Polymorphisms in the tumor necrosis factor-alpha gene at position -308 and the inducible 70 kd heat shock protein gene at position +1267 in multifetal pregnancies and preterm premature rupture of fetal membranes

OBJECTIVE: The purpose of this study was to determine the relationship between preterm premature rupture of membranes, tumor necrosis factor-alpha, and heat shock protein-70 gene polymorphisms in multifetal gestations. STUDY DESIGN: Buccal swabs from 101 mother-neonate pairs of multifetal pregnancies were tested for single nucleotide polymorphisms at position -308 of the tumor necrosis factor-alpha gene and +1267 of the heat shock protein-70 gene. Pregnancy outcome data were obtained subsequently. RESULTS: Tumor necrosis factor-alpha allele 2 carriage by the first-born occurred in 10 of 27 pregnancies (37.0%) that resulted in preterm premature rupture of membranes compared with 6 of 67 pregnancies (9.0%) without preterm premature rupture of membranes ( P = .002). The allele frequency of tumor necrosis factor-alpha allele 2 and heat shock protein-70 allele 2 in the first born was higher in pregnancies that were complicated by preterm premature rupture of membranes (18.5% vs 4.5%; P = .003; and 57.7% vs 41.3%; P = .04, respectively). There was no relationship between tumor necrosis factor-alpha allele 2 or heat shock protein-70 allele 2 carriage by the second fetus or mother and preterm premature rupture of membranes. CONCLUSION: Tumor necrosis factor-alpha allele 2 and/or heat shock protein-70 allele 2 carriage by the first-born fetus is associated with preterm premature rupture of membranes in multifetal pregnancies.     

Association of oligohydramnios in women with preterm premature rupture of membranes with an inflammatory response in fetal, amniotic, and maternal compartments.

OBJECTIVE: This study was undertaken to examine whether oligohydramnios in women with preterm premature rupture of membranes is associated with evidence of fetal, amniotic, and maternal inflammatory responses. STUDY DESIGN: Amniotic fluid index was measured before the performance of amniocentesis in patients with preterm premature rupture of membranes. Fifty-nine patients who were delivered of preterm neonates (gestational age 5 cm (positive amniotic fluid culture result, 79% [15/19] vs 30% [12/40]; clinical chorioamnionitis, 37% [7/19] vs 5% [2/40]; histologic chorioamnionitis, 100% [17/17] vs 69% [24/35]; median amniotic fluid interleukin 6 concentration, 13.5 ng/mL; range, 0.2-142.2 ng/mL vs 3.0 ng/mL and 0.001-115.2 ng/mL; median amniotic fluid interleukin 1beta concentration, 348.0 pg/mL; range, 0.7->80, 000 pg/mL vs 36.6 pg/mL and 0-2075 pg/mL; median amniotic fluid tumor necrosis factor alpha concentration, 132.0 pg/mL; range, 0-1600 pg/mL vs 11.2 pg/mL and 0-1305 pg/mL; median cord plasma interleukin 6 concentration, 49.7 pg/mL; range, 4.4-7400 pg/mL vs 9. 1 pg/mL and 0-5211 pg/mL; P <.05 for each). There was no significant difference between the 2 groups of patients in the mean umbilical artery pH at birth. CONCLUSION: Oligohydramnios in women with preterm premature rupture of membranes is associated with an inflammatory response in the fetal, amniotic, and maternal compartments.     

Recurrence of clinical chorioamnionitis in subsequent pregnancies

OBJECTIVE: To establish the role of clinical chorioamnionitis as an independent risk factor for recurrence in a subsequent pregnancy. 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.     

