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

Abstract

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, P O 2, P CO 2, 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 P O 2 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 P CO 2 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 P O 2 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.)