Download 4b. Rh Blood groups

Rh Blood Grouping
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’
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.
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
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.
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.
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
Rhesus Blood Group System
• 78 genotypes are possible. Most frequent
genotypes are –
– Cde/cde
– Cde/cDe
– Cde/cDE
– cDE/cde
– cde/cde
– cdE/cde
– Cde/cde
(33%)
(18%)
(12%)
(11%)
(15%)
(1%)
(1%)
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%
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%.
Antibodies for Rh factor
• ABO system antibodies are spontaneously
formed (Landsteiner law)
• Anti Rh antibodies are normally not
present in Rh+ or Rh – person
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.
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.
• Subsequent exposure to Rh positive blood
into the Rh negative person, transfusion
reaction is greatly enhanced and can be
immediate and severe.
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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
Pathogenesis
Rh Negative Women
Man Rh positive (Homo/Hetero)

Rh Neg Fetus

No problem


Fetus  
Mother previously sensitized
Secondary immune response

antibody (IgG)

Fetus

Haemolysis
 

 
Rh positive Fetus

Rh+ve R.B.C.s enter
Maternal circulation

Non sensitized Mother
  ?  Primary immune response

Fetus  unaffected, 1st
Baby usually escapes.
Mother gets sensitized? 

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.
• 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.
Erythroblastosis Fetalis
Blast
Cells
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 Rhmother in the first gestation after delivery for
immediate destruction of Rh+ cells of the baby
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
that have come from the mother have
been destroyed.
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 Rhpositive RBCs (approx 30 mL
whole blood)
Mechanism of Action
• Suppresses the immune response of Rhnegative individuals to Rh-positive RBC’s
• Is not effective once Rh immunization has
occurred
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.
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.
Erythroblastosis Fetalis
Thank-you
Questions ??