iron deficiency anemia

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Iron Deficiency Anemia



Anemia can be caused by iron deficiency, folate deficiency, vitamin B12 deficiency, and other causes. The term iron deficiency anemia means anemia that is due to iron deficiency. Iron deficiency anemia is characterized by the production of small red blood cells. When examined under a microscope, the red blood cells also appear pale or light colored. For this reason, the anemia that occurs with iron deficiency is also called hypochronic microcytic anemia.


Iron deficiency anemia is the most common type of anemia throughout the world. In the United States, iron deficiency anemia occurs to a lesser extent than in developing countries because of the higher consumption of red meat and the practice of food fortification (addition of iron to foods by the manufacturer). Anemia in the United States is caused by a variety of sources, including excessive losses of iron in menstrual fluids and excessive bleeding in the gastrointestinal tract. In developing countries located in tropical climates, the most common cause of iron deficiency anemia is infestation with hookworm.

Causes and symptoms

Infancy is a period of increased risk for iron deficiency. The human infant is born with a built-in supply of iron, which can be tapped during periods of drinking low-iron milk or formula. Both human milk and cow milk contain rather low levels of iron (0.5-1.0 mg iron/liter). However, the iron in human milk is about 50% absorbed by the infant, while the iron of cow milk is only 10% absorbed. During the first six months of life, growth of the infant is made possible by the milk in the diet and by the infant's built-in supply. However, premature infants have a lower supply of iron and, for this reason, it is recommended that preterm infants (beginning at 2 months of age) be given oral supplements of 7 mg iron/day, as ferrous sulfate. Iron deficiency can be provoked where infants are fed formulas that are based on unfortified cow milk. For example, unfortified cow milk is given free of charge to mothers in Chile. This practice has the fortunate result of preventing general malnutrition, but the unfortunate result of allowing the development of mild iron deficiency.
The normal rate of blood loss in the feces is 0.5-1.0 ml per day. These losses can increase with colorectal cancer. About 60% of colorectal cancers result in further blood losses, where the extent of blood loss is 2-10 ml/day. Cancer of the colon and rectum can provoke losses of blood, resulting in iron deficiency anemia. The fecal blood test is widely used to screen for the presence of cancer of the colon or rectum. In the absence of testing, colorectal cancer may be first detected because of the resulting iron deficiency anemia.
Infection with hookworm can provoke iron deficiency and iron deficiency anemia. The hookworm is a parasitic worm. It thrives in warm climates, including in the southern United States. The hookworm enters the body through the skin, as through bare feet. The hookworm then migrates to the small intestines where it attaches itself to the villi (small sausage-shaped structures in the intestines that are used for the absorption of all nutrients). The hookworm provokes damage to the villi, resulting in blood loss, and they produce anti-coagulants which promote continued bleeding. Each worm can provoke the loss of up to 0.25 ml of blood per day.
Bleeding and blood losses through gastrointestinal tract can be provoked by colorectal cancer and hookworms, as mentioned above, but also by hemorrhoids, anal fissures, irritable bowel syndrome, aspirin-induced bleeding, blood clotting disorders, and diverticulosis (a condition caused by an abnormal opening from the intestine or bladder). Several genetic diseases exist which lead to bleeding diorders, and these include hemophilia A, hemophilia B, and von Willebrand's disease. Of these, only von Willebrand's disease leads to gastrointestinal bleeding.
The symptoms of iron deficiency anemia include weakness and fatigue. These symptoms result because of the lack of function of the red blood cells, and the reduced ability of the red blood cells to carry iron to exercising muscles. Iron deficiency can also affect other tissues, including the tongue and fingernails. Prolonged iron deficiency can result in changes of the tongue, and it may become smooth, shiny, and reddened. This condition is called glossitis. The fingernails may grow abnormally, and acquire a spoon-shaped appearance.
Decreased iron intake is a contributing factor in iron deficiency and iron deficiency anemia. The iron content of cabbage, for example, is about 1.6 mg/kg food, while that of spinach (33 mg/kg), lima beans (15 mg/kg), potato (14 mg/kg), tomato (3 mg/kg), apples (1.5 mg/kg), raisins (20 mg/kg), whole wheat bread (43 mg/kg), eggs (20 mg/kg), canned tuna (13 mg/kg), chicken (11 mg/kg), beef (28 mg/kg), corn oil (0.6 mg/kg), and peanut butter (6.0 mg/kg), are indicated. One can see that apples, tomatoes, and vegetable oil are relatively low in iron, while whole wheat bread and beef are relatively high in iron. The assessment of whether a food is low or high in iron can also be made by comparing the amount of that food eaten per day with the recommended dietary allowance (RDA) for iron. The RDA for iron for the adult male is 10 mg/day, while that for the adult woman is 15 mg/day. The RDA during pregnancy is 30 mg/day. The RDA for infants of 0-0.5 years of age is 6 mg/day, while that for infants of 0.5-1.0 years of age is 10 mg/day. The RDA values are based on the assumption that the consumer eats a mixture of plant and animal foods.
The above list of iron values alone may be deceptive, since the availability of iron in fruits, vegetables, and grains is very low, while that the availability from meat is much higher. The availability of iron in plants ranges from only 1-10%, while that in meat, fish, chicken, and liver is 20-30%. The term availability means the percent of dietary iron that is absorbed via the gastrointestinal tract to the bloodstream. Nonabsorbed iron is lost in the feces.
Interactions between various foods can influence the absorption of dietary iron. Vitamin C can increase the absorption of dietary iron. Orange juice is a rich source of vitamin C. Thus, if a plant food, such as rice, is consumed with orange juice, then the orange juice can enhance the absorption of the iron of the rice. Vitamin C is also added to infant formulas, and the increased use of formulas fortified with both iron and vitamin C have led to a marked decline in anemia in infants and young children in the United States (Dallman, 1989). In contrast, if rice is consumed with tea, certain chemicals in the tea (tannins) can reduce the absorption of the iron. Phytic acid is a chemical that naturally occurs in legumes, cereals, and nuts. Phytic acid, which can account for 1-5% of the weight of these foods, is a potent inhibitor of iron absorption. The increased availability of the iron in meat products is partly due to the fact that heme-iron is absorbed to a greater extent than free iron salts, and to a greater extent than iron in the phytic acid/iron complex. Nearly all of the iron in plants is nonheme-iron. Much of the iron in meat is nonheme-iron as well. The nonheme-iron in meat, fish, chicken and liver may be about 20% available. The heme-iron of meat may be close to 30% available. The most available source of iron is human milk (50% availability).


