Portal de Periódicos da CAPES

Defining mechanisms of recurrence following apical prolapse repair based on imaging criteria

2021; Elsevier BV; Volume: 225; Issue: 5 Linguagem: Inglês

10.1016/j.ajog.2021.05.041

1097-6868

Shaniel T. Bowen, Pamela Moalli, Steven D. Abramowitch, Mark E. Lockhart, Alison C. Weidner, Cecile A. Ferrando, Charles W. Nager, Holly E. Richter, Charles R. Rardin, Yuko M. Komesu, Heidi S. Harvie, Donna Mazloomdoost, Amaanti Sridhar, Marie G. Gantz, Michael Albo, Marianna Alperin, Joann Columbo, Jodi Curry, Kimberly L. Ferrante, Kyle Herrala, Sherella Johnson, Anna C. Kirby, Emily S. Lukacz, Charles W. Nager, Erika Ruppert, Erika Wasenda, Gouri B. Diwadkar, Keisha Y. Dyer, Linda M. Mackinnon, Shawn A. Menefee, Jasmine Tan-Kim, Gisselle Zazueta‐Damian, Cindy L. Amundsen, Yasmeen Bruton, Notorious Coleman-Taylor, Robin Gilliam, Acacia Harris, Akira Hayes, Amie Kawasaki, Nicole Longoria, Shantae McLean, Mary Raynor, Nazema Y. Siddiqui, Anthony G. Visco, Alicia Ballard, Kathy Carter, David R. Ellington, Sunita K. Patel, Nancy Saxon, R. Edward Varner, V. N. B. Willis, Kathy Carter, Cassandra Carberry, Samantha B. Douglas, B. Star Hampton, Nicole B. Korbly, Ann S. Meers, Deborah L. Myers, Vivian W. Sung, Elizabeth-Ann Viscione, Kyle Wohlrab, Karen Box, Gena C. Dunivan, Peter C. Jeppson, Julia Middendorf, Rebecca G. Rogers, Lily A. Arya, Uduak U. Andy, Norman Butler, Doris Cain, Teresa Carney, Lorraine Flick, Kavita Desai Khanijow, Michelle Kingslee, Daniel Lee, Patricia O’Donnell, Ariana L. Smith, Donna Thompson, Michael Bonidie, Judy Gruss, Jerry L. Lowder, Jonathan P. Shepherd, Gary Sutkin, Halina M. Zyczynski, Matthew D. Barber, Kathleen Dastoli, Maryori Edington, Annette Graham, Geetha Krishnan, Eric Jelovsek, Marie Fidela R. Paraiso, Ly Pung, Cecile A. Ferrando, Mark D. Walters, Susan Meikle, Andrew Burd, Kate Burdekin, Kendra Glass, Tracey Grant, Scott F. Grey, Michael Ham, James D. Pickett, Dennis Wallace, Ryan Whitworth, Amanda Shaffer, Taylor Swankie,

