Development Of Stress Incontinence Research Articles

Pubovaginal sling and pelvic prolapse repair in women with occult stress urinary incontinence: effect on postoperative emptying and voiding symptoms

Objectives. To determine the perioperative morbidity of performing a concurrent pubovaginal sling with prolapse repair in women with occult (or potential) stress incontinence, particularly on voiding dysfunction and emptying. Methods. We reviewed the charts of 38 women with grade 3-4 pelvic prolapse and occult stress incontinence. All patients underwent video urodynamic testing with the prolapse unreduced and again with the prolapse reduced with a pessary or packing. The abdominal leak point pressure was determined. Appropriate surgical repair of all components of the prolapse was performed concurrently with pubovaginal sling placement. The outcomes were measured with respect to the time to spontaneous voiding, permanent urinary retention, development of stress incontinence or de novo urge incontinence, resolution of urge incontinence, and perioperative complications. Results. The mean age was 72 years, and the mean follow-up was 15 months (range 6 to 39). The mean time required before spontaneous voiding resumed without the need for catheterization was 11.8 days (range 2 to 46). No patient developed permanent urinary retention. Two (9.5%) of 21 women without preoperative urge incontinence developed de novo urge incontinence. However, existing urge incontinence resolved in 45%. One woman developed a suprapubic wound infection, which resolved with conservative management. Stress incontinence occurred in 2 women (7%) at 4 and 19 months postoperatively. Clinically significant prolapse (uterine) developed in 1 patient 2 years after surgery. Conclusions. Simultaneous pubovaginal sling placement for women with occult stress incontinence undergoing repair of a large pelvic prolapse is effective in preventing postoperative stress incontinence and has little negative effect on postoperative bladder emptying. It should be considered in all women with occult stress incontinence undergoing prolapse repair.

The Risk of Stress Incontinence 5 Years After First Delivery

To evaluate the risk of developing long-lasting stress incontinence after first delivery, the authors interviewed all women who had their first delivery at Glostrup County Hospital in 1989 (N = 305). Within a few days of delivery and again 3 months later, the women were interviewed by phone using a questionnaire that incorporated the International Continence Society standards for stress incontinence. The questionnaire included questions about urinary incontinence symptoms provoked by physical exertion, frequency of symptoms, and social or hygienic problems caused by stress incontinence. Five years later all patients were mailed the same questionnaire with additional questions about obstetric history and treatment for stress incontinence. Two hundred seventy-eight of the initial population of 305 women (91%) returned the follow-up questionnaire and form the basis of the analysis. For comparison, the women were divided into three groups. The 166 women who had no initial stress incontinence before, during, or 3 months after the first pregnancy were assigned to group 0. Eighty women experienced onset of stress incontinence symptoms with the first pregnancy; they form group 1. Group 2 includes 19 women who reported stress incontinence symptoms persisting 3 months after first delivery. Multivariate logistic regression analysis of possible contributing factors, including length of second stage of delivery, episiotomy, use of vacuum extraction, and fetal weight, was performed for all groups. One hundred seventy-two of the 278 women had a second delivery during the 5-year interval. Eighteen of these were delivered by cesarean delivery. Vacuum extraction was necessary in seven women delivering vaginally. Five women had a sphincter rupture at second delivery; 1 woman had a spontaneous rupture with no episiotomy, and 4 women in the group of 25 who had mediolateral episiotomy also sustained a sphincter rupture. Minor perineal lesions requiring sutures occurred in 75 women. There was only one perineal lesion among eight women who had a third delivery during the 5-year follow-up. At the 5-year point, 83 women (30%) had stress incontinence. Seventeen (6%) reported daily symptoms, and 23 (8%) reported social or hygienic problems due to stress incontinence. The likelihood of developing stress incontinence in the 5 years after first delivery was 3.8 times greater for women in group 1 than for women in group 0. After multivariate logistic regression analysis, only episiotomy at first delivery had borderline significance in predicting the development of stress incontinence. Compared with group 0, the risk of developing stress incontinence was 4.5 times greater for women in group 2. The use of vacuum extraction during the first delivery was the only significant risk factor remaining after analysis. Nineteen percent of the women in group 0 developed stress incontinence in the 5-year study period. No significant predicting factors were found in multivariate analysis. Among all 278 women, retrospective bivariate analysis found that episiotomy at first delivery was the only significant predicting factor for the presence of stress incontinence at 5 years. The women in group 1 had a 42% chance of stress incontinence symptoms recurring by the 5-year follow-up. In comparison, 92% of the women in group 2, those with persistent symptoms, had stress incontinence at 5 years.

