What is the role of intrinsic sphincter deficiency in the pathophysiology of urinary incontinence?

Updated: Jan 22, 2021
  • Author: Sandip P Vasavada, MD; Chief Editor: Edward David Kim, MD, FACS  more...
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Intrinsic sphincter deficiency is a condition in which the urethral sphincter is unable to coapt and generate enough resting urethral closing pressure to retain urine in the bladder. The anatomic support of the urethra may be normal.

Intrinsic sphincter deficiency is due to devascularization and/or denervation of the bladder neck and proximal urethra. The urethral sphincter may become weak after pelvic surgery (eg, failed bladder suspension surgery) because of nearby nerve damage or excessive scarring of the urethra and surrounding tissues. Additional causes of urethral dysfunction include pelvic radiation or neurologic injury, including myelomeningocele.

Women with severe intrinsic sphincter deficiency do not always have the usual urethral hypermobility during a Valsalva maneuver. Paradoxically, the urethra appears well supported. This results in so-called lead pipe urethra, where the urethra remains open at rest. Whenever intra-abdominal pressure exceeds proximal urethral pressure, involuntary urine loss ensues. Because the urethra cannot remain closed, the patient experiences almost continuous urinary incontinence.

Female urethral function is influenced by estrogen. The lack of estrogen at menopause leads to atrophy and replacement of submucosa (ie, vascular plexus) by fibrous tissue. When estrogen is administered to postmenopausal women with atrophic vaginitis, the mucosa regains its turgor, with simultaneous up-regulation of alpha-receptors and angiogenesis of vascular plexus. Lack of estrogen is a risk factor for developing intrinsic sphincter deficiency, but estrogen replacement may reverse its effects.

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