HISTORICAL EVIDENCE TYPES OF Rh ANTIGENS CRITERIA OF Rh POSITIVE AND NEGETIVE CONCENTRATION OF Rh POSITIVE AND NEGETIVE Rh AGGLUTININS INHERITANCE HEMOLYTIC DISEASE OF NEWBORN TREATMENT PREVENTION

2. HISTORICAL EVIDENCE
TYPES OF Rh ANTIGENS
CRITERIA OF Rh POSITIVE AND NEGETIVE
CONCENTRATION OF Rh POSITIVE AND NEGETIVE
Rh AGGLUTININS
INHERITANCE
HEMOLYTIC DISEASE OF NEWBORN
TREATMENT
PREVENTION

3. HISTORICAL EVIDENCE
“Rh” owes its name to the rhesus
monkey in whom Lansteiner and
Weiner discovered the Rh factor in
1940. They also demonstrated this
factor on the human RBCs
These were first discovered in
RBCs of rhesus monkeys

4. Rhesus monkey

5. There are 6 common types of Rh antigens. Each of
which is called as Rh factor. These types are
designated C, D, E, c, d, e.
Each person has 1 each of the three pairs of
antigens.
CRITERIA OF Rh POSITIVE AND
NEGETIVE
Type D antigen is commonest and more antigenic
so anyone having these type of antigen is regarded
as Rh positive and who does not have, regarded as
Rh negetive.

6. CONCENTRATION OF Rh POSITIVE AND NEGETIVE
About 85% of all white people are Rh positive and 15% are
Rh negetive.

7. Distribution of Rh group
About 85% of white people are Rh+ve.
95% of American blacks are Rh+ve and
virtually 100% of African blacks are Rh+ve.

8. Rh antigens inherited as dominant gene D.
Rh Positive individual maybe of two
genotypes DD (homozygous ) Dd
(heterozygous) . But the Rh negetive
individual is always dd.
Of 85% Rh positive individuals about 35%
have DD and 50% have Dd genotype.

9. The agglutinin that are formed is anti D. At
first exposure IgM type of antibodies are
formed.
On second exposure IgG types of
antibodies are formed.
But the person should be previously
exposed to antigen, then only the antibody
formation takes place.

10. Rh antibodies-
The Rh antibodies are not present
naturally in the blood, they’re formed-
1.When a Rh-ve mother conceives with a
Rh+ve fetus.
2.Transfusion/injection of
incompatible blood.
Anti-D is the most widely investigated
antibody all over the world.
It is produced mainly by the D-ve
subjects.

11. Erythroblastosis fetalis is a disease of the
fetus and newborn child and the father is
Rh positive. The baby has inheritated the Rh
positive antigen from the father.
During the time of parturition, a small
amount of fetal blood leaks and when it
enters the mother’s circulation, the mother
produces anti D antibody .
.

12. Erythroblastosis Fetalis
Disease of the fetus and newborn
characterized by agglutination and
phagocytosis of it’s RBCs.
Mother is Rh-ve and father is Rh+ve,
it is the father which inherits the
antigens to the fetus.
A Rh-ve mother has her first Rh+ve
child normal but about 3% of second
babies and 10% of third babies exhibit

13. When Rh+ cells enter into maternal
circulation after the first delivery-
Primary response- slow
destruction of Rh+ cells-primary
immune response detectable after 8-9
weeks.
Secondary response-following
primary response-rapid increase in

15. It occurs at the time of delivery but the fetus
is already out of the mother’s body. It affects
the next issue, if it is Rh positive again then
the antibodies from mother will enter into
fetal circulation and damage the fetal RBCs.
The incidence rises progressively with
subsequent pregnancies.

16. (Mild Hemolysis of fetal RBC
Hb is released
Hb is converted into billirubin
(unconjugated)
Jaundice of fetus

17. Hemolysis
So decrease in RBC count
Baby will be severe anemic
Stimulation of bone marrow
Erythropoiesis
Blastic (nucleated forms of RBC enters into
circulation)

18. In moderate form
Hemolysis
increase billirubin
Cross blood brain barrier
Accumulates into basal ganglia of the brain
Permanent motor damage known as
kernicterus

19. In severe case called as hydrops fetalis
Severe anemia
Tissue anoxemia
Metabolic acidosis
Generation of oedema
Bloated appearance of baby
It can be ascites, hydrothorax.

21. Treatment
Before birth, options for treatment
include intrauterine transfusion.
Blood is infused through the
umbilical vein or hepatic vein.
The procedure is repeated,
frequency depending upon severity
of the disease and the gestational
age of the fetus.

22. After birth the treatment depends
upon the severity of the disease.
If condition is not very severe,
phototherapy is given.
The therapy uses a blue light (420-470 nm) that
converts bilirubin so that it can be excreted in the
urine and feces.
Soft eye shields are placed on the baby to protect
their eyes from damage that may lead to
retinopathy due to the lights.

23. phototherapy

24. In severe cases,exchange transfusion is
given.
The neonate’s blood is replaced with Rh-ve
blood that is infused while the neonate’s Rh+ve
blood is being removed.
Procedure is repeated till first few weeks of
life,the fetal RH+ve RBCs replace the negative
ones over a period of time and the Rh antibodies
are destroyed.

25. severe cases,exchange
transfusion

26. It is to replace the neonate's blood with Rh
negetive blood . About 400 ml of Rh
negetive blood is infused over a period of
1.5 or more hrs.
This process requires 6 or more weeks and
by this time this transfused Rh negetive
cells are replaced with the infant’s own Rh
positive cell.

27. Prevention-
Anti D antibody is administered to the mother
starting at 28 to 30 weeks of gestation.
It is also given to the Rh-ve women who deliver
Rh+ve babies to prevent sensitization of the
mother.
Cases of erythroblastosis fetalis are
significantly decreased after the discovery of
the anti D sera.

28. Nowadays Rh negative mother is given an anti D injection
within 48 to 72 hrs of first delivery.
It can be injected starting at 28-30 weeks of gestation.

30. 1. Text book of medical physiology Indu Khurana
2. Text book of Physiology, Gyuton
3. Essentials of Haematology, Kawathalkar
4. Internet source

31. Thank you!!