IRON DEFICIENCY ANEMIA
A. Definition of the symptom
1. Anemia – reduction of RBC volume and hematocrit concentration below the normal range for
healthy children
2. Pallor is the result of anemia
i. It manifests in the mucus membranes when hemoglobin falls below 70-80mg/dL
B. Definition of the disease
1. Results from lack of sufficient iron to synthesize haemoglobin
2. It said to be the most common hematologic disease of infancy and childhood
C. Pathophysiology/Etiology
1. Early depletion of stored iron in low-birthweight infants or those with perinatal blood loss
2. Consumption of large amounts of cow's milk and of foods not supplemented with iron
3. Blood loss in older children
4. Chronic iron-deficiency anemia from occult bleeding may be caused by a lesion of the
gastrointestinal tract
i. milk protein–induced inflammatory colitis
ii. peptic ulcer
iii. Meckel diverticulum
iv. polyp
v. hemangioma
vi. inflammatory bowel disease.
5. Hookworm infestation and H. pylori infection
6. Pulmonary hemosiderosis - associated with unrecognized bleeding in the lungs and recurrent iron
deficiency after treatment with iron.
7. Chronic diarrhea in early childhood
8. Cow's milk–induced anemia may be expected simply from an inadequate intake of iron.
9. Histologic abnormalities of the mucosa of the gastrointestinal tract, such as blunting of the villi, are
present in advanced iron-deficiency anemia and may cause leakage of blood and decreased
absorption of iron, further compounding the problem.
10. Intense exercise conditioning, as in competitive athletics in high school, may result in iron depletion
in girls
D. Differential diagnosis
1. α- and β-thalassemia trait and other hemoglobinopathies
i. elevated RBC count despite the presence of a mild anemia and microcytosis
ii. RDW is not elevated
2. β-Thalassemia trait - occurs in people from the Mediterranean area, Africa, and Asia
i. characterized by elevated levels of hemoglobin A 2 and/or increased fetal hemoglobin
concentration
ii. serum iron, total iron-binding capacity (transferrin), and ferritin are normal
iii. no abnormal hemoglobin is seen on electrophoresis
3. α-Thalassemia trait - occurs in persons of African, Chinese, and Southeast Asian descent
i. assumed when a patient with a familial hypochromic microcytic anemia has normal results
of iron studies (including ferritin), normal levels of Hb A 2and Hb F, and a normal
hemoglobin electrophoresis.
4. Hb H disease
i. characterized by hypochromia and microcytosis
ii. Hb H is readily identified by hemoglobin electrophoresis
5. Anemia of chronic disease (ACD) and infection
i. normocytic although occasionally it may be slightly microcytic
ii. in contrast to iron-deficiency anemia, both the serum iron level and iron-binding capacity
(transferrin) are reduced, and serum ferritin levels are normal or elevated
iii. serum transferrin receptor (TfR) level is elevated in iron deficiency and is within the normal
range in anemia of chronic disease.
6. Lead poisoning
i. coarse basophilic stippling of the RBCs often is prominent
ii. elevated blood lead, FEP, and urinary coproporphyrin levels are seen
E. Laboratory Work-up
1. serum ferritin, an iron-storage protein – provides a relatively accurate estimate of body iron stores
in the absence of inflammatory disease
2. serum iron level – decreases
3. iron-binding capacity of the serum (serum transferrin) – increases
4.percent saturation (transferrin saturation) - falls below normal
5.bone marrow - hypercellular, with erythroid hyperplasia
i. normoblasts have scanty, fragmented cytoplasm with poor hemoglobination
ii. leukocytes and megakaryocytes are normal
iii. no stainable iron in marrow reticulum cells
6. occult blood – may be detected in the stool.
7. mean corpuscular hemoglobin (MCH) and mean cor-puscular volume (MCV) – hypochromic,
microcytic
8. peripheral blood smear
i. microcytosis, hypochromia, poikilocytosis, and increased RBC distribution width (RDW)
ii. nucleated RBCs
iii. white blood cell counts are normal
3
iv. thrombocytosis (600,000–1 million/mm ) - caused by increased erythropoietin, which is
known to have some structural homology with thrombopoietin. Very severe iron-deficiency
anemia occasionally may be associated with thrombocytopenia
F. Management
1. Oral administration of simple ferrous salts (e.g., sulfate, gluconate, fumarate)
i. therapeutic dose should be calculated in terms of elemental iron
ii. ferrous sulfate is 20% elemental iron by weight
iii. daily total dose of 4–6 mg/kg of elemental iron in 3 divided doses provides an optimal
amount of iron for the stimulated bone marrow to use
iv. parenteral iron preparation (iron dextran) is an effective form of iron when given in a
properly calculated dose
2. Diet
i. milk consumption should be limited to a reasonable quantity, preferably 500 mL (1 pint)/24
hr or less
ii. amount of iron-rich foods is increased
iii. iron-fortified formula or cereals during infancy
iv. iron and hormone therapy - in adolescent females secondary to abnormal uterine blood
flow loss
v. iron medication should be continued for 8 wk after blood values are normal
G. Some Guidelines*
*From: Guidelines for the Use of Iron Supplements to Prevent and Treat IDA. Rebecca Stoltzfus and Michele Dreyfuss.
International Nutritional Anemia Consultative Group. 1998.