Rh incompatibility occurs when a pregnant woman with Rh negative blood is carrying a baby with Rh positive blood. During pregnancy or delivery, the baby's Rh positive blood can enter the mother's bloodstream and trigger an immune response. This response produces antibodies that can destroy the baby's red blood cells if the mother has a subsequent Rh positive baby. Rh incompatibility can cause jaundice, anemia and in severe cases hydrops fetalis in the baby. Diagnosis involves blood tests to check the mother's Rh status and antibody levels. Treatment may include Rh immunoglobulin injections during pregnancy to prevent sensitization.

1. RH INCOMPATIBILITY

2. INTRODUCTION
 Hemolytic diseases of the fetus and newborn occurs as a result of
paternally derved RBC antigens presenting on fetal redcells
which is absent in the mother.Rhesus iso immunisation seen in Rh
negative pregnant mothers remains the most common cause of
haemolytic diseases of the fetus and newborn.
 When an Rh negative mother causes an Rh positive fetus,
transplacental haemorrhage from the fetus to the mother.
 Fetal RBC enter the mothers blood stream stay in the maternal
circulation for their normal lifespan, facilitating stimulation of
maternal immune response and production of antibodies , the
fetus if Rh positive is affected resulting erythroblastosis fetalis.

4. CAUSES
Factors that influence an Rh negative
pregnant female chance of developing
Rh incompatibility include the
following
 Ectopic pregnancy
 Placenta Previa
 Placental abruption
 Abdominal trauma
 In uterofetal death
 Spontaneous abortion
It is a condition that develops
when a pregnant women has Rh
negative blood and the baby in
her womb has Rh positive
blood.
DEFINITION

9. ETIO PATHOLOGY
Iso immunization can occur either following in compatible blood
transfusion.The normal serum in the human body contains small
amount of natural antibodies of IgM,IgG,Ig A isotypes that can react
with foreign or self antigens and these complexes may have the
potential to elicit an immune response.
The immune complexes between antigens and antibodies may form
at the onset and during the course of an immune response.
The initial response in case of a women exposed to the RhD antigen
is week.It is primarily composed of IgM , a large molecule that
cannot cross the placenta.

10. However this immune response changes to the production of IgG
within a period of 6 weeks to 6 months, which can cross the placenta
resulting in various complications in the fetus and the mother.Rh iso
immunization is generally observed n case of 2nd pregnancies .
As the maternal antibodies cross the placenta and destroy the fetal
Rh positive red cell, haemolytic anemia ensures along with
increased levels of bilirubin.
Severe anemia may be followed by erythroblastosis fetalis that is
characterized by extramedullary hematopoiesis,Heart failure,edema
and Percardial effusion.

12. PATHOGENESIS
 Hematopoisis in the fetus begin as early as 8th week of gestation up to 40% of
pregnancy.These cells pass through the placenta into maternal circulation.
 If the fetus is Rh positive and mother Rh negative, the mother forms
antibodies against fetal blood cells.
 First IgM antibodies that are too large to pass through the placenta and later
IgG antibodies that can cross the placenta.
 This process of antibody formation is called Maternal sensitization.
 During subsequent pregnancies antibodies form in response to repeated
contact with antigen from the fetal blood resulting in lysis.
 Severe Rh incompatibility results in marked fetal haemolytic anemia because
the fetal erythrocytes are destroyed by maternal Rh positive antibodies.

13.  Placenta usually clear the bilirubin generated by RBC
breakdown.In extreme cases fetal bilirubin level increases.This
results in fetal jaundice known as Icterus gravis.
 The fetus compensates for the anemia by producing large number
of immature erythrocytes to replace those hremolyzed called as
Erythroblastosis fetalis.
 Severe form ---Hydrops fetalis.
 The fetus has marked anemia cardiomegaly, hepatosplenomegaly,
cardiac decompression.
 Hypoxia results from the severe anemia because decreased
intravascular oncotic pressure involved.

14. CLINICAL MANIFESTATION OF
HEMOLYTIC DISEASES OF NEWBORN
ICTERUS
GRAVIS
NEONATORUM
HYDROPS
FETALIS
CONGENITAL
ANAEMIA OF
NEWBORN

15. ICTERUS GRAVIS NEONATORUM
 The baby is born without evidences of jaundice but soon develops within 24
hours.
 While fetus is in utero, there is destruction of fetal red cells with liberation of
un conjucated bilirubin which is mostly excreted the placenta in to the maternal
system.
 As the umbilical cord is clamped with continuing haemolysis, the bilirubin
concentration is increased. Sooner or later baby develops jaundice.
 If the bilirubin rises to the critical level of 20 mg per 100 ml (340micromol/l)
{normal—30 micromol/l}
 The bilirubin crosses the blood brain barrier to damage the basal nuclei of the
brain permanently producing the clinical manifestation of kernicterus

17. CONGENITAL ANEMIA OF THE
NEWBORN
 The destruction of the red cells continues up to 6 weeks after which the
antibodies are not available for Haemolysis. The liver and spleen are enlarged.
CAUSES: Rh incompatibility
 Risk factors:
 Pregnant woman with Rh negative blood who had a prior pregnancy with fetus
that was Rh positive.
 Pregnant woman who had a prior blood transfusion.
 Pregnant woman with Rh negative blood who did not receive Rh immunization
prophylaxis during a prior pregnancy with Rh positive fetus.

