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review of all CD. Rates of SSI were calculated, with significanceascribed to p � 0.05.RESULTS: During the time period 868 CD were performed. Therewere 509 cases that had SSI results by all four methods. A total of 31(6.09%) SSIs were diagnosed using any of the four methods, which isthe true SSI rate. Questionnaire completion rates were 80.53% forsurgeons and 79.38% for patient-report. SSI rates were 2.75% forsurgeon- and 5.11% for patient-report. Two facility SSI readmissionswere found (0.39%). The SSI rate for chart review was 3.1%.Detection of SSI via all four combined methods had a highersensitivity as compared to surgeon-report (p ¼ 0.014), chart review(p ¼ 0.035) or readmission rate (p ¼ 0.0001). SSI rates determinedby patient-report approximate the true SSI rate and did not signif-icantly differ from the combined method (p ¼ 0.59).CONCLUSION: SSI determined by a combination approach is mostaccurate, but is a cumbersome method for identification. Patient-report accurately identifies CD SSI, and may be the best methodsince it is relatively easy to implement. Reporting bias and recall bias,variation in the use of CDC SSI criteria, SSI diagnosed by physiciansother than the surgeon, and those reported by patients may explaindifferences between identification methods.

Rates of SSI by surgeon-report, patient-report, chart review, andpost-operative readmission individually as compared to all fourmethods combined.

Comparison of methods of SSI surveillance using Fisher’s ExactTest

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Cysteinyl leukotriene receptor antagonist montelukastfor the management of spontaneous preterm labour - a pilotrandomized controlled trialJean-Charles Pasquier1, Simon Blouin1, Stephanie Corriveau1,Marie-Eve Roy-Lacroix1, Nils Chaillet11Université de Sherbrooke, Obstetrics, Sherbrooke, QC, CanadaOBJECTIVE: Inflammation play a major role in preterm birth. Cys-teinyl leukotrienes (cys-LTs) are potent mediators of inflammationderived from arachidonic acid. Montelukast, a cys-LTs receptorantagonist and anti-inflammatory agent, is a consistent tocolytic invitro (Corriveau 2014). In this study, we aimed to prepare a rand-omised control trial (RCT) to evaluate the impact of Montelukast onthe rate of spontaneous preterm birth.STUDY DESIGN: The proposed trial was a two-arm, double-blindedRCT involving 60 pregnant women hospitalized for spontaneouspreterm labour occurring between 24 and 34 weeks of pregnancy. Inaddition to a prescription of nifedipine for tocolysis, participantswere asked to take a daily capsule of either montelukast (10 mg) orplacebo, until delivery or 35 weeks of pregnancy. The primaryoutcome was the time interval between the beginning of treatmentand delivery. Urine samples were collected to assess concentrationsof LTE4. Others secondary outcomes included the recruitment rate,the rate of preterm birth, and a composite determination of neonatalmortality and morbidity.RESULTS: We approached 105 eligible women, of whom 60 agreed toparticipate (57%). Five women stopped the treatment (Montelukastor placebo). Mean gestational age at randomization was 31.1 weeksfor both groups. Time interval between the beginning of treatmentand delivery were 30.5 days (21.6) and 23.8 days (17,3) in Mon-telukast and control group respectively (p¼0,21). Adverse perinataloutcome was not significantly different between the groups.CONCLUSION: For the first time the effectiveness of maintenancetocolysis with Montelukast was used in a clinical study. Our pilotstudy in women with threatened preterm labor showed that 1) aRCT is feasible, 2) a prolongation of pregnancy of 6.7 days could beexpected with Montelukast. In a perspective of personalized medi-cine, only women with higher concentrations of urinary LTE4 couldbe selected to receive Montelukast treatment.

