Hemolytic Disease of Newborn (HDN)

[Audio] "Welcome to this overview of Hemolytic Disease of the Newborn, or HDN. This immune-mediated condition occurs when a mother's antibodies attack her baby's red blood cells due to blood type mismatches, like Rh-negative mother with Rh-positive fetus . It affects about 1 in 59 live births overall, though Rh cases are rarer now..

[Audio] Hemolytic disease of the fetus and newborn is a condition where fetal red blood cells are destroyed by maternl antibodies due to blood group incompatibility, primarily involving Rh or ABO blood types..

[Audio] Under the blood group classifications, the most common types of red blood cell antigens are; ABO classification Rh classification.

ABO Classification. Majority of the Abs for AgA and AgB are IgM, but some IgG may be present..

Rh Classification. Presence of the D agglutinogen (DD or Dd) – Rh Positive Absence of the D agglutinogen (dd) - Rh Negative The majority of Rh antibodies are of the IgG type (some IgM). Abs for Rh don’t occur naturally; exposure to the Rh-positive blood is essential IgG is the only antibody class that crosses the placenta through the syncytiotrophoblast layer..

Rh incompatibility. When a Rh-negative mother carries a Rh-positive fetus, fetal blood can enter the maternal circulation at delivery. Mother develops Rh agglutinins. (IgG anti-Rh antibodies) In the subsequent pregnancies, these IgG antibodies will cross the placenta. If the fetus is again Rh positive, these antibodies will cause hemolysis of the fetal RBCs. This is the underlying pathophysiology of HDN/Erythroblastosis fetalis. https://www.ncbi.nlm.nih.gov /books/NBK557423/.

[Audio] "HDN stems from alloimmunization. In Rh HDN, fetal-maternal bleeding during pregnancy exposes the mother to RhD antigen, producing IgG anti-D antibodies. These cross the placenta in subsequent pregnancies, binding fetal RBCs and causing hemolysis. ABO HDN is milder, often in group O mothers with A/B babies, due to natural IgG antibodies..

[Audio] During fetal life, maternal liver clears bilirubin; post-birth, neonatal jaundice emerges within 24 hours "Severe cases show fetal anemia, hydrops fetalis, or neonatal hyperbilirubinemia risking kernicterus—brain damage from bilirubin deposition . Signs include pallor, hepatosplenomegaly, and rapid jaundice. Diagnosis uses maternal antibody screen, amniocentesis for bilirubin, or Doppler for fetal anemia.

[Audio] "Treatment escalates by severity: phototherapy for mild jaundice, exchange transfusion for moderate, or intrauterine transfusion for fetuses . Survival exceeds 90% with timely intervention, especially early IUT . IVIG reduces hemolysis needs "Prevention transformed HDN: Rh immunoglobulin (RhIg) at 28 weeks and postpartum for Rh-negative mothers halves sensitization to under 0.5% . Universal screening prevents most cases.

[Audio] "Thanks to prophylaxis, HDN deaths dropped dramatically. For updates, see recent reviews.