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* From the Departments of Anesthesiology,
Pathology,
Obstetrics and Gynecology, Magee-Womens Hospital, University of Pittsburgh School of Medicine, and
Quantitative Sciences (School of Business), Duquense University, Pittsburgh, Pennsylvania, USA.
Dr. Manuel C. Vallejo, Department of Anesthesiology, Magee-Womens Hospital, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Phone: 412-641-4260; Fax: 412-641-4766; E-mail: vallejomc{at}anes.upmc.edu
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Abstract |
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Methods: Data from 14,073 patients were entered into a database over a two-year period. From this database, 62 nulliparous parturients with clinical chorioamnionitis (amnionitis), but without LEA were identified (Group I). Two other groups who received LEA were matched for parity and gestation: Group II – LEA with concomitant amnionitis (n=50) and, Group III – LEA without concomitant amnionitis (n=201). The diagnosis of chorioamnionitis was confirmed by histologic examination. Results are expressed as mean ± SD and analyzed at P <0.05 using ANOVA or Chi-square.
Results: No differences were noted among the groups in the operative delivery rate or Apgar scores at five minutes. The percentage of patients with maternal fever during labour (38.0°C) with amnionitis was significantly less in Group III compared to the other groups (100% in both Groups I and II vs 1.0% in Group III; P=0.000). Likewise, Group III had a lower percentage of neonates with Apgar scores <7 at one minute (35.5% in Group I, 20.0% in Group II, 17.4% in Group III; P=0.010). The percentage of histologic chorioamnionitis was significantly higher in both amnionitis groups compared to Group III (67.7% in Group I, 56.0% in Group II, 4.0% in Group III; P=0.000).
Conclusion: LEA without chorioamnionitis is not associated with maternal fever (38.0°C), increased operative delivery rates or low Apgar scores.
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Methods |
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Epidural blocks are inserted at the request of the patient and with approval of the obstetrician. LEA blocks are performed in the sitting position at the L3–L4 to L4–L5 intervertebral space using the loss of resistance to air technique. Bupivacaine 0.25% or ropivacaine 0.2% is used for induction of analgesia to a T10 dermatomal level followed by a continuous infusion of 0.125% bupivacaine or 0.125% ropivacaine with fentanyl (2 µg•mL–1) at 10–12 mL•hr–1.
Diagnostic criteria used at our institution for the diagnosis of clinical chorioamnionitis (amnionitis) includes fever (38.0°C) plus one or more of the following: maternal tachycardia, fetal tachycardia, uterine tenderness, foul smelling amniotic fluid, or maternal leukocytosis. All patients admitted to the labour suite received an initial vaginal examination to determine cervical dilatation, station, effacement and were subsequently checked at the discretion of the attending obstetrician. Laboratory examination was ordered by the obstetrician as determined by medical history, obstetrical history and current clinical situation. Maternal temperature was measured every four hours or every hour if febrile. Maternal vital signs (heart rate, blood pressure, respiratory rate) were measured every hour as per institutional labour and delivery pathway protocol. External fetal heart rate was monitored continuously or by internal fetal scalp electrode if external fetal heart tones could not be monitored continuously.
From the CQI database, 62 nulliparous parturients who did not receive LEA, but had amnionitis at 34.0 ± 7.0 weeks gestation (Group I) were identified. In order to match other nulliparous parturients who did receive LEA, the 95% confidence interval was used to estimate the true mean gestation at 34 ± 2.0 weeks. The matched patients were then divided into two groups: LEA with concomitant amnionitis (Group II) and LEA without concomitant amnionitis (Group III).
Maternal data retrieved from the CQI database included: parity, gestation, age, weight, group B-ß hemolytic streptococcal colonization status (GBBS), preterm (<37 weeks gestation), premature rupture of membranes (PROM), oxytocin augmentation, maternal fever during labour (38.0°C), and mode of delivery (Cesarean section, vaginal delivery, and vacuum/forceps). Maternal temperature was measured orally using a sublingual thermometer (IVAC Corporation, San Diego, CA, USA).
Neonatal outcome data retrieved from the CQI database included; Apgar scores <7 at one minute, and <9 at five minutes, birth weight, and NSER. Indications for neonatal sepsis evaluation at our institution include; maternal fever during labour (38.0C), maternal diagnosis of clinical chorioamnionitis (amnionitis), prolonged rupture of membranes >24 hr, birth weight <2,500 grams, preterm gestational age <37 weeks gestation, meconium and/or respiratory distress at birth, hypothermia at birth, GBBS colonization, and maternal pre-ecclampsia and/or hypertension.
Statistics describing interval data are expressed as mean ± SD. Statistical comparison between the three groups was analyzed using one-way analysis of variance (ANOVA). Statistics describing nominal data are reported in percentages. Statistical comparison between the three groups' proportions was analyzed using the Chi-square method.5 The P-value for each univariate test are reported. A P-value less than 0.05 was considered statistically significant.
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Results |
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). Group II consisted of 50 parturients with LEA, and with concomitant amnionitis. Group III consisted of 201 parturients with LEA, but without concomitant amnionitis (Table I).
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Demographic data are presented in Table I
. No differences were noted with respect to gestational age and maternal age and weight. No differences were noted in the GBBS colonization rate or in the percentage of patients with PROM (Table I). More patients in both LEA Groups II and III presented preterm (<37 weeks gestation) compared to Group I (Table I).
Table II presents maternal labour and delivery outcome data. No differences were noted in the operative delivery rate. The percentage of patients with maternal fever plus one or more criterion used for the diagnosis of amnionitis was significantly less in Group III (Table II). Group III was more likely to receive oxytocin augmentation compared to Group I (Table II).