Changes in the urethral sphincter in relation to child birth and the development of stress incontinence

Changes in the urethral sphincter in relation to child birth and the development of stress incontinence

Current Concepts of Female Pelvic Anatomy and Physiology

The female urinary bladder and urethra are situated on the intrapelvic surface of the anterior vaginal wall, firmly anchored to the distal vagina by the urogenital diaphragm and to the superior vagina at the vesicocervicouterine junction. The anterior surface of the proximal urethra is firmly anchored to the posterior aspect of the symphysis pubis by the pubourethral ligaments and to the remaining distal vagina by the lower two thirds of the urogenital diaphragm. The lateral bladder wall derives its support from the anterior vaginal wall attachments to the pelvic sidewall. The anterior vaginal wall is strongly supported by pubococcygeus muscle fibers inserting on the vaginal wall and the genital hiatus and by the cardinal and uterosacral ligaments. Vaginal detachment from the lateral pelvic sidewall can result in herniation, with accompanying secondary posterior bladder descent. Levator ani weakness or injury may be a contributing etiologic factor in the genesis of vaginal wall detachment and the development of stress incontinence.

Is there a correlation between the degree of proliferation of vaginal and urethral epithelium and the incidence of stress incontinence? A contribution to estrogen therapy in stress incontinence

The extent of proliferation of the vaginal and urethral epithelium, as well as urodynamic parameters, were studied in 232 patients in order to determine whether there is a relation between the development of stress incontinence and hormone-related epithelial proliferation. A higher build-up of vaginal than of urethral epithelium was found in 74% of the patients. Even in post-menopause patients, epithelial atrophy in the vagina was only found in 29.3%, while in the urethra it was found in 61.3%. Therefore, the vaginal epithelium cannot with confidence be taken as a basis for conclusions concerning the condition of the urethral epithelium. In the group of 145 patients with urinary stress incontinence no link could be established between the extent of proliferation of the urethral epithelium, the urethral occlusion pressure and the functional length of the urethra: The occurrence of an age-related excessively low urethral occlusion pressure (hypotonic urethra) is independent of the extent of proliferation of the vaginal or urethral epithelium. Sedimentation phenomena are also seen equally frequently in cases with atrophic and eutrophic epithelium. Owing to the high percentage of overweight women among those with stress incontinence, the extent of proliferation of the vaginal and urethral epithelium often corresponds to premenopausal cell pictures even in perimenopausal and postmenopausal women; this is a consequence of increased estrogen production in the peripheral fatty tissue. Therefore, estrogen therapy is unsuccessful in women with pure urinary stress incontinence. However, the efficacy of an equivalent therapy, e.g., with estriol, has been confirmed in cases of active and combined incontinence.

SIMULTANEOUS INTRAURETHRAL AND INTRAVESICAL PRESSURE STUDIES IN NORMAL WOMEN AND THOSE WITH STRESS INCONTINENCE

M A N Y theories regarding normal urinary contineke and the development of stress incontinence in women have been advanced. Llntil quite recently normal urinary continence and micturition were thought to involve little more than an appropriate interaction of the bladder detrusor and urethral sphincter muscles.“’ Some gynecologists ha1.e tried to esplain the reason for urinary stress incontinence in equally simple terms based upon empiric observations such as the “short urethra”” or tht “inadequate posterior urethro\xxical angle.“” JeffcoatcaT and I>uttong have cmphasiztd that the inadequate posterior urcthrovcsical angle is a frequent accompanying sign of. not the reason for. stress incontincncc. However the sign is often misinterpreted as the cause of stress incontinence. It is now realized that normal urinary continence inl,olves a complicated mechanism. The functional result of this mechanism is that, in maintaining continence. the intraurethral pressure remains Kreater than the intravesical pressure. EnhGrning” has shown that in normal women and those with stress incontincncc at rest the intraurcthral pres-

Simultaneous intraurethral and intravesical pressure studies in normal women and those with stress incontinence

M A N Y theories regarding normal urinary contineke and the development of stress incontinence in women have been advanced. Llntil quite recently normal urinary continence and micturition were thought to involve little more than an appropriate interaction of the bladder detrusor and urethral sphincter muscles.“’ Some gynecologists ha1.e tried to esplain the reason for urinary stress incontinence in equally simple terms based upon empiric observations such as the “short urethra”” or tht “inadequate posterior urethro\xxical angle.“” JeffcoatcaT and I>uttong have cmphasiztd that the inadequate posterior urcthrovcsical angle is a frequent accompanying sign of. not the reason for. stress incontincncc. However the sign is often misinterpreted as the cause of stress incontinence. It is now realized that normal urinary continence inl,olves a complicated mechanism. The functional result of this mechanism is that, in maintaining continence. the intraurethral pressure remains Kreater than the intravesical pressure. EnhGrning” has shown that in normal women and those with stress incontincncc at rest the intraurcthral pres-