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

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.