Haemolytic Disease of Newborn (HDN)

- July 09, 2020

Haemolytic Disease of Newborn (HDN)

Disorder o the fetus or newborn where fetal red cells are destroyed by maternal IgG antibodies.
It is also called Erythroblastosis Fetalis.
The IgG antibodies cross the placenta and short red cell survival.
The prematurer red cell destruction results in disease varying from mild Anaemia to death in utero.

The most immunogenic RBC antigens belong to Rhesus blood group D, followed by C and E.
Hemolytic disease of Fetus can be also caused by Kell antigen sensitization.
Kell antigen can cause hypoproliferation of erythroid precursors leading to severe anaemia.
Other Non- RhD antibodies include Rhesus-c, Cotton, Diego, Duffy, etc.
HDN does not usually affect first pregnancy.
It is more common in "O" blood group mothers have been shown to have high titers of IgG than "A" or "B" group mothers.
In type "A" and "B" individuals, naturally occurring anti- B and anti-A isoantibodies which are largely IgM molecules; that do not cross placenta.
The alloantibodies present in type "O" patients are mainly of IgG antibodies.
For this reason, ABO incompatibility is largely limited to type "O" mothers having fetal blood group "A" or "B".

Symptoms Of HDN in a Newborn:

Severe anaemia with marked jaundice
Heart failure with markedly increased central venous pressure.
Hepatosplenomegaly.
Portal vein obstruction.
Ascites, Pleural and Pericardial effusion.
Marked generalized edema (Anasarca).
Ultimately leading to hydrops and even death of the fetus.

Maternal Management of HDN:

As part of routine prenatal or antenatal care, the blood type of the mother (ABO and Rh) is determined by a blood test.
A test for the presence of atypical antibodies in the Mother's serum is also performed. At present, RhD incompatibility is the only cause of HDN for which screening is routine.
To find out whether a pregnant Rh-D negative mother has been sensitized to the RhD antigen, an indirect coomb's test is done.
If anti-D is not found in the mother's serum, it is likely that she has not been sensitized to the Rh D antigen.
The risk of future sensitization can be greatly reduced by giving all unsensitized mother anti-D Ig, which "mops up" any fetal RBCs that may have leaked into the maternal circulation, reducing the risk of first time exposure to the D antigen.
Usually RhD-negative mothers receive an injection of anti D Ig at about 28 weeks gestation, which is about the time when fetal RBCs start to express the D antigen, and mothers receive another dose at about 34 weeks, a few weeks before labor begins during which the risk of fetomaternal hemorrhage is high.
A final dose of anti- D Ig is given after the baby has been delivered.
Monitoring includes regular ultrasound scans of the fetus and monitoring of the amount of anti-D in the mother's serum.
Active hemolysis is indicated by a rise in anti D.
If a fetal blood test confirms fetal anaemia, depending upon it's severity, a blood transfusion can be done in utero to replace the lysed fetal RBCs.
Blood transfusion may be needed to correct anaemia in the newborn period. During this period there may also be a sharp rise in the level of bilirubin in the neonate, which can be lowered by phototherapy and exchange transfusions.
If Mother is sensitised
Once the presence of maternal anti D has been confirmed, the next step is to determine whether the fetal RBCs are a target, i.e., confirm the Rh satatus of the fetus.
Test a sample of fetal cells taken from the amniotic fluid or umbilical cord.
If the fetus is Rh D positive, the pregnancy is carefully monitored for signs of HDN.