Hematologic Disorders and

Pregnancy
 Anemia and Pregnancy

• Since the blood volume expands during

pregnancy slightly ahead of the red cell
count, most women have a pseudoanemia of
early pregnancy.
• This should not be confused with the true
anemia that can occur as a complication of
pregnancy.
 The Woman with Iron-
Deficiency Anemia

• Most common anemia of pregnancy.

• Incidence of 15% to 25%.
 Women may enter pregnancy with
an existing deficit resulting from:

• A diet low in iron.

• Heavy menstrual periods.
• Unwise weight-reducing programs.
• Short interval between pregnancies.
• Low socioeconomic status.
• When the hemoglobin level is below
10mg/dl or hematocrit under 33%, iron
deficiency should be suspected.
• It is characterized by microcytic (small
RBC), hypochromic (less hemoglobin than
the average red cell) anemia. *
• Both hemoglibin and hematocrit will be
reduced.
• Serum transferrin will be under 100mg/dl,
and serum transferrin saturation level will
be under 5%.
• It is characterized by microcytic (small
RBC), hypochromic (less hemoglobin than
the average red cell) anemia.
• Both hemoglibin and hematocrit will be
reduced.
• Serum transferrin will be under 100mg/dl,
and serum transferrin saturation level will
be under 5%.
• Serum iron will be under 30 ug/dl.
• Mean corpuscular hemoglobin
concentration will be under 30.
• Iron binding capacity will be increased
( over 400 ug/dl)
• It is associated with low birthweight and
preterm birth.
• Women develop pica or eating substances
like ice or starch.
• Women experience fatigue and poor
exercise tolerance.
 Prophylaxis

• Pregnant women should be prescribed

prenatal vitamins containing 60 mg of
elemental iron as supplement to prevent
iron deficiency anemia.
 Treatment

• For women with iron-deficiency anemia, should

be prescribed 120 to 180 mg elemental iron as
ferrous sulfate or ferrous gluconate.
• It is best absorbed in an acid medium.
• A diet rich in iron and vitamins should be eaten.
• If anemia is severe or patient is non-compliant
with oral therapy, IM or IV iron can be
administered.
 Treatment Response

• New RBC should begin to increase or the

reticulocyte count should rise from a normal
range of 0.5% to 1.5% to 3% to 4% by 2
week’s time.
 Adverse Drug Reaction

• Constipation
• Gastric irritation

 To avoid these, advise them to increase

roughage in the diet and always take pills with
food.
 The Woman with Folic Acid-
Deficiency Anemia

• Necessary for RBC formation.

• Associated with preventing neural tube
defects in the fetus.
• Incidence of 1% to 5%.
 Occurs most often in:

• Multiple pregnancies
• Women with a secondary hemolytic illness
• In women who are taking hydantoin
• In women taking oral contraceptives.
 Characteristics

• Megaloblastic (enlarged RBC) anemia

develops. *
• The mean corpuscular volume will be
elevated.
• It becomes most apparent during the second
trimester of pregnancy.
• It may be a contributory factor in early
miscarriage or abruption.
 Characteristics

• Megaloblastic (enlarged RBC) anemia

develops.
• The mean corpuscular volume will be
elevated.
• It becomes most apparent during the second
trimester of pregnancy.
• It may be a contributory factor in early
miscarriage or abruption.
 Prophylaxis

