Rh Incompatibility a Gynecological disorder

for UG and PG Nursing Students

2. •Aconditionthatoccursduringpregnancyifa
bloodandher
blood.Mother’sbodycreateRh
antibodiesagainstthebaby’sblood.
•Alsoknownashaemolyticdiseaseofthe
fetusandnewborn (HDFN) or
erythroblastosisfetalis.
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3. INTRODUCTION:
Four blood types ( A, B, AB, and O)
Each blood type is additionally classified according to the
presence or absence of the Rhfactor into Rhnegative and Rh
positive.

4. Rh Incompatibility
Occurswhenthereisa
differentRhblood
typebetweenthatof
thepregnantmother
(Rhnegative)and
thatofthefetus(Rh
positive)

5. Rh Incompatibility
Exposuretofetal
ANTIGENScauses
themotherto
produce
ANTIBODIES

6. The placenta usually acts as a barrier to
fetal blood entering the maternal
circulation.

7. Fetal cells can enter the maternal
circulation through a “break” in the
“placental barrier”.

8. Maternal production of Rhesus antibodies
following introduction of Rhesus positive
blood

9. Maternal production of Rhesus antibodies
following introduction of Rhesus positive
blood

10. Introduction
•Rh-Agsare found on the surfaces of the RBCs may
cause isoimmunization.
•D-antigen, the most powerful Rhfactor. If the
RBCs carry the D antigen, the person is Rh
positive and the reverse is correct.
•Exposure of Rh-vegroup to even small amounts
of Rh+vecells can result in the production of anti-
D alloantibody–Rh sensitization/isoimmunization
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11. Pathogenesis
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1. Rh-vemother carrying Rh+ve
fetus
2. Entry of fetus Rh+veRBC into
maternal circulation
3. Development of Rhantibodies
by the mother

12. 1. Rh-vemother carrying Rh+ve
fetus
•The chance of having Rh+ve fetus from
Rh+ve father ranges from 50% (if the father
is heterozygous Dd) to 100% (if the father is
homozygous DD).
•All offspring of the homozygous Rh-positive
person will be Rh-positive. The offspring of
the heterozygous Rh-positive person may be
Rh-positive or negative.
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13. 2. Entry ofthe fetal Rh+veRBC into
maternal circulation
•Transfusion of incompatible blood (rare)
•Fetomaternalhemorrhage(through leaks in the
placenta-3
rd
stage):
Spontaneous/ induced abortion
Ectopic gestation
Antepartumhemorrhage: abruptioplacenta,
amniocentesis, abdominal trauma, external cephalic
version.
•Worsen fetomaternalbleeding during labourare manual
removal of placenta, twin delivery and caeseriansection.
•Fetal RBC are detected in the maternal circulation in 6%
in the 1
st
trimester, 15% in the 2
nd
trimester and 30% in
the 3
rd
trimester.
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14. 3. Development of Rhantibodies by
the mother
•Initially –IgM (big Igcan’t pass the placental
barrier).
•Fetomaternalbleeding in the subsequent
pregnancies results in the anamenstic
reaction(Abproduction against Ag) producing
IgG (can pass placental barrier)
•Transfer of IgG develops hemolytic disease of
the newborn and hydropsfetalis, antibodies
mediated destruction of the fetal RBCs.
•First neonate is usually spared but subsequent
Rh+vefetuses are affected.
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15. Risks of Rh incompatibility effect
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Rh+ve father Rh-ve mother
1
st
Rh+ve baby
Usually unaffected
Rh+vecells
Miscarriage/ Termination
of pregnancy
Ectopic pregnancy
Amniocentesis
Antepartumhaemorrhage
Delivery of placenta
Rhesus antibodies
Pass to 2
nd
Rh+ve baby
Hemolysis of Rh +ve cells
Fetal Anemia
Hydrops fetalisIntrauterine transfusion
Postnatal exchange transfusion
Treatment

16. Effects on the fetus and the newborn
•Hemolytic anemia
•Progressive anemia which eventually leads
to congestive HF and tissue hypoxia.
•Hydrop fetalis-generalized edema of the
fetus
•Kernicterus-unconjugated bilirubin crosses
the BBB(blood brain barrier) and damages
the basal ganglia manifested by convulsions
and paralysis
•Neonatal jaundice-⬆bilirubin in infant’s
blood
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17. Signs in a newborn baby
•Hemolytic anemia
₋Pale,
₋increased breathing rate,
₋poor feeding
•Jaundice
₋Yellow sclera, palms and soles
•Kernicterus
₋Motor sensory and mental deficiencies
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18. Investigations:
•Atthefirstantenatalvisit,allwomenare
screenedforABOandRhtype.
•IfawomanhasRh-negativeblood,the
paternalbloodtypeandzygosityare
determined.IfthefatherhasRh-positive
blood,maternalRhAnti-Dtitresaremeasured
at26to28weeks.
•Maternalserumantibodytitreisaguideto
diseaseseverity.
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19. Investigations:
•If antibody levels rise, the baby should be
examined for signs of anaemia.
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Anti-D level Outcome
<4IU/mL HDFN unlikely
4-15IU/mL Moderate risk ofHDFN
>15IU/mL High risk of hydropsfetalis

20. •Amniocentesis: is performed if the anti-D titre is 4
IU/ ormore. The AF is examined for bilirubin by
the spectrophotometer using the Liley chart. This
gives idea about the degree of haemolysis and the
severity of the disease.
•Ultrasoundexaminationofthefetusatriskfor
Rhincompatibilitymayrevealsubcutaneous
oedema,ascites,pleuraleffusion,orpericardial
effusion,allofwhichareconsistentwithsevere
fetalanaemiainanaffectedfetus.
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Investigations:

