Abstract

Neuraxial labor analgesia is associated with elevations in maternal temperature; the mechanism responsible is unknown. Proposed mechanisms have included infection, altered thermoregulation, and inflammation, potentially triggered by local anesthetics. Studies of the association between neuraxial labor analgesia and maternal fever have focused on epidural analgesia, and there have been no comparisons of the rate of maternal fever between continuous spinal and epidural labor analgesia. We performed a retrospective study to compare the rate of maternal fever between patients who received continuous spinal versus epidural labor analgesia between June 2012 and March 2020. Each patient who received continuous spinal analgesia was matched to 2 patients who received epidural analgesia and had the same nulliparous status. The primary outcome of our study was the incidence of intrapartum maternal fever, which we defined as any temperature ≥38 °C before delivery and compared between the continuous spinal and epidural groups using Fisher exact test. We identified 81 patients who received continuous spinal analgesia and 162 matched controls who received epidural analgesia. Demographic and obstetric characteristics of the patients were similar between groups. While the duration of analgesia did not significantly differ, there was markedly increased bupivacaine consumption in women with epidural analgesia. Eight of 81 (9.9%; 95% confidence interval [CI], 5.1-18.3) women with continuous spinal analgesia developed an intrapartum fever compared to 18 of 162 (11.1%; 95% CI, 7.1-16.9) of women with epidural analgesia ( P = .83; Fisher exact test). There was no significant difference in the rate of maternal fever between women with continuous spinal compared to epidural labor analgesia. While the route of administration and dose of bupivacaine differs between epidural and spinal labor analgesia, they are titrated to produce similar levels of neuraxial blockade. Our results are consistent with a model in which epidural related maternal fever is due to altered thermoregulation from a central neuraxial block and argue against a direct effect of bupivacaine or fentanyl, although we cannot rule out a concentration-independent effect of bupivacaine or fentanyl or an inflammatory effect of the catheter itself. These retrospective results highlight the importance of prospective and mechanistic study of neuraxial analgesia-related maternal fever.

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