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Hope the attached article is of use , the link
below is from A Guide to Effective Care in Pregnancy and
Childbirth
Cheers ,
David
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Volume 179(3) September 1998 pp 635-639 For the Term PROM Study Group Toronto, Ontario, Canada, Carshalton, United Kingdom, and Haifa, Israel From the Division of Maternal-Fetal Medicine, Departments of Obstetrics and Gynecology (Seaward, Hannah, Farine) and Paediatrics, (Ohlsson, Wang) the Maternal, Infant and Reproductive Health Research Unit, Centre for Research in Women's Health, (Seaward, Hannah, Myhr, Ohlsson, Hodnett, Weston) and the Faculty of Nursing, (Hodnett) University of Toronto, the Department of Pediatrics, St Helier, (Haque) and the Department of Obstetrics and Gynecology, Bnai Zion Medical Centre (Ohel). Supported by grant No MA-11392 from the Medical Research Council of Canada. Presented at the Seventeenth Annual Meeting of the Society of Perinatal Obstetricians, Anaheim, California, January 20-25, 1997. Received for publication August 26, 1997; revised October 8, 1997; accepted January 19, 1998. Reprint requests: P.G.R. Seaward, MB, BCh, Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Mt Sinai Hospital, Suite 775B, 600 University Ave, Toronto, Ontario, Canada M5G 1X5.
Outline Graphics Abstract^ OBJECTIVE: Our objective was to determine significant predictors for the development of neonatal infection in infants born to patients with premature rupture of membranes at term. STUDY DESIGN: Multivariate analysis was used to determine the significant predictors of neonatal infection in infants born to women with premature rupture of the membranes who were enrolled in the Term PROM Study. In a randomized, controlled trial, the Term PROM Study recently compared induction of labor with expectant management for premature rupture of membranes at term. RESULTS: The following variables were identified as independent predictors of neonatal infection: clinical chorioamnionitis (odds ratio 5.89, P < .0001), positive maternal group B streptococcal status (vs negative or unknown, odds ratio 3.08, P < .0001), 7 to 8 vaginal digital examinations (vs 0 to 2, odds ratio 2.37, P = .04), 24 to <48 hours from membrane rupture to active labor (vs <12 hours, odds ratio 1.97, P = .02), >or=to48 hours from membrane rupture to active labor (vs <12 hours, odds ratio 2.25, P = .01), and maternal antibiotics before delivery (odds ratio 1.63, P = .05). CONCLUSIONS: Among infants born to patients with premature rupture of membranes at term, clinical chorioamnionitis and maternal colonization with group B streptococci are the most important predictors of subsequent neonatal infection. (Am J Obstet Gynecol 1998;179:635-9.) Key words: Premature rupture of membranes, infant, neonatal infection, clinical chorioamnionitis, group B streptococci Premature rupture of the membranes results in an increase in pregnancy complications in both term and preterm gestations. The risk of infection after premature rupture of the membranes is of concern for both mother and fetus or neonate. [1] The incidence of neonatal infection after membrane rupture of more than 24 hours is approximately 1%, and when clinical chorioamnionitis is present the risk increases to between 3% and 5%. [2] A ten-fold increase in neonatal infection has been noted in uncomplicated cases of premature rupture of the membranes compared with neonates in general. [3] There is a wide spectrum of clinical appearance in infants with infection, and the early and efficient diagnosis of neonatal bacterial sepsis remains difficult. [2] It therefore seems reasonable to determine in which neonates infection is most likely to develop after premature rupture of the membranes at term so that effective management of pertinent aspects of labor and delivery can minimize subsequent neonatal infection and allow a reduction in inappropriate use of antibiotics in the neonatal period.
