What is the most common form of acquired anemia during pregnancy?

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When you're pregnant, you may develop anemia. When you have anemia, your blood doesn't have enough healthy red blood cells to carry oxygen to your tissues and to your baby.

During pregnancy, your body produces more blood to support the growth of your baby. If you're not getting enough iron or certain other nutrients, your body might not be able to produce the amount of red blood cells it needs to make this additional blood.

It's normal to have mild anemia when you are pregnant. But you may have more severe anemia from low iron or vitamin levels or from other reasons.

Anemia can leave you feeling tired and weak. If it is severe but goes untreated, it can increase your risk of serious complications like preterm delivery.

Here's what you need to know about the causes, symptoms, and treatment of anemia during pregnancy.

Several types of anemia can develop during pregnancy. These include:

Iron-deficiency anemia
Folate-deficiency anemia
Vitamin B12 deficiency

Here's why these types of anemia may develop:

Iron-deficiency anemia. This type of anemia occurs when the body doesn't have enough iron to produce adequate amounts of hemoglobin. That's a protein in red blood cells. It carries oxygen from the lungs to the rest of the body.

In iron-deficiency anemia, the blood cannot carry enough oxygen to tissues throughout the body.

Iron deficiency is the most common cause of anemia in pregnancy.

Folate-deficiency anemia. Folate is the vitamin found naturally in certain foods like green leafy vegetables A type of B vitamin, the body needs folate to produce new cells, including healthy red blood cells.

During pregnancy, women need extra folate. But sometimes they don't get enough from their diet. When that happens, the body can't make enough normal red blood cells to transport oxygen to tissues throughout the body. Man made supplements of folate are called folic acid.

Folate deficiency can directly contribute to certain types of birth defects, such as neural tube abnormalities (spina bifida) and low birth weight.

Vitamin B12 deficiency. The body needs vitamin B12 to form healthy red blood cells. When a pregnant woman doesn't get enough vitamin B12 from their diet, their body can't produce enough healthy red blood cells. Women who don't eat meat, poultry, dairy products, and eggs have a greater risk of developing vitamin B12 deficiency, which may contribute to birth defects, such as neural tube abnormalities, and could lead to preterm labor.

Blood loss during and after delivery can also cause anemia.

All pregnant women are at risk for becoming anemic. That's because they need more iron and folic acid than usual. But the risk is higher if you:

Are pregnant with multiples (more than one child)
Have had two pregnancies close together
Vomit a lot because of morning sickness
Are a pregnant teenager
Don't eat enough foods that are rich in iron
Had anemia before you became pregnant

The most common symptoms of anemia during pregnancy are:

Pale skin, lips, and nails
Feeling tired or weak
Dizziness
Shortness of breath
Rapid heartbeat
Trouble concentrating

In the early stages of anemia, you may not have obvious symptoms. And many of the symptoms are ones that you might have while pregnant even if you're not anemic. So be sure to get routine blood tests to check for anemia at your prenatal appointments.

Severe or untreated iron-deficiency anemia during pregnancy can increase your risk of having:

A preterm or low-birth-weight baby
A blood transfusion (if you lose a significant amount of blood during delivery)
Postpartum depression
A baby with anemia
A child with developmental delays

Untreated folate deficiency can increase your risk of having a:

Preterm or low-birth-weight baby
Baby with a serious birth defect of the spine or brain (neural tube defects)

Untreated vitamin B12 deficiency can also raise your risk of having a baby with neural tube defects.

During your first prenatal appointment, you'll get a blood test so your doctor can check whether you have anemia. Blood tests typically include:

Hemoglobin test. It measures the amount of hemoglobin -- an iron-rich protein in red blood cells that carries oxygen from the lungs to tissues in the body.
Hematocrit test. It measures the percentage of red blood cells in a sample of blood.

If you have lower than normal levels of hemoglobin or hematocrit, you may have iron-deficiency anemia. Your doctor may check other blood tests to determine if you have iron deficiency or another cause for your anemia.

Even if you don't have anemia at the beginning of your pregnancy, your doctor will most likely recommend that you get another blood test to check for anemia in your second or third trimester.

If you are anemic during your pregnancy, you may need to start taking an iron supplement and/or folic acid supplement in addition to your prenatal vitamins. Your doctor may also suggest that you add more foods that are high in iron and folic acid to your diet.

In addition, you'll be asked to return for another blood test after a specific period of time so your doctor can check that your hemoglobin and hematocrit levels are improving.

To treat vitamin B12 deficiency, your doctor may recommend that you take a vitamin B12 supplement.

