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ORIGINAL RESEARCH |
From the Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas.
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ABSTRACT |
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METHOD: This was a historical cohort study of pregnant women who had their first and second deliveries at our institution between January 1988 and May 2005. The index pregnancy was restricted to those who delivered vaginally. Data were collected from a continuously updated obstetric database and included demographic and labor characteristics and neonatal outcomes. Chorioamnionitis was diagnosed clinically.
RESULTS: The study population consisted of 23,397 women. During the index pregnancy, 10% of women developed chorioamnionitis. This group was significantly different from the rest of the cohort in terms of age, ethnicity, length of labor, epidural analgesia, use of internal monitors, and incidence of prolonged rupture of membranes. In the second pregnancy, 6% of those women again developed chorioamnionitis compared with 2% of women who did not have chorioamnionitis in the first pregnancy (odds ratio 2.93, 95% confidence interval 2.40–3.57). After adjusting for the above confounders, the increased risk of recurrence persisted (odds ratio 1.85, 95% confidence interval 1.49–2.30).
CONCLUSION: Women delivering vaginally who were diagnosed with chorioamnionitis during their first pregnancy are at increased risk for chorioamnionitis in a subsequent pregnancy. This supports the concept that there may be a predisposition to chorioamnionitis that should be further investigated.
LEVEL OF EVIDENCE: II-2
It has been suggested that the pro-inflammatory response associated with intra-amniotic infection is regulated genetically, thus placing some women at higher risk. Tumor necrosis factor 
(TNF-) is a pro-inflammatory cytokine important in the infection cascade. Simhan et al7 reported that carriage of the TNF-2 allele is associated with a threefold increased risk of clinical chorioamnionitis. Other studies have also reported an association between different polymorphisms in immunoregulatory genes and a woman's likelihood of developing chorioamnionitis.8,9 Thus, women with chorioamnionitis during their first pregnancy may be at higher risk in subsequent pregnancies.
Some women may be at increased risk of recurrent chorioamnionitis because of vaginal colonization with virulent bacteria. Abele-Horn et al10,11 demonstrated a significantly higher incidence of chorioamnionitis in women colonized with Ureaplasma urealyticum. Yancey et al12 reported similar results with group B streptococcal colonization. An association between bacterial vaginosis and chorioamnionitis has also been suggested.13
Dinsmoor and Gibbs14 did not find an increased incidence of intra-amniotic infection among women diagnosed with chorioamnionitis in a previous pregnancy, but their conclusion was limited by a small population size (n=70). In those patients who did have a recurrence, they found significantly longer labors, longer duration of internal monitors, and increased numbers of vaginal exams. These are known risk factors commonly associated with chorioamnionitis regardless of recurrence. The objective of this study was to evaluate clinical chorioamnionitis as an independent risk factor for recurrence in a subsequent pregnancy.
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MATERIALS AND METHODS |
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The index pregnancy was restricted to singleton pregnancies delivered vaginally, thus excluding elective cesarean deliveries for various indications and repeat elective cesarean deliveries. The second delivery was not limited by mode of delivery. Patients infected with the human immunodeficiency virus (HIV) were excluded, as were women with hypertension and diabetes mellitus. Patients with hypertension and diabetes were excluded because of their high rates of induction of labor. Selected obstetric and neonatal outcomes were obtained from a previously described, continuously updated, obstetric computerized database. Nurses attending each delivery completed an obstetric data sheet, and research nurses assessed the data for consistency and completeness before electronic storage.15
Obstetric characteristics of interest included those anticipated to impact the risk of chorioamnionitis: length of labor, need for induction or augmentation of labor, epidural analgesia, premature rupture of membranes (PROM), rupture of membranes for more than 24 hours, use of internal monitors, and a prolonged second stage. The length of labor was considered the period of time from admission to the labor and delivery floor to delivery of the fetus. A prolonged second stage was defined as more than 3 hours in a primiparous patient and more than 2 hours in a multiparous patient. Internal monitors were placed in cases of meconium, fetal heart rate decelerations, or inadequate labor progression.16,17
Chorioamnionitis was diagnosed clinically by a body temperature of 38°C (100.4ºF) or higher in the presence of other clinical findings, including maternal or fetal tachycardia, uterine tenderness, or malodorous vaginal discharge.17,18 Patients without contraindication were treated with ampicillin and gentamicin in accordance with hospital protocols. No bacterial cultures were performed.
