Damage to the muscles, fasciae, and sphincters of the pelvic floor that occurs at the time of birth is one of, if not the most important cause of stress urinary incontinence (SUI). Incontinent women have an odds ratio of 11.2 for having had a vaginal delivery compared with continent controls, twice the rate for any other factor. The mechanisms by which vaginal delivery causes SUI, however, are not understood. This study aims to clarify how damage caused by birth results in SUI. These insights will improve strategies for incontinence treatment and prevention. SUI is associated with defects in a) the urethral support systems and b) the sphincteric control system. Neither type of damage alone, however, adequately explains the occurrence of SUI. The hypothesis posed here is that vaginal birth causes SUI through a combination of damage to these two systems. To test this hypothesis, a case-control design is proposed enrolling as cases primiparous women with stress incontinence (SI; n=80), persisting 6 months postpartum. Negative controls will be nulliparous continent women (NC; n=80), and Positive controls; primiparous continent women (PC; n=80) delivered vaginally. They will quantify urethral support and sphincteric function in each of these groups using ultrasound, levator strength measurements and urethral pressure studies. For analysis of primary hypotheses, these data will be used to: 1) Show that measurements of either urethral support or sphincteric function alone will predict less than 30% of SI cases. 2) Identify which combinations of the three support parameters, three sphincter parameters, and their interactions have at least an 80% probability of correct prediction of SI compared with PC or NC by using discriminant analysis. 3) Construct a predictive model for SUI using discriminant functions and classification trees to indicate the relative importance of support parameters, sphincter parameters, and their interactions. Secondary hypotheses concern anatomical abnormalities visible on MRI responsible for functional problems. This project is expected to show that: 1) Loss of support involves connective tissue breaks and/or loss of levator ani bulk measurable on MRI as decrease in size of the levator ani, and 2) Sphincteric weakness results from quantifiable loss of sphincter bulk in the smooth and striated sphincter muscles. Correlation between anatomic measurements and functional parameters listed in the primary hypotheses will determine the cause of functional abnormalities.
Other aims i nclude 1) Using biomechanical models they will construct and validate a computer model of the fetal head and pelvic floor to test hypotheses concerning mechanisms of injury responsible for sphincter and support damage occurring during vaginal birth. 2) This project should establish the priority of obstetrical parameters associated with SUI. The importance of this research lies in its providing insights about the specific functional and anatomical defects caused by vaginal birth. This knowledge should help in devising future injury prevention at birth and help form the basis for more rational treatment selection in women with stress incontinence.
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|Brincat, Cynthia A; Delancey, John O L; Miller, Janis M (2011) Urethral closure pressures among primiparous women with and without levator ani muscle defects. Int Urogynecol J 22:1491-5|
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|Margulies, Rebecca U; Huebner, Markus; DeLancey, John O L (2007) Origin and insertion points involved in levator ani muscle defects. Am J Obstet Gynecol 196:251.e1-5|
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|Huebner, Markus; Margulies, Rebecca U; Fenner, Dee E et al. (2007) Age effects on internal anal sphincter thickness and diameter in nulliparous females. Dis Colon Rectum 50:1405-11|
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