Snapshot A 32-year-old G1P0 woman presents to the emergency room with contractions. She was found to be Rh-negative and her husband’s Rh status is unknown. Fetal ultrasound shows no signs of edema or ascites. After the Kleihauer-Betke test, she is given the appropriate dose of Rh IgG. Introduction Overview Rh hemolytic disease of the newborn is caused by Rh incompatibility maternal anti-Rh IgG antibodies cross the placenta and destroy fetal Rh-positive red blood cells Epidemiology incidence 15% of the population is Rh-negative risk factors history of prior blood transfusion previous pregnancy mother is Rh-negative, and father is Rh-positive or unknown prior administration of Rh IgG (RhoGam) history of invasive obstetric procedures Pathogenesis mechanism Rh factor is a red blood cell antigen when an Rh-negative mother is pregnant with an Rh-positive fetus, the mother is exposed to Rh-positive red blood cells and leads to maternal antibody production (IgG) against the foreign Rh antigen as IgG can cross the placenta, subsequent pregnancy with Rh-positive fetus will result in fetal alloimmune-induced hemolytic anemia development of antibody depends on volume of transplacental crossover of red blood cells, concurrent presence of ABO incompatibility, and extent of maternal immune response breakdown of red blood cells causes elevation of bilirubin Presentation Symptoms hemolytic anemia Physical exam inspection jaundice pallor Imaging Fetal ultrasound indication suspected Rh incompatibility findings fetal ascites and edema Studies Serum labs hyperbilirubinemia low hematocrit elevated reticulocyte count positive direct Coombs test in fetus; positive indirect Coombs test in the mother Rosette test initial test to test for fetal-maternal hemorrhage Kleihauer-Betke test measures fetal red blood cells in utero in maternal circulation to determine dose of RhoGAM Differential ABO incompatibility key distinguishing factor typically less severe Treatment Medical maternal anti-D immune globulin (Rh IgG or RhoGAM) administration indication if mother is Rh-negative and has not been sensitized previously, given at 28th week of pregnancy, if possible, and 72 hours after birth external cephalic version amniocentsis ectopic pregnancy any suspected / known exposure of Rh-positive blood exchange transfusion indications erythroblastosis fetalis hydrops fetalis kernictus Complications Kernicterus secondary to hyperbilirubinemia loss of Moro reflex posturing poor feeding seizures Erythroblastosis fetalis most severely, can manifest as hydrops fetalis with high output cardiac failure, edema, and death indication for immediate delivery and exchange transfusion