Is Acute Intrapartum Fetal Asphyxia Associated With an Increase in Fetal Nucleated Red Blood Cells? [28J]. (May 2018)

• Record Type: Journal Article
• Authors: Chu, Amanda; Divon, Michael; Guillaume, Stoffels; Kulla, Klea; Minior, Victoria; Bornstein, Eran
• Is Part Of: Obstetrics and gynecology. Volume 131(2018)Supplement 1
• Publication Date: 2018-05
• Subjects: Obstetrics -- Periodicals; Gynecology -- Periodicals; 618
• DOI: 10.1097/01.AOG.0000533493.07703.a6
• Languages: English
• ISSNs: 0029-7844

Abstract

Abstract : INTRODUCTION: Fetal heart rate abnormalities and elevated nucleated red blood cells (nRBCs) have been suggested as markers of fetal asphyxia. Animal studies suggest that the time between the onset of hypoxia and FHR abnormalities is short. The time interval in humans is unknown. Our study aims to evaluate the association between nRBCs and acute intrapartum fetal asphyxia. METHODS: Study patients included consecutive NICU admissions (2013–2017) with cord gases indicating severe fetal asphyxia (n=35). Controls without asphyxia were NICU patients matched for gestational age (n=72). All had a category I FHR tracing on admission. Fetal asphyxia was defined by an umbilical cord pH <7.0 with a base excess <−9. We examined the time interval from the last FHR acceleration to the time of delivery. Fetuses with congenital or genetic abnormalities were excluded. Statistical analysis included χ 2 testing, T-testing and Spearman correlations. RESULTS: There was no significant association between delta t and nRBCs in either group ( P =.70 and P =.71 in study and control patients, respectively). Several additional variables were studied including maternal BMI, gestational age, maternal age, parity, mode of delivery, fetal sex, standardized birth weight. We found that delta T was significantly associated with asphyxia in patients with increased BMI and in Cesarean Sections. CONCLUSION: It is highly unlikely that nRBCs can serve as a marker of acute intrapartum fetal asphyxia. We believe that fetal nRBCs are the result of antepartum compensatory mechanisms responding to chronic inadequate fetal oxygenation.