OBJECTIVE: To evaluate predictors of umbilical artery acidemia in term neonates with low Apgar score. STUDY DESIGN: From a cohort of term singleton deliveries over a 13-year period, we selected neonates with 5-min Apgar score < 7. Acidemia was defined as umbilical artery pH < 7.00 or base excess (BE) < or = -12 mmol/L. Three pathogenic processes of neonatal acidemia were evaluated: (1) intrauterine vascular disease, defined as preeclampsia, clinical diagnosis of placental abruption, birth weight < 10th centile, or histologic evidence of placental infarction or severe vascular pathology, (2) intrauterine infection, defined as clinical chorioamnionitis, histologic chorioamnionitis, or early neonatal sepsis, and (3) acute intrapartum events, which included cases of cord prolapse, amniotic fluid embolism, uterine rupture, sudden and sustained fetal bradycardia or absence of FHR variability with a previously normal pattern, shoulder dystocia or complicated breech extraction. The associations of such processes with umbilical artery evidence of acidemia were tested using chi(2), Fisher's exact test, Student's t-test, and logistic regression, with P < 0.05 or odds ratio (OR) with 95% confidence interval (CI) not inclusive of the unity considered significant. RESULTS: Among the 27,395 neonates in the cohort, an Apgar score at 5 min < 7 was recorded in 94 (0.32%) and it was associated with umbilical artery acidemia in 33 cases. Logistic regression analysis showed that intrauterine vascular disease was independently associated with umbilical cord acidemia (P=0.035, OR=3.2, 95% CI=1.1-9.7) whereas intrauterine infection (OR=1.1, 95% CI 0.4-3.4) and acute intrapartum events (OR=2.1 95% CI 0.6-7.0) were not. CONCLUSIONS: Umbilical artery evidence of acidemia is present in 38% of term babies with low Apgar score and it is predominantly associated with chronic antepartum vascular disease. Neither intrauterine infection nor acute intrapartum events are significantly associated with umbilical artery acidemia.
OBJECTIVE: To evaluate predictors of umbilical artery acidemia in term neonates with low Apgar score. STUDY DESIGN: From a cohort of term singleton deliveries over a 13-year period, we selected neonates with 5-min Apgar score < 7. Acidemia was defined as umbilical artery pH < 7.00 or base excess (BE) < or = -12 mmol/L. Three pathogenic processes of neonatal acidemia were evaluated: (1) intrauterine vascular disease, defined as preeclampsia, clinical diagnosis of placental abruption, birth weight < 10th centile, or histologic evidence of placental infarction or severe vascular pathology, (2) intrauterine infection, defined as clinical chorioamnionitis, histologic chorioamnionitis, or early neonatal sepsis, and (3) acute intrapartum events, which included cases of cord prolapse, amniotic fluid embolism, uterine rupture, sudden and sustained fetal bradycardia or absence of FHR variability with a previously normal pattern, shoulder dystocia or complicated breech extraction. The associations of such processes with umbilical artery evidence of acidemia were tested using chi(2), Fisher's exact test, Student's t-test, and logistic regression, with P < 0.05 or odds ratio (OR) with 95% confidence interval (CI) not inclusive of the unity considered significant. RESULTS: Among the 27,395 neonates in the cohort, an Apgar score at 5 min < 7 was recorded in 94 (0.32%) and it was associated with umbilical artery acidemia in 33 cases. Logistic regression analysis showed that intrauterine vascular disease was independently associated with umbilical cord acidemia (P=0.035, OR=3.2, 95% CI=1.1-9.7) whereas intrauterine infection (OR=1.1, 95% CI 0.4-3.4) and acute intrapartum events (OR=2.1 95% CI 0.6-7.0) were not. CONCLUSIONS: Umbilical artery evidence of acidemia is present in 38% of term babies with low Apgar score and it is predominantly associated with chronic antepartum vascular disease. Neither intrauterine infection nor acute intrapartum events are significantly associated with umbilical artery acidemia.
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