cause iron deficiency anemia. Metals that interfere with the gastrointestinal absorption of iron include lead, cobalt, and strontium. Of these, only lead is a significant problem. Iron deficiency increases the rate of uptake of both iron and lead from the gastrointestinal tract.








TABLE 289.1. NUTRITIONAL ANEMIAS






































Deficiency Prevalence Associated Laboratory Findings Treatment
Iron Common Low reticulocyte count Low MCV Replace iron PO, or IM 6 mg/kg of elemental iron
Low serum ferritin
Low iron/total iron-binding capacity
Folic acid Uncommon Low reticulocyte count Replace folic acid
Elevated MCV
Low serum folate levels
Normal serum vitamin B12 levels
Vitamin B12 Uncommon Low reticulocyte count Elevated MCV Replace B12 PO or IM depending on results from Schilling test
Low serum vitamin B12 levels
Normal serum folate levels
MCV, mean corpuscular volume.


Blood loss is the world’s leading cause of iron deficiency anemia. Blood loss caused by gastrointestinal lesions commonly causes iron deficiency. The most frequent congenital defect in the gastrointestinal tract is Meckel diverticulum. Other causes of occult gastrointestinal bleeding include peptic ulcer disease, polyps, or hemangiomas. Arteriovenous malformations involving the superficial blood vessels along the gastrointestinal tract occur with hereditary hemorrhagic telangiectasia. Whole cow’s milk contains proteins that may irritate the lining of the gastrointestinal tract in infants. Although cow’s milk contains iron at approximately the same concentration as does human milk, the bioavailability of iron in human milk is much greater.

The world’s leading cause of gastrointestinal blood loss is parasitic infestation. Hookworm infection, caused primarily by Necator americanus or Ancylostoma duodenale, is endemic to much of the world and is often asymptomatic. Microscopic blood loss leads to iron deficiency in more than 1 billion people. Once prevalent in the southeastern United States, hookworm infection has declined with better sanitation and the routine wearing of footwear when outside.


Clinical Manifestations

Anemia solely caused by inadequate dietary iron is unusual during the first 4 to 6 months of life, but it becomes more common from 9 to 24 months of age. The usual dietary pattern of infants with iron deficiency anemia is the consumption of large amounts of milk and carbohydrates not supplemented with iron. Pallor is the most frequent sign of iron deficiency anemia. In mild to moderate deficiency (i.e., hemoglobin level of 7 to 10 g/dL), few symptoms of anemia are seen. As the anemia progresses, tachycardia, cardiac dilation, and systolic murmurs occur. The spleen is palpable in 10% to 15% of patients. The child with iron deficiency anemia may be obese or overweight. Often other evidence of undernutrition is present.

Some children with iron deficiency anemia have pica. Iron deficiency anemia and even iron deficiency without significant anemia may adversely affect the attention span, behavior, and performance of affected children.


Laboratory Findings

Because iron is essential for hemoglobin synthesis, erythrocyte production is among the first casualties of iron deficiency. Prelatent iron deficiency occurs when stores are depleted without a change in hemoglobin or serum iron levels. This stage is rarely detected. Latent iron deficiency occurs when the serum iron level decreases and the total iron-binding capacity increases without a change in the hemoglobin. The level of serum ferritin provides a biochemical estimate of body iron stores. Serum ferritin levels in the range of 10 to 20 ng/mL indicate depletion of iron stores; levels of less than 10 ng/mL are diagnostic of iron deficiency. Frank iron deficiency anemia is associated with serum iron levels of less than 30 ng/dL, an increased serum iron-binding capacity, and a resulting serum transferrin saturation of less than 15%. As iron deficiency progresses, the erythrocytes become smaller than normal, with decreased hemoglobin content (microcytic and hypochromic) and abnormal shapes (poikilocytosis). The mean corpuscular volume (MCV) decreases to less than normal for age. The reticulocyte count is normal or minimally elevated, and the leukocyte counts are normal. Elevated platelet counts (greater than 600,000/μL) often are seen, although occasionally thrombocytopenia may be present.

Iron deficiency must be differentiated from other hypochromic, microcytic anemias (Fig. 289.1). In lead poisoning, the erythrocytes are morphologically similar, but coarse basophilic
stippling is prominent (Fig. 289.2). Evaluation reveals elevations of blood lead and marked elevation of free erythrocyte protoporphyrins. As described previously, many children with lead poisoning have concomitant iron deficiency anemia. Thalassemia trait (alpha- or beta-thalassemia) is sometimes confused with iron deficiency anemia. Alpha-thalassemia trait occurs in approximately 3% of blacks and in many people of Southeast Asian origin. Beta-thalassemia major with its organomegaly, erythroblastosis, and hemolytic component is usually clinically apparent. Beta-thalassemia trait is common in individuals of Mediterranean descent. The erythrocyte morphology of chronic inflammatory or infectious conditions may be microcytic. In these conditions, the serum iron and iron-binding capacity is reduced, and the serum ferritin levels are normal or elevated.

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Jul 24, 2016 | Posted by in ORTHOPEDIC | Comments Off on Nutritional Anemias

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