• Folic acid supplementation, in the form of

pills or folacin-rich foods, should be started
even before getting pregnant.
• All women of childbearing age should take
400 ug of folic acid daily.
• During pregnancy, the requirement
increases to 600 ug/day.
 The Woman with Sickle Cell
Anemia
• A recessively inherited hemolytic anemia caused by
abnormal amino acid in the beta chain of hemoglobin. *
• An individual who is heterozygous has the sickle cell
trait.
• An individual who is homozygous has sickle cell
disease.
• Approximately 1 in every 10 African Americans has the
sickle cell trait.
• 1 in 400 African Americans theoretically has the disease.
 The Woman with Sickle Cell
Anemia
• A recessively inherited hemolytic anemia caused by
abnormal amino acid in the beta chain of hemoglobin.
• An individual who is heterozygous has the sickle cell
trait.
• An individual who is homozygous has sickle cell
disease. *
• Approximately 1 in every 10 African Americans has
the sickle cell trait.
• 1 in 400 African Americans theoretically has the
disease.
 The Woman with Sickle Cell
Anemia
• A recessively inherited hemolytic anemia caused by
abnormal amino acid in the beta chain of hemoglobin.
• An individual who is heterozygous has the sickle cell
trait.
• An individual who is homozygous has sickle cell
disease.
• Approximately 1 in every 10 African Americans has
the sickle cell trait.
• 1 in 400 African Americans theoretically has the
disease.
 Pathophysiology

• With the disease, the majority of RBC are

irregular or sickle-shaped. *
• They cannot carry as much hemoglobin.
• When oxygen tension becomes reduced or blood
becomes viscid than usual, the RBC tend to
clump.
• This clumping can result to vessel blockage and
organ infarcts.
• The cells then will hemolyze causing anemia.
 Pathophysiology

• With the disease, the majority of RBC are

irregular or sickle-shaped.
• They cannot carry as much hemoglobin. *
• When oxygen tension becomes reduced or blood
becomes viscid than usual, the RBC tend to
clump.
• This clumping can result to vessel blockage and
organ infarcts.
• The cells then will hemolyze causing anemia.
 Pathophysiology

• With the disease, the majority of RBC are

irregular or sickle-shaped.
• They cannot carry as much hemoglobin.
• When oxygen tension becomes reduced or blood
becomes viscid than usual, the RBC tend to
clump. *
• This clumping can result to vessel blockage and
organ infarcts.
• The cells then will hemolyze causing anemia.
Normal red cells maintain
their shape as they pass
through the capillaries and
release oxygen to the
peripheral tissues (upper
panel). Hemoglobin
polymers form in the sickle
rell cells with oxygen
release, causing them to
deform. The deformed cells
block the flow of cells and
interrupt the delivery of
oxygen to the tissues
(lower panel).
 Pathophysiology

• With the disease, the majority of RBC are

irregular or sickle-shaped.
• They cannot carry as much hemoglobin.
• When oxygen tension becomes reduced or blood
becomes viscid than usual, the RBC tend to
clump.
• This clumping can result to vessel blockage and
organ infarcts.
• The cells then will hemolyze causing anemia.
 Effect on Pregnancy

• It does not influence the course of

pregnancy in terms of pregnancy-induced
hypertension, prematurity, miscarriage, or
perinatal mortality, women with the trait do
seem to have an increased incidence of
asymptomatic bacteriuria, resulting in an
increased incidence of pyelonephritis.
 Effect on Pregnancy

• Blockage to the placental circulation can

directly compromise the fetus, causing low
birthweight and possibly death.
• At anytime in life, sickle cell anemia is a
threat to life if vital blood vessels such as
those to the liver, kidneys, heart, lungs, or
brain become blocked.
 Assessment

• All African-American women should be

screened for sickle cell anemia.
• Hemoglobin levels for all women with the
disease should be obtained frequently.
• A woman with sickle-cell disease may
normally have a hemoglobin of 6 to 8
mg/100ml.
• Hemolysis may occur so rapidly that the
hemoglobin can fall to 5 or 6 mg/100ml in a
few hours.
• An increase in indirect bilirubin occurs
because she cannot conjugate the bilirubin
from the RBCs so quickly destroyed.
 During Pregnancy

• Because a pregnant woman with sickle cell

disease is more susceptible to bacteriuria, a
clean catch urine sample should be
collected periodically to detect developing
bacteriuria while still asymptomatic.
• Folic acid supplementation is esssential.
• Fluid intake should be carefully monitored.
 During Pregnancy

