Hemolytic Disease of the Fetus and Newborn

Abstract

Hemolytic disease of the fetus and newborn (HDFN) is the result of immune-mediated destruction of fetal or newborn red blood cells when such cells contain antigens that are not present in the maternal blood. HDFN is now the preferred term that replaces the historic term erythroblastosis fetalis. Sensitization of the mother to fetal-newborn red blood cells requires fetomaternal hemorrhage in most cases except in ABO incompatibility where naturally occurring antibodies against A and B antigens are present in mothers with O blood type. The most common antigen involved in HDFN is Rhesus D. Kell 1 HDFN is rare but commonly associated with severe anemia and lower titers of anti-Kell antibodies in maternal serum in severely affected infants. Prevention of Rhesus D HDFN with anti-D immunoglobulin during pregnancy, delivery, and fetal-maternal events that predispose to fetomaternal hemorrhage, have markedly decreased the incidence of the disorder but may not be available in low-income countries. An algorithm is available to manage affected pregnancies by using antibody titers, fetal middle cerebral artery velocities, intrauterine transfusions, and timed delivery. Infants who have mild to moderate anemia may tolerate normal labor, but severely affected infants may require transfusion or exchange transfusions at birth, and the delivery team needs to be prepared. Delayed anemia in the transfused infants is still a concern, and the infants need to be closely followed after delivery. Phototherapy has largely replaced exchange transfusion in the management of hyperbilirubinemia. With appropriate early detection and multidisciplinary planning, infants who have HDFN can be delivered in a timely manner with appropriate planning for postnatal resuscitation and postnatal therapy resulting in good neonatal outcomes.