18. SYMPTOMS
• High bilirubin level(greater than 18mg/cc)
• Extreme jaundice, absent startle reflex,Poor sucking
reflex, Lethargy
EARLY
• High pitch cry, Arched back with neck
Hyperextended backwards
• Bulging fontanel, Seizure
INTER
MEDIATE
• High pitched hearing loss, intellectual disability,
muscle rigidity, speech difficulties, seizures,
movement disorders
LATE

19. DIAGNOSIS: Blood test for Rh factor
TREATMENT:
IMMUNE GLOBULIN INJECTION: Give an injection of Rho immune globulin week 28th
of the pregnancy. This desensitizes mothers blood to Rh positive blood. Injection of
immune globulin within 72 hours after delivery .This is help ful for future pregnancy.

22. HYDROPS FETALIS
 Excessive destruction of the fetal red cells lead to severe anemia , tissue
anoxaemia and metabolic acidosis.
 Hyperplasia of the placental tissue occurs in an effort to increase the transfer of
oxygen but the available fetal red cells are progressively diminished due to
hemolysis.
 As a result of fetal anoxaemia, there is damage to the liver leading to
hupoproteinaemia which responsible for generalised edema, ascities and
hydrothorax.
 Fetal death occurs sooner due to cardiac failure. The baby is either still born or
macerated and even if born alive, dies soon after.

24. TREATMENT
 Amniocentesis to determine severity
 Intrauterine fetal transfusion
 Early induction of labour
 A direct transfusion of packed red cells and also exchange transfusion of the
newborn.
 This is done to rid the infants blood of the maternal antibodies that are
destroying the red blood cells.
 Control the congestive failure and fluid retention.

25. FACTORS INFLUENCING Rh
IMMUNIZATION
DURATION OF
PREGNANCY
AMOUNT OF
TRANSPLACENTAL
HEMORRHAGE
ABO
INCOMPATIBILITY
ANTI-D
PROPHYLAXIS
POST PARTUM
PROPHYLAXIS

26. DURATION OF PREGNANCY
 Entry of fetal cell (trans placental hemorrhage) in to the maternal
circulation mostly occurs at the time of expulsion of the fetus. It can
occur during pregnancy as well. Both the frequency and magnitude of
bleeding increases as pregnancy advances.
 Even spontaneous abortion is associated with transplacental
haemorrhage , but the incidence is less than 1%
 Abortion in first trimester—3%
 Abortion in second trimester--- 12%
 Maximum risk—46% in the time of delivery.
 As fetal Rh antigen can be detected early, when the fetus is only 38
days old, sensitisation can occur as early as 7 week of gestation.

27. AMOUNT OF TRANS PLACENTAL
HEMORRHAGE
 The volume of fetal blood cells entering the maternal circulation
is not uniform in all pregnancies.
 It may vary from 0.1 ml to more on average the blood may not be
more than 15 ml in term pregnancy.
 The risk of immunisation is 3% with 0.1ml of fetal red cells, 25%
with 0.25-1 ml and increases to 65% with more than 5 ml.

28. DIAGNOSIS
INDIRECT
COOMB’S TEST
USG
DOPPLER
STUDIES
CORDOCENTESIS

29. IDENTIFICATION OF Rh
INCOMPATIBILITY
 If the pregnant mother is Rh negative, then the husband’s blood
group is checked. In case husband Rh negative no further
investigation is required and pregnancy is managed as a normal
does not need any additional care.
 If the pregnant mother’s blood group is Rh negative, the husband
is Rh positive then at the first visit, Indirect coomb’s test is done
to detect maternal serum anti –D antibodies which unbound, If
antibodies are not detected, the test is repeated in the second and
third trimester.
 Anti partum prophylaxis with a dose of 300micro gram of anti-D
has been recommended.