A polymorphism in the promoter region of TNF and bacterial vaginosis: preliminary evidence of gene-environment interaction in the etiology of spontaneous preterm birth

OBJECTIVE: The rarer of 2 alleles of a polymorphism in the promoter of the tumor necrosis factor alpha gene (TNF) has been associated with spontaneous preterm birth following preterm premature rupture of the fetal membranes in some populations. The aim of this study was to assess if the presence of symptomatic bacterial vaginosis amplifies the risk of spontaneous preterm birth in those with a "susceptible" TNF genotype. STUDY DESIGN: A case-control study was performed at our institution. Cases (n=125) were defined as women who delivered before 37 weeks as a result of ruptured membranes or preterm labor, while control subjects (n=250) were defined as women who delivered after 37 weeks. DNA was collected from maternal blood and analyzed for the TNF genotype. Information on symptomatic bacterial vaginosis and other risk factors for preterm birth was obtained by review of the antenatal record. Multiple logistic regression was also used to test the interaction between bacterial vaginosis, the TNF genotype, and preterm birth. RESULTS: Maternal carriers of the rarer allele (TNF-2) were at a significantly increased risk of spontaneous preterm birth [odds ratio (OR) 2.7, 95% CI 1.7-4.5]. The association between TNF-2 and preterm birth was modified by the presence of bacterial vaginosis, such that those with a "susceptible" genotype and bacterial vaginosis had increased odds of preterm birth compared with those who did not (OR 6.1, 95% CI 1.9-21.0). CONCLUSION: This study provides preliminary evidence that an interaction between genetic susceptibilities (ie, TNF-2 carriers) and environmental factors (ie, bacterial vaginosis) is associated with an increased risk of spontaneous preterm birth.     

Tumor necrosis factor in preterm and term labor.

OBJECTIVE: Our objective was to determine if labor (term and preterm) and microbial invasion of the amniotic cavity were associated with changes in amniotic fluid concentrations of tumor necrosis factor. STUDY DESIGN: Amniotic fluid was retrieved by transabdominal amniocentesis from 269 women in the following groups: midtrimester (n = 38), preterm labor with intact membranes (n = 52), preterm premature rupture of membranes (n = 74), term in active labor (n = 84), and term not in labor (n = 21). Fluid was cultured for aerobic and anaerobic bacteria and for Mycoplasma species. Tumor necrosis factor was measured with a commercially available enzyme-linked immunosorbent assay validated for amniotic fluid (sensitivity 60 pg/ml). RESULTS: Amniotic fluid from pregnant women in the second and third trimesters who were not in labor did not contain tumor necrosis factor. Among women in preterm labor, 92.3% (12/13) of patients with a positive amniotic fluid culture had detectable tumor necrosis factor in the amniotic fluid (median 820 pg/ml, range less than 60 to 2340 pg/ml). In contrast, only 10.2% (4/39) of women with a negative amniotic fluid culture had detectable tumor necrosis factor. Histopathologic chorioamnionitis was found in all patients who had a positive amniotic fluid culture, and tumor necrosis factor was detectable in the amniotic fluid of all but one of these patients. Among women in active labor at term, 25% (21/84) had detectable tumor necrosis factor in the amniotic fluid. Tumor necrosis factor was detected more frequently in the amniotic fluid of patients with a positive amniotic fluid culture than in patients with a negative culture (46.6% [7/15] vs 20.2% [14/69], p = 0.047). Amniotic fluid concentrations of tumor necrosis factor were significantly higher in patients with preterm premature rupture of membranes, labor, and a positive amniotic fluid culture than in the other subgroups of patients with preterm premature rupture of membranes. CONCLUSION: Parturition in the setting of microbial invasion of the amniotic cavity is associated with activation of the cytokine network as demonstrated by the detection of tumor necrosis factor in human amniotic fluid.     