Patients and methods^ We wished to determine the important predictors of neonatal infection in infants born to women with premature rupture of the membranes at term who had either spontaneous or induced labor. Neonatal infection was classified as either definite or probable. Criteria for definite infection included the presence of clinical signs of infection and >or=to1 of the following: a positive culture result from blood, cerebrospinal fluid, urine, tracheal aspirate, or lung tissue; a positive Gram stain of cerebrospinal fluid; a positive antigen-detection test result from blood, cerebrospinal fluid, or urine; a chest radiograph compatible with pneumonia; or a histologic diagnosis of pneumonia. Probable neonatal infection was defined as the presence of clinical signs of infection and >or=to1 of the following: a high or low blood neutrophil count, a high immature-to-total neutrophil ratio, a high actual immature neutrophil count, or abnormal cerebrospinal fluid findings showing an elevated white blood cell count, a high level of protein, or a low level of glucose. To minimize bias in determination of neonatal infection, babies had blood taken for culture and complete blood cell count <or=to24 hours after birth and before treatment with antibiotics. In addition, an adjudication committee blinded to treatment group and to mode of labor onset determined whether neonatal infection was present. Data were collected prospectively at the collaborating centers by means of standardized forms. Patients were excluded from this secondary analysis if they had undergone prelabor cesarean section. The SAS (SAS Institute, Cary, NC) software package was used for statistical analysis. Univariate analyses were used to identify variables associated with the diagnosis of neonatal infection. Categoric data were tested for significance with the chi squared or Fisher's exact test. Continuous data were tested for significance with a 2-tailed Student t test or Wilcoxon rank sum test if not normally distributed. Multivariate analysis was performed by stepwise logistic regression. All variables from the univariate analysis with a P value <.1 were included in the subsequent stepwise logistic regression. Variables were also included in the regression model if there was previous evidence from the literature of an association between the variable and neonatal infection (clinically suspect variables) even if P was >or=to.1. Logistic regression analysis was performed with the diagnosis of neonatal infection as the dependent variable. Results of the multivariate analysis are expressed as odds ratios with their 95% confidence intervals. Where appropriate, results are also reported in terms of level of statistical significance. All P values were based on 2-tailed tests, with P values <.05 considered statistically significant. Variables included in the model to determine important predictors of neonatal infection were parity, history of maternal smoking, maternal group B streptococcal status, maternal antibiotics before delivery, internal fetal heart rate monitoring, time from membrane rupture to active labor, duration of active labor, induced versus spontaneous labor, mode of delivery (spontaneous vaginal, operative vaginal, or cesarean delivery), number of vaginal examinations before delivery, clinical chorioamnionitis, and meconium staining of the liquor.
Results^ Table I. Demographic data and perinatal outcomes for study population (N = 5028) Definite or probable neonatal infection occurred in 133 infants (2.6%). One of these babies died of infection, for a rate of <1%. Five variables were found to be independently associated with definite or probable neonatal infection (Table II). The strongest predictor of neonatal infection after premature rupture of the membranes at term was clinical chorioamnionitis (odds ratio 5.89, 95% confidence interval 3.68 to 9.43). Other independent predictors of definite or probable neonatal infection were positive maternal group B streptococcal status (vs negative or unknown) (odds ratio 3.08, 95% confidence interval 2.02 to 4.68), 7 or 8 vaginal digital examinations (vs 0 to 2) (odds ratio 2.37, 95% confidence interval 1.03 to 5.43), time from membrane rupture to active labor >or=to48 hours and 24 to <48 hours (vs <12 hours) (odds ratios 2.25 and 1.97, 95% confidence intervals 1.21 to 4.18 and 1.11 to 3.48, respectively), and maternal antibiotics before delivery (odds ratio 1.63, 95% confidence interval 1.01 to 2.62). Table II. Significant independent predictors of neonatal infection* with multiple logistic regression analysis The variables that were not independently associated with definite or probable neonatal infection were parity, history of maternal smoking, 2 to <7 or >8 (vs 0 to 2) digital vaginal examinations before delivery, 12 to <24 hours (vs <12 hours) from rupture of membranes to active labor, induced labor (vs spontaneous labor), duration of active labor (3 to <6, 6 to <9, 9 to <12 hours or >or=to12 vs <3 hours), internal fetal heart rate monitoring, cesarean section (vs spontaneous vaginal delivery), operative vaginal delivery (vs spontaneous vaginal delivery), and meconium staining of the liquor.
