Iron deficiency anemia

Iron deficiency anemia: Excerpt from Professional Guide to Diseases (Eighth Edition)

Iron deficiency anemia is caused by an inadequate supply of iron for optimal formation of red blood cells (RBCs), resulting in smaller (microcytic) cells with less color on staining. Body stores of iron, including plasma iron, decrease, as do levels of transferrin, which binds with and transports iron. Insufficient body stores of iron lead to a depleted RBC mass and, in turn, to a decreased hemoglobin (Hb) concentration (hypochromia) and decreased oxygen-carrying capacity of the blood. (See Absorption and storage of iron.)

Causes and incidence

Iron deficiency anemia may result from:

❑ inadequate dietary intake of iron (less than 1 to 2 mg/day), such as in prolonged unsupplemented breast-feeding or bottle-feeding of infants or during periods of stress such as rapid growth in children and adolescents

❑ iron malabsorption, such as in chronic diarrhea, partial or total gastrectomy, chronic diverticulosis, and malabsorption syndromes, such as celiac disease and pernicious anemia

❑ blood loss secondary to drug-induced GI bleeding (from anticoagulants, aspirin, and steroids) or due to heavy menses, hemorrhage from trauma, GI ulcers, esophageal varices, or cancer

❑ pregnancy, which diverts maternal iron to the fetus for erythropoiesis

❑ intravascular hemolysis-induced hemoglobinuria or paroxysmal nocturnal hemoglobinuria

❑ mechanical erythrocyte trauma caused by a prosthetic heart valve or vena cava filters.

A common disease worldwide, iron deficiency anemia affects 10% to 30% of the adult population of the United States. It occurs most commonly in premenopausal women, infants (particularly premature or low-birth-weight neonates), children, and adolescents (especially girls). Persons who are at increased risk for iron deficiency include those of low socioeconomic status who don’t get a well-balanced diet that includes iron-rich foods.

Signs and symptoms

Because of the gradual progression of iron deficiency anemia, many patients are initially asymptomatic except for symptoms of any underlying condition. They tend not to seek medical treatment until anemia is severe. At advanced stages, decreased Hb levels and the consequent decrease in the blood’s oxygen-carrying capacity cause the patient to develop dyspnea on exertion, fatigue, listlessness, pallor, inability to concentrate, irritability, headache, and a susceptibility to infection. Decreased oxygen perfusion causes the heart to compensate with increased cardiac output and tachycardia.

In chronic iron deficiency anemia, nails become spoon-shaped and brittle, the mouth’s corners crack, the tongue turns smooth, and the patient complains of dysphagia or may develop pica. Associated neuromuscular effects include vasomotor disturbances, numbness and tingling of the extremities, and neuralgic pain.

Diagnosis

Blood studies (serum iron levels, total iron-binding capacity, and ferritin levels) and stores in bone marrow may confirm iron deficiency anemia. However, the results of these tests can be misleading because of complicating factors, such as infection, pneumonia, blood transfusion, or iron supplements. Characteristic blood test results include:

❑ low Hb levels (in males, less than 12 g/ dl; in females, less than 10 g/dl)

❑ low hematocrit (in males, less than 39%; in females, less than 35%)

❑ low serum iron levels, with high binding capacity

❑ low serum ferritin levels

❑ low RBC count, with microcytic and hypochromic cells (in early stages, RBC count may be normal, except in infants and children)

❑ decreased mean corpuscular Hb in severe anemia.

Bone marrow studies reveal depleted or absent iron stores (done by staining) and normoblastic hyperplasia.

Diagnosis must rule out other forms of anemia, such as those that result from thalassemia minor, cancer, and chronic inflammatory, hepatic, and renal disease.

Treatment

The first priority of treatment is to determine the underlying cause of anemia. Once this is determined, iron replacement therapy can begin. Treatment of choice is an oral preparation of iron or a combination of iron and ascorbic acid (which enhances iron absorption). However, in some cases, iron may have to be administered parenterally — for instance, if the patient is noncompliant to the oral preparation, if he needs more iron than he can take orally, if malabsorption prevents adequate iron absorption, or if a maximum rate of Hb regeneration is desired.

Because total dose I.V. infusion of supplemental iron is painless and requires fewer injections, it’s usually preferred to I.M. administration. Pregnant patients and geriatric patients with severe anemia, for example, should receive a total dose infusion of iron dextran in normal saline solution over 8 hours. To minimize the risk of an allergic reaction to iron, an I.V. test dose of 0.5 ml should be given first. For more patient care information, see Supportive management of patients with anemia, page 1034.

Special considerations

❑ Monitor the patient’s compliance with the prescribed iron supplement therapy. Advise the patient not to stop therapy even if he feels better, because replacement of iron stores takes time.

❑ Tell the patient he may take iron supplements with a meal to decrease gastric irritation. Advise him to avoid milk, milk products, and antacids because they interfere with iron absorption; however, vitamin C can increase absorption.

❑ Warn the patient that iron supplements may result in dark green or black stools and can cause constipation.

❑ Instruct the patient to drink liquid supplemental iron through a straw to prevent staining his teeth.

❑ Tell the patient to report reactions, such as nausea, vomiting, diarrhea, constipation, fever, or severe stomach pain, which may require a dosage adjustment.

❑ If the patient receives I.V. iron, monitor the infusion rate carefully and observe for an allergic reaction. Stop the infusion and begin supportive treatment immediately if the patient shows signs of an adverse reaction. Also, watch for dizziness and headache and for thrombophlebitis around the I.V. site.

❑ Use the Z-track injection method when administering iron I.M. to prevent skin discoloration, scarring, and irritating iron deposits in the skin. (See How to inject iron solutions, page 1035.)

❑ Because an iron deficiency may recur, advise regular checkups and blood studies.

Health professionals can play a vital role in preventing iron deficiency anemia by:

❑ teaching the basics of a nutritionally balanced diet — red meats, green vegetables, eggs, whole wheat products, and iron-fortified bread. (However, no food in itself contains enough iron to treat iron deficiency anemia; an average-sized person with anemia would have to eat at least 10 lb of steak daily to receive therapeutic amounts of iron.)

❑ emphasizing the need for high-risk individuals — such as premature infants, children younger than age 2, and pregnant women — to receive prophylactic oral iron, as ordered by a physician. (Children younger than age 2 should also receive supplemental cereals and formulas high in iron.)

❑ assessing a family’s dietary habits for iron intake and noting the influence of childhood eating patterns, cultural food preferences, and family income on adequate nutrition.

❑ encouraging families with deficient iron intake to eat meat, fish, or poultry; whole or enriched grain; and foods high in ascorbic acid.

❑ carefully assessing a patient’s drug history because certain drugs, such as pancreatic enzymes and vitamin E, may interfere with iron metabolism and absorption and because aspirin, steroids, and other drugs may cause GI bleeding. (Teach patients who must take gastric irritants to take these medications with meals.)

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Book Source Details

• Book Title: Professional Guide to Diseases (Eighth Edition)
• Author(s): Springhouse
• Year of Publication: 2005
• Copyright Details: Professional Guide to Diseases (Eighth Edition), Copyright © 2005 Lippincott Williams & Wilkins.

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More About This Book: Title: Professional Guide to Diseases (Eighth Edition) Authors: Springhouse Publisher: Lippincott Williams & Wilkins Copyright: 2005 ISBN: 1-58255-370-X

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