ABSTRACT
I. INTRODUCTION Stress urinary incontinence is the involuntary loss of urine related to increases in abdominal pressure. It has been suggested that urethral hypermobility and/or intrinsic sphincter deficiency (ISD) contribute to most forms of stress urinary incontinence. Urethral hypermobility results when the vaginal musculofascial attachments that support the bladder neck and urethra in a retropubic position lose integrity. On increases in abdominal pressure, this loss causes the proximal urethra and bladder neck to descend into the vagina. ISD, on the other hand, refers to a deficiency in the function of the urethral sphincter that is unrelated to urethral support [1]. This leads to poor coaptation of the urethral mucosa and incontinence with minimal stress activities. Intrinsic sphincteric weakness can result from neurologic deficit, or it may merely be a secondary effect of aging. ISD may also be related to previous attempts at surgical repair or exposure to pelvic radiation. DeLancey proposed a unifying theory known as the “hammock hypothesis” that suggests that a poor muscular backing to the posterior aspect of the urethra results in failure of effective urethral coaptation, excessive urethral mobility, and urinary leakage [2].
