Association between umbilical blood gas parameters and neonatal morbidity and death in neonates with pathologic fetal acidemia

Objective: Our purpose was to correlate umbilical artery blood gas parameters with neonatal death and indicators of morbidity in neonates with pathologic fetal acidemia (pH <7.0). Study Design: We reviewed maternal and neonatal charts of 93 neonates with an umbilical artery pH <7.0 who were delivered at 2 university-based centers. The relationships between umbilical artery pH, PO2, PCO2, bicarbonate, base deficit, and neonatal variables—death, need for intubation, cardiopulmonary resuscitation, seizures, hypoxic-ischemic encephalopathy, respiratory distress syndrome, intraventricular hemorrhage, meconium, sepsis, and intrauterine growth restriction—were determined with the Student t test, Mann-Whitney U test, and multiple logistic regression analysis. Data are presented as either median with 25th-75th percentiles or mean ± SD. Results: The mean gestational age at delivery was 37.9 ± 3.6 weeks, and the mean birth weight was 3003 ± 866 g. There was no relationship between neonatal death, respiratory distress syndrome, intraventricular hemorrhage, necrotizing enterocolitis, patent ductus arteriosus, meconium, sepsis, and any umbilical artery blood gas parameter. The PO2 was not related to any of the variables studied. A lower umbilical artery pH was associated with hypoxic-ischemic encephalopathy (6.69 vs 6.93, P = .03), cardiopulmonary resuscitation (6.83 vs 6.93, P = .03), seizure (6.75 vs 6.93, P = .02), intubation (6.83 vs 6.94, P< .001), and intrauterine growth restriction (6.72 vs 6.93, P = .01). Greater mean base deficit was associated with seizure (20.6 vs 15, P = .01), intubation (18.0 vs 13.7, P< .001), cardiopulmonary resuscitation (18.5 vs 15.0, P = .03), intrauterine growth restriction (22.0 vs 14.0, P = .02), and hypoxic-ischemic encephalopathy (24.0 vs 14.5, P = .03). Arterial PCO2 was higher only in infants with hypoxic-ischemic encephalopathy (138 vs 95.5, P = .048), intubation (106.0 vs 90.5, P = .003), and cardiopulmonary resuscitation (106.5 vs 93.0, P = .04). After control for birth weight and gestational age in the multivariate analysis, base deficit and bicarbonate were independently related to death or morbidity. Conclusion: Our data suggest that “pathologic” fetal acidemia is indicated by an umbilical artery pH <7.00 with a metabolic component. The metabolic component of fetal acidemia (ie, base deficit and bicarbonate) is the most important variable in subsequent neonatal morbidity. As expected, the umbilical artery PO2 has no apparent clinical utility. The ability to predict more accurately which newborn infants with fetal acidemia are at risk of having complications may lead to a more efficient implementation of preventive measures. (Am J Obstet Gynecol 1999;181:867-71.)