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Effect of maternal betamethasone on the fetal peak middle cerebral artery Doppler velocity in a case of Duffy alloimmunization
Abstract Number: S-19
Abstract Type: Case Report/Case Series
Betamethasone has become the standard for mothers at risk of preterm labor to decrease neonatal morbidity and mortality. As middle cerebral artery peak systolic velocity (MCA PSV) is essential in the diagnosis and management of fetal anemia, it is important to understand the effect of betamethasone on MCA PSV. We report a case of transient and significant decrease in fetal MCA PSV after betamethasone administration in a case of anti-Fya alloimmunization. Our patient was a 37 year old G4, P2002 at 27 weeks' gestation with anti-Fya alloimmunization and elevated MCA PSV of greater than 1.5 multiples of median (MoM). During the pregnancy, the patient was followed with serial anti-Fya titers along with MCA Dopplers. The titer at 25 6/7 weeks was 128 and 256 by 27 weeks. Her MCA PSV trended from 1.65 MoM at 16 4/7 weeks to greater than 2.0 MoM at 26 4/7 weeks.
The patient received intramuscular betamethasone at 26 5/7 weeks gestation. Ultrasound revealed no evidence of fetal hydrops with a MCA PSV of 1.53 MoM. Based on the borderline value for her MCA and similar findings in her previous pregnancy, a second dose of betamethasone was administered. At 27 weeks, her MCA PSV was once again elevated to 1.8 MoM. Fetal echocardiogram revealed an increased RV cardiac dimension. Based on these findings, a decision was made to proceed with cordocentesis.
At 27 1/7 weeks, cordocentesis revealed a fetal hemoglobin of 5.2. Blood typing revealed the presence of the Fya antigen with a positive direct Coombs. The patient underwent a series of five uneventful intravascular transfusions, the last at 35 weeks. At 37 3/7 weeks, she underwent induction of labor with delivery of a 2891 g male infant with Apgars of 8 and 9. Initial neonatal hemoglobin was 16.6 and total bilirubin was 6.5 with a decline to 4.5 in 24 hours. Patient and infant were discharged on the second day of life.
Doppler measurement of the fetal MCA PSV has been adopted almost universally to evaluate for anemia. The MCA PSV is influenced primarily by fetal hemoglobin concentration. Previously, there have been conflicting reports on the effects of maternally administered corticosteroids on fetal hemodynamics. There are several possible mechanisms of a glucocorticoid-induced decrease in MCA PSV. Betamethasone partially crosses the placenta and binds to glucocorticoid receptors which are plentiful in the hippocampus, thus changing vascular tone. Another possible mechanism is that glucocorticoids induce synthesis and production of placental corticotropin releasing hormone, increasing nitric oxide expression and vasodilation, presumably affecting cerebral blood flow. In conclusion, our case describes a transient decline in the MCA PSV after maternal betamethasone that has not previously been described. If confirmed, MCA PSV should be interpreted cautiously, as anemic fetuses could be misdiagnosed when the Doppler MCA PSV normalizes after antenatal betamethasone.