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Postpartum weight retention: impact on perinataloutcomes in subsequent pregnancyJennifer Durst1, Methodius Tuuli1, Molly Stout1,George Macones1, Alison Cahill11Washington University School of Medicine, Obstetrics and Gynecology,Division of Maternal-Fetal Medicine, St. Louis, MOOBJECTIVE: Prior studies show that more than 50% of gravidas retain� 10 pounds at one year postpartum. We sought to estimate theassociation between interval pregnancy weight retention and adverseperinatal outcomes in a subsequent gestation.STUDY DESIGN: Within the first 2 years of a prospective cohort studyof consecutive term births, we studied the 560 patients who had 2term births. Prepregnancy BMI, BMI at delivery, and outcomes forboth gestations were collected. Interval pregnancy weight retentionwas defined as the difference between prepregnancy weight in thesecond gestation and prepregnancy weight in the first gestation.Pregnancy weight retention was considered as minimal (� 5 lbs),moderate (> 5 but < 18 lbs), or high (� 18 lbs). Outcomes assessedin the second pregnancy included pre-eclampsia, gestational weightgain (GWG), cesarean delivery (CD) and neonatal acidemia.Multivariable logistic regression was used to adjust for nulliparityand BMI.RESULTS: 301 (53.8%) women had minimal, 121 (21.6%) hadmoderate, and 138 (24.6%) had high weight retention betweenpregnancies. Women with high weight retention were younger, hadhigher starting BMI, and were more likely to be obese compared towomen with minimal retention. Nearly half of women gained weight

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above the Institute of Medicine (IOM) recommendations in theirsecond pregnancy. There were no significant differences in CD, pre-eclampsia, GWG above the IOM recommendations, and neonatalacidemia among women with moderate or high retention whencompared to those with minimal retention, with the exception ofbase excess� 8 which was higher in women with moderate retention(Table).CONCLUSION: While nearly half of women had moderate or highinterpregnancy weight retention, we found no increased risk ofadverse perinatal outcomes in a subsequent pregnancy. This suggeststhat the absolute maternal weight, rather than weight retention,drives pregnancy outcomes. Given these findings, more effortsshould be focused on achieving optimal maternal weight prior topregnancy.

Selected perinatal outcomes

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Prevalence of maternal cell contamination in amnioticfluid samplesJennifer Weida1, Avinash Patil1, Frank Schubert1,Stephen Dlouhy1, Gail Vance1, Holli Drendel1, Men Jean Lee11Indiana University School of Medicine, Indianapolis, INOBJECTIVE: Chromosomal microarray analysis is a growing compo-nent of invasive prenatal testing; however, this technique is suscep-tible to maternal cell contamination (MCC). Many practitionershave abandoned the practice of discarding the first few milliliters(mL) of amniotic fluid withdrawn during the amniocentesis sincethe reported rate of MCC in cultured cells is considered to benegligible (1-3%). We evaluated the incidence of MCC by molecularanalysis within the first 2 mL of amniotic fluid from amniocentesisto determine a more accurate risk of contamination.STUDY DESIGN: A prospective observational study was performedbetween May 2013 and July 2014. The initial 2ml of amniotic fluidwithdrawn during the amniocentesis was divided into cultured anduncultured samples for research analysis. A matching maternalbuccal swab was obtained for MCC testing. Maternal and fetal DNAwas isolated and amplified by PCR. MCC was determined by shorttandem repeat analysis. Primary outcomes included the presence orabsence of MCC. Additional data collection included gestational age,needle size, location of placenta, volume of amniotic fluid removed,and color of amniotic fluid.RESULTS: Twenty-four samples were acquired for the following in-dications: advanced maternal age (25%), fetal anomaly (21%),abnormal serum screening (13%), and other indications. Thirteensamples were obtained between 15-21 weeks and eleven > 24 weeks.Three samples did not yield an adequate amount of DNA and 4failed culture, leaving 17 samples for analysis. Of these samples, 10uncultured (58.8%) and 2 cultured (11.7%) samples had MCC. Bothcultured samples with MCC were obtained from pregnancies with aposterior placenta.CONCLUSION: Cultured amniotic fluid samples revealed a greaterincidence of MCC than previously reported (11.7% vs. 3%). Ourdata suggests that the practice of discarding the initial 2mL of am-niotic fluid from amniocentesis to reduce the risk of maternal cellcontamination should not be abandoned.

