Hemolytic disease of the fetus and newborn caused by ABO, Rhesus, and other blood group alloantibodies

Abstract

Introduction This chapter presents an overview of immune mediated hemolytic disease of the fetus and newborn (HDFN) due to ABO, Rh(D) and other red cell alloantibodies. Section I reviews the pathophysiology of immune mediated HDFN. Section II describes HDFN due to different antigen incompatibilities (ABO, Rh, and other antigens). Section III focuses on the management of the non-sensitized Rh(D) negative female, the alloimmunized mother, the fetus, and the neonate. Section I: Pathophysiology of hemolytic disease of the fetus and neonate (HDFN) The cause of hemolytic disease of the fetus and neonate (HDFN) is immune mediated destruction of fetal and/or newborn erythrocytes by maternal antibodies directed against fetal erythrocyte antigens inherited from the father. HDFN occurs as the result of five distinct events: (1) Fetal inheritance of a paternal erythrocyte antigen The gene for red cell antigen is inherited from the father. If the father is homozygous for the gene that the mother lacks, 100% of his offspring carry that gene and will be at the greatest risk for HDFN. The offspring of a heterozygous father will have 50% chance of carrying that gene and therefore will be at a lesser risk. Passage of fetal erythrocytes into the maternal circulation exposes the pregnant female to the “foreign” paternal erythrocyte antigen Any clinical situation that introduces the possibility of fetomaternal hemorrhage (FMH) may introduce fetal RBCs into maternal circulation and, thus, the possibility of maternal alloimmunization.