Iron deficiency anemia in infants is defined as a hemoglobin level below 109 mg/ml of whole blood, and a hematocrit of under 33%. Anemia in adult males is defined as a hemoglobin under 130 mg/ml and a hematocrit of under 38%. Anemia in adult females is defined as hemoglobin under 120 mg/ml and a hematocrit of under 32%. Anemia in pregnant women is defined as hemoglobin of under 110 mg/ml and hematocrit of under 31%.
When an abnormally high presence of blood is found in the feces during a fecal occult blood test, the physician needs to examine the gastrointestinal tract to determine the cause of bleeding. Here, the diagnosis for iron deficiency anemia includes the examination using a sigmoidoscope. The sigmoidoscope is an instrument that consists of a flexible tube that permits examination of the colon to a distance of 60 cm. A barium enema, with an x ray, may also be used to detect abnormalities that can cause bleeding.
The diagnosis of iron deficiency anemia should include a test for oral iron absorption, where evidence suggests that oral iron supplements fail in treating anemia. The oral iron absorption test is conducted by eating 64 mg iron (325 mg ferrous sulfate) in a single dose. Blood samples are then taken after 2 hours and 4 hours. The iron content of the blood serum is then measured. The concentration of iron should rise by an increment of about 22 micromolar, where iron absorption is normal. Lesser increases in concentration mean that iron absorption is abnormal, and that therapy should involve injections or infusions of iron.


Oral iron supplements (pills) may contain various iron salts. These iron salts include ferrous sulfate, ferrous gluconate, or ferrous fumarate. Injections and infusions of iron can be carried out with a preparation called iron dextran. In patients with poor iron absorption (by the gut), therapy with injection or infusion is preferable over oral supplements. Treatment of iron deficiency anemia sometimes requires more than therapy with iron. Where iron deficiency was provoked by hemorrhoids, surgery may prove essential to prevent recurrent iron deficiency anemia. Where iron deficiency is provoked by bleeding due to aspirin treatment, aspirin should be discontinued. Where iron deficiency is provoked by hookworm infections, therapy for this parasite should be used, along with protection of the feet by wearing shoes whenever walking in hookworm-infested soil.


