2. Rh Blood Grouping

3. Rh antigens
Rh antigens were originally discovered in the RBCs of Rhesus Monkey- Named as ‘Rh antigens’ or ‘Rh Factor’
Later on Rh antigens were also detected in most of the human beings
The people having Rh antigen or factor are called ‘Rh Positive’

4. Rhesus Blood Group System
First demonstrated by testing human blood with rabbit anti sera against red cells of Rhesus monkey & classifying Rh negative & Rh positive.

5. Rhesus Blood Group System
The genotype is determined by the inheritance of 3 pairs of (SIX) closely linked allelic genes situated on chromosome 9
Six common type of Rh antigens in human beings C,D,E, c, d, & e.
Person having C cannot have c antigen
Same is true for D-d & E-e groups

6. Rhesus Blood Group System
The gene ‘d’ has no antigenic expression. So there are only five effective antigens.
The foetus inherits one gene from each group as a set of Cde, cde etc from each parent
Subsequently less common antigens Cw, Du, Es have also been found.

7. Rhesus Blood Group System
C/c & E/e are weak antigens and impractical to match.
‘D’ antigen is by far the most immunogenic in the Rh system.

8. Rh antigens Antigen D is most widely present antigen
The persons having either of C, D, E antigens are Rh Positive
The persons having either of c, d, e antigens are Rh negative

9. Rhesus Blood Group System
78 genotypes are possible. Most frequent genotypes are –
Cde/cde (33%)
Cde/cDe (18%)
Cde/cDE (12%)
cDE/cde (11%)
cde/cde (15%)
cdE/cde (1%)
Cde/cde (1%)

10. Rhesus Blood Group System
For clinical & all practical purposes it is enough to know whether one is Rh POSITIVE or NEGATIVE against anti D sera.
Rh positive 85%
Rh negative 15%

11. Rhesus Blood Group System
Incidence of Rh negative varies in different races:
Mongoloids- nil,
Chinese & Japanese- 1-2%,
Indians-5%,
Africans-5-8%,
Causcasians-15-17%
Basques-30-35%.

12. Antibodies for Rh factor
ABO system antibodies are spontaneously formed (Landsteiner law)
Anti Rh antibodies are normally not present in Rh+ or Rh – person

13. Formation of anti Rh- antibodies:
RBCs containing Rh factor injected into Rh
Negative person.
Anti Rh antibodies develop slowly,
Maximum conc 2 to 4 months later.
Multiple exposures to Rh factor result in Rh negative person being strongly “sensitized”to Rh factor.

14. Characteristics of the transfusion reactions:
Rh negative never exposed to Rh positive blood—no immediate reaction.
Anti Rh antibodies formed in sufficient quantities during the next 2-4 weeks.
Agglutination of transfused cells.
RBCs hemolyzed by the tissue macrophage system.
Mild delayed transfusion reaction occurs.

15. Subsequent exposure to Rh positive blood into the Rh negative person, transfusion reaction is greatly enhanced and can be immediate and severe.

16. Erythroblastosis Fetalis
Hemolytic disease of the new born
Icterus Neonatorum
Rh- mother
Rh+ Fetus due to Rh+ father
No reaction in first pregnancy
Rh+ cells of baby may enter maternal blood during labor
Mother will develop Anti D
Next pregnancy with Rh+ baby will cause the disease

17. Pathogenesis Haemolysis Rh Negative Women
Man Rh positive (Homo/Hetero)
 
Rh Neg Fetus No problem
  Fetus    
Rh positive Fetus 
Rh+ve R.B.C.s enter Maternal circulation
Mother previously sensitized Secondary immune response    
Non sensitized Mother Primary immune response
antibody (IgG)     ?   
Fetus
Fetus  unaffected, 1st Baby usually escapes. Mother gets sensitized?  
Haemolysis 

18. Erythroblastosis Fetalis
Anti D cross placental barrier
Rh+ cells of baby react
Characterised by Agglutination and phagocytosis of the fetal RBCs.
Hemolysis, Hb released into blood.
Fetus macrophages convert Hb into bilirubin. ↑Bilirubin→ Jaundice.

19. Severe Anemia → ↑↑Erythropoiesis → Appearance of immature, even nucleated cells (Blast cells) in the blood
Hematopoietic tissues, liver and spleen get enlarged and produce RBCs trying to replace for the hemolyzed RBCs.
Because of rapid production, early forms of RBCs including nucleated blastic forms of RBCs are released into circulation.

20. Erythroblastosis Fetalis
Blast Cells

21. Erythroblastosis Fetalis
Death very common
Permanent mental impairment if the baby survives
Damaged motor area of brain due to precipitation of bilirubin in neurons (Kernicterus)
Exchange transfusion with Rh- blood just after birth is the only treatment
Prevention- Injection of anti D antibody to Rh- mother in the first gestation after delivery for immediate destruction of Rh+ cells of the baby

22. Treatment of erythroblastosis fetalis:
EXCHANGE TRANSFUSION:
400ml of Rh negative blood is infused over a period of 1.5 or more hours while the neonate’s own Rh positive blood is being removed.
This is done several times to keep bilirubin level low and prevent kernicterus.
By the time these transfused Rh negative cells are replaced by infant’s own Rh positive cells (6 weeks), anti Rh antibodies

23. that have come from the mother have been destroyed.

24. Prevention RhoGAM® Contains IgG anti-D (anti-Rh)
Prevents Rh immunization
Manufactured from human plasma that contains anti-D
A single 300mcg dose will suppress the immune response to 15 ml of Rh-positive RBCs (approx 30 mL whole blood)

25. Mechanism of Action
Suppresses the immune response of Rh-negative individuals to Rh-positive RBC’s
Is not effective once Rh immunization has occurred

26. Prevention of Rh Incompatibility
Premarital counseling?
Proper matching of blood in transfusions particularly in women before childbearing.
Blood grouping must for every woman, before 1st pregnancy.
On exposure to Rh +ve Blood Anti Rh Immunoglobulin should be given as early as possible
Proper management of unsensitised Rh negative pregnancies.

27. POSSIBLE MECHANISM OF ACTION OF ANTI –D ANTIBODY:
Anti-D antibody attaches to D antigen sites on Rh positive fetal red blood cells that may cross the placenta and enter the mother’s circulation thereby interfering with the immune response to the D antigen.

28. Erythroblastosis Fetalis

29. Thank-you
Questions ??