HAEMOLYTIC DISEASE
OF THE NEW BORN
(HDN)
Haemolytic disease of the newborn
(HDN) occurs when the mother has anti-
red-cell IgG antibodies in her plasma that
cross the placenta and bind to fetal red
cells bearing the corresponding antigen.
The three most common red cell
alloantibodies which cause significant
HDN are anti D, anti c and anti Kell (anti
K).
Fetal red cells binding sufficient maternally
derived antibody are destroyed in the fetal
reticuloendothelial system, producing
extravascular haemolysis and a variable
degree of fetal anaemia.
In severe cases the fetus may die in utero of
heart failure (hydrops fetalis). If the fetus
survives birth, the neonate rapidly develops
jaundice and is at risk of neurological
damage due to the high Bilirubin level.
• Development of red cell antibodies in the
mother may occur either as a result of:
1. Previous pregnancies (because fetal blood
displaying paternal red cell antigens
frequently enters the mother’s circulation
during pregnancy).
2. As a result of a previous blood transfusion.
The three most common red cell
alloantibodies which cause significant
HDN:
Antibody to the Rh antigen:
– The most common is anti D.
– This develops in RhD negative women who have
carried a RhD positive fetus.
– It rarely affects the first pregnancy although it can
sensitize the mother so that subsequent pregnancies
with RhD positive babies boost antibody production
progressively, putting later
pregnancies at increasing risk.
Smaller family sizes and the introduction
of prophylaxis with RhD immunoglobulin
have reduced the incidence and severity of
this condition.
The fetus is only at risk if its red blood
cells express the antigens against which the
antibody is directed (e.g. if a RhD negative
woman with anti D is carrying a RhD
positive fetus, there is a risk that the fetus
will be affected, but if the fetus is RhD
negative the baby will not be at risk of
HDN).
- The next most common causes of severe
HDN are the rhesus antibody anti c.
Treatment
Exchange transfusion
3-Antibodies of the ABO blood group
system
in a group O mother with naturally occurring
anti-A and anti-B of the IgG subclass which
can cross the placenta.
HDN due to ABO incompatibility occurs
when a group O mother with IgG anti-A or
IgG anti-B is carrying a fetus of blood group
A or blood group B respectively.
The most common presentation of ABO
HDN is jaundice (un-conjugated
hyperbilirubinaemia).
The direct antiglobulin test is usually
(but not always) positive.
Severe anaemia in HDN due to
maternal anti-A or anti-B is
uncommon in Caucasians in the UK,
but is commoner in some other ethnic
groups, especially among women of
African or Caribbean origin.
ABO haemolytic disease of the
new born
Child rarely requires treatment
by exchange transfusion
Blood film shows auto
agglutination and shperocytosis
Prevention of HDN due to anti RhD
Anti RhD immunoglobulin (anti D)
Anti-D immunoglobulin (Routine antenatal anti-D
prophylaxis) is prepared from plasma of donors
who have high levels of plasma anti-D due to
exposure to RhD positive cells following
pregnancy or intentional immunization.
Anti-D products contain specified levels of anti D
and are available for intramuscular or intravenous
administration.
Anti D is administered to RhD negative
women who may have been exposed to
RhD positive fetal red cells that have
entered the maternal circulation.
The anti D destroys the RhD positive red
cells and prevents active immunization,
thus preventing the production of RhD
antibodies.
Clinical features
Severe disease : intrauterine death
Moderate disease : the baby born with
severe anaemia and jaundise
Mild disease : mild anaemia
Treatment
Exchange transfusion
Management of pregnant women and prevention:
The ABO and Rh blood groups of all pregnant
mother determined early in pregnancy
The severity of the haemolytic disease can be
assessed by estimation the bile pigment derivatives
in the aminotic fluid
Suitable fresh blood should be available at the
time of induction for exchange transfusion
A birth the babies of Rh-negative who do not
have antibodies must have their Cord blood
grouped for ABO and Rh :
- If the baby Rh-negative ( no need for
treatment(
- If the baby Rh-positive (prophylactic
anti-D should be administered
5. Prevention of Rh immunization : by giving
(anti-D) to an Rh (D) negative mother giving
birth Rh-positive baby . The routine dose is
500 i.u of anti-D giving intramuscular within
72 hours of delivery.
Laboratory findings at birth
Cord blood
* variable anaemia (haemoglobin<16 g/dl)
– High reticulocyte count
– Baby Rh (D) positive
– Direct coombs test positive
– Increased serum bilirubin
– Presence of erythroblast in blood film
Mother : is Rh (D) negative with high plasma level
anti-Rh (D)
Why Does Rh Status Matter?
Fetal RBC cross to maternal circulation
Maternal immune system recognizes foreign
antigens if fetus Rh + and mother Rh –
Antibodies are formed against fetal antigens
Subsequent pregnancy with Rh+ fetus,
immune system activated
and large amounts of Ab formed
IgG Ab cross placenta & attack fetal RBC
Fetal anemia, hydrops, etc
Gold Standard Test
Indirect Coombs:
-mix Rh(D)+ cells with maternal serum
-anti-Rh(D) Ab will adhere
-RBC’s then washed & suspended in Coombs
serum (antihuman globulin)
-RBC’s coated with Ab will be agglutinated
Direct Coombs:
-mix infant’s RBC’s with Coombs serum
-maternal Ab present if cells agglutinate
Prevention
RhoGAM (120mcg or 300mcg)
Anti-D immune globulin
Previously 16% Rh(D)- women became
alloimmunized after 2 pregnancies, 2%
with routine PP dose, and 0.1% with added
dose @ 28 wks