The prognosis for treating and curing iron deficiency anemia is excellent. Perhaps the main problem is failure to take iron supplements. In cases of pregnant women, the health care worker may recommend taking 100-200 mg iron/day. This dose is rather high, and can lead to nausea, diarrhea, or abdominal pain in 10-20% of women taking this dose. The reason for using this high dose is to effect a rapid cure for anemia, where the anemia is detected at a mid-point during the pregnancy. The above problems of side-effects and noncompliance can be avoided by taking iron doses (100-200 mg) only once a week, where supplements are initiated some time prior to conception, or continuously throughout the fertile period of life. The problem of compliance is not an issue where infusions are used, however a fraction of patients treated with iron infusions experience side effects, such as flushing, headache, nausea, anaphylaxis, or seizures. A number of studies have shown that iron deficiency anemia in infancy can result in reduced intelligence, where intelligence was measured in early childhood. It is not certain if iron supplementation of children with reduced intelligence, due to iron-deficiency anemia in infancy, has any influence in allowing a "catch-up" in intellectual development.

Key terms

Hematocrit — The proportion of whole blood in the body, by volume, that is composed of red blood cells.
Hemoglobin — Hemoglobin is an iron-containing protein that resides within red blood cells. Hemoglobin accounts for about 95% of the protein in the red blood cell.
Protoporphyrin IX — Protoporphyrin IX is a protein. The measurement of this protein is useful for the assessment of iron status. Hemoglobin consists of a complex of a protein plus heme. Heme consists of iron plus protoporphyrin IX. Normally, during the course of red blood cell formation, protoporphyrin IX acquires iron, to generate heme, and the heme becomes incorporated into hemoglobin. However, in iron deficiency, protophoryrin IX builds up.
Recommended Dietary Allowance (RDA) — The Recommended Dietary Allowances (RDAs) are quantities of nutrients of the diet that are required to maintain human health. RDAs are established by the Food and Nutrition Board of the National Academy of Sciences and may be revised every few years.


In the healthy population, all of the mineral deficiencies can be prevented by the consumption of inorganic nutrients at levels defined by the RDA. Iron deficiency anemia in infants and young children can be prevented by the use of fortified foods. Liquid cow milk-based infant formulas are generally supplemented with iron (12 mg/L). The iron in liquid formulas is added as ferrous sulfate or ferrous gluconate. Commercial infant cereals are also fortified with iron, and here small particles of elemental iron are added. The levels used are about 0.5 gram iron/kg dry cereal. This amount of iron is about 10-fold greater than that of the iron naturally present in the cereal.



Walter, T., P. Pino, F. Pizarro, and B. Lozoff. "Prevention of Iron-deficiency Anemia: Comparison of High- and Low-iron Formulas in Term Healthy Infants after Six Months of Life." Journal of Pediatrics 132 (1998): 635-640.


a condition in which there is reduced delivery of oxygen to the tissues; it is not actually a disease but rather a symptom of any of numerous different disorders and other conditions. The World Health Organization has defined anemia as a hemoglobin concentration below 7.5 mmol/L (12 g/dL) in women and below 8.1 mmol/L (13 g/dL) in men.
 Peripheral blood smears from a patient with megaloblastic anemia (left) and from a normal subject (right), both at the same magnification. The smear from the patient shows variation in the size and shape of erythrocytes and the presence of macro-ovalocytes. From Goldman and Bennett, 2000.

Some types of anemia are named for the factors causing them: poor diet (nutritional anemia), excessive blood loss (hemorrhagic anemia), congenital defects of hemoglobin (hypochromic anemia), exposure to industrial poisons, diseases of the bone marrow (aplastic anemia and hypoplastic anemia), or any other disorder that upsets the balance between blood loss through bleeding or destruction of blood cells and production of blood cells. Anemias can also be classified according to the morphologic characteristics of the erythrocytes, such as size (microcytic, macrocytic, and normocytic anemias) and color or hemoglobin concentration (hypochromic anemia). A type called hypochromic microcytic anemia is characterized by very small erythrocytes that have low hemoglobin concentration and hence poor coloration. Data used to identify anemia types include the erythrocyte indices: (1) mean corpuscular volume (MCV), the average erythrocyte volume; (2) mean corpuscular hemoglobin (MCH), the average amount of hemoglobin per erythrocyte; and (3) mean corpuscular hemoglobin concentration (MCHC), the average concentration of hemoglobin in erythrocytes. adj., adj ane´mic.
Symptoms. Mild degrees of anemia often cause only slight and vague symptoms, perhaps nothing more than easy fatigue or a lack of energy. As the condition progresses, more severe symptoms may be experienced, such as shortness of breath, pounding of the heart, and a rapid pulse; these are caused by the inability of anemic blood to supply the body tissues with enough oxygen. Pallor, particularly in the palms of the hands, the fingernails, and the conjunctiva (the lining of the eyelids), may also indicate anemia. In very advanced cases, swelling of the ankles and other evidence of heart failure may appear.
Common Causes of Anemia. Loss of Blood (Hemorrhagic Anemia): If there is massive bleeding from a wound or other lesion, the body may lose enough blood to cause severe and acute anemia, which is often accompanied by shock. Immediate transfusions are generally required to replace the lost blood. Chronic blood loss, such as excessive menstrual flow, or slow loss of blood from an ulcer or cancer of the gastrointestinal tract, may also lead to anemia. These anemias disappear when the cause has been found and corrected. To help the blood replenish itself, the health care provider may prescribe medicines containing iron, which is necessary to build hemoglobin, and foods with high iron content, such as kidney and navy beans, liver, spinach, and whole wheat bread.