• During prenatal visits, you should assess the

woman’s lower extremities for pooling of
blood. Pooling of blood can lead to cell
destruction.
• Fetal health is monitored by ultrasound at
16 to 24 weeks to assess for IUGR.
• Weekly NST beginning 30 weeks.
• Doppler velocimetry to assess IUGR.
 Therapeutic Management

• Periodic exchange transfusion throughout

pregnancy to replace the sickle cells for
normal cells and to reduce the bilirubin
levels.
• Pain control, oxygen administration,
increase fluid volume.
• As a rule, iron cannot be given because they
cannot incorporate iron in the usual manner
resulting in excessive iron buildup.
 Therapeutic Management
• If a woman develops an infection that raises
her temperature or contracts a respiratory
infection, hospitalization may be necessary to
rule out the development of sickle cell crisis
and subsequent hemolysis of crowded cells.
• During labor, keep the parturient well
hydrated. Regional anesthesia is generally
given rather than a general anesthesia to avoid
hypoxia.
• If one of the parents has the disease and the
other is free of the disease and trait, the
chances that the child will inherit the disease
are zero.
• If the woman has the disease and her partner
has the trait, the chances that the child will be
born with the disease are 50%.
• If both parents have the disease, all their
children will also have the disease.
• Symptoms of the disease do not become
clinically apparent until the child’s fetal
hemoglobin has converted largely into the
adult pattern. (in 3 to 6 months)
• Fetal Hgb comprises 2 alpha and 2 gamma
chains. *
• Because the sickle cell trait is carried on the
beta chain, it will not manifest clinically
until it appears.
• Symptoms of the disease do not become
clinically apparent until the child’s fetal
hemoglobin has converted largely into the
adult pattern. (in 3 to 6 months)
• Fetal Hgb comprises 2 alpha and 2 gamma
chains.
• Because the sickle cell trait is carried on the
beta chain, it will not manifest clinically
until it appears.
• Newborns have approximately 15% adult
hemoglobin at birth, so electrophoresis
testing at birth can reveal if the disease is
present.
 Coagulation Disorders and
Pregnancy

• Most coagulation disorders are sex-linked

occuring only in males, so have little effect
on pregnancies.
 Von Willebrand Disease

• an autosomal dominant trait that does occur

in women.
• Symptoms
 Menorrhagia
 Frequent epistaxis
 Spontaneous miscarriage
 Postpartal hemorrhage
 Pathology

• Normal platelet count but bleeding time is

prolonged.
• Factor VIII-related antigen and Factor VIII
coagulation activity are both reduced.
• Replacement of these factors with
cryoprecipitate and FFP may be necessary
before labor to prevent excessive bleeding.
 Hemophilia B

• Christmas disease or Factor IX deficiency

• Sex-linked disorder, occurs only in males
• Females carriers may have reduced level of
factor IX (only 3% of normal) which may
lead to hemorrhage with labor or
spontaneous miscarriage.
• FFP or factor IX concentrate
 Idiopathic Thrombocytopenic Purpura

• Decreased number of platelets

• Cause is unknown, but it is assumed to be
an autoimmune illness.
• Symptoms appear after a viral illness.
 Minute petechiae or large ecchymoses appear. *
 Frequent epistaxis
• Lab studies show low platelet count (as low
as 20,000/mm3
 Idiopathic Thrombocytopenic Purpura

• Decreased number of platelets

• Cause is unknown, but it is assumed to be
an autoimmune illness.
• Symptoms appear after a viral illness.
 Minute petechiae or large ecchymoses appear.
 Frequent epistaxis
• Lab studies show low platelet count (as low
as 20,000/mm3
 Idiopathic Thrombocytopenic Purpura

• 1-3 month limited course.

• Platelet concentrate may be transfused.
• Oral prednisone is also active.
• Hemorrhage with labor is a complication.
• Also, the antiplatelet factor can cross the
placenta and destroy the fetal platelets.