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INTRODUCTION
 During Pregnancy, the mother and the fetus
have different Rh protein factors, this
condition is called Rh incompatibility.
 Like our blood type, we inherit our Rh factor
type from our parents. Most people are Rh-
positive, but a small percentage of people are
Rh-negative
 Rh factor doesn’t directly affect the health.
 However, Rh factor becomes important
during pregnancy.
Rh FACTOR
 • Proteins (antigens) occurring only on surface of
 RBC’s
 • Rh + if proteins present
 • Rh – if proteins absent
 • A+, A-, B+, B-, AB+, AB-, O+, O-
 • Most important for pregnancy
 • Inheritance is Autosomal Dominant
 • 15% Caucasian population are Rh-
Rh DISEASE?
 Rhesus disease is a condition where antibodies in a
pregnant woman's blood destroy her baby's blood
cells. It's also known as haemolytic disease of the
fetus and newborn (HDFN).
 If the mother is Rh-negative and her baby is Rh-
positive, during pregnancy (and especially during
labor and delivery) some of the fetus's Rh-positive red
blood cells may get into the mother's bloodstream.
 SENSITIZATION – The process in which mother’s
body will try to fight them off by producing antibodies
against them.
 Usually placenta acts as barrier to fetal blood entering
maternal circulation.However,sometimes during
pregnancy or birth,fetomaternal haemorrhage (FMH) can
occur. The woman’s immune system reacts by producing
anti-D antibodies that cause sensitisation
EVENTS FOR RHESUS DISEASE
 Miscarriage
 Termination of pregnancy
 Antepartum haemorrhage
 Invasive prenatal testing (amniocentesis cordocentesis
etc.)
 Delivery
 Ectopic pregnancy
PATHOPHYSIOLOGY
CAUSES
 A difference in blood type between a pregnant woman and
her baby causes Rh incompatibility. The condition occurs if
a woman is Rh-negative and her baby is Rh-positive.
RISK FACTORS
 This may have happened during:
 An earlier pregnancy (usually during delivery).
 An ectopic pregnancy, a miscarriage, or an induced
abortion. (An ectopic pregnancy is a pregnancy that starts
outside of the uterus, or womb.)
 A mismatched blood transfusion or blood and marrow
stem cell transplant.
 An injection or puncture with a needle or other object
containing Rh-positive blood.
SYMPTOMS
 Rh incompatibility can cause symptoms ranging from very
mild to deadly.
 Mildest form- Rh incompatibility:
1-Hemolysis (Destruction of the red blood cells) with the
release of free hemoglobin into the infant's circulation.
2- Jaundice (Hemoglobin is converted into, bilirubin which
causes an infant to become yellow.
 Severe form- Rh incompatibility
1- Hydrops fetalis (Massive fetal red blood cell
destruction).
2- It causes Severe anemia Fetal heart failure
Death of the infant shortly after delivery.
 Total body swelling.
 Respiratory distress (if the infant has been delivered)
 Circulatory collapse.
 Kernicterus. (Neurological syndrome in extremely
jaundiced infants)
 It occurs several days after delivery and is characterized
initially by...
A) Loss of the Moro reflex.
B)Poor Feeding.
C) Decreased activity
 At last it may lead to death of the child immediately after
its birth
Diagnosis
MCA doppler
Cell free DNA
Kleihauer test
Amniocentesis and liley graph
Direct coomb’s test
 SCREENING TESTS
 ABO & Rh Ab at 1st prenatal visit At 28 weeks
 Postpartum Bleeding
 Antepartum bleeding and before giving any immune globulin
 Neonatal bloods ABO, Rh
 GOLD STANDARD TESTS
• Indirect Coombs:
 mix Rh(D)+ cells with maternal serum
 anti-Rh(D) Ab will adhere
 RBC’s then washed & suspended in
 Coombs serum
 RBC’s coated with Ab will be agglutinated
• Direct Coombs:
 mix infant’s RBC’s with Coombs serum
 maternal Ab present if cells agglutinate
Ultrasound Parameters
 Non Reliable Parameters:
 Placental thickness
 Umbilical vein diameter
 Hepatic size
 Splenic size
 Polyhydramnios
 Visualization of walls of fetal bowel from small amounts
intra abdominal fluid may be 1st sign of impending
hydrops
 U/S reliable for hydrops (ascites, pleural effusions, skin
edema) – Hgb < 70
COMPLICATIONS
DURING PREGNANCY
 Mild anemia, hyperbilirubinemia and jaundice.
 Severe anemia with enlargement of the liver and spleen.
 Hydrops fetalis.
AFTER BIRTH
 Severe hyperbilirubinemia and jaundice.
 Kernicterus
Management
 Anti D immunoglobulin
 Fetal blood transfusion (fetal Hct <30%)
 Phototherapy
 Routes of administration-
 Into umbilical vein at the
point of cord insertion
 Into intrahepatic vein
 Into peritoneal cavity
 Into fetal heart
 Transfused blood-
 RhD negative
 Crossmatched with a maternal sample
 Densely packed (Hb around 30g/L)
 White cell depleted and irradiated
 Screened for infection including CMV
PROPHYLACTIC VACCINATIONS
 During every pregnancy
 After a miscarriage or abortion
 After prenatal tests such as amniocentesis
and chorionic villus biopsy
 After injury to the abdomen during
pregnancy

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Rh incompatibility

  • 1.
