Abstract

The objectives of this study were to determine if infants delivered with severe acidemia (cord umbilical arterial pH < 7.0) had short-term neurologic effects and whether infants with persistent bradycardia who received cardiopulmonary resuscitation (CPR) in the delivery room would be at greatest risk for subsequently developing neonatal seizures. Forty-seven infants (39 term, 8 preterm) delivered with severe fetal acidemia were studied. The mean (± S.D.) for pH, PaCO 2, and base deficit for the 47 infants was 6.86 ± 0.11, 97 ± 22 mm Hg, and −17 ± 4, respectively. Labor complications were common and included placental abruption in 8, ruptured uterus in 4, cord prolapse in 3, fetal heart rate decelerations in 12, and other (n = 14). Most infants were delivered via emergency cesarean section (n = 29). Delivery room interventions included oxygen and bag/mask ventilation only (n = 20) and intubation and ventilation (n = 22); 7 of 22 infants received CPR and epinephrine for persistent bradycardia (heart rate < 80 beats/min despite ventilatory support). Five infants required no intervention. Eight infants (17%) had seizures; 6 of these infants received CPR in the delivery room. Short-term outcomes were abnormal in 7 of 8 infants (i.e., death in 5, abnormal neurologic examination at discharge in 2). In 39 infants without seizures, 32 had transient neurologic abnormalities (i.e., irritability, hyperreflexia, proximal hypotonia) which resolved by discharge, and 2 had abnormal and 5 normal examinations. By univariate analysis, adverse outcome was related to 1 min ( P < .001) and 5 min Apgar scores ( P = .019) and CPR in the delivery room ( P < .0001). The odds ratio estimate for CPR is 234. These data indicate that CPR and epinephrine intervention in the delivery room for persistent bradycardia identifies infants at greatest risk for short-term adverse outcome and that therapeutic strategies to preserve brain function in severe fetal acidemia should focus on such infants.

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