Wednesday, June 12, 2024

Hemolytic Disease of the Newborn

Background

A French midwife was the first to report hemolytic disease of the newborn (HDN) in a set of twins in 1609. In 1932, Diamond and colleagues described the relationship among fetal hydrops, jaundice, anemia, and erythroblasts in the circulation, a condition later called erythroblastosis fetalis. Levine later determined the cause after Landsteiner and Weiner discovered the Rh blood group system in 1940. In 1953, Chown subsequently confirmed the pathogenesis of Rh alloimmunization to be the result of passage of Rh-positive fetal RBCs after transplacental hemorrhage into maternal circulation that lacked this antigen.

In 1966, 2 groups from the United Kingdom and the United States demonstrated, in a combined study, that anti-D immunoglobulin G (IgG) prophylaxis soon after delivery prevented sensitization in Rh-negative women. The World Health Organization (WHO) technical report in 1971 recommended that a dose of 25 mcg (125 IU) of anti-D immunoglobulin G (IgG) should be given intramuscularly for every 1 mL of fetomaternal hemorrhage of Rh-positive packed RBCs or 2 mL of whole blood.

In 1998, this recommendation was reinforced by the American Association of Blood Banks and the American College of Obstetrics and Gynecologists with inclusion of prophylaxis at 28 weeks’ gestation.
Routine use of Rh IgG prophylaxis resulted in a significant decline in the incidence of RhD alloimmunization,
and erythroblastosis fetalis has become rare. The perinatal effects of maternal Rh alloimmunization are now referred to as hemolytic disease of the fetus and newborn, and fetal manifestations of the disease are more appreciated with newer technologies such as cordocentesis and fetal ultrasonography.

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