  • 2. INTRODUCTION  During Pregnancy, the mother and the fetus have different Rh protein factors, this condition is called Rh incompatibility.  Like our blood type, we inherit our Rh factor type from our parents. Most people are Rh- positive, but a small percentage of people are Rh-negative  Rh factor doesn’t directly affect the health.  However, Rh factor becomes important during pregnancy.
  • 3. Rh FACTOR  • Proteins (antigens) occurring only on surface of  RBC’s  • Rh + if proteins present  • Rh – if proteins absent  • A+, A-, B+, B-, AB+, AB-, O+, O-  • Most important for pregnancy  • Inheritance is Autosomal Dominant  • 15% Caucasian population are Rh-
  • 4. Rh DISEASE?  Rhesus disease is a condition where antibodies in a pregnant woman's blood destroy her baby's blood cells. It's also known as haemolytic disease of the fetus and newborn (HDFN).  If the mother is Rh-negative and her baby is Rh- positive, during pregnancy (and especially during labor and delivery) some of the fetus's Rh-positive red blood cells may get into the mother's bloodstream.  SENSITIZATION – The process in which mother’s body will try to fight them off by producing antibodies against them.
  • 5.  Usually placenta acts as barrier to fetal blood entering maternal circulation.However,sometimes during pregnancy or birth,fetomaternal haemorrhage (FMH) can occur. The woman’s immune system reacts by producing anti-D antibodies that cause sensitisation
  • 6.
  • 7. EVENTS FOR RHESUS DISEASE  Miscarriage  Termination of pregnancy  Antepartum haemorrhage  Invasive prenatal testing (amniocentesis cordocentesis etc.)  Delivery  Ectopic pregnancy
  • 8.
  • 10.
  • 11. CAUSES  A difference in blood type between a pregnant woman and her baby causes Rh incompatibility. The condition occurs if a woman is Rh-negative and her baby is Rh-positive. RISK FACTORS  This may have happened during:  An earlier pregnancy (usually during delivery).  An ectopic pregnancy, a miscarriage, or an induced abortion. (An ectopic pregnancy is a pregnancy that starts outside of the uterus, or womb.)  A mismatched blood transfusion or blood and marrow stem cell transplant.  An injection or puncture with a needle or other object containing Rh-positive blood.
  • 12. SYMPTOMS  Rh incompatibility can cause symptoms ranging from very mild to deadly.  Mildest form- Rh incompatibility: 1-Hemolysis (Destruction of the red blood cells) with the release of free hemoglobin into the infant's circulation. 2- Jaundice (Hemoglobin is converted into, bilirubin which causes an infant to become yellow.
  • 13.  Severe form- Rh incompatibility 1- Hydrops fetalis (Massive fetal red blood cell destruction). 2- It causes Severe anemia Fetal heart failure Death of the infant shortly after delivery.
  • 14.  Total body swelling.  Respiratory distress (if the infant has been delivered)  Circulatory collapse.  Kernicterus. (Neurological syndrome in extremely jaundiced infants)  It occurs several days after delivery and is characterized initially by... A) Loss of the Moro reflex. B)Poor Feeding. C) Decreased activity  At last it may lead to death of the child immediately after its birth
  • 15. Diagnosis MCA doppler Cell free DNA Kleihauer test Amniocentesis and liley graph Direct coomb’s test
  • 16.  SCREENING TESTS  ABO & Rh Ab at 1st prenatal visit At 28 weeks  Postpartum Bleeding  Antepartum bleeding and before giving any immune globulin  Neonatal bloods ABO, Rh  GOLD STANDARD TESTS • Indirect Coombs:  mix Rh(D)+ cells with maternal serum  anti-Rh(D) Ab will adhere  RBC’s then washed & suspended in  Coombs serum  RBC’s coated with Ab will be agglutinated • Direct Coombs:  mix infant’s RBC’s with Coombs serum  maternal Ab present if cells agglutinate
  • 17.
  • 18. Ultrasound Parameters  Non Reliable Parameters:  Placental thickness  Umbilical vein diameter  Hepatic size  Splenic size  Polyhydramnios  Visualization of walls of fetal bowel from small amounts intra abdominal fluid may be 1st sign of impending hydrops  U/S reliable for hydrops (ascites, pleural effusions, skin edema) – Hgb < 70
  • 19. COMPLICATIONS DURING PREGNANCY  Mild anemia, hyperbilirubinemia and jaundice.  Severe anemia with enlargement of the liver and spleen.  Hydrops fetalis. AFTER BIRTH  Severe hyperbilirubinemia and jaundice.  Kernicterus
  • 20. Management  Anti D immunoglobulin  Fetal blood transfusion (fetal Hct <30%)  Phototherapy
  • 21.  Routes of administration-  Into umbilical vein at the point of cord insertion  Into intrahepatic vein  Into peritoneal cavity  Into fetal heart  Transfused blood-  RhD negative  Crossmatched with a maternal sample  Densely packed (Hb around 30g/L)  White cell depleted and irradiated  Screened for infection including CMV
  • 22. PROPHYLACTIC VACCINATIONS  During every pregnancy  After a miscarriage or abortion  After prenatal tests such as amniocentesis and chorionic villus biopsy  After injury to the abdomen during pregnancy