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ORIGINAL RESEARCH |
From the Departments of Obstetrics and Gynecology and Pathology, University of Texas Southwestern Medical Center, Dallas, Texas.
Address reprint requests to: Jodi S. Dashe, MD, University of Texas Southwestern Medical Center, Department of Obstetrics and Gynecology, 5323 Harry Hines Boulevard, Dallas, TX 75235-9032
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Abstract |
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Methods: Placentas collected prospectively from women with singleton gestations, who delivered 6 hours or more after membrane rupture, were evaluated systematically for histologic inflammation by an investigator blinded to all clinical information. Maternal and neonatal markers of infection were assessed in the cohorts who did and did not receive epidural analgesia.
Results: One hundred forty-nine consecutive placentas were analyzed, and 80 (54%) of these women received epidural analgesia. On univariate analysis, significant differences between epidural and no epidural groups were found with respect to maternal fever 38C or greater (46% versus 26%, P = .01), placenta inflammation (61% versus 36%, P = .002), and length of labor (11.8 hours versus 9.6 hours, P = .03). The combination of maternal fever plus placental inflammation was significantly more common in the epidural group (35% versus 17% P = .02). However, maternal fever in the absence of supporting evidence of infection, in the form of placental inflammation, was not increased after epidural analgesia (11% versus 9%, P = .61).
Conclusion: Epidural analgesia is associated with intrapartum fever, but only in the presence of placental inflammation. This suggests that the fever reported with epidural analgesia is due to infection rather than the analgesia itself.
Several investigators found that maternal temperature tends to increase in some women after they receive epidural analgesia for labor pain. Fusi et al1 and Camann et al2 first described this increase in temperature, although in both series, the average maternal temperature remained below 38C. More recently, labor epidural analgesia was associated with overt maternal fever. Herbst et al3 found that the odds of overt fever (at least 38C) in labor increased four-fold, and Lieberman et al4 found it increased more than 14 times after labor epidural analgesia. In the latter series,4 diagnosis of maternal fever was linked to a four-fold increase in neonatal sepsis evaluations.
Although it is clear that maternal temperature increases in some women who receive labor epidural analgesia, the cause of the increase is controversial. One view is that the rise in temperature is a side effect of the analgesia, possibly indicating a decrease in sweating from sympathetic blockade, a decrease in hyperventilation from the pain relief, or reactive upper body vasoconstriction.1 Another explanation for fever in labor is intrapartum infection, because women who choose epidural analgesia might have risk factors that predispose them to infection, such as longer labor.3 Women with subclinical infections might choose epidural analgesia because their labors are dysfunctional.
It is difficult to establish incontrovertibly the cause of fever among women in labor. For example, traditional supporting signs of maternal infection, such as white blood cell (WBC) count, often are elevated in labor regardless of infection. Transvaginal uterine cultures are difficult to collect without contamination from normal cervical-vaginal microbes. Similarly, uterine tenderness, often found with uterine infection, will likely be eliminated by epidural analgesia. Such difficulties in interpretation of signs and symptoms make empiric diagnosis of intrapartum infection problematic in laboring women. The goal of this study was to determine whether placental examination for acute inflammation might permit a better understanding of the relationship, if any, between epidural analgesia and maternal fever in labor.
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Materials and Methods |
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Placentas were collected from all women who delivered singletons weighing at least 2500 g during June 1997 at Parkland Memorial Hospital, Dallas, TX. Those who delivered within 6 hours of membrane rupture were excluded because of their very low incidence of intrapartum fever (less than 1%) and because some delivered before epidural analgesia could be considered. Smaller infants (less than 2500 g) were excluded to avoid the confounding effects of prematurity-related intrauterine infection.
Each placenta was labeled with a study number at delivery and refrigerated immediately. One pathologist (BR) evaluated every placenta within 48 hours of delivery. From each placenta, one section of chorionic plate, one roll of free membranes (chorion and amnion, with attached decidua capsularis), and two sections of umbilical cord were examined systematically for inflammation. We used the histologic grading system devised by Salafia and colleagues,5 which includes four grades of inflammation of the amnion, chorion-decidua, umbilical cord, and chorionic plate. We used grade 2 or more leukocytic infiltration of the chorionic plate as the marker for significant placental inflammation, because this was reported to be the most sensitive indicator of culture-proven amnionic fluid infection.6 Grade 2 inflammation was characterized by multiple foci of five or more polymorphonuclear leukocytes or one focus of five to 20 polymorphonuclear leukocytes in the subchorionic fibrin. Grade 3 was multiple or confluent foci of grade 2 inflammation. Grade 4 was diffuse or dense acute inflammation. Figure 1
shows grade 4 accumulation of leukocytes within the subchorionic fibrin of the chorionic plate.
