To the Editor, A recent article proposes urethral support failure rather than urethral function failure as the principal cause of urodynamically proven stress urinary incontinence (SUI). The article's author cites… Click to show full abstract
To the Editor, A recent article proposes urethral support failure rather than urethral function failure as the principal cause of urodynamically proven stress urinary incontinence (SUI). The article's author cites many earlier papers on a “Urethral Hanging Theory (UHT).” Another earlier study by Gleadell and Zacharin on upper urethral support failure is supported, in particular, laxity of the pubourethral ligaments. A strong relation between mid‐urethral mobility and SUI was found, at one stage, to be a relevant. A separate review and a recent inconclusive debate favored urethral function (e.g., abnormally low closure pressure) failure as the predominant cause of SUI. As is well‐known, different aspects of prolapse, particularly anterior vaginal prolapse, can conceal SUI. The mid‐urethral sling (MUS or tension‐free vaginal tape) has revolutionized the management of SUI, though the mechanism of success has been widely debated. Successful sling operations are claimed to be associated with decreased urethral mobility as a prime factor in that success rather than improved urethral function. Is there a simple mechanism by which SUI occurs and/or is improved or cured, or indeed, fails to be cured? That mechanism, we believe, irrespective of bladder neck mobility, function or a myriad of other theories, is bladder neck closure (BNC). If the bladder neck is sufficiently closed, SUI will not be present; if the bladder neck is not sufficiently closed, it will be present. For a number of years, the first author has observed a significant degree of BNC as an end result of MUS surgery. A pilot study was performed with forty consecutive women with SUI who were consented for: (i) MUS (Advantage Fit©‐ Boston Scientific) under spinal block (to allow cough testing) and pre‐ and post‐ MUS insertion observations of the (ii) sign of SI and; (iii) BNC (by cystoscopy at standardized bladder volume of 300 ml). Stress incontinence grading (SIG) was scored (multiple maximal coughs): 0: cough, no SI; 1: cough, few drops SI; 2: cough, small leak; 3: cough, moderate leak; 4: cough, large leak; 5: no cough, large leak. BNC: was scored: 1: 0%–25%; 2: 25%–50%; 3: 50%–75%; 4: 75%–100% closure. This represents the degree of reduction of the bladder neck aperture from a full bladder neck circumference image before withdrawing the cystoscope by an approximated 5 mm. Multiple observers were involved in an aim to reduce the subjective nature of these new observations. Mean SIG pre‐MUS insertion was 3.6 (range: 2–5); mean SIG post‐MUS insertion was 0.5 (range: 0–3; p< 0.001). This indicates a mean reduction of the sign of SI from a moderate/large leak with coughing to a few drops (max) with coughing. Mean BNC pre‐MUS insertion was 1.9 (range: 1–3); mean BNC post‐MUS insertion was 3.9 (range: 3–4, p< 0.001). This indicates a mean improvement in BNC from 25% to 50% pre‐MUS insertion to 75%–100% post‐MUS insertion. All women with a BNC over 75% achieved satisfactory intraoperative continence (see Table 1 and Figure 1). Our preliminary conclusion is that BNC (over 75%) is associated with the intraoperative cure of stress incontinence by MUS insertion. At early (6 weeks) follow‐up, success rates
               
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