erythroblastosis fetalis
Summary
Erythroblastosis fetalis (hemolytic disease of the newborn) is fetal/neonatal hemolytic anemia caused by maternal IgG antibodies against fetal RBC antigens, most classically Rh(D) incompatibility. It occurs when an Rh-negative mother is sensitized to Rh-positive fetal blood, producing anti-D IgG that crosses the placenta in subsequent pregnancies and destroys fetal RBCs. Prevention via RhoGAM (anti-D immunoglobulin) has made ABO incompatibility now the more common, but milder, cause.
Detail
Pathophysiology: Rh-negative mothers can become sensitized to Rh-D antigen during a prior pregnancy with an Rh-positive fetus (via fetomaternal hemorrhage at delivery, miscarriage, trauma, or invasive procedures) or via prior Rh-incompatible transfusion. Sensitization produces maternal anti-D IgG antibodies, which do not cause issues in the first pregnancy (too little exposure) but can cross the placenta in subsequent Rh-positive pregnancies, binding fetal RBCs and causing extravascular hemolysis (via splenic macrophages). This leads to fetal anemia, compensatory extramedullary hematopoiesis (hepatosplenomegaly, release of immature RBCs = erythroblasts, hence the name), and in severe cases, hydrops fetalis (high-output heart failure, generalized edema, ascites) due to severe anemia and hypoproteinemia from hepatic dysfunction.
After birth, continued hemolysis causes unconjugated hyperbilirubinemia (since the neonatal liver clears bilirubin inefficiently and placental clearance is lost), risking kernicterus (bilirubin deposition in basal ganglia, causing irreversible neurologic damage) if untreated.
ABO incompatibility (usually maternal type O, fetal type A or B) can cause a similar but typically milder hemolytic disease because anti-A/B antibodies are often IgM (don't cross placenta) or lower-affinity IgG, and it can occur in the first pregnancy since anti-A/B antibodies are naturally occurring (not requiring prior sensitization).
Clinical significance: Screening involves maternal blood type/Rh status and indirect Coombs test to detect anti-D antibodies. Rh-negative mothers receive anti-D immunoglobulin (RhoGAM) at 28 weeks gestation and within 72 hours postpartum (if baby is Rh-positive) to prevent sensitization by binding fetal Rh-positive cells before the maternal immune system can react. Direct Coombs test on neonatal blood confirms antibody-coated RBCs. Treatment of affected neonates includes phototherapy (converts bilirubin to water-soluble lumirubin) or exchange transfusion in severe cases.
Key associations: Rh-D incompatibility = more severe, preventable with RhoGAM, usually not first pregnancy. ABO incompatibility = milder, can occur in first pregnancy, direct Coombs may be weakly positive or negative.
Sources
- First Aid for the USMLE Step 1
- Robbins and Cotran Pathologic Basis of Disease
- Williams Obstetrics
- UpToDate: Hemolytic disease of the fetus and newborn
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