Tumor necrosis factor-alpha promotor polymorphisms and endometriosis

To explore whether having the mutant tumor necrosis factor (TNF)2 (G-308*A) and TNFA-A (G-238*A) alleles in the TNF-alpha gene promotor region is higher in women with endometriosis, we determined the respective genotype and allele frequencies in a retrospective case-control study.Polymerase chain reaction was performed to identify the G-308A and G-238A promotor polymorphisms in 92 women with surgically and histologically confirmed endometriosis. A series of 69 healthy women without a history of endometriosis served as clinical controls.The allele frequencies of the TNF2 polymorphism were 0.13 and 0.16 in women with endometriosis and in the control group, respectively, and the frequencies of the TNFA-A polymorphisms in women with endometriosis and in the control group were 0.04 and 0.05, respectively, with no significant difference between the study and control groups. The TNF2 polymorphism was present in the homozygous form (TNF(2/2)) in 4.3% of women with endometriosis and in 2.9% of controls (P=.7). No TNFA-A homozygotes (TNFA(A/A)) were detected.We studied TNF-alpha promotor gene variants among women with endometriosis and found that having the G-308A TNF-alpha and the G-238A TNF-alpha polymorphism was not associated with endometriosis in a white population.     

Predictive value of serum interleukin-6 and -8 levels in preterm labor or rupture of the membranes

BACKGROUND: The aim of this prospective study was to examine if serum concentrations of cytokines are of value in the identification of patients at risk for preterm delivery. METHODS: Interleukin- 1beta,2,4,6,8 and tumor necrosis factor alpha were determined between 25 and 37 weeks of gestation in the serum of 72 consecutive patients with preterm labor, 38 patients with preterm rupture of the membranes, and 24 healthy pregnant women as a control group. Material was collected within 18 hours after hospitalization and was immediately centrifuged and shock frozen. RESULTS: Significantly increased serum levels were found for interleukin-6 and -8 in patients with preterm labor or preterm rupture of the membranes when compared to the control group (p<0.001 and p<0.005, respectively). In patients with preterm rupture of the membranes and interleukin-6 levels above the median of 4.0 pg/ml the delivery occurred significantly earlier than in patients with lower levels (1 versus 5.5 days; p=0.005). Patients of both pathology groups with detectable (>18 pg/ml). Interleukin-8 levels had a shorter pregnancy duration when compared to other patients (p=0.05 for preterm labor and p=0.04 for preterm rupture of the membranes). Interleukin-1beta,2,4, and tumor necrosis factor alpha were not correlated with clinical outcome. CONCLUSIONS: Increased serum interleukin-6 and -8 levels are associated with a shorter interval between onset of preterm rupture of the membranes and delivery and should therefore be further evaluated for their use in clinical practice.     

Chorioamnionitis increases neonatal morbidity in pregnancies complicated by preterm premature rupture of membranes

OBJECTIVE: To compare morbidities of neonates born to women who developed chorioamnionitis after premature preterm rupture of membranes versus those who did not. STUDY DESIGN: We reviewed outcomes in singleton pregnancies with confirmed premature preterm rupture of membranes at 24 weeks or beyond that resulted in delivery less than 37 weeks. Management of premature preterm rupture of membranes included the use of antibiotics, betamethasone if less than 32 weeks, and expectant management with induction at 34 weeks or greater. Composite neonatal major and minor morbidity rates were compared between pregnancies complicated by chorioamnionitis and those that were not. RESULTS: From August 1998 to August 2000, 430 cases of premature preterm rupture of membranes were identified among 6003 deliveries (7.2%). Thirteen percent of women (56/430) with premature preterm rupture of membranes developed chorioamnionitis. The incidence of chorioamnionitis increased significantly with decreasing gestational age. The composite neonatal major morbidity rate was significantly higher in neonates whose mothers developed chorioamnionitis (55%) versus those who did not (18%, P < .0001). In a multiple logistic regression model, chorioamnionitis ( P < .0001), infant gender ( P = .007), latency ( P = .03), and gestational age at delivery ( P < .0001) were significantly associated with composite neonatal morbidity. CONCLUSION: Neonatal morbidities are significantly higher among pregnancies with premature preterm rupture of membranes complicated by chorioamnionitis when compared with pregnancies that were not.     