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At our hospital, labor is managed according to formalized, written protocol. Amniotomy is done routinely in active labor (defined as cervical dilation 3–4 cm) once the fetal head is applied to the cervix, and pelvic examinations are performed routinely every 2 hours. Dystocia is diagnosed if adequate uterine activity (200–250 Montevideo units for 2–4 hours) does not result in progressive cervical dilation and fetal descent. Oxytocin is administered according to written protocol,7 starting at 6 mU/minute and increasing by 6 mU/minute every 40 minutes, to a maximum of 42 mU/minute. Internal monitors are placed if there is inadequate progress of labor, fetal heart rate decelerations, or meconium staining of the amnionic fluid. Use of forceps is limited to inadequate voluntary pushing or fetal heart rate abnormalities.
Women in active labor who request pain medication are given the choice of epidural analgesia or IV meperidine (50–100 mg every 2 hours as needed). To be eligible for epidural analgesia, women must be afebrile with no evidence of infection. Epidural analgesia is administered by an obstetric anesthesiologist according to written protocol. A bolus of 500 mL IV fluids is administered, and an indwelling catheter is placed in the lumbar epidural space using a 17 gauge Tuohy needle. After a test dose of 3 mL 1.5% lidocaine with epinephrine 1:200,000, analgesia is achieved with 3-mL increments of 0.25% bupivacaine to a bilateral T-10 sensory level. A continuous epidural infusion of 0.125% bupivacaine with 2 µg/mL fentanyl is infused at 8–10 mL/hour to maintain a T-10 sensory level. Maternal blood pressure is recorded every 5 minutes for 30 minutes, then every 30 minutes until delivery. Hypotension is treated initially with IV fluids, followed by 5 mg IV ephedrine as needed. After epidural placement, temperature is recorded every 15 minutes for 1 hour, then hourly for the duration of labor.
Groups were compared by Student t test and Mann-Whitney U test for continuous outcomes, and 
2 for categoric outcomes. P < .05 was considered significant.
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Results |
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. Overt fever (38C or greater) was significantly more likely to develop either in labor or within 6 hours postpartum in women who received labor epidural analgesia (46% versus 26%, P = .01). The maximum temperature (mean ± standard deviation [SD]) recorded in women without overt fever was 37.3 ± 0.5C in the epidural group and 37.1 ± 0.4C in those who did not receive epidural (P = .06). Women with epidural were significantly more likely to have evidence of placental inflammation (61% versus 36%, P = .002). The combination of fever and placental inflammation was present significantly more often in women in the epidural group compared with those in the no-epidural group (35% versus 17%, P = .02). Among women without placental inflammation, epidural analgesia was not associated with intrapartum fever. Specifically, in nine women (11%) who received epidural analgesia, fever developed without placental inflammation, compared with six women (9%) who had not received epidural analgesia (P = .61).
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. Most women from whom placentas were collected were not in active labor at admission (defined as cervical dilation 4 cm or more), which was true for both groups. The median (± SD) duration of membrane rupture was significantly longer in those who received epidural analgesia compared with those who did not (13 ± 3 hours versus 10 ± 4 hours, P = .017). The admission to delivery interval, our estimate of length of labor, averaged approximately 2 hours longer (11.8 ± 4 hours versus 9.6 ± 4 hours, P = .03) in the epidural group than in the no-epidural group.
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Discussion |
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However, when clinical fever occurs with placental inflammation, the placental findings should buttress the clinical diagnosis of intrapartum infection. We analyzed our results by combining clinical fever with placental inflammation, and found that epidural analgesia was associated with this combination. The corollary, fever without placental inflammation, did not appear to be related to epidural analgesia. We found that women who received epidural analgesia had only a 2% higher incidence of fever without placental inflammation. Although it is not clear what would constitute a clinically significant difference, our study had a power of 80% (2-sided 
= .05) to detect a difference of 11% between these groups.
