Download Rh NEGATIVE PREGNANCY

Rh NEGATIVE PREGNANCY
The individual having the antigen on the
human red cells is called Rh positive and
in whom it is not present is called Rh
negative.
Incidence :In India 5% to 10%
South India 5%
North India 10%
In general 60% of Rh Positive men are
heterozygous and 40% are homozygous
Overall Rh Negative women have the
chance of having an Rh positive fetus is
60% irrespective of father’s genotype.
Mechanism of antibody formation in the mother
Antibody formation occurs by iso immunization, which is defined as
the production of immune antibodies in an individual in response
to an antigen derived from another individual of the same species
provided first one lacks the antigen.
This occurs in two stages
Sensitisation
Immunisation
In ABO - blood groups naturally occurring anti-A, anti-B antibodies
are present in the serum.
But in Rh group there is no such naturally occurring antibodies. So
for the first time when Rh positive fetal red cells enter mother’s
blood, they remain in the circulation for their remaining life span.
There after they are removed by the reticulo-endothelial tissues
and are broken down with liberation of antigen which triggers the
iso immunization.
Since it takes as long as 6 months for detectable antibodies to
develop the immunization in 1st pregnancy is unlikely.
If the feto-maternal bleed is less than 0.1 ml the anti body
production sufficient to produce iso immunization is unlikely
The main effect of Rh antibodies is on the baby
in the form of hemolytic disease of the new
born. If the baby is Rh positive and the mother
is Rh negative, in the sensitized mother the
antibody becomes attached to the antigen on
the surface of fetal erythrocytes.
The effected fetal cells are rapidly removed
from the circulation by the RE system.
Depending upon the degree of agglutination
and destruction of the fetal red cells various
types of fetal hemolytic diseases appear.
They are
Congenital anemia of new born
Icterus gravis Neonatorum
Hydrops fetalis
Congenital anemia of new born: It is the mildest form of the
disease where hemolysis is going on slowly. The destruction of the
red cells continues up to six weeks after which the antibodies are
not available for hemolysis. So the neonate may require blood
transfusion for its survival.
Icterus gravis Neonatorum: The baby is born alive without
evidence of jaundice but soon develops it with in 24 hrs of birth. If
Bilirubin level rises to the critical level of 20 mg/100ml then
Bilirubin crosses the blood brain barrier to damage the basal nuclei
of the brain producing clinical manifestations of Kernicterus and
may require exchange transfusion.
Hydrops fetalis: Excessive destruction of the fetal RBC leads to
severe anemia, tissue anoxaemia and metabolic acidosis. These
have got adverse effects on the fetal heart, brain and on the
placenta.
Hyperplasia of the placental tissue occurs in an effort to increase
the transfer of oxygen.
As a result of fetal anoxaemia there is damage to the liver leading
to hypoproteinemia which is responsible for generalized oedema
ascites and hydrothorax. Fetal death occurs sooner or later due to
cardiac failure. Baby is either still born or macerated and even if it
is born alive dies soon after.
Affection in the mother
Increased incidence of pre-eclampsia,
Polyhydramnios
Big size of the baby
Hypofibrinogenemia due to prolonged
retention of dead fetus.
Maternal syndrome or mirror
syndrome with generalized oedema
proteinurea and pruritis.
Repeated still births
Repeated abortions.
Past history
History of previous transfusions
History of previous normal fetus and in Subsequent
pregnancies fetus presenting as hemolytic diseases of
new born.
History of receiving Anti D after delivery
Signs
Generalised oedema
PIH
Jaundice may be present
Pruritis
On abdominal examination
Polyhydramnios may be present.
Size of the uterus may be more than the expected.
In case of a intra-uterine death of fetus FHS absent.