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Evolving Strategies in the Diagnosis and Management of Hemolytic Disease of the Fetus and Newborn

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Evolving Strategies in the Diagnosis and Management of Hemolytic Disease of the Fetus and Newborn SUPPLEMENT TO FREE CME Credit To receive CME credit, please read the articles and go to www.omniaeducation.com/HDFN to access the posttest November 2020 and evaluation. CME CREDITS: .25 CREDITS To receive CME credit, please read the articles and go to www.omniaeducation.com/HDFN to access the post-test Evolving Strategies in the and evaluation. Diagnosis and Management OVERVIEW: Hemolytic disease of the fetus and newborn (HDFN) of Hemolytic Disease of the is a rare condition with an estimated 3 to 80 cases per 100,000 persons annually in the United States. Nonetheless, Fetus and Newborn the complexity and increased risk for adverse outcomes in such cases requires more targeted approaches to HDFN that minimize or negate the risks associated with intrauterine transfusion. Kenneth J. Moise, Jr., MD Department of Obstetrics, Gynecology and This article focuses on the pathophysiology underlying Reproductive Sciences fetal/newborn allo- and autoimmune diseases, especially McGovern School of Medicine – UT Health HDFN and the current/evolving diagnostic and treatment The Fetal Center regimens for HDFN. Children’s Memorial Hermann Hospital REVIEWERS/CONTENT PLANNERS/AUTHORS: Houston, Texas • Sean T. Barrett has nothing to disclose. • Barry A. Fiedel, PhD has nothing to disclose. • Amanda Hilferty has nothing to disclose. Once a significant cause of perinatal loss, alloimmu- • Kenneth J. Moise, Jr., MD receives royalties from Up-To-Date, Inc. and has contracted research with Momenta nization to red cell antigens is infrequently encoun- Pharmaceuticals Inc. tered in obstetrical practice today. Although maternal • Robert Schneider, MSW, has nothing to disclose. alloimmunization to the rhesus blood group D (RhD) • Lee Philip Shulman, MD, FACOG, FACMG, receives antigen remains the leading cause of fetal anemia, consulting fees from Biogix, Celula, Cooper Surgical, Natera, and Vermillion/Aspira, is a speaker for Bayer, more than 50 different red cell antigens have been Lupin Pharmaceuticals, Inc., and Myriad. associated with hemolytic disease of the fetus and newborn (HDFN). Sensitization to any one of these LEARNING OBJECTIVES: After participating in this educational activity, participants antigens occurs in approximately 1% of pregnan- should be better able to: cies.1 Most of these anti-red cell antibodies result in • Explain the pathophysiology underlying fetal/newborn the need for only phototherapy or simple transfusions allo- and autoimmune diseases, with a focus on HDFN. after birth. However, after anti-RhD, only a few red cell • Identify current diagnostic and treatment regimens for HDFN. antibodies are associated with profound HDFN neces- • Explain the role of the neonatal Fc receptor pathway sitating fetal therapy. A review of one large series of as a therapeutic means to address HDFN. intrauterine transfusions (IUTs) from a national referral ACCREDITATION AND CREDIT DESIGNATION center indicated that 10% of IUTs were secondary to STATEMENTS: Kell disease, and 3.5% of IUTs were secondary to anti-c Global Learning Collaborative is accredited by the alloimmunization.2 In another large series of IUTs, anti- Accreditation Council for Continuing Medical Education E, anti-e, and anti-Fya were reported to require IUT in (ACCME) to provide continuing medical education single cases.3 Significant advances in diagnostic tools for physicians. for the management of red cell alloimmunization Global Learning Collaborative designates this enduring have occurred with the addition of genetic testing of material for a maximum of .25 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate the parents and fetus and the use of Doppler ultraso- with the extent of their participation in the activity. nography for the detection of fetal anemia. Pregnant women routinely undergo red cell typ- COMMERCIAL SUPPORT: This activity is supported by an independent educational grant ing and an antibody screen at their first prenatal visit. from Momenta Pharmaceuticals. Identification of an antibody associated with HDFN EVOLVING STRATEGIES IN THE DIAGNOSIS AND MANAGEMENT OF HEMOLYTIC DISEASE OF THE FETUS AND NEWBORN should result in a reflex determination of the maternal artery peak systolic velocity (MCA-PSV) of the fetus titer. Until recently, titers were performed manually by to detect moderate to severe anemia.8 Once a critical laboratory technicians using an indirect Coombs test maternal titer has been reached in an alloimmunized on serial dilutions of the patient’s serum combined pregnancy and the fetus is found to be at risk based on with indicator red cells. Gel technology now allows its antigen status, MCA Dopplers