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L-arginine prevents hypoxia-induced vasoconstriction inthe fetal vasculature: a potential intervention in chronicuteroplacental ischemiaJimmy Espinoza1, Andrey Bednov1, Ancizar Betancourt1,Julia Chernis1, Ignatia Ven den Veyver1, Michael Belfort1,Chandrasekhar Yallampalli11Baylor College of Medicine, Obstetrics and Gynecology, Houston, TXOBJECTIVE: Chronic hypoxia in the uteroplacental unit is associatedwith increased impedance to blood flow in the fetal-placental cir-culation. These changes may be compensatory in nature, but they areassociated with fetal heart remodeling and long term cardiovasculareffects. This study was designed to determine if L-arginine [a nitricoxide (NO) substrate] and BQ123 (an endothelin A receptorantagonist) administration can reverse hypoxia-induced increases offetal vascular pressure in dual-perfused human placental cotyledons.STUDY DESIGN: Dual-perfused placental cotyledons (n¼16) wereprepared from uncomplicated term pregnancies. Following equili-bration with 95% O2 and 5% CO2 (normoxia) the maternalcompartment was sequentially perfused with Krebs solution withhypoxia (95% N2 and 5% CO2) and normoxia. Changes in theperfusion pressure in the fetal compartment were continuouslyrecorded. L-arginine (n¼3), BQ123 (n¼3) or normal saline (n¼10)were administered to the fetal compartment prior to the initiation ofhypoxia in the maternal compartment. Perfusion pressure changes inthe fetal compartment were compared among groups.RESULTS: Hypoxia in the maternal compartment was associated withincreased (mean delta: 3.17 + 1.33 mm Hg) perfusion pressure in thefetal compartment, which returned to baseline following reoxyge-nation. L-arginine administration to the fetal compartment bluntedthe effect of maternal hypoxia on the fetal perfusion pressure (meandelta: 0.40 + 0.6 mm Hg; p¼0.006). In contrast, BQ123 did notsignificantly change the hypoxic effect on the fetal vasculature (meandelta: 2.23 + 0.9; p¼0.7).CONCLUSION: 1) L-arginine, but not BQ123, reduces the hypoxia-induced vasoconstriction in the fetal compartment suggesting thatNO, but not endothelin, signaling participate in hypoxia-inducedvasoconstriction of the fetal vasculature; 2) L-arginine administra-tion could potentially reduce the fetal cardiovascular changes asso-ciated with chronic uteroplacental ischemia.

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Funisitis more common in incompetent cervix than inpreterm laborJoohee Choi1, Jeong Woo Park3, Ye-Jin Choi3, Byoung Jae Kim2,Seung Mi Lee21Seoul National University College of Medicine, Obstetrics and Gynecology,Seoul, Republic of Korea, 2Seoul Metropolitan Government Seoul NationalUniversity Boramae Medical Center, Department of Obstetrics andGynecology, Seoul, Republic of Korea, 3Inje University College of Medicine,Isan-Paik Hospital, Department of Obstetrics and Gynecology, Gyeonggi,Republic of KoreaOBJECTIVE: Substantial evidences indicate that infection and/orinflammation is associated with the risk of preterm birth and adverseneonatal outcomes, and ascending infection is the major route ofinfection. Microbial invasion to amniotic cavity from lower genitaltract can occur by uterine contraction (preterm labor, PTL), in theabsence of intact membranes (preterm premature rupture ofmembrane, PROM), or in the absence of cervix as a barrier(incompetent internal os of cervix, IIOC), but there is a paucity ofinformation regarding which component is essential in this route ofinfection. In this context, we compared the frequency of histologicchorioamnionitis (HCA) and funisitis based on three leading causesof spontaneous preterm birth (PTB): PTL, PROMand IIOC.STUDY DESIGN: This retrospective cohort study included singletonpregnant women who were delivered at �36 weeks of gestation. Thecauses of PTB were defined as the diagnosis made at the time of

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