The doctor may also recommend that you include more animal foods in your diet, such as:

Your OB may refer you to a hematologist, a doctor who specializes in anemia/ blood issues. The specialist may see you throughout the pregnancy and help your OB manage the anemia.

To prevent anemia during pregnancy, make sure you get enough iron. Eat well-balanced meals and add more foods that are high in iron to your diet.

Aim for at least three servings a day of iron-rich foods, such as:

lean red meat, poultry, and fish
leafy, dark green vegetables (such as spinach, broccoli, and kale)
iron-enriched cereals and grains
beans, lentils, and tofu
nuts and seeds
eggs

Foods that are high in vitamin C can help your body absorb more iron. These include:

citrus fruits and juices
strawberries
kiwis
tomatoes
bell peppers

Try eating those foods at the same time that you eat iron-rich foods. For example, you could drink a glass of orange juice and eat an iron-fortified cereal for breakfast.

Also, choose foods that are high in folate to help prevent folate deficiency. These include:

leafy green vegetables
citrus fruits and juices
dried beans
breads and cereals fortified with folic acid

Follow your doctor's instructions for taking a prenatal vitamin that contains a sufficient amount of iron and folic acid.

Vegetarians and vegans should talk with their doctor about whether they should take a vitamin B12 supplement when they're pregnant and breastfeeding.

Sickle cell hemoglobinopathies include those abnormalities resulting from an alteration in the structure, function, or production of hemoglobin (Hb). Hemoglobin S (HbS) results from substitution of thymine for adenine in the beta-globin gene, which leads to the substitution of the neutral amino acid valine for the negatively charged glutamic acid at the sixth position from the N terminus in the beta chain. Hemoglobin C (HbC) results from substitution of lysine for glutamic acid.

HbAS is also known as sickle cell trait and occurs in 1 in 12 African Americans. HbS is also found in other populations, such as Greeks, Italians (particularly Sicilians), Turks, Arabs, Southern Iranians, and Asian Indians.

Major sickle disorders with severe clinical symptoms include sickle cell anemia (HbSS), sickle cell hemoglobin C (HbSC) disease, and sickle cell beta-thalassemia (HbS beta-Thal). HbSS is the most common of these, occurring in 1 in 625 African Americans. Minor disorders include hemoglobin C disease (HbAC), hemoglobin SE (HbSE), hemoglobin SD (HbSD), and hemoglobin S-Memphis (HbS-Memphis). Heterozygosity for hemoglobin A and hemoglobin S (HbAS) is the most common disorder. These hemoglobinopathies are diagnosed by hemoglobin electrophoresis.

Anemia occurs as a result of the sickle hemoglobinopathies. Deoxygenation of the abnormal red blood cells (RBCs) results in sickling. These permanently damaged RBCs are then removed by the reticuloendothelial system, with the average RBC lifespan reduced to 17 days. The result is a chronic compensated anemia, with Hb typically measured between 6.5 and 9.5 g/dL.

The sickle shape also results in altered motion through the microvasculature. This altered motion can predispose the patient to vascular stasis, hypoxia, acidosis, and increased 2,3-diphosphoglycerate, which perpetuates the cycle by resulting in further deoxygenation and, thus, more sickling. The microvascular injury can result in ischemic necrosis and end-organ infarction.

Organs affected by chronic sickling include the spleen, lungs, kidneys, heart, and brain. Patients with sickle cell anemia are functionally asplenic. Therefore, immunization for encapsulated organisms (pneumococcus and meningococcus) is recommended. Likewise, aggressive treatment should be instituted when encapsulated bacterial infections are diagnosed in sickle cell disease.

In general, treating a pregnant woman who has sickle cell disease requires close observation. Obtain blood cell counts frequently because anemia can worsen quickly. Folic acid supplementation is recommended because of the quick turnover of erythrocytes. One should monitor the pregnancy with serial sonograms for assessment of fetal growth, and implementation of fetal surveillance in the third trimester is reasonable. Pneumococcal and meningococcal vaccines should be provided.

Prophylactic RBC transfusions, once standard in patients who were pregnant and had sickle cell disease, is no longer routinely advised. In 1988, a National Institutes of Health (NIH)–sponsored, multicenter, randomized, controlled trial of 72 patients with HbSS disease showed no significant difference in overall maternal or perinatal outcome of patients who received transfusions and those who did not, except for a lower incidence of painful crises in patients who received transfusions. [7]

The risks incurred with multiple blood transfusions include infection and alloimmunization, which have their own implications for pregnancy. Similar findings have been reported in a more heterogenous group of patients from the United Kingdom (including patients with HbSS, HbSC, and HbS beta-Thal), although some evidence indicates that the subset of women with sickle hemoglobinopathies carrying twins or higher-order multiples may benefit from prophylactic transfusion.