21. •Cordocentesis:Bloodisobtainedfromthe
umbilicalveintodeterminetheHBconc.,Hct,
bloodgroup,directcoomb’stestandbilirubin
level.Thisisdoneusinganeedlepassedunder
ultrasoundcontrol.
•Atdeliverythecordbloodisexaminedfor:ABO
andRhgroup,Hb%,levelofbilirubinanddirect
Coombstesttodetectthepresenceofantibodies
onthesurfaceoffetalRBCs.
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Investigations:

22. Management
Management
Unsensitized
pregnancy
Identification
Management
Sensitized
pregnancy
Management
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23. Management of Rh-veunsensitized
pregnancy
•Provide anti D prophylaxis in cases with amniocentesis, APH,
external cephalic version.
•Following delivery determine blood group of the newborn and
antibody screening.
•If the newborn is Rhnegative no further treatment is needed.
•If antibody screen is positive monitor the newborn for
haemolysisand manage next pregnancy as sensitized.
•If newborn is Rh positive and antibody screen is negative,
provide anti D gamma globulin within 72 hours. The usual
dose is 300 micrograms but ideally should be determined by
the extent of fetomaternalhemorrhage.This is done by
performing KleihauerBetketest (acid elusion test). For
abortion of less than 12 weeks gestation the dose is 50
micrograms.
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24. Management of sensitized mother
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•Measurement of antibody levels in titers at
regular intervals,
•Amniocentesis for bilirubin levels
•Serial ultrasound for detection of hydrops and
management of neonatal anemia and
hyperbilirubinemia.
•Therefore, referral of these women is the
correct approach at health center level.

25. Treatment
•Intrauterine transfusion.
•Elect time of delivery.
•Maternal plasmapheresis(therapeutic
intervention –extracorporeal removal
,return,exchange of blood plasma and its
component).
•Exchange transfusion after delivery.
•Phototherapy after delivery.
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26. Intrauterine transfusion
•The fetus can die in utero from severe anaemiaand
hydropsbefore he can be delivered.
•An intrauterine transfusion can prolong the life in
uteroof a fetus to a gestation where the risks of
prematurity are estimated as being less than those
of the Rhdisease. This can be done by an:
1. Intraperitonealtransfusion guided by ultrasound.
2. Umbilical vein transfusion guided by ultrasound.
•Group O, Rh-negative blood is transfused under
ultrasound control.
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27. Choose time of induction and best
method of delivery
•Balance the risks of prematurity (too soon) with
that of worsening Rh disease (too late).
•Usually done only after 34 weeks of gestation.
Before this time the fetus is too premature to
survive after delivery.
•The paediatric team should be in close and a
senior paediatrician present at the delivery
•fresh Rh-negative blood available.
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28. Maternal plasmapheresis
•Towashantibodiesfrommaternalblood.
Indicatedforseverecasesbetween12and
16weeksofpregnancywhenintrauterine
transfusioncannotbecarriedout.Itiscostly
andtimeconsuming.
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29. Resuscitation and Exchange transfusion
•Good resuscitation is
essential. In an anaemicand
premature infant, lung
disease is common. It can
be due to:
Surfactant deficiency at
very early delivery.
Pulmonary oedemafrom
anaemiaand
hypoproteinaemia.
Hypoplasticlungs
secondary to pleural
effusions.
•In severe Rhhaemolytic
disease of the newborn, an
umbilical artery catheter
should be inserted as soon
as possible to assess and
control PaO2 and pH.
•Central venous pressure
should be measured.
Drain pleural effusions and
ascitesat resuscitation.
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30. Indication for exchange
Transfusion:
1.Early: Decision mainly based
on cord haemoglobin
(in addition consider history of
previously affected babies).
•Cord haemoglobin<12g/dl.
•Strongly positive Coombs’ test.
•Dangerous level of cord
serum bilirubinwhich varies
according to weight of the
baby.
2.Late: Usually done for
hyperbilirubinaemia.
•The aims:
Treat anaemia.
Washes out IgGantibodies.
Supply of Rh-negative cells
which will not haemolyse
Removes bilirubin.
Prevents kernicterus.
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Resuscitation and Exchange transfusion

31. Phototherapy
•Placing newborn baby under a halogen or
fluorescent lamp with their eyes covered to avoid
retinal damage.
•Lowers the bilirubin levels in the baby’s blood
through photo-oxidation.The blue or blue green light
converts the insoluble unconjugated bilirubin into a
soluble form which is rapidly excreted in bile and
urine.
•With phototherapy, it is rarely necessary to need
exchange transfusion.June:6 Rhesus Incompatibility 31

32. Prevention and Prophylaxis
•anti-D immunoglobulin to all Rh-negative women at 28
and 34 weeks routinely.
•Or give anti-D immunoglobulin
if she has a:
Therapeutic abortion.
Spontaneous abortion/ectopic pregnancy.
Amniocentesis.
Any bleeding in pregnancy/threatened miscarriage.
ECV.
After delivery at any gestation within 72Hours.
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33. Precautions after delivery
•After delivery, the cord is not milked and
immediately clamped to avoid further passage
of antibodies to the fetus.
•The cord is divided 3 inches from the
umbilicus to facilitate exchange transfusion
when needed.
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34. ABO-incompatibility
•Erythroblastosis fetalis may occur if the mother is
group O and the fetus is group A or B or AB like the
father.
•The Group O mother has naturally occurring anti A
and anti B antibodies which can cross the placenta
and destroy fetal cells of group A, B or AB. So HDFN
from ABO incompatibility may occur during the 1
st
pregnancy as the maternal antibodies are already
present.
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