Study of interleukin-6 and tumor necrosis factor-alpha levels in maternal serum and amniotic fluid of patients with premature rupture of membranes

To study the change and clinical significance of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) levels in the maternal serum and amniotic fluid of pregnant women with chorioamnionitis and with premature rupture of membranes. Twenty-six normal-term pregnant women formed the control group, and forty-six pregnant women with premature rupture of membranes were enrolled for the study. Maternal serum and amniotic fluid IL-6 and TNF-alpha levels were measured using a sensitive radioimmunoassay and enzyme-linked immunosorbent assay (ELISA); chorioamnionitis was diagnosed by fetal membrane pathology. The maternal serum IL-6 levels and amniotic fluid IL-6 and TNF-alpha levels were higher than those of the control (P < 0.01). There was a significant relationship between maternal serum IL-6 and maternal serum and amniotic fluid IL-6 and TNF-alpha with the time of the premature rupture of membranes, i.e. the longer the time, the higher the maternal serum and amniotic fluid IL-6 and TNF-alpha. There were 12 patients with chorioamnionitis in premature rupture of membranes and their maternal serum and amniotic fluid IL-6 and TNF-alpha levels were higher than that of non-chorioamnionitis patients (P < 0.01-0.05). IL-6 and TNF-alpha levels in maternal and amniotic fluids are a valuable index in identification of the chorioamnionitis in patients with premature rupture of membranes.     

Adverse outcomes after preterm labor are associated with tumor necrosis factor-alpha polymorphism -863, but not -308, in mother-infant pairs

OBJECTIVE: Two single-base polymorphisms of the tumor necrosis factor-alpha gene (TNF-alpha) at positions -863 and -308 are associated with variation in production of TNF-alpha (TNF-alpha). TNF-alpha genotypes were tested for association with adverse outcomes in mother-infant pairs with preterm labor. STUDY DESIGN: We analyzed a cohort of 118 mother-infant pairs with preterm labor before 34 weeks' gestation. Polymerase chain reaction was used on extracted deoxyribonucleic acid for polymorphism assay. Outcomes included amniotic fluid TNF-alpha concentration, histologic chorioamnionitis, delivery gestational age, and composite neonatal morbidity. Statistical significance was determined by chi 2 and Kruskal-Wallis analysis of variance. RESULTS: Mothers homozygous for the -863 polymorphism (AA) had significantly earlier deliveries ( P = .02), more chorioamnionitis ( P = .03), and greater composite neonatal morbidity ( P = .03). Neither maternal nor fetal carriage of the -308 polymorphism was associated with adverse outcome. CONCLUSION: In women with preterm labor before 34 weeks' gestation, maternal homozygous carriage of the -863 polymorphism may be associated with preterm delivery and adverse neonatal outcome.     

Further observations on the fetal inflammatory response syndrome: a potential homeostatic role for the soluble receptors of tumor necrosis factor alpha

