The Association of Fetal Acidemia With Adverse Neonatal Outcomes at Time of Scheduled Cesarean Delivery

Abstract

ABSTRACT Up to 30% of term labor deliveries experience fetal acidemia, a condition usually caused by hypoxia that is associated with adverse neonatal outcomes. The American College of Obstetricians and Gynecologists and American Academy of Pediatrics recommend assessing fetal umbilical artery (UA) blood gases at delivery when fetal metabolic status is in question. Although a UA pH of 7.24 to 7.28 is considered normal, the degree of acidemia associated with neonatal death is unclear. Recent data suggest that mild acidemia (UA pH of 7.0–7.2) and certain types of acidemia (metabolic, mixed, or respiratory) also indicate increased risk for adverse outcomes. Most cases of acidemia follow labor when the placental gas exchange is interrupted during contractions. But fetal acidemia is rare in cases of scheduled prelabor cesarean delivery (CD) and not well described in the literature. This study aims to determine if fetal acidemia at the time of scheduled, prelabor CD is associated with neonatal morbidity. This was a retrospective cohort study comparing patients with and without fetal acidemia, defined as a UA pH <7.2. Included were singleton neonates delivered via scheduled CD at a single tertiary care center from June 2004 to December 2014. Excluded were those who delivered before 37 weeks of gestation, were diagnosed with major anomalies, or underwent CD due to labor, rupture of membranes, or nonreassuring fetal status. Also excluded were cases in which data on validated umbilical cord gases were unavailable. The primary outcome was a composite of neonatal outcomes, including neonatal death, encephalopathy, therapeutic hypothermia, seizures, intubation, and respiratory distress. A total of 2081 neonates met the inclusion criteria, with fetal acidemia present at the time of delivery in 252 cases (12.1%). Acidemia occurred more frequently in breech neonates and those born to mothers with gestational diabetes mellitus or obesity. Intraoperative maternal hypotension, use of vasopressor therapy, and increased times from anesthesia induction and skin incision to delivery were also more likely to occur in cases of acidemia. The primary composite outcome was observed in 176 (8.5%) of neonates. This outcome was significantly higher in those with acidemia than those without (7.6% vs 15.1%; adjusted risk ratio [aRR], 2.95; 95% confidence interval [CI], 2.03 to 4.12). Intubation (aRR 3.50; 95% CI, 1.27–9.13) and respiratory distress (aRR, 2.93; 95% CI, 2.00–4.13) also occurred more frequently among those with acidemia. As the rate of UA pH categories decreased, the proportion of neonates with the primary outcome increased: 13.5% morbidity if UA pH was 7.0 to 7.19 versus 42.9% morbidity if UA pH was <7.0. Compared with neonates with a UA pH ≥7.2, the risk for adverse outcomes rose 3.2-fold in those with a UA pH <7.1 (aRR, 3.23; 95% CI, 1.73–5.24) and 6.6-fold in those with a UA pH <7.0 (aRR, 6.64; 95% CI, 3.23–8.96). The primary outcome was observed in 24.7% of neonates with respiratory acidemia, 27.5% with mixed, and 25% with other acidemia. There were no cases of metabolic acidemia. Compared with neonates without acidemia, the risk for adverse outcomes after controlling for confounders increased 2.7-fold in those with respiratory acidemia (adjusted odds ratio, 2.77; 95% CI, 1.74–4.15) and 3-fold in those with mixed acidemia (adjusted odds ratio, 3.08; 95% CI, 1.72–4.93). In conclusion, there was an increased risk of adverse neonatal outcomes in cases with mild fetal acidemia at the time of scheduled CD. Most cases in this study were attributed to respiratory acidemia.