Rh-incompatibility is the discordant pairing of maternal and foetal Rh type. It is a condition where maternal Rh-negative blood type is exposed to foetal Rh-positive blood cells which in turn leads to alloimmunization and formation of anti-D antibodies(1). This process may cause the maternal alloantibodies to persist for life and these can move across placenta freely into foetal circulation causing the destruction of foetal erythrocytes due to formation of antigen-antibody complexes with the surface D antigen. This is turn causes alloimmnune haemolytic anaemia which is called Erythroblastosis Fetalis.
The prevalence of Rhesus negative type individuals is varying around the globe. It is around 15% in the North Americans and Europeans, 4%-8% in Africans and 0.1%-0.3% in Asians. The risk of death and stillbirths are 24% and 11% respectively among these affected newborns, while 13% of affected neonates develop kernicterus with the highest reported mortality rates in the Eastern Europe/Central Asian region with 38 deaths per 100,000 live births(2). The incidence of Rh-Negative blood group is 3%-5.7% in India(3).
The pathophysiology is very simple. When the Rh-positive fetal RBCs enter the maternal circulation due to breaking of the embryonic chorion, the immune system of Rh-negative women considers these cells as foreign and creates a primary immune response by producing IgM antibodies initially. The first pregnancy is event free due to IgM antibodies but in the subsequent pregnancies, the exposure as less as 0.03ml of Rh-positive cells cause anti-D formation and thus leading to the diseases(2).