Learning Objective

Explain the pathophysiology, clinical presentation, and prevention of ABO and Rh hemolytic disease of the fetus and newborn (erythroblastosis fetalis).

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Hemolytic Disease of the Fetus and Newborn (Erythroblastosis Fetalis)

Hemolytic disease occurs when maternal antibodies attack fetal RBCs due to blood group incompatibility. It can involve major blood groups (ABO, Rh) or minor groups (e.g., Kell). Disease severity ranges from mild jaundice to hydrops fetalis.

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ABO Hemolytic Disease

Interaction:

• Type O mother; Type A or B fetus.

Mechanism:

• Preexisting maternal anti-A or anti-B IgG antibodies cross the placenta → destroy fetal RBCs → hemolysis.

Presentation:

• Mild jaundice in neonates often occurs within 24 hours of birth. It can occur in firstborns and is usually less severe.

Treatment:

• Phototherapy or, rarely, exchange transfusion.

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Rh Hemolytic Disease

Interaction:

• Rh-negative mother; Rh-positive fetus.

Mechanism:

• First pregnancy: Maternal exposure to fetal Rh⁺ RBCs (often during delivery) → formation of anti-D IgG.
• Subsequent pregnancies: Maternal anti-D IgG crosses the placenta → attacks fetal RBCs → hemolysis.

Presentation:

• Severe anemia, hydrops fetalis, jaundice shortly after birth, and risk of kernicterus.

Prevention:

• Administer anti-D IgG (Rho(D) immunoglobulin) to Rh⁻ mothers during:
  • Third trimester
  • Early postpartum period

After miscarriage, ectopic pregnancy, abdominal trauma, or antepartum hemorrhage (if fetus is Rh⁺) → Prevents maternal anti-D IgG production.

Treatment:

Phototherapy or exchange transfusion for affected neonates.

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Activity

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Activity