Insight into the abnormal cardiotocographic patterns following neuraxial analgesia for pain management in labor

Background: Neuraxial analgesia (NA) is widely used for pain management in labor but may be associated with abnormal fetal heart rate patterns, including prolonged decelerations. Objective: To investigate decelerations and fetal bradycardia following neuraxial analgesia (NA; epidural, combined spinal-epidural, or spinal) in labor, in terms of frequency, associated factors, and outcomes. The primary objective was to determine whether maternal hypotension (SBP<100 mmHg or DBP<60 mmHg), uterine hyperstimulation (ie, exaggerated response to uterine stimulants presenting as a prolonged contractions for over 2 minutes), or other potentially implicated factors are associated with prolonged deceleration (lasting more than 3 minutes) after NA (PDAA). Study design: We retrospectively analyzed data of 898 singletons term pregnant women who underwent NA during labor. Data were retrieved from a prospectively collected database and medical records. All cardiotocographic tracings were manually reviewed from at least 10 minutes before NA to delivery. Univariate and multivariable logistic regression analyses were used to explore the associations between demographic, obstetric, and clinical characteristics and the occurrence of PDAA within 30 minutes after NA. Results: PDAA occurred in 6.57% (59/898; 95% CI 5.08%-8.44%) of women within 30 minutes after NA. Uterine hyperstimulation was significantly more frequent in those with PDAA [39% (23/59) vs 5.4% (45/839); P<.001], who also reported higher preanalgesia pain scores [9.7 (0.94) vs 8.9 (2.04); P=.003]. No significant differences were found between groups in systolic/diastolic blood pressure or the prevalence of maternal hypotension. Nulliparity (OR 2.27, 95% CI 1.01-1.06; P=.048), uterine hyperstimulation (OR 11.4, 95% CI 5.48-23.7; P<.001), and higher pain intensity at time 0 (OR 1.50, 95% CI 1.10-2.30; P=.007) were independently associated with PDAA. Conclusion: Uterine hyperstimulation appeared to be the strongest factor associated with PDAA. The role of uterine hyperstimulation due to a rapid drop in catecholamines in the occurrence of PDAA may be further supported by the association with higher preanalgesia pain intensity and nulliparity. Conversely, postanalgesia hypotension did not appear to be a key factor.