Presented by:

Group 86
Chow Jun Wing
Lui Siau Ting
• A condition that occurs during pregnancy if
a blood and her
blood. Mother’s body create Rh
antibodies against the baby’s blood.
• Also known as haemolytic disease of the
fetus and newborn(HDFN).

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 Introduction
• Rh-Ag 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.
possess it- Rh +ve ; lack- Rh –ve
• Exposure of Rh-ve ppl 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

1.Rh-ve mother carrying Rh+ve

fetus

2.Entry of fetus Rh+ve RBC into

maternal circulation

3.Development of Rh antibodies
by the mother

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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) to 100% (if the father is
homozygous).
• Non paternity explains the development of
hemolytic disease of the newborn.

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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

Treatmen Postnatal exchange transfusion
t
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Effects on the fetus and the newborn
• Hemolytic anemia
• Progressive anemia which eventually leads
to congestive HF and tissue hypoxia
• Portal HPT ~ obstruction of the portal
veins
• Hydrop fetalis- generalized edema
• Kernicterus- unconjugated bilirubin crosses
the BBB and damages the basal ganglia
• Jaundice-⬆bilirubin in infant’s blood
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 Signs in an unborn baby
• If the baby develops rhesus disease while still
in the womb, they may become anaemic
because their RBCs are being destroyed faster
than usual by the antibodies. If the anaemic is
severe, internal swelling may result.

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 Signs in a newborn baby
• Hemolytic anemia
₋ Pale,
₋ increased breathing rate,
₋ poor feeding
• Jaundice
₋ Dark skin
₋ Yellow sclera, palms and soles
• Kernicterus
₋ Motor sensory and mental
deficiencies
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 Complications
• Repetitive miscarriage
• Fetal anemia
• Hydrop fetalis
• Intrauterine fetal death

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 Investigations:
• At the first antenatal visit, all women are
screened for blood and Rh type.
• If a woman has Rh-negative blood, the
paternal blood type and zygosity (if paternity
is certain) are determined. If the father has
Rh-positive blood, maternal Rh antibody 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:
• Spectral photometry of amniotic fluid - used to measure
the level of bilirubin as an indirect indicator of fetal
haemolysis.
• 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.
• A rosette test can be used to rule out significant
fetomaternal haemorrhage. If results are positive, a
Kleihauer-Betke (acid elution) test or flow cytometry can
measure the amount of fetal blood in the maternal
circulation.

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 Management

Identification
Unsensitized
pregnancy
M
a
n
Sensitized a
gManagement
pregnancy e
m
e
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n 16
 Management of Rh-ve unsensitized
pregnancy
I. Identification of pregnancies at risk at the initial
ANC visit.
– Determine blood group & Rh factor and indirect
coombs test for antibody screening for all
pregnant mothers.
II. Management of unsensitized pregnancy
• Repeat indirect coombs test at 28 weeks and at
36 weeks. If negative consider antepartum
prophylaxis with 300 micrograms of anti D
gamma globulin at 28 weeks. If positive manage
as sensitized pregnancy.

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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 negative 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
• Exchange transfusion after delivery
• Phototherapy after delivery
• Top-up transfusion
(Hb falls below 7g/dl, prophylactic :oral folate)

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 Intrauterine transfusion
• The fetus can die in utero from severe anaemia and
hydrops before he can be delivered.
• 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.
• Rh-negative blood is either transfused under ultrasound
control. Repeat as necessary, according to amniotic
optical density, or fetal haematocrit. The intravenous
route is becoming increasingly the preferred method.

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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).
• Consider the risks of vaginal delivery and be
prepared for a lower segment Caesarean section
(LSCS).
• Usually done only after 34 weeks of gestation.
• The paediatric team should be in close and a
senior paediatrician present at the delivery
• fresh Rh-negative blood available.

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 Resuscitation and Exchange transfusion
• Good resuscitation is • In severe Rh haemolytic
essential. In an anaemic and disease of the newborn, an
premature infant, lung umbilical artery catheter
disease is common. It can should be inserted as soon
be due to: as possible to assess and
 Surfactant deficiency control PaO2 and pH.
• Central venous
at very early delivery.
 Pulmonary oedema pressure should be
from anaemia and  measured.
Drain pleural effusions
hypoproteinaemia. and ascites at
 Hypoplastic resuscitation.
lungs secondary to
pleural effusions.

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 Resuscitation and Exchange transfusion
Indication for exchange
Transfusion: 2. Late: Usually done
1. Early: Decision mainly for
based on cord haemoglobin hyperbilirubinaemia.
(in addition consider history of • The aims:
previously affected babies).  Treat anaemia.
• Cord haemoglobin <12g/dl.  Washes out IgG
• Strongly positive Coombs’ test. antibodies.
• Cord bilirubin >85mmol/l.  Decreases
degree of
haemolysis.
 Removes bilirubin.
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 Prevents
 Phototherapy
• Placing newborn baby under a halogen
or fluorescent lamp with their eyes
covered.
• Lowers the bilirubin levels in the baby’s blood
through photo-oxidation.
• During phototherapy, intravenous hydration is
required.

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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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