Dietary Deficiencies and Abnormalities of Red Blood Cell Production (Nutritional Anemia, Aplastic Anemia, and Hypoplastic Anemia): Anemia may develop if the diet does not provide enough iron, protein, vitamin B12, and other vitamins and minerals needed in the production of hemoglobin and the formation of erythrocytes. The combination of poor diet and chronic loss of blood makes for particular susceptibility to severe anemia. Anemias associated with folic acid deficiency are very common.

Excessive Destruction of Red Blood Cells (hemolytic anemia): Anemia may also develop related to hemolysis due to trauma, chemical agents or medications (toxic hemolytic anemia), infectious disease, isoimmune hemolytic reactions, autoimmune disorders, and the paroxysmal hemoglobinurias.
Patient Care. Assessment of patients with some form of anemia will depend to some extent on the specific type of blood dyscrasia presented. In general, these patients do share some common problems requiring special assessment skills and interventions. Anemia can affect many different body systems
(see table). Although pallor of the skin is a sign of anemia, it is not the most reliable sign; many other factors can affect complexion and skin color. Jaundice of the skin and sclera can occur as a result of hemolysis and the release of bilirubin into the blood stream, where it eventually finds its way into the skin and mucous membranes. (See also jaundice.) Bleeding under the skin and bruises in response to the slightest trauma often are present in anemic and leukemic patients. A bluish tint to the skin (cyanosis) can indicate hypoxia due to inadequate numbers of oxygen-bearing erythrocytes.

Activity intolerance is a common problem for patients with anemia. Physical activity increases demand for oxygen, but if there are not enough circulating erythrocytes to provide sufficient oxygen, patients become physically weak and unable to engage in normal physical activity without experiencing profound fatigue. This can result in some degree of self-care deficit as the fatigue interferes with the patient's ability to carry on regular or enjoyable activities.
acute posthemorrhagic anemia hemorrhagic anemia.
aplastic anemia see aplastic anemia.
autoimmune hemolytic anemia (AIHA) an acquired disorder characterized by hemolysis due to the production of autoantibodies against one's own red blood cell antigens.
Blackfan-Diamond anemia congenital hypoplastic anemia (def. 1).
congenital hypoplastic anemia
idiopathic progressive anemia occurring in the first year of life, without leukopenia and thrombocytopenia; it is due to an isolated defect in erythropoiesis and is unresponsive to hematinics, requiring multiple blood transfusions to sustain life. For those responding to steroid therapy the prognosis is good. Called also Blackfan-Diamond anemia or syndrome, Diamond-Blackfan anemia or syndrome, and erythrogenesis imperfecta.
Cooley's anemia tthalassemia major.
deficiency anemia nutritional anemia.
Diamond-Blackfan anemia congenital hypoplastic anemia (def. 1).
drug-induced hemolytic anemia (drug-induced immune hemolytic anemia) a form of immune hemolytic anemia induced by the taking of drugs, involving one of four different mechanisms:

Immune complex problems: Ingestion of any of a large number of drugs is followed by immunization and the formation of a soluble drug–anti-drug complex that adsorbs nonspecifically to the erythrocyte surface.

Drug absorption: Drugs bind firmly to erythrocyte membrane proteins, inducing the formation of specific antibodies; the drug most commonly associated with this mechanism is penicillin.

Membrane modification: A nonimmunologic mechanism whereby the drug involved is able to modify erythrocytes so that plasma proteins can bind to the membrane.

