Mother-child blood group incompatibility

and its complication

Alifah Anggraini
Outline
• ABO Incompatibility
• Rh Incompatibility
ABO incompatibility
Background
• Isoimmune hemolytic anemia may result when ABO incompatibility
occurs between the mother and the newborn infant.
• Most common: blood type A or B infants born to type O mothers.
• The hemolytic process begins in utero and is the result of active
placental transport of maternal isoantibody.
• Incidence:
• Symptomatic ABO hemolytic disease occurs in <1% of all newborn infants ~
two-thirds of observed cases of hemolytic disease in the newborn.
ABO blood group antigens present on red blood cells and IgM antibodies present in the serum
Risk factors
• A1 antigen in the infant.
• A1 antigen: greatest antigenicity → greater risk of symptomatic disease.
• Hemolytic activity: anti-B antibodies > anti-A antibodies → more severe disease (in
particular among infants of African American descent).
• Elevated isohemagglutinins.
• Antepartum intestinal parasitism or third-trimester immunization with tetanus toxoid
or pneumococcal vaccine may stimulate isoantibody titer to A or B antigens.
• Maternal immune serum globulin anti-A/B titers.
• Anti-A/B titers >512% are significantly associated with the risk of ABO hemolytic
disease of the newborn and may be an early indicator for therapy.
• Birth order.
• Birth order is not considered a risk factor. Maternal isoantibody exists naturally and is
independent of prior exposure to incompatible fetal blood group antigens.
Clinical presentation
• Jaundice.
• sole physical manifestation of ABO incompatibility with a clinically significant
level of hemolysis.
• onset: the first 24 hours of life.
• The jaundice evolves at a faster rate over the early neonatal period than
nonhemolytic physiologic pattern jaundice.
• Anemia.
• Exaggerated physiologic anemia may occur at 8 to 12 weeks of age,
particularly when treatment during the neonatal period required
phototherapy or exchange transfusion.
• Additional signs of clinical disease: hepatosplenomegaly or hydrops
fetalis
• Unusual but may be seen with a more progressive hemolytic process.
Diagnosis
• Blood type and Rh factor in the mother and the infant.
• Reticulocyte count.
• Direct Coombs test (direct antiglobulin test).
• Blood smear: microspherocytes, polychromasia, normoblastosis
• Bilirubin levels: indirect hyperbilirubinemia
• Additional laboratory studies: Antibody identification (indirect
Coombs test).
Post Partum Management
• General measure:
• adequate hydration
• evaluation for potentially aggravating factors (e.g sepsis)
• Phototherapy
• Exchange transfusion
• Intravenous immunoglobulin
Rh incompatibility
Background
• Rh incompatibility is a condition that occurs during pregnancy when a
mother with Rh-negative blood [who is previously sensitized to the
Rh(D) antigen] is exposed to her fetus who is Rh-positive leading to
the development of Rh antibodies and resulting in fetal isoimmune
hemolytic anemia of variable severity.
Incidence
• (RhoGAM) prophylaxis → reduced the incidence of Rh sensitization
to <1% of Rh-incompatible pregnancies
• In developing countries without prophylaxis: stillbirth still occurs in
14% of affected pregnancies, and 50% of pregnancies survivors either
die in the neonatal period or develop cerebral injury.
https://medmovie.com/portfolio-item/rh-factor-sensitization/
Risk factors
• Birth order.
• The first-born infant is at minimum risk (<1%) unless sensitization has occurred previously. Once sensitization
has occurred, subsequent pregnancies are at a progressive increased risk for fetal disease.
• Fetomaternal hemorrhage.
• The volume of fetal erythrocytes entering the maternal circulation correlates with the risk of sensitization.
The risk is approximately 8% with each pregnancy but ranges from 3% to 65%, depending on the volume of
fetal blood (3% with 0.1 mL compared with 22% with >0.1 mL) that passes into the maternal circulation.
• ABO incompatibility.
• Coexistent incompatibility for either the A or B blood group antigen reduces the risk of maternal Rh
sensitization to 1.5% to 3.0%. Rapid immune clearance of these fetal erythrocytes after their entry into the
maternal circulation exerts a partial protective effect. It confers no protection once sensitization has occurred.
• Obstetric factors.
• Cesarean delivery or trauma to the placental bed during the third stage of labor increases the risk of
significant fetomaternal transfusion and subsequent maternal sensitization.
• Gender.
• Male infants are reported to have an increased risk of more severe disease than females, although the basis
for this observation is unclear.
• Ethnicity.
• Approximately 15% of whites are Rh negative compared with 7% of blacks and almost 0% of Asiatic Chinese
and Japanese. The risk to the fetus varies accordingly.
Clinical presentation
• Jaundice.
• Unconjugated hyperbilirubinemia
• Within the first 24 hours of life
• Anemia
• Approximately 50% of cases
• Hepatosplenomegaly.
• Hydrops fetalis
Diagnosis
• Blood type and Rh factor in the mother and the infant.
• Reticulocyte count.
• Direct Coombs test (direct antiglobulin test).
• Blood smear: polychromasia, normoblastosis
• Bilirubin levels:
• indirect hyperbilirubinemia
• hydrop: direct bilirubin (5 - 6 days of age)
• Glucose and blood gas levels
• Additional laboratory studies: Antibody identification (indirect
Coombs test).
Post Partum Management
• Resuscitation
• Phototherapy
• Exchange transfusion
• Intravenous immunoglobulin
• Management for hydrops
• Partial exchange transfusion with type O Rh-negative packed erythrocytes.
• Central arterial and venous catheterization
• Positive-pressure mechanical ventilation
• Therapeutic thoracentesis or paracentesis
• Volume expanders
• Drug treatment: diuretics, pressor agents (such as dopamine)
• Electrocardiography or echocardiography.
Thank You