Williams Manual of Pregnancy Complications, 23 ed.

CHAPTER 68. Anemia

A modest fall in hemoglobin levels is observed during pregnancy in healthy women who are not deficient in iron or folate (Figure 68-1). This is caused by a relatively greater expansion of plasma volume compared with the increase in hemoglobin mass and red blood cell volume that accompany normal pregnancy. Early in pregnancy and again near term, the hemoglobin level of most healthy women with iron stores is 11 g/dL or higher. The hemoglobin concentration is lower in midpregnancy. For these reasons, the Centers for Disease Control and Prevention (CDC) have defined anemia as less than 11 g/dL in the first and third trimesters, and less than 10.5 g/dL in the second trimester.


FIGURE 68-1 Mean hemoglobin concentrations (black line) and 5th and 95th percentiles (blue lines) for healthy pregnant women taking iron supplements. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010. Data from Centers for Disease Control and Prevention: CDC criteria for anemia in children and childbearing-aged women. MMWR 38:400, 1989.)


Any disorder causing anemia encountered in childbearing-age women may complicate pregnancy. A classification based primarily on etiology and including most of the common causes of anemia in pregnant women is shown in Table 68-1. In this chapter, we focus on the more common causes of anemia during pregnancy. The reader is referred to Chapter 51 of Williams Obstetrics, 23rd ed., for information on the rare hemolytic and aplastic or hypoplastic anemias.

TABLE 68-1. Causes of Anemia during Pregnancy



The two most common causes of anemia during pregnancy and the puerperium are iron deficiency and acute blood loss. Not infrequently, the two are intimately related, because excessive blood loss with its concomitant loss of hemoglobin iron and exhaustion of iron stores in one pregnancy can be an important cause of iron-deficiency anemia in the next pregnancy.

In a typical gestation with a single fetus, the total maternal need for iron induced by pregnancy averages close to 1000 mg, which considerably exceeds the iron stores of most women. Unless the difference between the amount of stored iron available to the mother and the iron requirements of normal pregnancy is compensated for by absorption of iron from the gastrointestinal tract, iron-deficiency anemia develops. Because the amount of iron diverted to the fetus from an iron-deficient mother is not much different from the amount normally transferred, the newborn infant of a severely anemic mother does not suffer from iron-deficiency anemia.


The initial evaluation of a pregnant woman with moderate anemia (hematocrit of 22 to 29 volume percent) should include measurements of hemoglobin, hematocrit, and red blood cell indices; careful examination of a peripheral blood smear; sickle-cell preparation if the woman is of African origin; and measurement of serum iron concentration or ferritin, or both. Pragmatically, the diagnosis of iron deficiency in moderately anemic pregnant women usually is presumptive and based largely on the exclusion of other causes of anemia.


The objectives of treatment are correction of the deficit in hemoglobin mass and eventually restitution of iron stores. Both of these objectives can be accomplished with orally administered, simple iron compounds—ferrous sulfate, fumarate, or gluconate—that provide a daily dose of approximately 200 mg of elemental iron. To replenish iron stores, oral therapy should be continued for 3 months or so after the anemia has been corrected. When the pregnant woman with moderate iron-deficiency anemia is given adequate iron therapy, a hematological response is detected by an elevated reticulocyte count.

Transfusions of red blood cells or whole blood seldom are indicated for the treatment of iron-deficiency anemia unless hypovolemia from blood loss coexists or an emergency operative procedure must be performed on a severely (hematocrit less than 20 volume percent) anemic woman.


Massive acute hemorrhage demands immediate treatment to restore and maintain perfusion of vital organs such as the kidney. Even though the amount of blood replaced commonly does not completely repair the hemoglobin deficit created by the hemorrhage; in general, once dangerous hypovolemia has been overcome and hemostasis has been achieved, the residual anemia should be treated with iron. For the moderately anemic woman whose hemoglobin is more than 7 g/dL, whose condition is stable, who no longer faces the likelihood of further serious hemorrhage, and who can ambulate without adverse symptoms, iron therapy for at least 3 months rather than blood transfusions is the best treatment.


During pregnancy, a number of chronic diseases may cause anemia. Some of these are chronic renal disease, inflammatory bowel disease, systemic lupus erythematosus, granulomatous infections, malignant neoplasms, and rheumatoid arthritis. Such anemias are typically intensified as plasma volume expands out of proportion to red cell mass expansion.

Treatment with recombinant erythropoietin has been used successfully to treat chronic anemia in women with chronic renal insufficiency and is usually initiated when the hematocrit approximates 20 percent. One worrisome side effect is hypertension, which is already prevalent in women with renal disease. In addition, pure red cell aplasia and formation of antierythropoietin antibodies has been reported.


In the United States, megaloblastic anemia beginning during pregnancy almost always results from folic-acid deficiency. It usually is found in women who do not consume fresh green leafy vegetables, legumes, or animal protein. The treatment of pregnancy-induced megaloblastic anemia should include folic acid, a nutritious diet, and iron. As little as 1 mg of folic acid administered orally once daily produces a striking hematological response. By 4 to 7 days after beginning treatment, the reticulocyte count is increased appreciably. The fetus and placenta extract folate from maternal circulation so effectively that the fetus is not anemic even when the mother is severely anemic from folate deficiency.

A great deal of attention has been devoted to the role of folate deficiency in the genesis of neural-tube defects. These findings led the Centers for Disease Control and Prevention (CDC) and the American College of Obstetricians and Gynecologists (Neural tube defects, Practice Bulletin No. 44, July 2003) to recommend that all childbearing-age women consume at least 0.4 mg of folic acid daily. Additional folic acid is given in circumstances where folate requirements are unusually excessive, as in multifetal pregnancy or hemolytic anemia, such as sickle-cell disease. Other indications include Crohn disease, alcoholism, and some inflammatory skin disorders. There is evidence that women who previously have had infants with neural-tube defects have a lower recurrence rate if folic acid, 4 mg daily, is given prior to and through early pregnancy.

Megaloblastic anemia caused by lack of vitamin B12 during pregnancy is exceedingly rare. In our limited experience, vitamin B12 deficiency in pregnant women is more likely encountered following partial or total gastric resection. Other causes are Crohn disease, ileal resection, and bacterial overgrowth in the small bowel.

For further reading in Williams Obstetrics, 23rd ed.,

see Chapter 51, “Hematological Disorders.”