Autoantibody formation: Methyldopa (Aldomet) induces the production of autoantibodies that recognize erythrocyte antigens and are serologically indistinguishable from those seen in patients with warm autoimmune hemolytic anemia.
Fanconi's anemia (Fanconi's hypoplastic anemia) Fanconi's syndrome (def. 1).
hemolytic anemia see hemolytic anemia.
hemorrhagic anemia anemia caused by the sudden and acute loss of blood; called also acute posthemorrhagic anemia.
hypochromic anemia anemia in which the decrease in hemoglobin is proportionately much greater than the decrease in number of erythrocytes.
hypochromic microcytic anemia any anemia with microcytes that are hypochromic (reduced in size and in hemoglobin content); the most common type is iron deficiency anemia.
hypoplastic anemia anemia due to incapacity of blood-forming organs.
immune hemolytic anemia an acquired hemolytic anemia in which a hemolytic response is caused by isoantibodies or autoantibodies produced on exposure to drugs, toxins, or other antigens. See also autoimmune hemolytic anemia, drug-induced immune hemolytic anemia, and erythroblastosis fetalis.
iron deficiency anemia a type of hypochromic microcytic anemia that results from the presence of greater demands on stored iron than can be met, usually because of chronic blood loss, dietary deficiency, or defective absorption; it is characterized by low or absent iron stores, low serum iron concentration, low transferrin saturation, elevated transferrin (total iron-binding capacity), and low hemoglobin concentration or hematocrit. Iron deficiency anemia is the most common nutritional disorder in the United States.
macrocytic anemia anemia characterized by macrocytes (erythrocytes much larger than normal).
Mediterranean anemia thalassemia major.
megaloblastic anemia any of various anemias characterized by the presence of megaloblasts in the bone marrow or blood; the most common type is pernicious anemia.
microangiopathic hemolytic anemia thrombotic thrombocytopenic purpura.
microcytic anemia anemia characterized by microcytes (erythrocytes smaller than normal); see also hypochromic microcytic anemia and microcythemia.
myelopathic anemia (myelophthisic anemia) leukoerythroblastosis.
normochromic anemia that in which the hemoglobin content of the red blood cells is in the normal range.
normocytic anemia anemia characterized by proportionate decrease in hemoglobin, packed red cell volume, and number of erythrocytes per cubic millimeter of blood.
nutritional anemia anemia due to a deficiency of an essential substance in the diet, which may be caused by poor dietary intake or by malabsorption; called also deficiency anemia.
pernicious anemia see pernicious anemia.
sickle cell anemia see sickle cell anemia.
sideroachrestic anemia (sideroblastic anemia) any of a heterogenous group of acquired and hereditary anemias with diverse clinical manifestations, commonly characterized by large numbers of sideroblasts in the bone marrow, ineffective erythropoiesis, variable proportions of hypochromic erythrocytes in the peripheral blood, and usually increased levels of tissue iron.
spur cell anemia anemia in which the erythrocytes are acanthocytes (spur cells) and are destroyed prematurely, primarily in the spleen; it is an acquired form occurring in severe liver disease in which there is increased serum cholesterol and increased uptake of cholesterol into the erythrocyte membrane, causing the abnormal shape.

i·ron de·fi·cien·cy a·ne·mi·a

hypochromic microcytic anemia characterized by low serum iron, increased serum iron-binding capacity, decreased serum ferritin, and decreased marrow iron stores.
Synonym(s): hypoferric anemia

iron deficiency anemia

a microcytic hypochromic anemia caused by inadequate supplies of iron needed to synthesize hemoglobin. Symptoms are pallor, fatigue, anorexia, malaise, and weakness. Laboratory diagnosis includes hemoglobin, hematocrit, transferrin saturation, ferritin, and serum iron concentration. Iron deficiency may be the result of an inadequate dietary supply of iron, poor absorption of iron by the digestive system, chronic bleeding, or compensated hemolytic anemia. Replacement iron can be supplied by oral ferrous sulfate. The anemia corrects in 2 months, but therapy is continued for another 4 months to replace tissue stores. Compare hemolytic anemia, hypoplastic anemia. See also iron metabolism, nutritional anemia, red cell indexes.

iron de·fi·cien·cy a·ne·mia

(ī'ŏrn dĕ-fish'ĕn-sē ă-nē'mē-ă)
Hypochromic microcytic anemia characterized by low serum iron, increased serum iron-binding capacity, decreased serum ferritin, and decreased marrow iron stores.