Group comparisons between those with chorioamnionitis in the index pregnancy and those without were made by using the 
2 test for categorical data and Student t test for continuous measures. Regression was done to control for significant variables. Wilcoxon rank-sum was performed for data known to be statistically nonnormal. Breslow-Day statistic was used to compare odds ratios between term (estimated gestational age more than 36 weeks) and preterm (estimated gestational age 36 weeks or less) groups. P<.05 was considered statistically significant. All analyses were performed with SAS 9.1 (SAS Institute, Cary, NC).
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RESULTS |
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In the second pregnancy, 6% of those women diagnosed with chorioamnionitis in the index pregnancy again developed chorioamnionitis, compared with 2% of women who did not have chorioamnionitis in the first pregnancy (odds ratio 2.93, 95% confidence interval 2.40–3.57). Demographic characteristics for the second pregnancy are listed in Tables 2 and 3. The group of women with chorioamnionitis in both pregnancies was significantly different from the group of women who had chorioamnionitis only in the index pregnancy in terms of length of labor, inductions or augmentations, length of rupture of membranes, length of second stage of labor, use of internal monitors, and rate of cesarean delivery. These differences were also seen between the group of women not diagnosed with chorioamnionitis in either pregnancy and the group of women diagnosed with chorioamnionitis only in the second pregnancy.
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DISCUSSION |
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In this study, the recurrence of chorioamnionitis in a subsequent pregnancy was significantly increased among women diagnosed with chorioamnionitis in their first pregnancy. The risk was increased twofold and was independent of known risk factors for intra-amniotic infection, including ethnicity, length of labor, length of rupture of membranes, use of internal monitors, and length of second stage. In addition, there was no difference between patients delivering at term and those delivering preterm.
The strengths of this study include a large population size followed over an extended period of time. All patients were managed in a similar manner, using the same definition of chorioamnionitis as well as the same intrapartum management strategies. Patients were examined, generally, every 2–3 hours while in active labor. Internal monitors were used only in the setting of strict obstetric indications. By limiting the index pregnancy to a vaginal delivery, patients undergoing a cesarean delivery electively, and thus at lower risk for chorioamnionitis, could be avoided. This also resulted in the exclusion of primiparous women whose first viable pregnancy resulted in a cesarean delivery for an alternative reason, such as dystocia. Satin et al19 in 1992 suggested that women with chorioamnionitis may have some preexisting disposition to dystocia and abnormal labor. The structure of this cohort eliminates that potential bias.
There are, however, several limitations to this study that are worth mentioning. The actual number of vaginal examinations, a known risk factor for chorioamnionitis, was not available. Therefore, length of labor had to be used as a surrogate marker. Another limitation was that bacterial cultures of the intrauterine cavity or placenta were not performed. Because clinical chorioamnionitis is polymicrobial, it is felt that culture results would not aid in management.20,21 For research purposes, however, it could have provided some insight into why some women get chorioamnionitis several times while others do not. Likewise, patients were not cultured antepartum for group B streptococcus. Instead, prophylaxis was administered when intrapartum risk factors were present.22
After controlling for known risk factors, the occurrence of chorioamnionitis at the time of first vaginal delivery increases the risk of recurrence twofold in the next pregnancy. This indicates that women with chorioamnionitis during several pregnancies are perhaps, in some way, predisposed to this complication. A multitude of factors could influence this. A genetic predisposition to intrauterine infection is one. Colonization of the upper and lower genital tract with more virulent bacterial organisms is another. Further research is needed in this area to determine the etiologies involved. Chorioamnionitis is likely a multifactorial complication possibly influenced by a genetic predisposition.
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Footnotes |
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doi:10.1097/01.AOG.0000247647.88489.b0
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REFERENCES |
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2. Verma U, Tejani N, Klein S, Reale MR, Beneck D, Figueroa R, et al. Obstetric antecedents of intraventricular hemorrhage and periventricular leukomalacia in the low-birth-weight neonate. Am J Obstet Gynecol 1997;176:275–81.[Medline]
3. Wu YW, Escobar GJ, Grether JK, Croen LA, Greene GD, Newman TB. Chorioamnionitis and cerebral palsy in term and near-term infants. JAMA 2003;290:2677–84.
