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3. Parenteral iron. Parenteral iron in the form of iron-dextran may be given intramuscularly or intravenously, but does not lead to a more rapid hematologic response than oral iron and rare anaphylactic reactions have been reported. In general it should be reserved for individuals with malabsorption or intractable non-compliance with oral therapy.
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4. Blood transfusion. Blood transfusion should be avoided if at all possible, but may be necessary for individuals with anemia so severe as to cause cardiorespiratory embarrassment; in this case it should be given as packed red cells with a potent diuretic administered concomitantly.

D. Prevention of iron deficiency. Iron deficiency is such a prevalent problem that it is appropriate to approach prevention on a population basis. Efforts to increase heme protein in the diet may be useful, especially for young children after weaning. Iron supplementation with a therapeutic iron preparation to improve the iron status of a segment of the population in a relatively short period of time is beneficial in pregnant women and may be considered for infants, school children, and groups of workers. Iron fortification, the addition of iron to a common food to increase the iron intake of the population as a whole, is practiced in western countries by adding iron to flour and likely would be of benefit in developing countries.
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E. Differential diagnosis of microcytic anemia. Other causes of a microcytic hypochromic anemia include thalassemias, lead poisoning, hereditary sideroblastic anemia, and the anemia of chronic inflammation.

1. Identify the cause. Iron deficiency as the cause of anemia is suspected on epidemiologic grounds. As discussed above, the condition is a common cause of low hemoglobin in infants, adolescents, women of childbearing age, individuals with hookworm infestation and patients with chronic blood loss from the gastrointestinal tract or other sites. Before treatment, consideration should be given to the cause of iron deficiency which may be deduced from history and physical examination or examination of the stool for occult blood and parasites. If possible, the underlying cause should be corrected. A search must be made for the presence of a potentially curable malignancy giving rise to blood loss.
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2. Oral iron therapy. Iron deficiency anemia is almost always treated with oral iron preparations. The typical adult dose is 200 mg of elemental iron per day, for example one 300 mg ferrous sulfate tablet three times a day (300 mg ferrous sulfate = 65 mg elemental iron). The pediatric dose is 5 mg/kg of elemental iron per day in tablet or elixir form. Iron is best absorbed if given without food. Side effects of iron therapy include constipation, diarrhea, nausea and abdominal pain, and if these limit compliance the medication can be administered with food or the dose reduced by one-half. Oral iron therapy usually corrects anemia within four to six weeks, but should be continued for an additional three to six months to replenish iron stores. All iron tablets must be kept out of the reach of young children, because iron ingestion is a common cause of poisoning and as little as I0 ferrous sulfate tablets can prove fatal for an infant.
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Carbonyl iron is an elemental iron powder that may be given in capsule form and has similar efficacy to iron salts in correcting iron deficiency. Elemental iron has the advantage of having remarkably reduced toxicity when compared to iron salts, and it would be reasonable to consider the substitution of carbonyl iron for therapeutic uses.
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A presumptive diagnosis of iron deficiency is sufficient to begin a trial of oral iron therapy in a menstruating woman who presents with microcytic hypochromic indices, a low reticulocyte count, a low serum ferritin, and guaiac-negative stools. A menstrual source of blood loss can then be safely assumed. The earliest response to oral iron therapy is a moderate reticulocytosis and increase in hemoglobin concentration occurring within l0 days, and this response confirms the diagnosis.
In a man or in a non menstruating woman with laboratory evidence for iron deficiency in whom the source of blood loss is not clear, the situation is more complicated. If the patient’s stool is guaiac positive, it is reasonable to assume that the anemia is caused by iron deficiency, and a search for the site of bleeding should be undertaken. If no blood loss is detected, despite laboratory findings compatible with iron deficiency, a bone marrow examination should be performed. The patient may or may not have a history suggesting a potential bleeding source (eg, alcohol abuse, the use of aspirin or nonsteroidal antiinflammatory drugs, or peptic ulcer disease). In any case, an exhaustive search for a bleeding site such as colorectal cancer is indicated if the bone marrow reveals a decrease in stainable iron stores.
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The treatment of iron deficiency anemia is oral iron replacement. The most commonly used agent, ferrous sulfate, is inexpensive and well absorbed. Most patients respond to oral iron therapy if they are compliant, and intramuscular or intravenous iron dextran is rarely necessary. Some patients receiving parenteral iron therapy experience severe allergic reactions, and all patients receiving parenteral iron should be monitored carefully. Ferrous sulfate is a leading cause of medicinal iron poisoning in small children, and in the future oral therapy with carbonyl iron, a bioavailable but non toxic elemental iron powder, may replace ferrous sulfate as standard therapy for iron deficiency.