Iron Deficiency Anemia

DRG Category:812
Mean LOS:3.4 days
Description:MEDICAL: Red Blood Cell Disorders Without Major CC

Iron deficiency anemia (IDA), the most common form of anemia, is a condition in which there is a decrease in normal body stores of iron and hemoglobin levels. IDA is caused by inadequate intake of iron, inadequate storage of iron, excessive loss of iron, or some combination of these conditions. The red blood cells (RBCs), which become pale (hypochromic) and small (microcytic), have a decreased ability to transport oxygen in sufficient quantities to meet body needs. Anemia is defined as a decrease in circulating RBC mass; the usual criteria for anemia are hemoglobin of less than 12 g/dL with a hematocrit less than 36% in women and hemoglobin less than 14 g/dL with a hematocrit less than 41% in men.

Generally, IDA is more common in people who are economically disadvantaged because of the high cost of a well-balanced diet with iron-rich foods. Complications from IDA include infection and pneumonia. For patients suffering from pica (the urge to eat clay and other inappropriate items), lead poisoning may result from increased intestinal absorption of lead. Although it is a rare condition, Plummer-Vinson syndrome (IDA associated with difficulty swallowing, enlarged spleen, and spooning of the nails) may occur in severe cases of IDA, especially in middle-aged women who have recently had their teeth extracted.


The most common causes of IDA are menstrual blood loss and the increased iron requirements of pregnancy. Pathological bleeding, particularly gastrointestinal (GI) bleeding, is a common cause of iron depletion in men. Iron malabsorption can lead to IDA. Pathological causes include GI ulcers, hiatal hernias, malabsorption syndromes such as celiac disease, chronic diverticulosis, varices, and tumors. Other causes include surgeries such as partial gastrectomy and the use of prosthetic heart valves or vena cava filters.

Genetic considerations

There are no documented heritable syndromes that cause an isolated iron deficiency, but the possibility has not been excluded. There are known causes of iron overload including hereditary hemochromatosis (HHC), which follows an autosomal recessive transmission pattern.

Gender, ethnic/racial, and life span considerations

Infants under age 2 may develop IDA in situations of prolonged unsupplemented breastfeeding or bottle feeding; breast milk has some iron, but cow’s milk has none. During periods of rapid growth in childhood, adolescence, and pregnancy, patients may ingest inadequate supplies of iron. Young women, in particular, are at risk as a result of heavy menses or unwise weight-reduction plans, and in the United States, females have a higher incidence of IDA than males. During childbearing years, adult females lose an average of 2 mg of iron daily that must be replaced nutritionally, whereas men lose only 1 mg of iron per day. Women at highest risk for IDA are women who live in urban poverty. Elderly patients with a poor diet and people who are alcohol dependent who fail to eat a well-balanced diet may also ingest inadequate supplies of iron.

Global health considerations

In areas of the globe where meat is not a routine part of the diet, iron deficiency anemia is more prevalent than in developed nations where meat is plentiful and culturally part of dietary patterns. In certain underresourced regions of the world, intestinal parasites make iron deficiency worse because of gastrointestinal blood loss.



Inquire about recent weight loss, fatigue, weakness, dizziness, irritability, inability to concentrate, sensitivity to cold, heartburn, loss of appetite, diarrhea, or flatulence. Establish a history of difficulty in swallowing, which is a sign of long-term oxygen deficit, as esophageal webbing ensues. Elicit any history of neuromuscular effects, including vasomotor disturbances, tingling or numbness of the extremities, or pain along a nerve. Ask if the patient has experienced difficulty in breathing on exertion, rapid breathing, or palpitations. With infants and children, ask the parents to establish a history of growth patterns. With premenopausal women, ask about heavy bleeding during menses. Ask female patients for a pregnancy history.

Take a complete diet and illness history. Ask if the patient regularly eats foods that are rich in iron, such as whole grains, seafood, egg yolks, legumes, green leafy vegetables, dried fruits, red meats, and nuts; ask if she or he takes iron in vitamin supplements. Elicit the patient’s history of alcohol use. With infants, ask if breastfeeding or bottle feeding has been used and if any iron supplements have been added to the diet. Establish any history of frequent nosebleeds. With elderly patients, elicit a history of food preparation and diet planning to find out who takes responsibility for the patient’s diet. Ask the patient if she or he has had recent cravings for strange food (especially clay, laundry starch, or ice). Pagophagia is a form of pica involving compulsive eating or sucking of ice.