30. DOPPLER STUDIES
 DOPPLER USG of the middle cerebral artery of the fetus to determine the
Middle Cerebral Artery Peak Systolic Velocity (MCA-PSV )is being studied
fetal anemia.
 The wave forms of the MCA are observed using colour Doppler and highest
point of the Doppler waveform is measured as MCA-PSV.
 It has been propose that absolute MCA-PSV may be helpful in the
management od red cell iso immunization and rate of change in MCA-PSV
over time help predict fetal anemia.
 It is advised periodically for evaluation of fetal heart size, edema, pericardial effusion,
ascites and AFI
ULTRA SONOGRAPHY

31. MANAGEMENT OF UNSENSITIZED
PREGNANCY-STANDARD PROTOCOL
 Repeat Rh antibody titre.
 USG examination of fetus.
 IM Rh immunoglobulin 300 micro gram.
 Analysis of the husband’s blood type.
 To prevent this from occurring , an injection of Rh –D immunoglobulin is offered
to all unsensitised Rh negative women during the 28th week if a repeat Rh
antibody titre is still negative.
 No need to perform an USG examination of the fetus.
 The antibody screening must be repeated at 35th week gestation and if negative ,
the women kept on observation .If positive, she should be managed on the lines of
a sensitised patient.

32. VARIOUS DIAGNOSTIC MODALITIES
Rh ANTIBODY
ASSAY
USG EVALUATION
OF THE FETUS
MIDDLE
CEREBRAL
ARTERY
DOPPLER
AMNIOCENTESIS
AND
EXAMINATION OF
AMNIOTIC FLUID

33. Rh ANTIBODY ASSAY
 Maternal titre
 Human antiglobulin titre(Indirect coomb’s test)-to determine the degree of allo
immunisation.
 Critical titre-the titre associated with high risk for fetal Hydrops.
 If the coomb’s test is positive in dilution of further evaluation of the fetus is
required1:16.
 If the titre is less than it is repeated every trimester.
 Titre are repeated every 2 weeks thereafter to determine whether there is
trend.

34. METHOD OF TERMINATION
Indication:
 Previous H/O still birth with father being homozygous.
 Sudden rise in maternal antibody titre.
 Sonographic features of fetal affection.
 Mild affection-Pregnancy may be continue up to 38 weeks.
 Severe affection-terminate the pregnancy before 34 weeks.

35. METHOD OF TERMINATION
AMNIOTOMY(LOW RUPTURE OF THE MEMBRANE)
 Termination is done near term –vaginal PG E2 to make cervix ripe. Oxytocin
drip may be added.
 If it is fail-caesarean section is preferred.
CAESAREAN SECTION:
 When termination has to be done prematurely (34-37 weeks) if it is
unfavourable.
CARE DURING VAGINAL DELIVERY:
 Careful fetal monitoring.
 Prophylactic ergometrine during second stage.
 Gentle handling of the uterus in third stage
 To take care of PPH.

36. INTRA UTERINE FETAL TRANSFUSION
INTRA
PERIOTONEAL
TRANSFUSION
INTRA
VASCULAR
TRANSFUSION

37. INTRA PERITONEAL TRANSFUSION
 Blood is transfused to fetal peritoneal cavity under USG guidance.
 Correct the fetal anemia when transfuse the erythrocytes are taken up by sub-
diaphragmatic lymphatics.
 It can be started at 18 weeks and repeated at intervals of 1-3 weeks to 32-34
weeks.
 Type and amount of blood –blood group “o”.
 Rh negative packed cell cross matched with the mother are to be transfused.
 The quantity of blood is to be calculate as number of weeks of gestation.
 The blood is to be infused slowly(5-10ml) through a polythene tube that has
been threaded through an introducing needle inserted in to the fetal abdomen
under guidance.

38. INTRA VASCULAR TRANSFUSION
 Transfusion is made through umbilical cord vessel near its insertion in to the placenta
under guidance of USG.
 Blood group “o” Rh negative packed cells compatible with mothers blood are
transfused.
 Check the Hematocrit value at intervals during the procedure to determine the volume.
 Goal: Achieve haematocrit of 50% ;Repeat transfusion is given 2 weeks.
 Volume overload –fetal injury, preterm labour, fetal maternal hemorrhage,.
 Fetal surveillance with USG and continuous electronic fetal monitoring.
 Betamethasone (24 mg in divided dose) should be administered to the mother 24 hours
before transfusion from 26 weeks onwards to enhance pulmonary maturity.

39. PREVENTION
 Anti-D immunoglobulin 300 micro gram of D Antibody is given to D-negative
, non sensitized mothers to prevent the hazards f sensitization.
 Anti-D globulin is provided to D-negative mothers after miscarriage ,
evacuation of molar pregnancy or ectopic pregnancy.
 It is also administered when there is heavy feto maternal bleeding such as
placental abruption, intrauterine manipulation.
 Dose of 300 micro gram D-antibody will neutralize about 15ml of red cells.
 Rosette test is done to all such mothers to know the accurate amount of
Anti-D required.