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Anemia in Pregnancy
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, O 2 -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
Obstetricians, in consultation with a perinatologist, should evaluate anemia in pregnant Jehovah's Witness patients (who are likely to refuse blood transfusions) as soon as possible.
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 begins with CBC; usually, if women have anemia, subsequent testing is based on whether the MCV is low (<79 fL) or high (> 100 fL):
For microcytic anemias: Evaluation includes testing for iron deficiency (measuring serum ferritin) and hemoglobinopathies (using hemoglobin electrophoresis). If these tests are nondiagnostic and there is no response to empiric treatment, consultation with a hematologist is usually warranted.
For macrocytic anemias: Evaluation includes serum folate and B 12 levels.
For anemia with mixed causes: Evaluation for both types is required.
Treatment is directed at reversing the anemia (see below).
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.
About 95% of anemia cases during pregnancy are due to iron deficiency (see Iron Deficiency Anemia). The cause is usually
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.
Folate deficiency (see Folate Deficiency and 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.
During pregnancy, hemoglobinopathies, particularly sickle cell disease (see Sickle Cell Disease), Hb S-C disease (see Hemoglobin S-C Disease), β-thalassemia disease, and α-thalassemia (see Thalassemias), can worsen maternal and perinatal outcomes (for genetic screening for some of these disorders, see Table: 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.
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