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8/12/2019 5rh Negative Pregnancy
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Rh NEGATIVE PREGNANCY
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The individual having the antigen on thehuman red cells is called Rh positive and
in whom it is not present is called Rhnegative.
Incidence :In India 5% to 10%
South India 5%North India 10%
In general 60% of Rh Positive men are
heterozygous and 40% are homozygousOverall Rh Negative women have thechance of having an Rh positive fetus is60% irrespective of fathers genotype.
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Mechanism of antibody formation in the mother
Antibody formation occurs by iso immunization, which is defined asthe production of immune antibodies in an individual in response
to an antigen derived from another individual of the same speciesprovided first one lacks the antigen.This occurs in two stages
SensitisationImmunisation
In ABO - blood groups naturally occurring anti-A, anti-B antibodiesare present in the serum.But in Rh group there is no such naturally occurring antibodies. Sofor the first time when Rh positive fetal red cells enter mothersblood, they remain in the circulation for their remaining life span.There after they are removed by the reticulo-endothelial tissuesand are broken down with liberation of antigen which triggers the
iso immunization.Since it takes as long as 6 months for detectable antibodies todevelop the immunization in 1st pregnancy is unlikely.If the feto-maternal bleed is less than 0.1 ml the anti bodyproduction sufficient to produce iso immunization is unlikely
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The main effect of Rh antibodies is on the babyin the form of hemolytic disease of the newborn. If the baby is Rh positive and the mother
is Rh negative, in the sensitized mother theantibody becomes attached to the antigen onthe surface of fetal erythrocytes.
The effected fetal cells are rapidly removed
from the circulation by the RE system.Depending upon the degree of agglutinationand destruction of the fetal red cells varioustypes of fetal hemolytic diseases appear.
They are
Congenital anemia of new born
Icterus gravis Neonatorum
Hydrops fetalis
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Congenital anemia of new born:It is the mildest form of thedisease where hemolysis is going on slowly. The destruction of thered cells continues up to six weeks after which the antibodies arenot available for hemolysis. So the neonate may require bloodtransfusion for its survival.
Icterus gravis Neonatorum: The baby is born alive withoutevi
dence of jaundice but soon develops it with in 24 hrs of birth. IfBilirubin level rises to the critical level of 20 mg/100ml thenBilirubin crosses the blood brain barrier to damage the basal nucleiof the brain producing clinical manifestations of Kernicterus andmay require exchange transfusion.
Hydrops fetalis: Excessive destruction of the fetal RBC leads tosevere anemia, tissue anoxaemia and metabolic acidosis. Thesehave got adverse effects on the fetal heart, brain and on theplacenta.
Hyperplasia of the placental tissue occurs in an effort to increasethe transfer of oxygen.As a result of fetal anoxaemia there is damage to the liver leadingto hypoproteinemia which is responsible for generalized oedemaascites and hydrothorax. Fetal death occurs sooner or later due tocardiac failure. Baby is either still born or macerated and even if it
is born alive dies soon after.
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Affection in the mother
Increased incidence of pre-eclampsia,
PolyhydramniosBig size of the baby
Hypofibrinogenemia due to prolongedretention of dead fetus.
Maternal syndrome or mirrorsyndrome with generalized oedemaproteinurea and pruritis.
Repeated still birthsRepeated abortions.
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Past historyHistory of previous transfusions
History of previous normal fetus and in Subsequent
pregnancies fetus presenting as hemolytic diseases ofnew born.
History of receiving Anti D after delivery
SignsGeneralised oedema
PIH
Jaundice may be present
Pruritis
On abdominal examinationPolyhydramnios may be present.
Size of the uterus may be more than the expected.
In case of a intra-uterine death of fetus FHS absent.