Comment^ By means of stepwise logistic regression analysis this study identified important maternal variables independently associated with definite or probable neonatal infection as clinical chorioamnionitis, maternal group B streptococcal colonization, the number of vaginal digital examinations, time from membrane rupture to active labor (latent interval), and maternal antibiotics before delivery. We found clinical chorioamnionitis to be the most important independent predictor of definite or probable neonatal infection. This result confirms a similar association reported by others. [2,5,6] In a retrospective review, Haque [5] noted that chorioamnionitis was 1 of 3 variables predictive of neonatal infection (of a total of 30 variables tested). When symptoms and signs of clinical chorioamnionitis are present in patients with premature rupture of the membranes, the risk of proven neonatal sepsis is reported to increase to between 3% and 5%. [2] In our study 16% of the infants born to mothers with clinical chorioamnionitis had neonatal infection. Hauth et al [7] reported a 23.5% incidence of congenital pneumonia among term infants born to mothers with clinical chorioamnionitis. Seo et al [8] reported an increase in neonatal mortality in the presence of chorioamnionitis at all gestational ages >28 weeks. In addition, neonatal morbidity in the presence of chorioamnionitis appears to be increased, and an association between clinical chorioamnionitis and cerebral palsy was noted in the National Institute of Neurological and Communicative Disorders and Stroke studies, which reported a 2.6 times increased risk for infants >2500 g. [9] The risk of neonatal infection was increased threefold in this study among mothers colonized with group B streptococci. The prevalence of maternal group B streptococcal colonization in our study may have been under-reported because of variations among centers in collection and culture techniques. The protocol did not require the routine collection of both vaginal and rectal group B streptococcal swabs. In the absence of other risk factors, maternal colonization with group B streptococci is reported to impart a neonatal infection risk between 0.5% and 1%, similar to the rate of neonatal infection associated with uncomplicated premature rupture of the membranes. [2] Risk factors that increase the risk of neonatal infection in a mother with group B streptococcal colonization include premature rupture of the membranes >18 hours, maternal fever during labor, and prematurity. [10] In previous studies a combination of premature rupture of the membranes and maternal group B streptococcal colonization was associated with an incidence of definite neonatal infection between 4% and 6% and an incidence of definite or probable neonatal infection between 7% and 11%. [11] Merenstein and Weisman [6] reported an increase of 40 times in expected mortality rate with group B streptococcal sepsis in term infants. We found a time from membrane rupture to active labor (latent interval) of >or=to24 hours to be an independent risk factor for subsequent neonatal infection, but the odds ratio was only moderately increased (1.97 to 2.25) compared with those of other predictors. Others have noted the association between duration of membrane rupture and neonatal infection in both premature and term infants, with the risk of infection being inversely related to the gestational age. [2,12] However, such other factors as chorioamnionitis and group B streptococcal colonization are more important predictors of neonatal infection. Induction with oxytocin appears to reduce the risk of neonatal infection in infants born to women with group B streptococcal colonization and this is probably related to the shorter duration of labor and lower number of vaginal examinations. [13,14] The number of vaginal digital examinations was an independent predictor of neonatal infection in our study, with the effect being statistically significant when >or=to7 vaginal examinations were performed during labor. This effect was in addition to the association between the number of vaginal examinations and the occurrence of clinical chorioamnionitis. [14] This association has not