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. The percentage of neonates with one minute Apgar scores <7 was significantly less in Group III compared to Group I. No differences were noted in the percentage of neonates with Apgar scores <9 at five minutes. Group I had the highest mean birth weight and the lowest percentage of low birth weight (LBW) <2.5 kg neonates. The overall NSER was highest in Group III compared to Groups I and II (Table III). However, 100% of the neonates in Groups I and II weighing less than 2.5 kg had a neonatal sepsis evaluation compared to only 76% of the neonates in Group III (Table III).
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shows the percentage of parturients with histologic acute chorioamnionitis in all groups. Group III had the lowest percentage of parturients with histologic acute chorioamnionitis compared to the other two groups.
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Discussion |
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The incidence of aminionitis in our institution is comparable to that in other tertiary care centers.8 Looff and Hager describe amnionitis as a significant cause of maternal fever in obstetrics.9 Our data concurs with this fact in that all patients in Groups I and II with amnionitis also had fever during labour compared to only 1% in Group III.
Epidural analgesia can elevate maternal temperature, but not enough to cause maternal fever (38.0°C).3,10 This is evidenced by the low incidence of maternal fever in Group III (LEA without concomitant amnionits). The highest rates of maternal fever occurred in both amnionitis groups. Morishima has shown that a greater than 2°C increase in maternal temperature above baseline is associated with decreased uterine blood flow and significant fetal compromise.11 However, small increases in maternal temperature (0.5–1.5°C) that normally occur with LEA, are advantageous to fetal well being in that uterine blood flow is increased, uterine vascular resistance is decreased, fetal blood oxygen tension is increased, with no changes in fetal carbon dioxide tension or pH.10
Our data confirm the results of Dashe et al.4 who found epidural analgesia to be associated with maternal fever, but only in the presence of histologic chorioamnionitis. However, our study is different from Dashe's in that we also looked at both maternal and neonatal outcome. Both amnionitis groups had a significantly higher incidence of histologic chorioamnionitis compared to Group III (Figure). Even though amnionitis was not suspected in Group III, the main reason for placental histologic examination was the high incidence of preterm labour.
Negishi et al.12 believe inflammation and/or infection causes hyperthermia, and not epidural analgesia itself, which is consistent with our study and Dashe's results. Negishi found that small concentrations of iv narcotics inhibit the febrile response, while epidural analgesia with or without narcotic does not attenuate this response.12 Hyperthermia during epidural analgesia should not be considered a result of the epidural alone, and potential sources of inflammation/infection (chorioamnionitis) should be aggressively pursued and treated.
Groups II and III had a higher percentage of parturients who presented in preterm labour compared to Group I (Table I), and hence a lower mean birth weight and a higher percentage of babies with LBW (Table III). Raghavan et al. identified both preterm delivery and LBW as major factors associated with neonatal sepsis.13 Groups II and III had a higher NSER due to the higher percentage of prematurity and LBW compared to Group I.
Patients with GBBS colonization are given iv penicillin during labour. Antibiotic coverage explains why the GBBS colonization rate does not make a difference in the febrile response to epidural analgesia and chorioamnionitis in our institution. More parturients in Group III received oxytocin augmentation than Group I. This is explained by the fact that oxytocin augmentation is often used in conjunction with epidural analgesia at our institution.
In conclusion, LEA without concomitant chorioamnionitis is not associated with elevated maternal fever, increased operative delivery rate or lower Apgar scores. On the other hand, chorioamnionitis with, or without concomitant LEA is associated with a higher percentage of maternal fever during labour. Any study comparing the effect of LEA on maternal thermoregulation should consider the issue of chorioamnionitis.
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Acknowledgments |
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Revision received August 29, 2001. Accepted for publication July 18, 2001.
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References |
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2 Philip J, Alexander JM, Sharma SK, Leveno KJ, McIntire DD, Wiley J. Epidural analgesia during labor and maternal fever. Anesthesiology 1999; 90: 1271–5.[Medline]
3 Vinson DC, Thomas R, Kiser T. Association between epidural analgesia during labor and fever. J Fam Pract 1993; 36: 617–22.[Medline]
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Dashe JS, Rogers BB, McIntire DD, Leveno KJ. Epidural analgesia and intrapartum fever: placental findings. Obstet Gynecol 1999; 93: 341–4.
5 Glantz SA. Primer of Biostatistics, 4th ed. New York: McGraw Hill, 1997.
6 Gilbert S. Labor pain relief tied to problems for infants. The New York Times. New York, NY: The New York Times Company, 1997.
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Alexander JM, McIntire DM, Leveno KJ. Chorioamnionitis and the prognosis for term infants. Obstet Gynecol 1999; 94: 274–8.
9 Looff JD, Hager WD. Management of chorioamnionitis. Surg Gynecol Obstet 1984; 158: 161–6.[Medline]
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Camann WR. Epidural analgesia in labor and fetal hyperthermia (Letter). Obstet Gynecol 1993; 81: 316–7.
11 Morishima HO, Glaser B, Niemann WH, James LS. Increased uterine activity and fetal deterioration during maternal hyperthermia. Am J Obstet Gynecol 1975; 121: 531–8.[Medline]
12 Negishi C, Lenhardt R, Ozaki M, et al. Opiods inhibit febrile responses in humans, whereas epidural analgesia does not. An explanation for hyperthermia during epidural analgesia. Anesthesiology 2001; 94: 218–22.[Medline]
13 Raghavan M, Mondal GP, Bhat VV, Srinivasan S. Perinatal risk factors in neonatal infections. Indian J Pediatr 1992; 59: 335–40.[Medline]
This article has been cited by other articles:
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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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