RhD haemolytic disease of the fetus and the newborn

Abstract

When an RhD negative mother is exposed to the RhD positive red cells (usually as transplacental haemorrhage), she develops allo-anti-D which crosses the placenta and then results in the destruction of fetal red cells. Clinical manifestations of RhD haemolytic disease (HDN) range from asymptomatic mild anaemia to hydrops fetalis or stillbirth associated with severe anaemic and jaundice. HDN was a significant cause of fetal mortality and morbidity until the introduction of amniocentesis, intrauterine transfusion, controlled early delivery and exchange transfusion in the management of severely alloimmunised women and their fetuses. The objective of monitoring alloimmunised women is to identify fetal anaemia and prevent the development of life-threatening hydrops. Evaluation involves assessing the history of previous pregnancies; serial estimation of maternal anti-D levels; serial ultrasound measurements; serial amniocentesis; fetal blood sampling, and intrauterine transfusion when indicated. Diagnostic genotyping by DNA-based methods can identify at-risk RhD positive fetuses early in gestation. Identification of transplacental haemorrhage (TPH) as the stimulus for anti-D antibody production led to the development of anti-D immunoglobulin prophylaxis for at-risk RhD negative women who are not already alloimmunised. Prevention includes administration of anti-D immunoglobulin for any event associated with TPH during pregnancy, and at delivery of an RhD positive infant. Prophylactic routine administration of anti-D immunoglobulin at 28 (and 34) weeks gestation, in addition to the above, has reduced alloimmunisation to < 1% of RhD negative women carrying an RhD positive fetus. (C) 2000 Harcourt Publishers Ltd.