been previously reported. Vaginal examinations may predispose toward the development of subclinical chorioamnionitis or may introduce bacteria directly into the uterus that do not proliferate or invade until they have reached the fetus. Maternal antibiotics before delivery were found to be independently predictive of neonatal infection in our study. In this case use of antibiotics is most likely a marker of clinical chorioamnionitis, and the increased risk of neonatal infection is related to the underlying infection rather than to the chemoprophylaxis. The neonates in whom infection is most likely to develop after premature rupture of the membranes at term include those in whom the intrapartum course is complicated by clinical chorioamnionitis. Maternal group B streptococcal colonization has an independent effect on subsequent neonatal infection. Strategies aimed at reducing the incidence of clinical chorioamnionitis (such as limiting the number of digital vaginal examinations after premature rupture of the membranes and during active labor) [14] should reduce the incidence of subsequent neonatal infection. In addition patients with group B streptococcal colonization and premature rupture of the membranes at term may benefit from (1) a routine policy of immediate induction of labor with oxytocin [13] and (2) routine intrapartum antibiotic prophylaxis. [10]
REFERENCES^ 2. Gerdes JS. Clinicopathologic approach to the diagnosis of neonatal sepsis. Clin Perinatol 1991;18:361-79. [Medline Link] [BIOSIS Previews Link] [Context Link] 3. Belady PH, Farkouh LJ, Gibbs RS. Intra-amniotic infection and premature rupture of the membranes. Clin Perinatol 1997;24:43-57. [Medline Link] [BIOSIS Previews Link] [Context Link] 4. Hannah ME, Ohlsson A, Farine D, Hewson SA, Hodnett E, Myhr TL, et al. Induction of labor compared with expectant management for prelabor rupture of membranes at term. N Engl J Med 1996;334:1005-10. [Fulltext Link] [Medline Link] [BIOSIS Previews Link] [Context Link] 5. Haque KN. Indications for antimicrobial therapy in babies after PROM: the Saudi Arabian experience. Post Grad Doctor 1993;16:342-7. [Context Link] 6. Merenstein GB, Weisman LE. Premature rupture of the membranes: neonatal consequences. Semin Perinatol 1996;20:375-80. [Medline Link] [BIOSIS Previews Link] [Context Link] 7. Hauth JC, Gilstrap LC 3d, Hankins GD, Connor KD. Term maternal and neonatal complications of acute chorioamnionitis. Obstet Gynecol 1985;66:59-62. [Medline Link] [BIOSIS Previews Link] [Context Link] 8. Seo K, McGregor JA, French JI. Preterm birth is associated with increased risk of maternal and neonatal infection. Obstet Gynecol 1992;79:75-80 [Medline Link] [BIOSIS Previews Link] [Context Link] 9. Nelson KB, Ellenberg JH. Antecedents of cerebral palsy. I. Univariate analysis of risks. Am J Dis Child 1985;139:1031-8. [Medline Link] [BIOSIS Previews Link] [Context Link] 10. Centers for Disease Control and Prevention. Prevention of perinatal group B streptococcal disease: a public health perspective. MMWR Morb Mortal Wkly Rep 1996;45(RR-7):1-24. [Context Link] 11. Boyer KM, Gotoff SP. Prevention of early onset group B streptococcal disease with selective intrapartum chemoprophylaxis. N Engl J Med 1986;314:1665-9. [Medline Link] [BIOSIS Previews Link] [Context Link] 12. Oshiro BT, Monga M, Blanco JD. Intra-amniotic infections. Semin Perinatol 1993;17:420-5. [Medline Link] [BIOSIS Previews Link] [Context Link] 13. Hannah ME, Ohlsson A, Wang E, Myhr T, Farine D, Hewson S, et al. Inducing labor with oxytocin may reduce the risk of neonatal infection in GBS positive women with PROM at term. Am J Obstet Gynecol 1997;177:780-5. [Fulltext Link] [Medline Link] [BIOSIS Previews Link] [Context Link] 14. Seaward PG, Hannah ME, Myhr TL, Farine D, Ohlsson A, Wang E, et al. International Multicenter Term PROM Study: evaluation of predictors of chorioamnionitis and postpartum fever in patients with prelabor rupture of membranes at term. Am J Obstet Gynecol 1997;177:1024-9. [Fulltext Link] [Medline Link] [BIOSIS Previews Link] [Context Link] Accession Number: 00000447-199809000-00014 Copyright (c) 2000-2002 Ovid Technologies, Inc. Version: rel5.0.0, SourceID 1.6100.1.111 |
