Hemolytic Disease Of The Newborn

Hemolytic disease of the newborn (HDN), also known as erythroblastosis fetalis, arises from maternal-fetal blood group incompatibility, primarily Rh factor mismatch between an Rh-negative mother and Rh-positive baby. The mother's immune system produces antibodies against fetal red blood cells (RBCs) that cross into her circulation during pregnancy or delivery, leading to their destruction (hemolysis) in subsequent pregnancies. This results in fetal or neonatal anemia as RBCs break down faster than they can be replaced.

Causes and Risk Factors

HDN most commonly stems from Rh(D) incompatibility, though ABO mismatches or other antigens can contribute. Sensitization typically occurs if fetal blood mixes with maternal blood during miscarriage, trauma, or invasive procedures, prompting antibody production. It affects second or later pregnancies more severely, with a higher incidence in Caucasian infants.

Symptoms and Complications

Newborns exhibit pallor from anemia, jaundice within 24-36 hours, enlarged liver/spleen, and edema in severe hydrops fetalis cases. Excess bilirubin risks kernicterus, causing brain damage, seizures, or death if untreated. Prenatal signs include ultrasound-detected organ enlargement or fluid buildup.

Diagnosis

Diagnosis involves maternal antibody screening, ultrasound, amniocentesis for bilirubin, and postnatal cord blood tests for hemolysis markers like a positive Coombs test.

Treatment and Prevention

Intrauterine transfusions treat severe fetal cases; postnatally, options include phototherapy, exchange transfusion, IVIG, or simple transfusions. RhoGAM prophylaxis at 28 weeks and postpartum prevents sensitization in Rh-negative mothers.