OBJECTIVE: The fetal inflammatory response syndrome is a subclinical condition frequently present in preterm labor and preterm premature rupture of the membranes and is associated with increased perinatal morbidity and mortality. Tumor necrosis factor alpha is a mediator of septic shock and death, and it exerts its biologic effects by interacting with 2 receptors, TNF-R1 and TNF-R2. Soluble tumor necrosis factor receptors can buffer the biologic activity and protect against the deleterious effects of tumor necrosis factor alpha. The purpose of this study was to determine the behavior of soluble tumor necrosis factor receptors in fetuses with and without fetal inflammatory response syndrome. STUDY DESIGN: Fetal blood sampling was performed in patients with preterm labor (n = 95) and preterm premature rupture of the membranes (n = 39). Control samples were obtained from fetuses who were undergoing blood sampling for clinical indications and had normal outcomes (n = 21). Fetal inflammatory response syndrome was defined as a fetal plasma interleukin 6 concentration >11 pg/mL. Concentrations of interleukin 6 and TNF-R1 and TNF-R2 were determined by use of sensitive and specific immunoassays. Analysis of covariance was used for statistical analysis. RESULTS: (1) TNF-R1 and TNF-R2 were detectable in all samples, and their concentrations decreased with advancing gestational age (r = -0.8 and r = -0.7; P<.0001 and P<.001, respectively). (2) The mean fetal plasma concentrations of TNF-R1 and TNF-R2 were significantly higher in fetuses with fetal inflammatory response syndrome than in those without the syndrome after adjustment for gestational age and fetal membrane status (TNF-R1: no fetal inflammatory response syndrome, mean +/- SE, 3473.7+/-128.8 pg/mL; vs fetal inflammatory response syndrome, mean +/- SE, 4079.9+/-190.7 pg/mL; P<.005; TNF-R2: no fetal inflammatory response syndrome, mean +/- SE, 6033.2+/-235.4 pg/mL; vs. fetal inflammatory response syndrome, mean +/- SE, 7783.1+/-342.8 pg/mL; P<.0001). (3) Fetuses of patients who delivered within 72 hours of cordocentesis had significantly higher concentrations of TNF-R1 and TNF-R2 receptors than those with longer latency periods (P<.05 for each). CONCLUSION: The fetal inflammatory response syndrome is associated with increased availability of the soluble receptors of tumor necrosis factor alpha in fetal plasma. These factors may attenuate the deleterious effects of tumor necrosis factor alpha.     

Interleukin-1 receptor antagonist gene polymorphism and multifetal pregnancy outcome

OBJECTIVE: The purpose of this study was to determine whether interleukin-1 receptor antagonist and/or interleukin-1beta gene polymorphisms influence multifetal pregnancy outcome. STUDY DESIGN: Maternal and neonatal buccal swabs from 51 multifetal gestations were analyzed for interleukin-1 receptor antagonist and interleukin-1beta alleles. Outcome data were obtained subsequently. RESULTS: Fetal carriage of interleukin-1 receptor antagonist allele 1 was more than twice as prevalent as the carriage of allele 2. Preterm premature rupture of membranes was observed in 12 of 24 pregnancies (50.0%) in which 2 fetuses tested positive for interleukin-1 receptor antagonist allele 2, as opposed to only 3 of 27 pregnancies (11.1%) in which 1 or neither fetus tested positive for interleukin-1 receptor antagonist allele 2 (P=.005). Similarly, 20 of 26 neonates (76.9%) with documented morbidity tested positive for interleukin-1 receptor antagonist allele 2, as compared with 36 of 78 neonates (46.2%) without morbidity (P=.007). Fetal or maternal interleukin-1beta polymorphisms or maternal interleukin-1 receptor antagonist polymorphisms were unrelated to pregnancy outcome. CONCLUSION: Fetal carriage of interleukin-1 receptor antagonist allele 2 was associated with both preterm premature rupture of membranes and neonatal morbidity in women with multifetal pregnancies.     

Acute myometritis and chorioamnionitis during cesarean section of asymptomatic women

Postoperative endomyometritis develops in as many as 85% of women undergoing cesarean section, which is 10- to 30-fold higher than after vaginal delivery. The timing and mechanism by which the infecting organisms gain access to the uterine cavity are unclear. One possibility is that the infection may occur postpartum by ascending colonization of the wound. Alternatively, myometritis may be already present at the time the cesarean section is performed in asymptomatic patients. With tissue necrosis, the stage is then set for puerperal endomyometritis. To study this second alternative mechanism, myometrial and placental biopsy specimens were obtained in 91 asymptomatic patients at the time of cesarean section. Histologic evidence of chorioamnionitis was identified in 10% (9/91) of patients. Acute myometritis was present in 11% (10/91) of the myometrial biopsy specimens. Seven of the nine women (77%) with subclinical acute chorioamnionitis demonstrated extension of the inflammation into the myometrium. Thirty-two percent (8/25) of women in labor and 31% (5/16) of those with rupture of membranes for greater than 6 hours had acute chorioamnionitis or myometritis, which is significantly higher (p less than 0.01) than in women without these risk factors. These findings suggest that approximately one third of asymptomatic women with rupture of the membranes for more than 6 hours or who are in labor at the time of cesarean section demonstrate histologic evidence of subclinical chorioamnionitis. In most of these patients the myometrium is also involved. The uterine incision is then performed through infected myometrium, possibly setting the stage for puerperal endomyometritis.     

