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Normally during pregnancy, erythroid hyperplasia of the marrow occurs, and RBC mass increases. However, a disproportionate increase in plasma volume results in hemodilution (hydremia of pregnancy): Hct decreases from between 38 and 45% in healthy women who are not pregnant to about 34% during late single pregnancy and to 30% during late multifetal pregnancy. Thus during pregnancy, anemia is defined as Hb < 10 g/dL (Hct < 30%). If Hb is < 11.5 g/dL at the onset of pregnancy, women may be treated prophylactically because subsequent hemodilution usually reduces Hb to < 10 g/dL. Despite hemodilution, O2-carrying capacity remains normal throughout pregnancy. Hct normally increases immediately after birth.
Anemia occurs in up to one third of women during the 3rd trimester. The most common causes are iron deficiency and folate deficiency.
Symptoms and Signs
Early symptoms are usually nonexistent or nonspecific (eg, fatigue, weakness, light-headedness, mild dyspnea during exertion). Other symptoms and signs may include pallor and, if anemia is severe, tachycardia or hypotension. Anemia increases risk of preterm delivery and postpartum maternal infections.
Diagnosis
Diagnosis begins with CBC; usually, if women have anemia, subsequent testing is based on whether the MCV is low (< 79 fL) or high (> 100 fL):
Treatment
Treatment is directed at reversing the anemia. Transfusion is usually indicated for any anemia if severe constitutional symptoms (eg, light-headedness, weakness, fatigue) or cardiopulmonary symptoms or signs (eg, dyspnea, tachycardia, tachypnea) are present; the decision is not based on the Hct.
Iron Deficiency Anemia in Pregnancy
About 95% of anemia cases during pregnancy are due to iron deficiency (see Anemias Caused by Deficient Erythropoiesis: Iron Deficiency Anemia). The cause is usually inadequate dietary intake (especially in adolescent girls), a previous pregnancy, or the normal recurrent loss of iron in menstrual blood (which approximates the amount normally ingested each month and thus prevents iron stores from building up).
Diagnosis
Typically, Hct is ≤ 30%, and MCV is < 79 fL. Decreased serum iron and ferritin and increased serum transferrin levels confirm the diagnosis.
Treatment
One 325-mg ferrous sulfate tablet taken midmorning is usually effective. Higher or more frequent doses increase GI adverse effects, especially constipation, and one dose blocks absorption of the next dose, thereby reducing percentage intake. About 20% of pregnant women do not absorb enough supplemental oral iron; a few of them require parenteral therapy, usually iron dextran 100 mg IM every other day for a total of ≥ 1000 mg over 3 wk. Hct or Hb is measured weekly to determine response. If iron supplements are ineffective, concomitant folate deficiency should be suspected.
Neonates of mothers with iron deficiency anemia usually have a normal Hct but decreased total iron stores and a need for early dietary iron supplements.
Prevention
Although the practice is controversial, iron supplements (usually ferrous sulfate 325 mg po once/day) are usually given routinely to pregnant women to prevent depletion of body iron stores and prevent the anemia that may result from abnormal bleeding or a subsequent pregnancy.
Folate Deficiency Anemia in Pregnancy
Folate deficiency (see Vitamin Deficiency, Dependency, and Toxicity: Folate Deficiency and see Anemias Caused by Deficient Erythropoiesis: Megaloblastic Macrocytic Anemias) increases risk of neural tube defects and possibly fetal alcohol syndrome. Deficiency occurs in 0.5 to 1.5% of pregnant women; macrocytic, megaloblastic anemia is present if deficiency is moderate or severe. Rarely, severe anemia and glossitis occur.
Diagnosis
Folate deficiency is suspected if CBC shows anemia with macrocytic indices or high RBC distribution width (RDW). Low serum folate levels confirm the diagnosis.
Treatment
Treatment is folate 1 mg po bid. Severe megaloblastic anemia may warrant bone marrow examination and further treatment in a hospital.
Prevention
For prevention, all pregnant women are given folate 0.4 mg po once/day. Women who have had a fetus with spina bifida should take 4.0 mg once/day, starting before conception.
Hemoglobinopathies in Pregnancy
(see Sidebar 1: Anemias Caused by Hemolysis: Hemoglobinopathies )
During pregnancy, hemoglobinopathies, particularly sickle cell disease, Hb S-C disease, β-thalassemia disease, and α-thalassemia, can worsen maternal and perinatal outcomes (for genetic screening, see Table 1: Prenatal Genetic Counseling and Evaluation: Genetic Screening for Some Ethnic Groups ).
Preexisting sickle cell disease, particularly if severe, increases risk of maternal infection (most often, pneumonia, UTIs, and endometritis), pregnancy-induced hypertension, heart failure, and pulmonary infarction. Fetal growth restriction, preterm delivery, and low birth weight are common. Anemia almost always becomes more severe as pregnancy progresses. Sickle cell trait increases the risk of UTIs but is not associated with severe pregnancy-related complications.
Treatment of sickle cell disease during pregnancy is complex. Painful crises should be treated aggressively. Prophylactic exchange transfusions to keep Hb A at ≥ 60% reduce risk of hemolytic crises and pulmonary complications, but they are not routinely recommended because they increase risk of transfusion reactions, hepatitis, HIV transmission, and blood group isoimmunization. Prophylactic transfusion does not appear to decrease perinatal risk. Therapeutic transfusion is indicated for the following:
Hb S-C disease may first cause symptoms during pregnancy. The disease increases risk of pulmonary infarction by occasionally causing bony spicule embolization. Effects on the fetus are uncommon but, if they occur, often include fetal growth restriction.
Sickle cell–β-thalassemia is similar to Hb S-C disease but is less common and more benign.
α-Thalassemia does not cause maternal morbidity, but if the fetus is homozygous, hydrops and fetal death occur during the 2nd or early 3rd trimester.
Last full review/revision December 2008 by Sean C. Blackwell, MD
Content last modified February 2012
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