A woman who is pregnant is at risk of developing sickle cell crisis (SCC). These crises typically are vasoocclusive and may be precipitated by infection. They may be associated with thrombophlebitis or preeclampsia. Commonly, a pattern of sudden recurrent attacks of pain involving the abdomen, chest, vertebrae, or extremities occurs. These crises are more common in HbSS disease than in HbSC and HbS beta-Thal disease.

Laboratory tests that may be helpful to distinguish between SCC and other possible etiologies of pain include a white blood cell (WBC) count with differential and lactic dehydrogenase (LDH) determinations. An elevated WBC count may be observed in cases of SCC, but a left shift should not be observed unless triggered by an underlying infection. Patients with SCC have elevated LDH levels. Other laboratory tests that should be ordered upon patient admission include a complete blood count (CBC) count, type and cross-match, and arterial blood gas determinations as indicated.

Therapeutic measures for SCC are primarily supportive, with the initiation of intravenous (IV) fluid administration to decrease blood viscosity and pain control as standard pillars of care. If a sudden drop in hematocrit (Hct) occurs, therapeutic transfusion may be advisable. Identification and treatment of any underlying infection is of paramount importance. If the fetus is viable, fetal heart rate monitoring is necessary if maternal oxygenation is compromised. If clinical evidence of hypoxia is present, mother and fetus may benefit from supplemental oxygen.

During a sickle cell crisis, fetal heart rate tracings may be nonreactive and the blood pressure and pulse may be abnormal; blood pressure and pulse typically revert to normal when the crisis resolves. Umbilical artery Doppler study findings have also been noted as frequently being normal during crisis, even in the setting of abnormal uterine artery Doppler study results.

Overall, improvement has occurred in maternal and fetal outcome in patients with sickle cell disease. A widely quoted study from West Africa in the early 1970s reported an 11.5% mortality rate in mothers who are homozygous. [8] Other investigators noted a decrease in maternal death rates at Los Angeles County Hospital, from 4.1% in the era before 1972 to 1.7% from 1972-1982, with all deaths occurring in patients with HbSS or HbS beta-Thal disease. [9]

A decade later, the NIH-sponsored Cooperative Study of Sickle Cell Disease reported 2 deaths in 445 (0.6%) pregnancies; both of these deaths occurred in patients with HbSS. [10] Few reported maternal deaths have been associated with HbSC disease in the past 2 decades.

The Cooperative Study also found earlier gestational ages at delivery, smaller birth weights, and an increased rate of stillbirths (0.9%) in the HbSS group, as well as a greater rate of painful crises (50%). [10] No difference in the rates of preeclampsia existed among the different genotypes, and surprisingly pyelonephritis occurred infrequently (< 1%). First trimester miscarriage occurred in approximately 6% of women with HbSS; however, correctly ascertaining this rate in the modern era is difficult, because many women with this disease electively terminate their pregnancies.

The most recent data on sickle cell disease in pregnancy come from a 2008 study by Chakravarty et al and Villers et al, who examined Nationwide Inpatient Sample data. They found increased risks of antenatal hospitalization, hypertensive disorders, intrauterine growth restriction (IUGR), and cesarean delivery among women with sickle cell disease. [11] The following odds ratios were significantly increased for women with sickle cell disease: pneumonia (9.8), sepsis (6.8), cerebral venous thrombosis (4.9), eclampsia (3.2), IUGR (2.9), DVT (2.5), stroke (2.0), pulmonary embolism (1.7), postpartum infection (1.4), and pyelonephritis (1.3). The mortality rate for women with sickle cell disease was 6 times that for women without sickle cell disease. [12]

Acute chest syndrome can occur in 10% of sickle cell patients in sickle cell crisis. This presents with pleuritic chest pain, fever, cough, lung infiltrates, and hypoxia. Up to 15% of patients require intubation, and it has up to a 3 % mortality rate. [13]

The improvement in both maternal and fetal survival notwithstanding, it is important to remember that patients with the sickle hemoglobinopathies remain at risk for renal insufficiency, cerebrovascular accidents, cardiac dysfunction, leg ulcers, and sepsis, particularly from encapsulated organisms.

Go to Sickle Cell Anemia for complete information on this topic.