Urethral function and failure: A review of current knowledge of urethral closure mechanisms, how they vary, and how they are affected by life events

Abstract

Introduction: A critical appraisal of the literature regarding female urethral function and dysfunction is needed in light of recent evidence showing the urethra's role in causing stress and urge urinary incontinence. Methods: An evidence assessment was conducted using selected articles from the literature that contained mechanistic data on factors affecting urethral function and failure.Results: Maximal urethral closure pressure (MUCP) is 40% lower in stress urinary incontinence (SUI) than normal controls. Evidence from five women shows relatively equal contributions to MUCP from striated/smooth muscle, vascular-plexus, connective tissue. MUCP varies twofold in individuals of similar age and declines 15% per decade even in nulliparous women. Age explains 57% of the variance in MUCP. This parallels with striated/smooth muscle loss and reduced nerve density. Factors influencing pressure variation minute-to-minute and decade-to-decade are poorly understood. Connective tissue changes have not been investigated. MUCP in de novo SUI persisting 9-months postpartum is 25% less than in age and parity-matched controls.Longitudinal studies do not show significant changes in urethral function after vaginal birth suggesting that changes in urethral support from birth may unmask pre-existing sphincter weakness and precipitate SUI. Mechanisms of interaction between support injury, pre-existing urethral weakness, and neuropathy are unclear. Conclusion:Urethral failure is the predominant cause of SUI and a contributing factor for UUI; potentially explaining why mixed symptoms predominate in epidemiological studies. Age-related striated muscle loss and differences between women of similar age are prominent features of poor urethral closure. Yet, connective tissue changes, vasculature function, and complex interactions among factors are poorly understood.

Stress urinary incontinence is caused predominantly by urethral support failure

“…Successful sling operations are known not to increase the MUCP but to decrease urethral mobility. The previously reported results [9,10] contradict these facts; nevertheless, the authors have concluded that urethral function failure (MUCP), not urethral support failure (mobility), is the predominant cause of SUI. A 1997 statement may explain this paradoxical reasoning.…”

“…In a recently published critical appraisal of the literature regarding female urethral function and failure [9], the authors have reviewed the ROSE study (2008), the "cough game" study (2009) and the TOMUS study (2010), among others.…”

“…The authors claim [9] that it is a hydraulic fact that urethral closure pressure must exceed the bladder pressure for continence to be maintained. However, this claim is false for the urethra, because the closed m.i.…”

“…According to DeLancey et al [9], "in the absence of interventions targeting low urethral closure pressure, surgical results from support operations are bound to remain imperfect" and "not addressing urethral failure" explains why success rates are only objectively 80% and subjectively 60%. These statements contradict the UHT, which states that most failed operations depend on sustained uncorrected suburethral support; a closed m.i.…”

Stress urinary incontinence: Bladder neck closure (BNC)—The real bottom line rather than urethral support or function failure

“…A strong relation between mid-urethral mobility and SUI 4 was found, at one stage, to be a relevant. A separate review 5 and a recent inconclusive debate 6 favored urethral function (e.g., abnormally low closure pressure) failure as the predominant cause of SUI. 5 As is well-known, different aspects of prolapse, particularly anterior vaginal prolapse, can conceal SUI.…”