Transcript Rh Immunozation

DR. RAZAQ MASHA, FRCOG
Consultant, Ob/Gyn Dept.
Rh IMMUNIZATION
• Rh haemolytic disease (RHD) is a
common condition and affects 1 in
250 live births in Europe and North
America although it is much less
frequent in other parts of the world
such as Asia, where the Rhnegative blood group is
uncommon.
TRANSPLACENTAL HAEMORRHAGE (TPH)
• The Rh antigen is limited to the red cell
surface and maternal Rh immunization, can,
therefore, only take place if fetal red cells
cross the placental barrier into the maternal
circulation.
• Occasional breaks in continuity will occur in
the placental barrier, during the stress of
labour, with consequent admixture of small
quantities of maternal and fetal blood.
• Kleihauer test – citric-phostphate buffer- an
elution technique which is capable of
detecting very small TPHs of the order of 0.1
ml of fetal blood.
DELIVERY:
• The placenta is subjected to maximal
trauma during delivery and it has been
deduced that TPH would mainly occur
during delivery rather than during the
course of pregnancy.
ABORTION:
• TPH occurs after abortion. The risk is
greater with induced as compared with
spontaneous abortion .TPH of 0.2 ml of
fetal blood has been recorded in about
5 percent of abortion.
THE NATURAL HISTORY OF Rh
IMMUNIZATION
• The process by which the body responds to an
antigen by producing the appropriate antibody is
called immunization and there are two types of
immunity:
a) Humoral immunity – associated with free antibody
b) Cellular immunity – cell bound antibody
Rhesus antibodies are humoral antibodies or free
antibody
1 gm – large, unable to cross the placenta
1gG – small, able to cross the placenta and
attach itself to Rh positive red cells
leading to haemolytic anaemia
IMMUNE RESPONSES ARE:
a) Primary – first response to an antigen
b) Secondary
For the D-antigen, the primary response appears after
several weeks and is IgM.
When exposed to the D- antigen for the second time a
secondary immune response takes place. If already
primed, antibody will appear within a few days or if
antibody is already present, the strength will increase
rapidly and the antibody will change its character to
IgG.
Generally, the quantity of antigen required to produce a secondary
immune response is very much smaller than that required to
initiate the primary immune response.
THE IMMUNIZING PREGNANCY:
• The first pregnancy is usually
unaffected by RHD because TPHs of
sufficient magnitude to induce primary
immunization do not usually take place
until delivery.
• Only about 5 percent of all Rh-negative
mothers form antibodies.
Reasons:
a) A TPH of sufficient magnitude to induce
primary immunization may not take place.
b) 50 percent of individuals do not produce
Rh antibodies even after a massive TPH
c) Reduced chance of immunization if there
are no complications of delivery.
•
Vast majority of TPHs after delivery are
small and are in the order of about 0.1 ml of
fetal blood, but about 0.2% of mothers have
larger bleeds of 30 ml or more. The risk of
Rh immunization is proportional to the size
of the TPH.
ABO INCOMPATIBILITY
• When the mother and the baby are ABO
incompatible such as an O mother and
an A baby any fetal red cell (Group A)
entering the maternal circulation
(Group O) is destroyed, in an exactly
similar way to that occurring in an ABO
incompatible blood transfusion.
PREGNANCY:
• TPH does occur during pregnancy but
is much less common than following
delivery. Most of the bleeds occur in
the last trimester when the placenta is
degenerating and the barrier may
become a little more pervious.
COMPLICATIONS:
• Anything which damages the placenta is
liable to increase the risk of TPH. The
incidence and magnitude of TPH is therefore
increased in:
 Caesarean section
 Complicated and difficult deliveries
 External version
 Toxaemia
 Hypertension
 Amniocentesis
ABORTIONS:
• Abortions with a gestational age above 14
weeks carry a risk of inducing immunization.
Rh IMMUNOGLOBULIN
The prevention of RHD is dependent on the
fact that, D-positive TPHs can be neutralized
by passively administered anti-D antibody
(Rh immunoglobulin) taken together with the
realization that Rh priming is usually due to a
TPH occurring at delivery in the preceeding
D-positive pregnancy.
FAILURE RATE:
About 1 percent of Rh-negative women become
immunized after two D-positive pregnancies despite
treatment with Rh immunoglobulin
a) Those already primed, even though overt
antibody is undetectable by present techniques.
b) Large TPHs before delivery e.g. epileptic or
eclamptic patients.
c) Extreme sensitivity to the D-antigen: thus small
bleeds will produce primary response.
d) Large TPHs after delivery more than the amount
that can be taken care of by standard dose of
immunoglobulin.
e) Failure to give the immunoglobulin – patients
who slip through the net.
AMNIOCENTESIS AND
AMNIOTIC FLUID ANALYSIS.
• When erythroblastosis fetalis is severe, the
amniotic fluid becomes bright yellow from
the bilirubin derived from fetal haemolysis.
Amniotic fluid bilirubin concentration can be
quantified by spectrophotometry by
assessing the change in optical density at
450nm ( OD 450)
• Amniocentesis is started after 24 weeks
under continuous ultrasound control.
COMPLICATIONS FOLLOWING
INTRAUTERINE TRANSFUSION:
1.
2.
3.
4.
5.
6.
Premature labour
Pre-labour ruptured membrane
Fetal haemorrhage
Fetal bradycardia
Failure to obtain a sample
Increase in maternal iso immunization
by inducing feto-maternal
haemorrhage
MANAGEMENT OF RED BLOOD
CELL ISOIMMUNIZATION
• Pregnancies complicated by clinically
relevant maternal RBC antibodies are
managed in regional blood transfusion
centers and fetal medicine units. These
centres maintain expertise in the
diverse clinical presentation of these
cases, follow them non-invasively and
perform invasive tests or therapy as the
case requires.
Cont.
a)
b)
c)
d)
e)
f)
g)
Maternal antibody quantification
Paternal blood group genotyping
Fetal blood group genotyping
Ultrasound assessment
Amniotic fluid spectrophotometry
Fetal blood sampling
Fetal blood transfusion
ULTRASOUND ASSESSMENT:
• The severely anaemic fetus is readily
identifiable on scan by the detection of
skin oedema, ascites, pleural or
pericardial effusions, cardiomegaly and
an oedematous placenta.
• Fetal heart rate changes have been
noted with severe anaemia. A
sinusoidal pattern with the loss of
normal baseline variability of the CTG
is highly suggestive of severe aneamia.