Pelvic and Acetabular Injuries

Background Prolapse recurrence after transvaginal surgical repair is common; however, its mechanisms are ill-defined. A thorough understanding of how and why prolapse repairs fail is needed to address their high rate of anatomic recurrence and to develop novel therapies to overcome defined deficiencies. Objective This study aimed to identify mechanisms and contributors of anatomic recurrence after vaginal hysterectomy with uterosacral ligament suspension (native tissue repair) vs transvaginal mesh (VM) hysteropexy surgery for uterovaginal prolapse. Study Design This multicenter study was conducted in a subset of participants in a randomized clinical trial by the Eunice Kennedy Shriver National Institute of Child Health and Human Development Pelvic Floor Disorders Network. Overall, 94 women with uterovaginal prolapse treated via native tissue repair (n=48) or VM hysteropexy (n=46) underwent pelvic magnetic resonance imaging at rest, maximal strain, and poststrain rest (recovery) 30 to 42 months after surgery. Participants who desired reoperation before 30 to 42 months were imaged earlier to assess the impact of the index surgery. Using a novel 3-dimensional pelvic coordinate system, coregistered midsagittal images were obtained to assess study outcomes. Magnetic resonance imaging–based anatomic recurrence (failure) was defined as prolapse beyond the hymen. The primary outcome was the mechanism of failure (apical descent vs anterior vaginal wall elongation), including the frequency and site of failure. Secondary outcomes included displacement of the vaginal apex and perineal body and change in the length of the anterior wall, posterior wall, vaginal perimeter, and introitus of the vagina from rest to strain and rest to recovery. Group differences in the mechanism, frequency, and site of failure were assessed using the Fisher exact tests, and secondary outcomes were compared using Wilcoxon rank-sum tests. Results Of the 88 participants analyzed, 37 (42%) had recurrent prolapse (VM hysteropexy, 13 of 45 [29%]; native tissue repair, 24 of 43 [56%]). The most common site of failure was the anterior compartment (VM hysteropexy, 38%; native tissue repair, 92%). The primary mechanism of recurrence was apical descent (VM hysteropexy, 85%; native tissue repair, 67%). From rest to strain, failures (vs successes) had greater inferior displacement of the vaginal apex (difference, −12 mm; 95% confidence interval, −19 to −6) and perineal body (difference, −7 mm; 95% confidence interval, −11 to −4) and elongation of the anterior vaginal wall (difference, 12 mm; 95% confidence interval, 8–16) and vaginal introitus (difference, 11 mm; 95% confidence interval, 7–15). Conclusion The primary mechanism of prolapse recurrence following vaginal hysterectomy with uterosacral ligament suspension or VM hysteropexy was apical descent. In addition, greater inferior descent of the vaginal apex and perineal body, lengthening of the anterior vaginal wall, and increased size of the vaginal introitus with strain were associated with anatomic failure. Further studies are needed to provide additional insight into the mechanism by which these factors contribute to anatomic failure. Prolapse recurrence after transvaginal surgical repair is common; however, its mechanisms are ill-defined. A thorough understanding of how and why prolapse repairs fail is needed to address their high rate of anatomic recurrence and to develop novel therapies to overcome defined deficiencies. This study aimed to identify mechanisms and contributors of anatomic recurrence after vaginal hysterectomy with uterosacral ligament suspension (native tissue repair) vs transvaginal mesh (VM) hysteropexy surgery for uterovaginal prolapse. This multicenter study was conducted in a subset of participants in a randomized clinical trial by the Eunice Kennedy Shriver National Institute of Child Health and Human Development Pelvic Floor Disorders Network. Overall, 94 women with uterovaginal prolapse treated via native tissue repair (n=48) or VM hysteropexy (n=46) underwent pelvic magnetic resonance imaging at rest, maximal strain, and poststrain rest (recovery) 30 to 42 months after surgery. Participants who desired reoperation before 30 to 42 months were imaged earlier to assess the impact of the index surgery. Using a novel 3-dimensional pelvic coordinate system, coregistered midsagittal images were obtained to assess study outcomes. Magnetic resonance imaging–based anatomic recurrence (failure) was defined as prolapse beyond the hymen. The primary outcome was the mechanism of failure (apical descent vs anterior vaginal wall elongation), including the frequency and site of failure. Secondary outcomes included displacement of the vaginal apex and perineal body and change in the length of the anterior wall, posterior wall, vaginal perimeter, and introitus of the vagina from rest to strain and rest to recovery. Group differences in the mechanism, frequency, and site of failure were assessed using the Fisher exact tests, and secondary outcomes were compared using Wilcoxon rank-sum tests. Of the 88 participants analyzed, 37 (42%) had recurrent prolapse (VM hysteropexy, 13 of 45 [29%]; native tissue repair, 24 of 43 [56%]). The most common site of failure was the anterior compartment (VM hysteropexy, 38%; native tissue repair, 92%). The primary mechanism of recurrence was apical descent (VM hysteropexy, 85%; native tissue repair, 67%). From rest to strain, failures (vs successes) had greater inferior displacement of the vaginal apex (difference, −12 mm; 95% confidence interval, −19 to −6) and perineal body (difference, −7 mm; 95% confidence interval, −11 to −4) and elongation of the anterior vaginal wall (difference, 12 mm; 95% confidence interval, 8–16) and vaginal introitus (difference, 11 mm; 95% confidence interval, 7–15). The primary mechanism of prolapse recurrence following vaginal hysterectomy with uterosacral ligament suspension or VM hysteropexy was apical descent. In addition, greater inferior descent of the vaginal apex and perineal body, lengthening of the anterior vaginal wall, and increased size of the vaginal introitus with strain were associated with anatomic failure. Further studies are needed to provide additional insight into the mechanism by which these factors contribute to anatomic failure.