Lack of association of severe preeclampsia with maternal and fetal mutant alleles for tumor necrosis factor alpha and lymphotoxin alpha genes and plasma tumor necrosis factor alpha levels

OBJECTIVE: The purpose of this study was to determine whether the increased frequency of mutant alleles of the gene for tumor necrosis factor alpha and elevated maternal and fetal plasma levels of tumor necrosis factor alpha were associated with severe preeclampsia. STUDY DESIGN: We performed a prospective cross-sectional study involving 112 patients with severe preeclampsia matched for gestational age with 106 normotensive pregnant women. Deoxyribonucleic acid for restriction fragment length polymorphism analysis was extracted from maternal and fetal blood. Two mutations associated with the gene for tumor necrosis factor alpha were assayed by polymerase chain reaction. Polymerase chain reaction products were digested with the restriction enzyme Ncol and then fractionated by gel electrophoresis. Genotypic frequencies were calculated. Maternal and fetal plasma tumor necrosis factor alpha levels were assayed by the dual monoclonal antibody sandwich enzyme-linked immunosorbent assay technique. The chi2 test, the Fisher exact test, the Student t test, and the Mann-Whitney test were performed to calculate statistical significance. RESULTS: The differences in the genotypic frequencies of the two loci were not significant in either maternal or fetal samples between control women and women with pregnancies complicated by severe preeclampsia. There was no statistical difference in median maternal plasma levels of tumor necrosis factor alpha between control subjects (0.0 pg/mL) and patients with severe preeclampsia (2.5 pg/mL; P =.36). Unexpectedly, fetal plasma tumor necrosis factor alpha levels were found to be significantly elevated in control women (18.4 pg/mL) relative to women with severe preeclampsia (9.1 pg/mL; P <.0001). CONCLUSION: Neither the genotypic frequencies for tumor necrosis factor alpha mutant alleles nor maternal tumor necrosis factor alpha plasma levels were increased in patients with severe preeclampsia.     

Preterm premature rupture of membranes: vascular endothelial growth factor and its association with histologic chorioamnionitis

OBJECTIVE: We hypothesize that vascular endothelial growth factor, a known angiogenic and permeability factor that is locally expressed in fetal membranes and decidua, may be the primary regulator in the pathway that eventually leads to preterm premature rupture of membranes. Our objective was to test the hypothesis that, both in the presence and in the absence of histologic chorioamnionitis, there is an increased expression of the vascular endothelial growth factor gene and its receptor Flt-1 in the human fetal membranes. STUDY DESIGN: Membranes were sampled from a region that was distinct as the rupture site from three groups of patients with preterm premature rupture of membranes. Groups 1 and 2 differed only in the length of the latency period from rupture of the membranes to delivery. Group 3 included preterm patients with intact membranes, who acted as control subjects. All patients who were selected for the study lacked clinical signs of chorioamnionitis and were delivered by cesarean delivery. Tissue samples were analyzed for interleukin-6 gene expression by Northern blot analysis and for the presence of interleukin-6 protein by immunocytochemistry. The expression of vascular endothelial growth factor and Flt-1 genes was analyzed by in situ hybridization. RESULTS: All tissue samples from group 1 and five tissue samples from group 2 (designated as group 2A) showed expression of the interleukin-6 gene and the presence of interleukin-6 protein in the fetal membranes (P <.001) and were therefore identified as inflamed. Five tissue samples from the patients in group 2 (designated as group 2B) and all control tissue samples showed neither evidence of interleukin-6 gene expression nor the presence of its protein and therefore were identified as not inflamed. Vascular endothelial growth factor and Flt-1 gene expression were increased significantly in the fetal membrane and decidua samples that were obtained from the noninflamed tissues from group 2B (P <.005) yet showed further enhancement in expression in the inflamed tissues. CONCLUSION: The expression patterns of vascular endothelial growth factor and Flt-1 genes are indicative of a molecular pathologic condition of fetal membranes, regardless of their inflammatory status, which suggests their role as a primary regulator of preterm premature rupture of membranes.     

