Rhesus (Rh) incompatibility is a crucial topic in the realm of pregnancy and childbirth. This condition arises when a pregnant woman, who is Rh-negative, carries a fetus with Rh-positive blood, causing a potential mismatch that can lead to serious complications. Understanding the mechanisms and implications of Rh incompatibility is paramount for healthcare providers and expecting parents alike. Let's delve into this intricate interplay between blood types, antibodies, and pregnancy, to grasp the significance of Rh incompatibility and its management.
5. Term Meaning
IgA Found in body secretion like breast milk and saliva and prevent antigen
crossing epithelial membranes and invading deeper tissues.
IgD This is made by B-cells and displayed on their surface. Antigens bind
here to activate B-cells.
IgE Found on cell membrane of basophilis and mast cells and if it binds its
antigen, activates the inflammatory response. This antibody is often
found in excess in allergy.
IgG This is the largest and most common antibody type. It attacks many
different pathogens and crosses the placenta to protect fetus
IgM Produce in large quantities in the primary response and is potent
activator of complement
Primary
response
Antigen encountered for the first time, primary response follows, in
which low level of antibodies can be detected in the blood after 2
weeks.
Secondary
response
Second encounter to antigen produce a secondary response
characterized by rapid memory B-cell response, resulting in a marked
increase in antibody production.
6. Rh incompatibility
• Rh incompatibility occurs when a
woman with an Rh- negative blood type
is exposed to Rh+ positive blood cells,
leading to the development of Rh
antibodies
7. Pathogenesis Of Rh Iso-immunisation
Rh Negative Women Man Rh positive (Homo/Hetero)
Fetus
Rh Neg Fetus
No problem
Rh positive Fetus
Rh+ve R.B.C.s enter
Maternal circulation
Mother previously sensitized
Secondary immune response
? Iso-antibody (IgG)
Non sensitized Mother
Primary immune response
Fetus unaffected, 1st
Baby usually escapes.
Mother gets sensitised?
Fetus
Haemolysis
?
8.
9. ABO incompatibility
• Haemolysis associated with ABO
incompatibility exclusively occurs in type
O mothers with fetuses who have type A
or type B blood although it has rarely been
documented in type A mothers with type
B infants with a high titer of anti B IgG.
10. • Type O mother have a high titer of the
antibodies of IgG class against both type
A and type B they cross the placenta and
cause haemolysis in the fetus.
11. Situation where incompatibility may
happen between the blood types of the
mother and the infant
Mother’s
blood type
O A B
Infant’s
blood type
A or B B A
12. Comparison of Rh and ABO incompatibility
Characteristics Rh ABO
Clinical aspects First born
Later pregnancy
Stillborn/hydrops
Severe anemia
Jaundice
Late anemia
5%
More sever
Frequent
Frequent
Moderate to
severe, frequent
Frequent
50%
No increased
severity
Rare
Rare
Mild
Rare
Laboratory
findings
Direct antibody
test
Indirect comb
test
Spherocytosis
Positive
Positive
Rare
Weakly positive
Usually positive
Frequent
13. Antenatal investigation protocol of
Rh negative mothers
• During first antenatal visit blood investigation for Rh and
ABO grouping
• Collect obstetric history
• In case of Rh negative women IgG antibody is detected by
indirect coomb’s test.
• If test found negative at 12th week, repeat test at 28th and 36th
week in primigravida. In multigravida test repeat monthly up
to 24 weeks and every 2 weeks thereafter.
• Fetal Rh status: amniotic fluid or chorionic villi to detect fetal
blood group.
14.
15. • Quantitative estimation of IgG antibody at
weekly interval.
- Sudden rise in titer from 1:8 to 1:256 is
very much suggestive of fetal affection.
- Antibody in maternal serum <4IU/Ml is safe
- Antibody in maternal serum >4IU/Ml but
<15 IU/mL is Moderate risk
-If anti D antibody is >15 IU/Ml is severe
HDFN
• Doppler ultrasound to assess fetal anemia.
16. Plan for delivery
• UNIMMUNIZED MOTHERs
No detectable antibody found during
pregnancy, an expectant attitude is
followed till term. Tendency of
pregnancy to overrun expected date
should not be allowed.
17. • IMMUNIZED MOTHERS
If there is evidence of hemolytic process in the fetus
in utero, the patient should be shifted to an equipped
center specialized to deal with Rh problems.
- Mild affection
- Severe affection
18. • Amniotomy (AROM)
• Careful fetal monitoring
• during 2nd stage should withheld
• Gentle handle of uterus in 3rd
stage
• Take care of PPH
19. • Cesarean section in case of prematurity.
- Avoid spillage of blood into peritoneal
cavity
- Routine manual removal of placenta
should be withheld.
21. Condition arise in fetus
• Hydrops fetalis
• Icterus gravis neonatrum
• Congenital anemia of the
newborn
22. Pathology Of Iso-immunisation
HAEMOLYSIS
IN UTERO
AFTER BIRTH
BILLIRUBIN
ANAEMIA
HEPATIC
ERYTHROPOESIS
& DYSFUNCTION
PORTAL & UMBILICAL VEIN
HYPERTNSION, HEART FAILURE
BIRTH OF AN AFFECTED INFANT - Wide spectrum of presentations. Rapid
deterioration of the infant after birth. May continue for few days to few months.
Chance of delayed anemia at 6-8 weeks probably due to persistence of anti Rh
antibodies.
Jaundice
Kernicterus
Hepatic Failure
DEATH
ERYTHROBLASTOSIS
FETALIS
IUD
23. After delivery
• Anti D administered within 72 hr or
preferably earlier following delivery or
abortion.
• In some case when specified time is
over (>72 hr), she may given up to 14-
28 days after delivery to avoid
sensitization.
• Anti D administered IM to mother 300
µg following delivery.
24. • Rh negative unsensitized woman
should receive 50 µg of Rh immune
globulin within 72 hr of induced or
spontaneous abortion, ectopic or
molar pregnancy or CVS in first
trimester.
25. SUMMARY
We discussed in class about basics of
blood, blood grouping system, ABO
compatibility and pathogenesis of in-
compatibility, protocol followed during
pregnancy, delivery and after delivery.
26. CONCLUSION
• ABO incompatibility has become a more
significant cause of hemolytic disease of
the fetus and newborn since the
introduction of effective anti-D prophylaxis.
• The condition is common and, if clinically
significant at all, causes only mild
jaundice, which can be treated with
phototherapy (PT)