are performed every for automation of the process of performing antibody 1 to 2 weeks starting as early as 16 weeks’ gestation screens and determining antibody titers. Gel titers (see FIGURE). An increasing value that reaches a typically provide results 2 to 3 dilutions higher than threshold of 1.5 multiples of the median for the cor- conventional tube titers (eg, 1:8 is found to be 1:64 responding gestational age warrants the need for cor- with gel), making the threshold for a critical titer more docentesis and probable IUT. difficult to determine.4 Obstetricians and maternal- Since its introduction in the mid-1960s, IUT of fetal medicine specialists should discuss the results of compatible red cells to the anemic fetus has proven a titer with their local blood bank to better understand to be the most effective fetal therapy to date. In the the methodology and to decide if further fetal surveil- mid-1980s, improvements in ultrasound technol- lance is warranted. ogy allowed for direct access to the fetal circulation Paternal antigen and subsequent zygosity testing through a puncture of the umbilical vein at either is an important next step in the evaluation process. An the cord insertion into the placenta or as the vein RhD-negative paternal blood type indicates the fetus courses through the fetal liver. Survival rates have is not at risk for HDFN as long as paternity is assured. improved to more than 95% in experienced centers, DNA technology is now the preferred approach to with reports of complications in 1.2% of procedures.9 determine if 1 or 2 copies of the paternal RhD gene are The widespread adoption of the MCA-PSV to detect present.5 A heterozygous result (only one RhD gene fetal anemia earlier in gestation before the onset of present) indicates a 50% chance of an affected fetus. hydrops fetalis has probably been the major factor in For other cases of red cell alloimmunization, paternal improved outcomes.10 However, a growing concern testing through serologic methods can still be used to is that the decreasing incidence of disease due to the determine zygosity. For example, a Kell-positive part- implementation of antenatal and postpartum pro- ner can have his red cells tested with anti-K and anti-k phylaxis for RhD alloimmunization will lead to fewer reagents. A reaction to anti-K indicates the individual training opportunities to maintain the availability of is Kell positive. If the anti-k serology test is also posi- skilled fetal interventionists. A recent study found that tive, the individual is heterozygous for Kell, which is between 30 and 50 IUT procedures were required for true for the majority of individuals. If the anti-k reac- a physician in training to achieve an optimal perinatal tion is negative, the individual is homozygous for Kell, outcome.11 An annual case rate of 10 procedures was which is a rare phenotype. Direct DNA testing can also required to maintain that expertise. determine paternal zygosity in these cases. Early-onset severe HDFN (EOS-HDFN) presents a Another advance in the field is the ability to deter- greater challenge to even the most experienced fetal mine the fetal antigen status through free fetal DNA. medicine specialist. In these cases, technical issues Often employed in clinical practice for determining with the puncture of small-diameter fetal vessels and the risk for chromosomal abnormalities, free fetal DNA a fragile fetal cardiovascular physiology contribute to after approximately 12 weeks’ gestation can be used a higher rate of perinatal mortality. Prior to 22 weeks’ to determine the fetal RhD status when the patient’s gestation, fetal loss can complicate up to 20% of partner is heterozygous or paternity is unknown.6 procedures.12 Should a perinatal loss occur, the man- European reference labs have expanded this technol- agement of a subsequent pregnancy is even more dif- ogy to determine the fetal antigen status for other ficult, because fetal anemia typically occurs earlier in important red cell antigens associated with severe gestation. In such cases characterized by EOS-HDFN, HDFN, namely Kell, RhC, and RhE7; however, these nonspecific immunomodulation has been used in tests are currently unavailable in the United States. the form of intravenous immunoglobulin (IVIG) with Measurement of amniotic levels of bilirubin or without the use of serial plasmapheresis to lower (ΔOD450), once the mainstay for surveillance of the maternal titer.13 Proposed mechanisms of action of pregnancies at risk for HDFN, has been relegated to IVIG include suppression of the maternal titer, partial the annals of the history of Rh disease. Two decades placental blockade through competition for transport have passed since the first reported use of a Dop- sites, and transplacental passage with suppression of pler ultrasound measurement of the middle cerebral the fetal reticuloendothelial system
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