The serum ferritin is a very helpful measure of total body iron stores and a low level (<12 mg/L) is diagnostic of iron deficiency. The serum ferritin is a positive acute phase reactant and may not reflect iron deficiency in a patient with both lack of iron and an inflammatory process. Typically the transferrin saturation is less than 15% (normal 20-50%) with iron deficiency anemia, but this measurement may not be a reliable test for the presence of iron deficiency. Transferrin saturation is decreased in the presence of acute and chronic inflammation and it is raised with marrow dysfunction due to alcohol, cancer chemotherapy, or a megaloblastic process. Transferrin saturation can also be affected by diurnal variations, typically being higher in the morning and lower in the evening. Early in the course of iron deficiency, the anemia may be normochromic and normocytic, but, in the absence of other systemic processes, the transferrin saturation and serum ferritin will be low. In an unexplained anemia with the serum ferritin >12 µg/L, the bone marrow can be stained to reveal the presence or absence of iron; if the anemia is the result of iron deficiency, iron stores are absent. Typically, the automated blood count reveals decreased mean corpuscular volume (<80 fl) and increased red cell distribution width (>15%).
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Iron studies usually indicate low serum iron, increased total iron binding capacity, low transferrin saturation (<10%) and low serum ferritin. The serum ferritin and transferrin saturation are unreliable tests for iron deficiency if an inflammatory condition is present. In many parts of the tropics there is a high prevalence of thalassemia trait which also causes a mild microcytic, hypochromic anemia and which may be difficult to distinguish from iron deficiency anemia. If there is doubt as to the diagnosis, the definitive test to document iron deficiency is a bone marrow aspirate stained with Perl’s reagent: the blue-staining iron normally present in macrophages is absent in iron deficiency. The differential diagnoses for low transferrin saturation and serum ferritin concentration are shown in Table 6.
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Symptoms. Even in the absence of anemia, iron deficiency may have adverse effects. Non-anemic children with prolonged iron deficiency in the second year of life were later found to have impaired mental and motor development at five years of age. In pregnancy, maternal iron deficiency may be associated with low fetal birth weight and increased prematurity. In adults with iron deficiency, reduced capacity for strenuous work and exercise has been reported. In addition to these findings, iron deficiency anemia is associated with increased maternal and fetal morbidity and mortality, growth retardation, reduced worker productivity, and symptoms of weakness, dizziness and dyspnea. Pica, a craving for and the ingestion of clay, starch or ice, is a common finding in iron deficiency.
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Physical findings. Physical findings of iron deficiency may include koilonychia, papillary atrophy of the tongue, angular stomatitis, esophageal web, achlorhydria and gastritis. Slight splenic enlargement, cause unknown, occurs in about 10% of patients.

Laboratory findings. Iron deficiency in the absence of anemia is characterized by low serum ferritin concentration (<12 µg/L). Iron deficiency is also typically accompanied by reductions in serum iron concentration and transferrin saturation (ratio of serum iron to total serum iron binding capacity). The condition is typically associated with elevations in red cell distribution width, free erythrocyte protoporphyrin concentration, transferrin concentration, total iron binding capacity, and circulating transferrin receptors (Table 4 at Canadian pharmacy news).
With iron deficiency anemia, the red cell count, hemoglobin concentration and hematocrit are below the normal range, and review of the peripheral blood smear shows hypochromia and microcytosis (Table 5). In addition, there is a low or normal reticulocyte count.
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Inadequate dietary iron for high physiologic requirements. Iron deficiency is the most common nutritional deficiency in the world. Infants, adolescents and women of child bearing age are at the highest risk of iron deficiency and may become iron deficient because of inadequate dietary iron to meet physiologic needs. Infants one to two years of age and adolescents have increased iron requirements due to the demands of rapid growth. Women need more iron because of the loss of hemoglobin with menstruation and the high iron demands of pregnancy.
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Blood loss. Other than in children and women of child bearing age, the finding of iron deficiency almost always signifies pathological blood loss of some sort. Populations with hookworm infestation have an increased incidence of iron deficiency due to chronic intestinal blood loss. Individuals with gastrointestinal bleeding due to ulceration, tumors, diverticulas, polyps and vascular malformations are prone to develop iron deficiency. Both women and men who are frequent blood donors have a high prevalence of iron deficiency. About 50% of hemodialysis patients develop iron deficiency due to blood lost during the procedure and with frequent diagnostic tests. The finding of iron deficiency should always prompt the consideration that the patient may have a gastrointestinal cancer (esophageal, gastric or colorectal are the most common) and intensive efforts should be made to find a curable malignancy. Hemoptysis and bleeding from a bladder tumor may lead to iron deficiency.
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Malabsorption, hemoglobinuria, pulmonary hemosiderosis. Iron deficiency also may in patients with defective absorption of food iron due to tropical sprue and other tropical enteropathies, achlorhydria and gastric resection. The condition may develop in the setting of intravascular hemolysis with associated hemoglobinuria- paroxysmal nocturnal hemoglobinuria and anemia in long distance runners are examples. Alveolar hemorrhage leads to iron-loading of pulmonary macrophages; because this iron cannot be utilized for hemoglobin synthesis, the process can lead to iron deficiency.
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Clinical features of iron deficiency. These include fatigue, irritability, headaches, paresthesias, glossitis (a smooth red tongue), angular cheilitis, pallor, and koilonychia (spooning of the nails). Pica, the craving to eat unusual substances such as ice, clay or dirt, can be a characteristic feature.

Iron deficiency is the most common cause of anemia in many parts of the world and is usually the result of blood loss, often combined with inadequate dietary iron. Iron deficiency occurs most commonly in menstruating women. When iron deficiency occurs in men or non menstruating women, the most likely site of blood loss is the gastrointestinal tract, and the specific site and cause must be sought.

When iron requirements or the loss of iron exceed the quantity of iron absorbed, the individual experiences a state of negative iron balance. With this negative balance, iron stores decrease progressively and synthesis of hemoglobin is impaired after storage iron is exhausted. Lack of body iron can be divided into two categories. (1) In iron deficiency without anemia, storage iron is absent but the deficit in iron is not sufficiently large to decrease the hemoglobin below the normal level. (2) In iron deficiency anemia, the deficit in iron is so severe that stores are absent and the hemoglobin is frankly below the normal range.
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