This chapter discusses the role of fetal therapy for fetal anemia, which has been one of the success stories of fetal medicine. There is a risk of red cell alloimmunization in any pregnancy where the mother is exposed to fetal red cells that possess antigens for which her own red cells are negative. A number of pregnancy-related events are associated with a risk of fetomaternal hemorrhage (FMH). A number of techniques have evolved over time to facilitate assessment of pregnancies at risk of 'hemolytic disease of the fetus and newborn' (HDFN). The aim of assessment is to identify the anemic fetus requiring intrauterine transfusion (IUT) before hydrops fetalis develops. However, monitoring an identified at-risk pregnancy to the point at which hydrops fetalis develops would be considered a management failure. Although less common than RhD disease, profound fetal anemia, hydrops, and intrauterine death can result from Kell alloimmunization.

This chapter focuses on red cell alloimmunization that is the immune-mediated destruction of erythrocytes initiated by maternal red cell antibodies which reach the fetal circulation by transportation across the placenta, onwards from approximately 12 weeks' gestation. Hemolytic disease of the newborn (HDN) describes the consequences of the antenatal pathogenic process which continues on into the newborn period. Prevention of Rhesus D (RhD) isoimmunization, and improvements in the ante-natal and neonatal care of isoimmunized women and their babies, has all but eradicated serious morbidity and mortality associated with this condition. Exogenous anti-D is produced by exposing RhD negative volunteers to the RhD antigen. The use of intravenous immunoglobulin is well established now in the treatment of neonatal alloimmune thrombocytopenia and HDN. Phenotypic tests of RhD status examine how blood from an individual behaves when it is added to serum containing anti-D antibodies.