A Clinical Audit of the Number of Vaginal Examinations in Labor: A NOVEL Idea

Introduction : Clinical practice audits present an opportunity for providers to examine and reflect on their practice. Vaginal examinations are an integral part of intrapartum care but can be uncomfortable for women and can increase the risk of chorioamnionitis. Thus, vaginal examinations should be performed thoughtfully and for necessary reasons. Methods : A busy midwifery service at a large academic center underwent an audit of the number of vaginal examinations performed in labor for 205 women admitted in spontaneous labor or with spontaneous rupture of membranes. The retrospective chart audit was performed by research midwives who queried 2 electronic medical record databases, 1 for provider progress notes and 1 for nursing notes. Results : On average, a woman underwent 4 vaginal examinations during labor, a rate greater than the World Health Organization recommendation of 1 examination every 4 hours during the first stage. The rate of presumed chorioamnionitis in this group of healthy, low‐risk women was 6%, and women with this diagnosis averaged 7 vaginal examinations. Discussion : After presentation and discussion of the audit findings, the midwives expressed appreciation for the opportunity to explore such a fundamental element of clinical practice and a heightened awareness of the importance of performing and documenting vaginal examinations. Audits of a similar nature in other midwifery practices are needed, as are studies exploring rates and possible modifiable causes of chorioamnionitis in low‐risk women.     

Amniotic fluid index values after preterm premature rupture of the membranes and subsequent perinatal infection

OBJECTIVE: Our purpose was to determine whether an amniotic fluid index (AFI) <5 cm after preterm premature rupture of the membranes is associated with an increased risk of perinatal infection. STUDY DESIGN: We performed a nonconcurrent prospective analysis of 225 singleton pregnancies complicated by preterm premature rupture of the membranes, with delivery between 24 and 32 weeks' gestation. All included patients received 2 doses of betamethasone antenatally, in the first 24 hours after admission, and broad-spectrum antibiotic prophylaxis. Patients were categorized into 2 groups on the basis of a 4-quadrant AFI <5 cm (n = 131) or > or =5 cm (n = 94). Perinatal outcomes analyzed included latency until delivery, mode of delivery, and frequencies of clinical chorioamnionitis, postpartum endometritis, and culture-proved early neonatal sepsis. Continuous data were evaluated for normal distribution and tested for significance with the Student t test. Categoric data were tested with the chi(2) and Fisher exact tests. Multiple logistic regression analyses were performed with chorioamnionitis, endometritis, and early-onset neonatal sepsis each as the dependent variable in separate analyses. All 2-sided P values <.05 were considered significant. RESULTS: Both groups were similar with respect to selected demographics, gestational age at rupture of the membranes, birth weight, and maternal group B streptococcal colonization. Patients with an AFI <5 cm demonstrated a shorter mean latency until delivery (5.5 +/- 4.0 vs 14.1 +/- 5.2) (mean +/- SD) days (P =.02), greater frequency of amnioinfusion therapy (23.6% vs 5.3%) (P <.001), and cesarean delivery for nonreassuring fetal testing (18.3% vs 4. 3%) (P =.01). Multiple logistic regression analysis showed that an AFI <5 cm was the only significant risk factor independently associated with early-onset neonatal sepsis (P =.004) and chorioamnionitis (P =.024). CONCLUSIONS: An AFI <5 cm after preterm premature rupture of the membranes between 24 and 32 weeks' gestation is associated with an increased risk of perinatal infection and a shorter latency preceding delivery.