Management of Red Cell Alloimmunization in Pregnancy

Abstract

Haemolytic disease of the foetus and newborn, also known as erythroblastosis foetalis, used to be one of the main causes of perinatal mortality for many centuries. Although the clinical picture of extremely hydropic and icteric stillborns was already described in the 17 century, the pathogenesis of the disease was not understood until the early 1940s. Darrow published in 1934 an extensive overview on the clinical picture and etiologic considerations of neonatal haemolytic disease [1]. From the observation that the disease frequently occurred in the offspring in one family, Darrow hypothesized that the placenta may be the means of transmission of a destructive influence from mother to foetus [1]. Subsequently, Levine and Stetson managed to identify an unknown red-cell antigen in the blood of a woman who was delivered from a stillborn hydropic baby [2]. The woman had massive uterine bleeding and appeared to suffer from a life-threatening transfusion reaction, after being transfused with her husbands blood. As husband and wife both had blood type 0, Levine and Stetson called this unknown phenomenon “intra-group agglutination” [2],[3]. Simultaneously, Landsteiner and Weiner discovered an agglutinating factor in th serum of rodents, sensitised with blood from a Macacus Rhesus monkey [4]. As this factor caused agglutination of the blood of 85% of New York’s population, it was initially assumed to be similar to the human antibody causing erythroblastosis foetalis. Eventually, the antibody appeared comparable, though not identical to the human antibody, but by that time it had been erroneously called “Rhesus”.