EFFECTS OF A PRESSURE DRESSING ON THE POST-CESAREAN SECTION INCISION ANJALI KAIMAL, JAMES PHILLIP, JAMES GREENBERG, Brigham and Women’ s Hospital, Department of Obstetrics and Gynecology, Boston, Massachusetts, Brigham and Women’s Hospital, Department of Anesthesia, Boston, Massachusetts, Brigham and Women’s Hospital, Department of Obstetrics and Gynecology, Boston, Massachusetts OBJECTIVE: Application of a pressure dressing is intended to compress dead space and prevent hematoma and seroma formation, leading to decreased wound disruption, a complication that causes significant morbidity and cost. Theoretically, the pressure dressing improves hemostasis by preventing venous capillary blood loss and exudate. Conversely, pressure dressings may cause increased patient discomfort and their removal can be associated with skin trauma. Given the paucity of data supporting the benefit of a pressure dressing for an abdominal incision and the potentially deleterious effects, this pilot study seeks to determine the increase in pressure exerted by a pressure dressing after a primary cesarean section. STUDY DESIGN: After undergoing routine cesarean section via a Pfannenstiel skin incision, the wound pressures in five subjects were measured in three different states. Using a Stryker Intra-Compartmental Pressure Monitor System, subcutaneous tissue pressures were measured immediately after wound closure, after application of a simple Telfa dressing, and after application of a pressure dressing. A t-test was used to compare the measurements. RESULTS: Mean baseline pressure in the subcutaneous tissue in an undressed wound was 1.4 mmHg. After application of a Telfa dressing, the mean pressure was 1.8 mm Hg. After application of a pressure dressing, the mean pressure was 6.6 mm Hg. Application of a pressure dressing resulted in an average increase in pressure in the subcutaneous tissue of 4.8 mm Hg (P ! .005) as compared with a Telfa dressing alone. CONCLUSION: Application of a pressure dressing significantly increases the pressure in the subcutaneous tissue of a cesarean section incision. However, the increase in pressure demonstrated by this study may not be sufficient to overcome capillary venous pressure; therefore, the pressure dressing may not be able to decrease hematoma and seroma formation. Until there is data that a dressing can impact the pathophysiology of wound disruption, surgeons may want to reconsider the use of a pressure dressing in this setting. 221 LABOR INDUCTION AND AUGMENTATION: INDEPENDENT RISK FACTORS FOR UTERINE RUPTURE? GEORGE MACONES, DAVID STAMILIO, EMMANUELLE PARE, JEFFREY PEIPERT, ANTHONY SCISCIONE, HARISH SEHDEV, SARAH RATCLIFFE, MARY SAMMEL, University of Pennsylvania, Obstetrics and Gynecology, Philadelphia, Pennsylvania, Brown University, Obstetrics & Gynecology, Providence, Rhode Island, Drexel University, Obstetrics and Gynecology, Philadelphia, Pennsylvania, Pennsylvania Hospital, Obstetrics & Gynecology, Philadelphia, Pennsylvania, University of Pennsylvania, Biostatistics, Philadelphia, Pennsylvania OBJECTIVE: To determine whether induction and augmentation of labor with specific agents independently increases the risk of uterine rupture in women attempting VBAC. STUDY DESIGN: A case-control study, nested within a cohort study of 13,706 women who attempted VBAC at 17 participating institutions (community and tertiary), was performed. Cases of uterine rupture were compared to randomly selected controls for a variety of obstetrical, historical, and intrapartum factors. Information was collected from the inpatient medical record by trained research nurses. We used both bivariate and multivariate techniques to determine whether induction/augmentation and the use of specific agents increased the risk of uterine rupture. RESULTS: We identified 133 cases of uterine rupture (incidence = 0.98%) and compared them to 665 randomly selected controls. After adjustment for confounding factors, neither labor induction (adjusted OR= 1.0, 95% CI 0.42.3) nor labor augmentation (adjusted OR= 1.7, 95% CI 0.8-3.6) were independently associated with uterine rupture. The use of prostaglandins alone was not associated with an increased risk of uterine rupture (adjusted OR= 1.4, 95% CI 0.2-8.2). The use of sequential prostaglandin and pitocin was, however, associated with a 3 fold increase in the risk of rupture (adjusted OR= 3.1, 95% CI 1.0-9.8). CONCLUSION: In contrast to a prior report and ACOG’s recent opinion, prostaglandins alone do not appear to be associated with uterine rupture. The need for sequential prostaglandins and pitocin, signifying a more difficult induction, appears modestly associated with rupture.