Physical examination

While the condition may be asymptomatic, common symptoms include leg cramps and craving for ice or cold foods (pagophagia). Inspect the patient’s mouth for signs of inflammation (stomatitis) or eroded, tender, and swollen corners (angular stomatitis). Observe the tongue to see if it is inflamed and smooth because of atrophy of the papillae (glossitis). Note the color of the patient’s skin to see if it is pale with poor turgor. Note the color of the patient’s sclera, which may be pearly white to bluish. Inspect the patient’s fingernails to check for brittleness; note the shape of the fingernails, which may be spoon-shaped with central depressions and raised borders. Check the patient’s hair to see if it is brittle and easily broken. In later stages, ankle edema may be present. Note any breathlessness or rapid breathing. Auscultate for heart sounds, noting rapid heart rate or a functional systolic murmur.


Patients may be anxious or fearful about symptoms that have made it difficult for them to function at their usual level of energy. Discomfort from oral mucosa symptoms may prove upsetting. A pregnant patient may have additional stress over the well-being of her baby. Some patients may be resistant to proposed changes that would disrupt long-held eating patterns. Patients may also be upset about body changes such as pallor and weight loss.

Diagnostic highlights

TestNormal ResultAbnormality With ConditionExplanation
Bone marrow biopsyNormal cellsCells show absent staining for ironCells are iron deficient
Complete blood countRBCs 4–5.5 million/μLDecreased; normal unless infection is presentCells are iron deficient; as hematocrit falls below 30%, hypochromic microcytic cells appear, followed by a decrease in MCV
White blood cells (WBCs) 4,500–11,000/μLUsually the WBC count is normal unless other conditions, such as infection, occur
Hemoglobin 12–18 g/dLDecreasedCells are iron deficient
Hematocrit 37%–54%DecreasedCells are iron deficient
Mean corpuscular volume (MCV) 82–93/mm3DecreasedCells are iron deficient
Serum ferritin11–200 ng/dL< 10 ng/dL in women; < 20 ng/dL in menCells are iron deficient

Other Tests: Serum iron, total iron-binding capacity, reticulocyte hemoglobin content, hemoglobin electrophoresis, hemoglobin A2, fetal hemoglobin

Primary nursing diagnosis


Activity intolerance related to imbalance between oxygen supply and demand


Energy conservation; Endurance; Self-care: Activities of daily living; Ambulation: Walking; Circulation status; Immobility consequences: Physiological; Mobility level; Nutritional status: Energy; Symptom severity


Nutritional management; Medication management; Energy management; Exercise promotion; Exercise therapy: Ambulation; Surveillance; Vital signs monitoring

Planning and implementation


The two primary goals of treatment are to diagnose and correct the underlying cause of the iron deficiency and to correct the iron deficit. Medication therapy involves administering supplemental iron, which often shows results in the form of increased patient energy within 48 hours. Blood transfusions are not recommended for iron supplementation and should not be used to treat IDA unless there is cerebrovascular or cardiopulmonary compromise. Dietary supplementation of iron-rich food is needed to complement therapy and serve as a preventive model against future recurrence of the anemia. Pregnant women may also need to take prenatal vitamins and iron supplements.

Pharmacologic highlights

Medication or Drug ClassDosageDescriptionRationale
Supplemental ironVaries with drugOral therapy: Ferrous sulfate (Feosol); ferrous gluconate (Fergon)Increases iron stores; oral preparations should be taken with water or a straw to avoid staining teeth; oral iron supplements may cause gastric irritation; irritation may be reduced by administering the supplement with meals as long as eggs, dairy products, coffee, tea, and antacids are avoided; foods containing ascorbic acid, however, aid absorption
Supplemental iron25-100 mg IV or deep IM dailyParenteral therapy: Iron dextran complexIron dextran complex (INFeD) is the preferred medication for intramuscular injections; pregnant and elderly patients with severe iron deficiency anemia; drug may be given as total-dose IV infusion of iron dextran complex in a sodium chloride solution after a small test dose is given to check for allergic reaction


Nursing interventions focus on preventing infections, promoting comfort, and teaching the patient. Patients with IDA are apt to have other nutritional deficiencies that place them at risk for infection. Use good hand-washing techniques and encourage the patient to avoid contact with people with known upper respiratory infections. If the patient experiences discomfort from oral lesions, provide mouth care. To limit activity intolerance, allow rest periods between all activities. Before the patient’s discharge, arrange for home health follow-up if needed.

