Hemolytic Disease of the New Born occurs when an RhD negative mother produces a RhD positive child. The child is RhD positive because it inherited the RhD gene from the father. HDN is not a problem in the first pregnancy of the mother. It becomes a problem in any subsequent pregnancies of the mother especially if she is already sensitized to the RhD antigen in her first child.
Sensitization is the process wherein the mother produces antibodies (immunoglobulin M, IgM) against the RhD antigen of the child’s RBCs. IgM antibodies are produced once RBCs of the child is mixed with the mother’s blood. IgM antibodies are incapable of crossing the placenta so the first child is safe from hemolytic disease.
The exposure of the mother to RhD positive RBCs of her second child triggers the production of immunoglobulin G (IgG) antibodies that are capable of crossing of the placenta and mix with the child’s blood. IgG antibodies destroys the child’s RBCs until the level of RBCs is inadequate to meet the child’s oxygen demand. The child develops severe anemia and the bone marrow and spleen are forced to produce red blood cells that are immature and non-functional. These two organs became enlarged as the level of RBCs is dropping. The destruction of the RBCs also result from the production of too much bilirubin in the body, a condition called hyperbilirubinemia. Bilirubin, a yellow colored substance, causes yellowing of the infant, a condition commonly known as jaundice.
