ABO and Rh Incompatability1

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ABO and Rh incompatability

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Rh-incompatability #1
• The fetus may have different blood groups than
those of its mother
• Some blood groups may act as antigens in
individuals not possessing those blood groups
• The antigens reside on red blood cells.

• If enough fetal cells cross into the maternal blood,


a maternal antibody response may be provoked
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Rh #2
• If these maternal antibodies cross the placenta,
they then can enter the fetal circulation and
destroy the fetal erythrocytes, causing hemolytic
anemia. This leads to fetal responses to meet the
challenge of enhanced blood cell breakdown.
• These changes in the fetus and newborn are called
erythroblastosis fetalis.
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Rh #3
• If these maternal antibodies cross the placenta, they
then can enter the fetal circulation and destroy the
fetal erythrocytes, causing hemolytic anemia. This
leads to fetal responses to meet the challenge of
enhanced blood cell breakdown.
• These changes in the fetus and newborn are called
erythroblastosis fetalis.
• The Rh antigens are grouped in 3 pairs: Dd, Cc, and Ee.
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Rh #4
• The major antigen in this group, Rho (D), or Rh
factor, is of particular concern.
• Rh-negative woman may carry an Rh-positive
fetus.
• If fetal RBCs pass into the mother's circulation in
sufficient numbers, maternal antibodies to the Rh-
positive antigen may develop and cross the
placenta, causing hemolysis of fetal blood cells
• Hemolytic disease of the newborn may occur, and
severe disease may cause fetal death
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Rh #5
• When the father is Rh-positive, 2 possibilities exist:
• he is either homozygous or heterozygous.
• 45% of Rh-positive persons are homozygous for D
and 55% are heterozygous.
• If the father is homozygous, all of his children will
be Rh-positive; if he is heterozygous, his children
will have a 50% chance of being Rh-positive.
• Rh-negative individual is always homozygous.

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Pathogenesis #1
• Isoimmunization may occur by 2 mechanisms:
following incompatible blood transfusion or
following fetomaternal hemorrhage between a
mother and an incompatible fetus.
• Fetomaternal hemorrhage may occur during
pregnancy or at delivery.
• Fetal red cells have been detected in maternal
blood in 6.7% of women during the first trimester,
15.9% during the second trimester, and 28.9%
during the third trimester.
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Pathogenesis #2
• Feto maternal hemorrhage happen during:
– spontaneous or induced abortion,
– amniocentesis,
– chorionic villus sampling,
– abdominal trauma (eg, due to motor vehicle
accidents or external version),
– placenta previa, abruptio placentae,
– fetal death,
– multiple pregnancy,
– manual removal of the placenta and CS
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Pathogenesis #3
• The initial maternal immune response to Rh
sensitization is low levels of immunoglobulin (Ig) M.
• Within 6 weeks to 6 months, IgG antibodies
become detectable.
• In contrast to IgM, IgG is capable of crossing the
placenta and destroying fetal Rh-positive cells

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Effects of Rh-isoimmunization #1

• Fetomaternal hemorrhage

• hyperbilirubinemia

• Hydrops fetalis

• Perinatal mortality

Fig. Hydrops fetalis 10


Management #2
 Visit at 28 Weeks: Antibody screening

 If negative, give 300g of Rh immunoglobulin

(RhIG)
 If positive, the pt should be managed as Rh-

sensitized

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Management #3
 Visit at 35 Weeks: Antibody screening is repeated.

 If negative, the patient is merely observed.

 If screening is positive, the patient is managed as

Rh-sensitized.

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Management #4
 Postpartum:

 If the infant is Rh-positive, 300g of RhIG is administered to

the mother (provided maternal antibody screening is negative).


 Although RhIG should generally be given within 72 hours after

delivery, it has been shown to be effective in preventing


isoimmunization if given up to 28 days after delivery.
 If positive, the patient is managed as if she will be Rh-

sensitized during the next pregnancy.

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Management
 Fetal blood transfusion incase of anemia
 Delivery of fetus if matured
 Photo therapy if hyperbilirubinemia

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