Moderate or severe neonatal encephalopathy (NE) has adverse outcomes and heterogeneous causes. Perinatal asphyxia is associated with encephalopathy (hypoxic ischemic encephalopathy [HIE]), but the proportion of cases that arise in labor has not been established. Diagnosis of asphyxia at the time of birth requires umbilical artery blood gas and acid-base assessment. A normal cardiotocographic (CTG) pattern at delivery represents normal central nervous fetal behavior and absence of hypoxia, whereas an abnormal CTG pattern implies an antenatal, possibly hypoxic, event. This retrospective study was performed to categorize admission CTG patterns and metabolic acidemia at birth to determine the proportion of moderate and severe NE cases attributable to asphyxia events before or after hospital admission, to assess the proportion that evolved during labor, and to determine the association between admission CTG patterns and neonatal outcomes.
Data on neonates with moderate or severe NE at 34 weeks’ gestation or greater were obtained from a previous study of 71,189 births. Fifty-six infants had moderate, and 24 had severe NE, for an incidence of 1.1 per 1000 infants. Infants with NE were categorized as having a normal or abnormal admission CTG pattern. A normal CTG pattern had a normal baseline fetal heart rate (110-150 beats/min), variability of 5 to 25 beats/min, 2 or more accelerations, and no decelerations. The CTG patterns not meeting these criteria were considered abnormal. Cases were classified as HIE or non-HIE, with HIE cases having umbilical artery or arterial samples indicating metabolic acidemia. Intrapartum HIE cases had spontaneous or induced labor and a normal admission CTG pattern; antepartum HIEs were considered to be those with an abnormal admission CTG pattern. Neurologic impairments included cerebral palsy, epilepsy, and mental retardation.
Of 80 infants with NE, 51 (64%) had a normal and 29 (36%) had an abnormal CTG pattern. Forty-eight infants (60%) had metabolic acidemia at birth (overall HIE incidence, 0.67/1000 infants); of these, 43 cases had spontaneous or induced labor. Forty-three (54%) of 80 infants had HIE evolving during labor, for an incidence of intrapartum HIE of 0.6 per 1000 cases. Most pregnancies were uncomplicated (92%), but previous cesarean deliveries were more frequent in cases with an abnormal admission CTG pattern. Spontaneous labor occurred in 77% of cases, more often among those with a normal admission CTG pattern. During the last 2 hours before delivery, 57 cases (71%) had CTG patterns of sufficient quality to interpret. A pathologic intrapartum CTG pattern was seen in 30 cases (81%) with a normal admission CTG pattern and in 19 cases (95%) with an abnormal admission CTG pattern. Late decelerations and decreased variability were significantly more frequent in cases with an abnormal admission CTG pattern. No differences were seen for tachycardia, bradycardia, or variable decelerations or between normal and abnormal CTGs in the median durations of these patterns. Adverse neonatal outcomes were more prevalent in HIE cases with an abnormal admission CTG pattern (78% vs 48%; P = 0.045). Severe NE and neonatal death were more common in cases with abnormal admission CTG patterns; moderate NE was more prevalent in cases with asphyxia that evolved during labor. Adverse neonatal outcomes at follow-up were similar (55%). In the 32 neonates without HIE or with missing acid-base data, neuroimaging revealed a perinatal hypoxic ischemic event in 13 neonates, an older lesion in 3, and perinatal cerebral infarction in 2, with others having meconium aspiration, sepsis, fetal anemia, cord prolapse, shoulder dystocia, and neuronal migration disorder; no cause was found in 3 of the cases.
Asphyxia was the main cause of moderate to severe HE and was strongly related to labor. An abnormal admission CTG pattern indicates a higher risk of neonatal death or adverse neurologic outcomes, particularly when metabolic acidemia is present. Because labor onset was spontaneous for most women, cases were not identified based on prenatal characteristics, limiting the opportunities for prevention during pregnancy. Future preventive strategies must focus on events related to labor.
Department of Women’s and Children’s Health, Uppsala University, Uppsala (M.J., J.Å., S.N.-L., U.H.); and Department of Pediatrics, Örebro University Hospital, Örebro (A.O.), Sweden