RH IMMUNISATION

Harika Priyanka. K
Asst. Professor
ACON
ABO SYSTEM

• Consists of 3 major allelic genes: A, B and O, located on

the long arm of chromosome 9.
• There are four main types of blood group‐ A, B, AB,
and O.
• Antigens of ABO system are: A (A1, A2), B and H.
• In addition to RBC, they are also expressed on WBC,
platelets and various body secretions.
• Acc to Landsteiner’s law, anti‐A or anti B antibodies are always
present in plasma of individual who lack corresponding antigen
on their red cells.

• These antibodies are usually of IgM class

• An O group individual who inherits A or B genes but
fails to inherit H gene from either parent is called Oh
phenotype or Bombay blood group.
• These individuals contain anti ‐A, anti ‐ B and anti ‐H.
• Therefore, Oh blood group persons should be
transfused only with Oh blood.
RHESUS SYSTEM

• The Rh allelic genes are C or c, D or d and E or e, located on

chromosome

1. The importance of this system lies in high immunogenecity of

Rh D antigen, which can cause severe hemolytic reaction.
• The presence of D in either homozygous or
heterozygous state make the individual Rh positive,
while Rh neg individuals are homozygous for d (d/d).
• Rh antigens are expressed on RBCs only and not on
any other tissue.

• There are no naturally‐occurring Rh antibodies

• 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.
• Antibody formation occurs by iso immunization
• Definition: The iso immunization is defined as a
production of immune antibodies in an individual in
response to an antigen derived from another
individual of the same species provided, the first one
lacks the antigen.
• In this condition, the Red Cells Of The Fetus Or
Newborn Are Destroyed By Maternally Derived
Alloantibodies
• Iso immunization occurs in two stages:
a. Sensitization
b. Immunization
• The Antibodies arise in the mother as the direct result
of a blood group incompatibility between the mother
and fetus
e.g. when an RhD negative mother carries an RhD
positive fetus.
• In The Fetus: Erythroblastosis Fetalis
• In The Newborn: HDN.
Incidence :In India 5% to 10%
• South India 5%
• North India 10%
• Overall Rh Negative women have the chance of
having an Rh positive fetus is 60% irrespective of
father’s genotype.
• 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 affected 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
1. Congenital anemia of new born
2. Icterus Gravis Neonatorum
3. Hydrops Fetalis

Kernicterus (Lethargy, Hypertonicity, Hearing Loss,

Cerebral Palsy And Learning Disability)
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.
• On X Ray abdomen, Buddha’s position of the fetus
with a halo around the head due to edematous scalp.
Budha’s position of the fetus on X - ray
How the mother is affected

• Increased incidence of pre-eclampsia,

Polyhydramnios

• Big size of the baby

• Hypofibrinogenemia due to prolonged retention of

dead fetus.
•  "Mirror syndrome" refers to the similarity between
maternal oedema and fetal hydrops. It was first
described in 1892 by John William Ballantyne
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.
LABORATORY FINDINGS

• Anaemia with reticulocytosis,

• Increased nucleated RBC and polychromasia

• elevated serum bilirubin

• positive direct Coombs’ test (fetus)

• Mother’s blood ‐ Indirect Coomb’s test ‐ anti ‐ D

antibodies.
 Fetal blood sampling

• Is the gold standard for detection of fetal anemia.

• Reserved for cases with: an increased MCA-PSV (Middle

Cerebral Artery Peak Systolic Velocity)
• Complications:
 Total Risk of Fetal Loss Rate 2.7% (Fetal death is
1.4% before 28 weeks and The perinatal death rate is
1.4% after 28 weeks).
 Bleeding from the puncture site in 23% to 53% of
cases.
 Bradycardia in 3.1% to 12%.
 Fetal-maternal hemorrhage: occur in 65.5% if the placenta is
anterior and 16.6% if the placenta is posterior.
 Infection and abruptio placentae are rare complications
Sensitising events

• Threatened miscarriage,
• Ectopic pregnancy,
• Any invasive prenatal procedure (chorionic villous sampling,
amniocentesis, etc),
• Antepartum haemorrhage,
• External cephalic version,
• Closed abdominal injury, and

• Intrauterine injury.
 Guidelines

Route of
1st Trimester
(< 12 weeks
Treatm administrat
gestation) ent ion
Indication:
●
●
Rh (D) Given slowly
●
immunoglobulinVF
Potential ●
250 IU for singleton by deep
pregnancies
sensitising ●
625 IU for multiple
intramuscula
pregnancies r injection
event.
 2nd and 3rd Route of
Trimester (≥ Treatm administrat
12 weeks
gestation) ent ion
Indication:
●
Given slowly
●
Rh (D)
●

Potential by deep
immunoglobu
sensitising intramuscular
linVF 625 IU
event. injection
 Route of
Antena Treatm administrat
tal ent ion
Indication: All Rh
Rh (D) Given slowly
●
● ●
(D) negative women
at 28 and 34 weeks Immunoglob by deep
gestation with no ulinVF intramuscular
preformed anti-D
antibodies.
●
625 IU. injection
 Route of
Postnat Treatm administrat
al ent ion
Indication: All Rh (D)
Product & Given slowly
●
● ●
negative women who give
birth to a Rh (D) positive
baby unless it has been Dose Rh (D) by deep
clearly documented that the
woman already has
●
Immunoglobul intramuscular
preformed antibodies
(alloimmunisation). inVF 625 IU injection
Treatment

• Exchange transfusion

• Phototherapy‐ converts unconjucated bilirubin into

soluble form, that is excreted in urine.

• Infusion of bile‐ binds free bilirubin in plasma and thus

decreases the risk of kernicterus.
Nursing management

• High risk for intra uterine fetal demise r/t

isoimmunization as evidenced by fetal anemia
• High risk for maternal complications such as
polyhydramnios secondary to Rh incompatibility

• High risk for fetal anoxemia

• High risk for PIH secondary to Rh isoimmunization.