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Surgical management of stress urinary incontinence in women: Preoperative evaluation for a primary procedure

J Eric Jelovsek, MD, MMEd, FACOG, FACS
Jhansi Reddy, MD
Section Editor
Linda Brubaker, MD, FACOG
Deputy Editor
Kristen Eckler, MD, FACOG


Stress urinary incontinence (SUI), the involuntary leakage of urine on effort or exertion, or on sneezing or coughing, affects 4 to 35 percent of women [1,2]. Conservative approaches to treatment of SUI include pelvic floor muscle training and incontinence pessaries. However, for women who fail or decline conservative therapy, there are a variety of surgical treatments. Preoperative evaluation of women with SUI helps to exclude other diagnoses and guide the choice of a surgical procedure.

The preoperative evaluation of women with SUI will be reviewed here. General principles of evaluation of women with urinary incontinence and conservative and surgical treatment of SUI, as well as evaluation of women with recurrent SUI after surgery, are discussed separately. (See "Evaluation of women with urinary incontinence" and "Treatment of urinary incontinence in women" and "Surgical management of stress urinary incontinence in women: Choosing a primary surgical procedure" and "Stress urinary incontinence in women: Persistent/recurrent symptoms after surgical treatment".)


Continence is achieved when the urethra maintains a pressure greater than bladder pressure (eg, during a detrusor muscle contraction or an increase in intraabdominal pressure). Loss of the urethra's ability to maintain the required pressure results from anatomic or neurologic defects.

The anatomic contribution to continence involves the anterior vaginal wall and overlying connective tissue, which provide the urethra with a stable base upon which to rest (hammock theory [3]). Upon an increase in bladder or intraabdominal pressure, the urethra is compressed onto this base, thereby closing the lumen and maintaining urethral pressure. When the support structures are weakened, the urethra loses its underlying support and becomes hypermobile. Thus, the normal mechanism of continence through urethral compression is compromised.

Etiologies of loss of urethral support include pregnancy/childbirth, aging, and repetitive stress on the pelvic floor (eg, repetitive heavy lifting, chronic cough, or obesity). Genetic factors may also contribute to a loss of pelvic support through deficient collagen structure.

The neurologic component of continence is mediated through both bladder and urethral innervation. The bladder storage and filling phase is controlled through a spinal sympathetic reflex that (1) stimulates beta adrenergic receptors within the bladder wall causing relaxation of the smooth muscle and (2) activates alpha adrenergic receptors in the urethra which contract the urethra and increase its pressure. The urethra is also innervated through efferent pathways from the pudendal nerve, which increases the tone of the pelvic diaphragm and striated urethral sphincter. Pregnancy, childbirth, and aging can result in pudendal neuropathy leading to urinary incontinence.

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Literature review current through: Nov 2017. | This topic last updated: Jun 13, 2016.
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