• A decrease in hemoglobin production due to an insufficient supply of iron that results in a microcytic, hypochromic anemia.

• Decreased dietary intake
• Decreased iron absorption
• Rapid growth causing increased red cell production. Seen in low birth weight infants and adolescents.
• Blood loss either overt or occult. Commonly associated with cow’s milk enteropathy in infants. In older children it is associated with inflammatory bowel disease, Meckel’s diverticulum, and menorrhagia.

• Impaired cognitive and motor development in infants and toddlers.
• Positive correlation between cognitive and motor deficits and severity and duration of anemia.
• Impaired lymphocyte and neutrophil function leading to an increased risk of infection.
• Short term memory impairment and poor exercise performance in adolescents

• Anemia readily corrected with iron replacement.
• Developmental delay may be long lasting or irreversible.

• Recent infection
• Lead poisoning
• Thalassemia trait
• Anemia of chronic disease (JRA, IBD, renal failure)

• Evaluate dietary intake of iron, including breast or formula feeding and type of formula
• Age of introduction of cow’s milk
• Amount of cow’s milk during the day
• Blood loss from stool, urine, menorrhagia
• Birth history for prematurity or blood loss
• Pica
• Lead exposure

• Usually normal exam
• Pallor, irritability
• Tachycardia, flow murmur
• Blue sclera
• Glossitis or stomatitis
• Stool test for occult blood

• Low hemoglobin. Hemoglobin less than 2 standard deviations below the age specific mean. (AAP recommends screening Hgb at 9 months, 5 years, and 14 years.)
• Low MCV (red cell volume) and MCH (hemoglobin concentration) for age.
• High red cell distribution width (RDW) >14.5%. Measures the variation in red cell size. Earliest laboratory sign.
• Low serum ferritin reflects tissue iron stores. May be normal or increased with concurrent infection.
• Low serum iron
• Increased transferrin (total iron binding capacity)
• Low transferrin saturation. Measures the iron available for hemoglobin synthesis
• Increased free erythrocyte protporphyrin (FEP), a precursor molecule to hemoglobin synthesis. Also increased in lead poisoning and chronic inflammation.
• Peripheral blood smear with microcytosis, hypochromia, poikilocytosis, and anisocytosis
• Bone marrow with decreased iron stores by hemosiderin staining (rarely done)

• Iron supplementation as ferrous sulfate orally at 4–6 mg/kg/day of elemental iron divided into two or three doses. Iron should be given on an empty stomach or with a Vitamin C-containing juice to increase absorption.
• Parenteral (IM or IV) iron dextran is rarely used. Associated with pain on injection and anaphylaxis.
• Educate family regarding age-appropriate diet including adequate iron
• May require initial inpatient observation in cases of severe anemia
• Red cell transfusion only if evidence of cardiovascular compromise (rarely indicated)

• Reticulocyte count should double in 1–2 weeks
• Hemoglobin concentration should be increased at least 1.0 grams per deciliter in 2–4 weeks
• Check CBC and reticulocyte count at 2 weeks to assess response
• Continue iron for 3 months to replete body stores

• Maintain breast-feeding for the first five to six months of life when possible. Although the concentration of iron is lower in breast milk than in formula, iron in breast milk is much more available. For infants who are exclusively breast fed beyond six months, give iron supplementation (1 mg/kg/day).
• Give infants who are not breast fed iron-fortified formula for the first 12 months of life.
• Give low birth weight and premature infants iron supplementation after 2 months of life because of decreased iron stores and increased growth rate.
• Encourage iron-enriched cereal when infants are started on solid food.
• Avoid whole cow’s milk during the first year of life.

• Noncompliance (most common)
• Ongoing blood loss
• Insufficient duration of therapy
• High gastric pH
• Concurrent lead intoxication
• Incorrect diagnosis (Thalassemia trait and anemia of chronic disease are not iron responsive.)

Q: What dietary changes can help prevent the reoccurrence of iron deficiency?
A: Limit milk to not more than 24 ounces a day so that your child has a better appetite for iron-containing foods. Foods rich in iron include meats, fish, and poultry. Other foods that contain iron are raisins, dried fruit, sweet potatoes, lima beans, chili beans, green peas, peanut butter and enriched foods. Give iron on an empty stomach along with an ascorbic acid-containing juice to increase absorption of iron. Foods that decrease iron absorption include bran, vegetable fiber, tannins found in tea, and phosphates

Q: What are the side effects of iron therapy?
A: Iron can cause temporary staining of the teeth, which can be decreased by diluting the iron with a small amount of juice. Iron will also change the color of bowel movements to greenish black.

Q: What are the most important tests to do to establish the diagnosis of iron deficiency?
A: For patients with a history of dietary deficiency or known blood loss, a complete blood count that shows a low Hgb and MCV and an elevated RDW is very suggestive of iron deficiency. A therapeutic trial of iron without further laboratory testing is an appropriate next diagnostic step. An increase in the hemoglobin concentration of 1 g/dl or greater after one month of therapy confirms the diagnosis. If this does not occur, further laboratory testing is necessary and other diagnoses should be considered.

Q: How does a concurrent infection affect the diagnosis of iron deficiency?
A: Common childhood infections can be associated with a mild microcytic anemia that resembles iron deficiency. Laboratory tests to diagnose iron deficiency can be misleading while a child is acutely ill. Acute infection is associated with a shift of iron from serum to storage sites causing a decrease in serum iron and an increase in ferritin. It is therefore more helpful to screen a child for iron deficiency 3–4 weeks after an acute infection.

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