A comparison of criteria for defining metabolic acidemia in liveborn neonates and its effect on predicting serious adverse neonatal outcomes.

BACKGROUND: Metabolic acidemia is a known risk factor for serious adverse neonatal outcomes in both preterm and term infants.

OBJECTIVE: To evaluate the clinical significance of delivery umbilical cord gas measurements and serious adverse neonatal outcomes and to determine if distinct thresholds for defining metabolic acidemia differ in their ability to predict such adverse neonatal complications.

STUDY DESIGN: This is a retrospective cohort study of singleton liveborn deliveries between 1/2011 - 12/2019. Stratification was performed by gestational age at birth (≥ 35 weeks of gestation and < 35 weeks of gestation) and comparisons of maternal characteristics, obstetric complications, intrapartum events, and adverse neonatal outcomes were made between those neonates with metabolic acidemia and those without. Metabolic acidemia (based on delivery umbilical cord gas analyses) was defined utilizing both ACOG and NICHD criteria. A primary outcome of interest was hypoxic ischemic encephalopathy requiring whole-body hypothermia.

RESULTS: 91,694 neonates born ≥ 35 weeks of gestation met inclusion criteria. By ACOG criteria, 2,659 (2.9%) infants had metabolic acidemia. Neonates with metabolic acidemia were at significantly increased risk for NICU admission, seizures, need for respiratory support, sepsis, and neonatal death. Metabolic acidemia by ACOG criteria was associated with an almost 100-fold increased risk of hypoxic ischemic encephalopathy requiring whole-body hypothermia (RR, 92.69; 95% CI, 64.42 - 133.35) in neonates born ≥ 35 weeks of gestation. Diabetes, hypertensive disorders of pregnancy, post-term deliveries, prolonged second stages, chorioamnionitis, operative vaginal deliveries, placental abruption and cesarean deliveries were significantly associated with metabolic acidemia in neonates born ≥ 35 weeks of gestation. The highest relative risk was in those diagnosed with placental abruption (RR 9.07; 95% CI 7.25-11.36). The neonatal cohort born < 35 weeks of gestation had similar findings. When comparing those infants born > 35 weeks of gestation with metabolic acidemia by ACOG criteria versus NICHD criteria, the NICHD criteria identified more neonates at risk for serious adverse neonatal outcomes. In particular, 4.9% more neonates were diagnosed with metabolic acidemia, and 16 more term neonates were identified as requiring whole-body hypothermia. Mean 1-minute and 5-minute Apgar scores were similar, and reassuring, among those neonates with and without metabolic acidemia born > 35 weeks of gestation defined by both ACOG and NICHD criteria (8 vs 8 and 9 vs 9 respectively, p < 0.001). The sensitivity and specificity of the NICHD criteria were 86.7% and 92.2% respectively, while sensitivity and specificity of the ACOG criteria were 74.2% and 97.2%.

CONCLUSIONS: Infants with metabolic acidemia identified on cord gas collection at delivery are at a significantly greater risk of serious adverse neonatal outcomes, including an almost an almost 100-fold increased risk of HIE requiring whole-body hypothermia. Use of the more sensitive NICHD criteria for defining metabolic acidemia identifies more neonates born > 35 weeks of gestation at risk for adverse neonatal outcomes including hypoxic ischemic encephalopathy requiring whole-body hypothermia.