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INTRODUCTION:
Four blood types ( A, B, AB, and O)

Each blood type is additionally classified according to the

presence or absence of the Rh factor into Rh negative and Rh
positive.
 Rh Incompatibility
Occurs when there is a
different Rh blood
type between that of
the pregnant mother
(Rh negative) and
that of the fetus (Rh
positive)
 Rh Incompatibility

Exposure to fetal
ANTIGENS
causes the
mother to
produce
ANTIBODIES
The placenta usually acts as a barrier to
fetal blood entering the maternal
circulation.
 Fetal cells can enter the maternal
circulation through a “break” in the
“placental barrier”.
 Maternal production of Rhesus
antibodies following introduction of
Rhesus positive blood
 Maternal production of Rhesus
antibodies following introduction of
Rhesus positive blood
 Introduction
• Rh-Ags are found on the surfaces of the RBCs
may cause isoimmunization.
• System used to designate Rh-Ag is the Fisher CDE
system.
• D-antigen, the most powerful Rh factor. If the
RBCs carry the D antigen, the person is Rh
positive and the reverse is correct.

• Exposure of Rh-ve group to even small amounts

of Rh+ve cells can result in the production of anti-
D alloantibody– Rh sensitization/isoimmunization
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 Pathogenesis

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 1. Rh-ve mother 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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 2. Entry of the fetal Rh+ve RBC into
maternal circulation
• Transfusion of incompatible blood (rare)
• Fetomaternal hemorrhage(through leaks in the
placenta- 3rd stage):
 Spontaneous/ induced abortion
 Ectopic gestation
 Antepartum hemorrhage: abruptio placenta,
amniocentesis, abdominal trauma, external cephalic
version.
• Worsen fetomaternal bleeding during labour are manual
removal of placenta, twin delivery and caeserian section.
• Fetal RBC are detected in the maternal circulation in 6%
in the 1st trimester, 15% in the 2nd trimester and 30% in
the 3rd trimester.
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 3. Development of Rh antibodies by
the mother
• Initially – Ig M (big Ig can’t pass the placental
barrier).
• Fetomaternal bleeding in the subsequent
pregnancies results in the anamenstic reaction
producing Ig G (can pass placental barrier)
• Transfer of Ig G develops hemolytic disease of
the newborn and hydrops fetalis, antibodies
mediated destruction of the fetal RBCs.
• First neonate is usually spared but subsequent
Rh +ve fetuses are affected.
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 Risks of Rh incompatibility effect
Rh+ve father Rh-ve mother

Rhesus antibodies

Rh+ve cells
Miscarriage/ Termination
of pregnancy Pass to 2nd Rh+ve baby
Ectopic pregnancy
Amniocentesis
Hemolysis of Rh +ve cells
Antepartum haemorrhage
1st Rh+ve baby Delivery of placenta
Usually unaffected Fetal Anemia

Intrauterine transfusion Hydrops fetalis

Treatment Postnatal exchange transfusion

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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
due to HF
• Kernicterus- unconjugated bilirubin crosses the
BBB and damages the basal ganglia manifested
by convulsions and paralysis
• Neonatal jaundice-⬆bilirubin in infant’s blood

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 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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 Investigations:
• At the first antenatal visit, all women are
screened for ABO and Rh type.
• If a woman has Rh-negative blood, the
paternal blood type and zygosity are
determined. If the father has Rh-positive
blood, maternal Rh Anti-D titres are measured
at 26 to 28 weeks. 
• Maternal serum antibody titre is a guide to
disease severity.

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 Investigations:
Anti-D level Outcome
<4IU/mL HDFN unlikely
4-15IU/mL Moderate risk of HDFN
>15IU/mL High risk of hydrops fetalis

• If antibody levels rise, the baby should be

examined for signs of anaemia.
• Fetal middle cerebral artery (MCA) blood flow is
measured at intervals of 1 to 2 weeks depending
on titres and patient history. The purpose is to
detect high-output heart failure and fetal anaemia.
• Using MCA doppler: the peak of MCA velocity
– Rise - high probability of anemia

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 Investigations:

• Amniocentesis: is performed if the anti-D titre is 4

IU/ or more. 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.

• Ultrasound examination of the fetus at risk for

Rh incompatibility may reveal subcutaneous
oedema, ascites, pleural effusion, or pericardial
effusion, all of which are consistent with severe
fetal anaemia in an affected fetus.
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Oct-15 Rhesus Incompatibility 22
 Investigations:

• Cordocentesis: Blood is obtained from the

umbilical vein to determine the HB conc., Hct,
blood group, direct coomb’s test and bilirubin
level. This is done using a needle passed under
ultrasound control.

• At delivery the cord blood is examined for: ABO

and Rh group, Hb %, level of bilirubin and direct
Coombs test to detect the presence of antibodies
on the surface of fetal RBCs.
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 Management

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 Management of Rh-ve unsensitized
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 Rh negative no further treatment is needed.

• If antibody screen is positive monitor the newborn for haemolysis and

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 fetomaternal hemorrhage.
This is done by performing Kleihauer Betke test (acid elusion test). For
abortion of less than 12 weeks gestation the dose is 50 micrograms.

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 Management of sensitized mother
• 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.

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 Treatment
• Intrauterine transfusion.
• Elect time of delivery.
• Maternal plasmapheresis.
• Exchange transfusion after delivery.
• Phototherapy after delivery.

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 Intrauterine transfusion
• The fetus can die in utero from severe anaemia and
hydrops before he can be delivered. It is indicated if
TOP is needed before 34 weeks.
• An intrauterine transfusion can prolong the life in
utero of a fetus to a gestation where the risks of
prematurity are estimated as being less than those
of the Rh disease. This can be done by an:
1. Intraperitoneal transfusion guided by ultrasound.
2. Umbilical vein transfusion guided by ultrasound.
• Group O, Rh-negative blood is transfused under
ultrasound control.
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 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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 Maternal plasmapheresis

• To wash antibodies from maternal blood.

Indicated for severe cases between 12 and
16 weeks of pregnancy when intrauterine
transfusion cannot be carried out. It is
costly and time consuming.

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 Resuscitation and Exchange transfusion

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 Resuscitation and Exchange transfusion

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 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.

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 Prevention and Prophylaxis
• anti-D immunoglobulin to all Rh-negative women at 28
and 34 weeks routinely-RAADP;
• 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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 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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 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 1st pregnancy
as the maternal antibodies are already present.

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