Teach the patient and significant others the causal relationships between bleeding tendencies and poor diet in relation to this anemia. Discuss the need to pace activities and allow for periods of rest. Emphasize to the patient the need for a well-balanced diet rich in iron; provide a list of iron-rich foods. Explain that any excess in iron stores may cause toxicity. Teach the patient that certain foods and medications—such as milk and antacids—interfere with the absorption of iron. Explain that stools normally turn greenish to black in color with iron therapy and that constipation may occur. Iron-rich foods, such as fresh vegetables and red meat, tend to be expensive, so budget planning activities or assistance in attaining food stamps or other assistive programs may be essential. A social service referral or arranging of home care needs may be necessary. Parents of infants may need follow-up home visits to ensure that the growth and development of the child are progressing normally.

Evidence-Based Practice and Health Policy

Silverberg, D.S., Schwartz, D., Schwartz, I., & Ben Assa, E. (2013). The missed opportunities to diagnose and treat iron deficiency in patients hospitalized with heart failure. International Journal of Cardiology, 168(3), 2164–2166.

  • Although iron deficiency anemia is common among heart failure patients, investigators suggest that there are missed opportunities to identify and treat the condition.
  • In a retrospective analysis of 76 records of recently hospitalized heart failure patients, anemia was identified in 55.3% of patients. However, less than 20% of the total sample received a complete iron work-up. More than 60% of the patients with anemia received no iron work-up.
  • Iron deficiency anemia was identified in 80% of patients who did receive a complete work-up, yet only 18.4% of the total sample was prescribed iron at the time of discharge.

Documentation guidelines

  • Physical findings: Oral mucosa alterations; weight loss; skin turgor
  • Response to activity; ability to maintain activities of daily living
  • Laboratory results: Reduced level of hemoglobin, RBCs, hematocrit, MCV
  • Response to iron supplement therapy, side effects

Discharge and home healthcare guidelines

Teach the patient that a well-balanced diet rich in both iron and iron supplements is necessary to prevent a recurrence of the anemia and provide a list of iron-rich foods. Advise continuation of iron supplementation therapy even after the patient begins to feel better. Teach the route, dosage, side effects, and indications for use of iron supplements. Infection is a possibility because of the patient’s weakened condition. Therefore, stress the importance of meticulous wound care, good hand-washing techniques, and periodic dental checkups. Emphasize the need for the patient to immediately report any signs of infection to the physician, such as fever or chills.

iron de·fi·cien·cy a·ne·mia

(īŏrn dĕ-fishĕn-sē ă-nēmē-ă)
Hypochromic microcytic anemia characterized by low serum iron, increased serum iron-binding capacity, decreased serum ferritin, and decreased marrow iron.
References in periodicals archive ?
Final report research project to investigate the prevalence of iron deficiency anemia in women aged 15 to 45.
When supplementation is inadequate, iron deficiency and iron deficiency anemia develop rapidly (15,16).
As mentioned earlier, iron deficiency anemia is commonly associated with pica and is often viewed as a physiological response to preexisting iron deficiency anemia.
Iron deficiency anemia is a frequent by-product of a dietary consisting largely of milk and unsupplemented by fortified food products during the early years of development.
Iron deficiency anemia in infancy is associated with altered temporal organization of sleep states in childhood.
Assuming that your diagnosis of iron deficiency anemia is correct, a three-month course of iron therapy should restore your red blood cell count to normal and replenish your iron stores.
This approach has proven the most inexpensive method of protecting donors against the development of progressive iron deficiency anemia.
In the meantime, he is excited about the finding because "it has proven very difficult to prevent the onset of iron deficiency anemia or to correct the problem once it develops.
The sNDA requests FDA approval to expand the indication for ferumoxytol beyond the current indication for the treatment of iron deficiency anemia (IDA) in adult patients with chronic kidney disease (CKD) to all adult patients with IDA who have failed or could not tolerate oral iron treatment.
LONDON, April 2, 2015 /PRNewswire/ -- Summary GlobalData's clinical trial report, "Iron Deficiency Anemia Global Clinical Trials Review, H2, 2014" provides data on the Iron Deficiency Anemia clinical trial scenario.
an innovative intravenous iron replacement therapy under development for the treatment of Iron Deficiency Anemia.
Objectives: The aim of this study was to evaluate the prevalence of subclinical and clinical iron deficiency with iron deficiency anemia in primary antiphospholipid syndrome (PAPS).