4. Grether JK, Nelson KB. Maternal infection and cerebral palsy in infants of normal birth weight [published erratum appears in JAMA 1998;279:118]. JAMA 1997;278:207–11.[Abstract]
5. Soper DE, Mayhall CG, Dalton HP. Risk factors for intraamniotic infection: a prospective epidemiologic study. Am J Obstet Gynecol 1989;161:562–6.[Medline]
6. Newton ER, Prihoda TJ, Gibbs RS. Logistic regression analysis of risk factors for intra-amniotic infection. Obstet Gynecol 1989;73:571–5.
7. Simhan HN, Krohn MA, Zeevi A, Daftary A, Harger G, Caritis SN. Tumor necrosis factor- promoter gene polymorphism -308 and chorioamnionitis. Obstet Gynecol 2002;102:162–5.
8. Annells MF, Hart PH, Mullighan CG, Heatley SL, Robinson JS, McDonald HM. Polymorphisms in immunoregulatory genes and the risk of histologic chorioamnionitis in caucasoid women: a case control study. BMC Pregnancy Childbirth 2005;5:4–13.[Medline]
9. Roberts AK, Monzon-Bordonaba F, Van Deerlin PG, Holder J, Macones GA, Morgan MA, et al. Association of polymorphism within the promoter of the tumor necrosis factor gene with increased risk of preterm premature rupture of the fetal membranes. Am J Obstet Gynecol 1999;180:1297–302.[Medline]
10. Abele-Horn M, Scholz M, Wolff C, Kolben M. High-density vaginal Ureaplasma urealyticum colonization as a risk factor for chorioamnionitis and preterm delivery. Acta Obstet Gynecol Scand 2000;79:973–8.[Medline]
11. Abele-Horn M, Peters J, Genzel-Boroviczeny Wolff C, Zimmerman A, Gottschling W. Vaginal Ureaplasma urealyticum colonization: influence on pregnancy outcome and neonatal morbidity. Infection 1997;25:286–91.[Medline]
12. Yancey MK, Duff P, Clark P, Kurtzer T, Frentzen BH, Kubilis P. Peripartum infection associated with vaginal group B streptococcal colonization. Obstet Gynecol 1994;84:816–9.
13. Gravett MG, Nelson HP, DeRouen T, Critchlow C, Eschenbach DA, Holmes KK. Independent associations of bacterial vaginosis and Chlamydia trachomatis infection with adverse pregnancy outcome. JAMA 1986;256:1899–903.[Abstract]
14. Dinsmoor MJ, Gibbs RS. Previous intra-amniotic infection as a risk factor for subsequent peripartal uterine infections. Obstet Gynecol 1989;74:299–301.
15. McIntire DD, Bloom SL, Casey BM, Leveno KJ. Birth weight in relation to morbidity and mortality among newborn infants. N Engl J Med 1999;340:1234–8.
16. 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]
17. Alexander JM, Sharma SK, McIntire DD, Leveno KJ. Epidural analgesia lengthens for Friedman active phase of labor. Obstet Gynecol 2002;100:46–50.
18. Cunningham FG, Leveno KJ, Hauth JC, Gilstrap LC Bloom SL, Wenstrom KD. Williams obstetrics. 22nd ed. New York (NY): McGraw-Hill; 2005. p. 427–39.
19. Satin AJ, Maberry MC, Leveno KJ, Sherman ML, Kline DM. Chorioamnionitis: a harbinger of dystocia. Obstet Gynecol 1992;79:913–5.
20. Romero R, Nores J, Mazor M, Sepulveda W, Oyarzun E, Parra M, et al. Microbial invasion of the amniotic cavity during term labor. prevalence and clinical significance. J Reprod Med 1993;38:543–8.[Medline]
21. Gibbs RS, Blanco JD, St Clair PJ, Castaneda YS. Quantitative bacteriology of amnionic fluid from women with clinical intraamnionic infection at term. J Infect Dis 1982;145:1–8.[Medline]
22. Wendel GD Jr, Leveno KJ, Sanchez PJ, Jackson GL, McIntire DD, Siegel JD. Prevention of neonatal group B streptococcal disease: a combined intrapartum and neonatal protocol. Am J Obstet Gynecol 2002;186:618–26.[Medline]
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