To begin, normal female urinary continence is achieved when the urethra maintains a greater pressure than the bladder during states of rest and activity. During bladder filling and during increases in abdominal pressure, the anterior vaginal wall and surrounding connective tissues and muscles, which comprise the female pelvic floor, compress the urethra. Urethral closure pressures are therefore elevated relative to the bladder pressures that are generated, and continence is maintained. Additionally, the urethral sphincter itself has an intrinsic closure mechanism that increases during exertion and further prevents urinary leakage.

Stress urinary incontinence occurs when these normal mechanisms of continence are compromised. Repetitive pelvic stress experienced throughout pregnancy or pelvic stress experienced during the course of prolonged labor, constipation, or chronic respiratory conditions can lead to significant weakening and disruption of the pelvic floor nerves and musculature. Urethral hypermobility often results in this setting when the pelvic floor musculature is unable to provide sufficient support and compress the urethra. The bladder neck and proximal urethra normally maintain a high retropubic position, and increases in intra-abdominal pressures are transmitted equally to the bladder and urethra [7]. However, when pelvic floor muscle laxity occurs, the bladder neck and urethra cannot maintain their normal anatomic position, and the bladder neck and urethra rotate posteriorly and descend caudally which can lead to reduced urethral closing pressures and urinary incontinence (Fig. 5.1). Intrinsic sphincteric deficiency (ISD ) is a second mechanism that leads to female stress urinary incontinence. ISD is a condition in which the bladder neck and/or proximal urethra remains partially open at rest. Urinary incontinence in this case develops despite normal pelvic floor musculature and despite minimal or no urethral descent during stress. ISD is often seen in patients due to atrophy of the sphincteric muscles from aging or in patients with persisting SUI following urethral sling surgery. All patients with SUI are believed to have some degree of ISD [5].

One of the problems clinicians often face when evaluating patients with SUI is identifying the primary etiology of incontinence. While it is clear that SUI can occur secondary to urethral hypermobilit y as well as ISD, the distinction of the two is not clinically relevant in most cases since treatment is generally the same. Patients with pure stress incontinence seen during an office stress test can be treated successfully with a urethral sling regardless of whether ISD or urethral hypermobility is the primary cause of their incontinence. However, patients with mixed urinary incontinence or patients with prior incontinence surgery and continued leakage should be evaluated more thoroughly. These patients may have urge-predominant symptoms due to detrusor overactivity or may have continued ISD despite prior sling placement with leakage . Urodynamics therefore can serve as a valuable diagnostic tool for these more complicated cases of SUI.

Urodynamics provides important information regarding the functionality of the bladder as well as the quality of the bladder outlet . The most important urodynamic studies for patients with SUI are leak point or urethral pressure profiles, opening detrusor pressures, as well as filling cystometry. These studies provide important information regarding the competence of the urethral sphincter and can shed light on the relative importance of contributory factors (i.e., detrusor instability, small bladder capacity, etc.) that may also exist along with SUI. These studies provide crucial information that can influence treatment options and help predict overall outcomes particularly in cases of urge-predominant mixed urinary incontinence, prior failed urethral slings, and pelvic organ prolapse.