Our findings suggest that the overt clinical fever associated with epidural analgesia is infection-mediated. Although we did not perform bacterial cultures, studies indicated that acute inflammation of the chorionic plate is associated with bacterial infection of amniotic fluid.6 Further evidence supporting our view that clinical fever linked to epidural analgesia is related to infection is provided by our findings that women with epidural analgesia had longer periods of ruptured membranes and longer labor times. Both of these are known risk factors for intrauterine infection in laboring women.3
Labor epidural analgesia inducing temperature elevation was first reported by Fusi and colleagues,1 who suggested that increase in maternal temperature resulted from thermoregulatory and vascular modifications caused by analgesia. However, the temperature increases attributed to epidural analgesia were subclinical, because temperatures never exceeded 38C. Camann and colleagues2 also identified subclinical fever in laboring women given epidural analgesia, compared with those not so treated.2 The mean maximum temperature after 9 hours of labor was 37.2C in women given epidural analgesia, compared with 36.4C in women not given epidural analgesia. In contrast, Herbst and colleagues3 analyzed overt maternal fever (38C or greater) in 250 women who were matched to 250 other women without fever.3 More women in the fever group received epidural analgesia (83% versus 53% in the control group, P = <.01), circumstantially implicating epidural analgesia as a cause not only of subclinical temperature elevation but also overt, clinical fever. Lieberman and colleagues4 observed that epidural analgesia was associated with overt maternal fever during labor, which caused an increase in neonatal work-ups for sepsis. Both Herbst and colleagues3 and Lieberman and colleagues4 found that independent risk factors for intrapartum infection, such as longer labor, also were linked to epidural analgesia. Our results support the latter conclusion. Such findings raise the likelihood that maternal fever linked to epidural analgesia is not a side effect of the analgesia, but a consequence of longer labor that predisposes these women to intrapartum infection.
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Footnotes |
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Received May 20, 1998. Received in revised form August 27, 1998. Accepted September 10, 1998.
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References |
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2. Camann WR, Hortvet LA, Hughes N, Bader AM, Datta S. Maternal temperature regulation during extradural analgesia for labour. Br J Anaesth 1991;67:565–8.
3. Herbst A, Wolner-Hanssen P, Ingemarsson I. Risk factors for fever in labor. Obstet Gynecol 1995;86:790–4.[Abstract]
4. Lieberman E, Lang JM, Frigoletto F Jr, Richardson DK, Ringer SA, Cohen A. Epidural analgesia, intrapartum fever, and neonatal sepsis evaluation. Pediatrics 1997;99:415–9.
5. Salafia CM, Weigl C, Silberman L. The prevalence and distribution of acute placental inflammation in uncomplicated term pregnancies. Obstet Gynecol 1989;73:383–9.
6. Romero R, Salafia CM, Athanassiadis AP, Hanaoka S, Mazor M, Sepulveda W, et al. The relationship between acute inflammatory lesions of the preterm placenta and amniotic fluid microbiology. Am J Obstet Gynecol 1992;166:1382–8.[Medline]
7. Satin AJ, Leveno KJ, Sherman ML, Brewster DS, Cunningham FG. High-versus low-dose oxytocin for labor stimulation. Obstet Gynecol 1992;80:111–6.
This article has been cited by other articles:
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  Y. Garnier, A. B. C. Coumans, A. Jensen, T. H. M. Hasaart, and R. Berger Infection-Related Perinatal Brain Injury: The Pathogenic Role of Impaired Fetal Cardiovascular Control Reproductive Sciences, December 1, 2003; 10(8): 450 - 459. [Abstract] [PDF]
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 H. K. Eltzschig, E. S. Lieberman, and W. R. Camann Regional Anesthesia and Analgesia for Labor and Delivery N. Engl. J. Med., January 23, 2003; 348(4): 319 - 332. [Full Text] [PDF]
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 Y. Cohen, M. C. Vallejo, B. Kaul, and S. Ramanathan Epidural analgesia and maternal fever Can J Anesth, August 1, 2002; 49(7): 760 - 760. [Full Text]
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M. C. Vallejo, B. Kaul, L. J. Adler, A. L. Phelps, C. M. Craven, T. A. Macpherson, R. L. Sweet, and S. Ramanathan Chorioamnionitis, not epidural analgesia, is associated with maternal fever during labour : [La chorio-amnionite est associee a la fievre puerperale pendant le travail, mais non l'analgesie epidurale] Can J Anesth, December 1, 2001; 48(11): 1122 - 1126. [Abstract] [Full Text] [PDF]
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