Published 2019/09/06
The urethral sphincter plays a significant role in releasing urine. Its function is inhibited when nerve and muscle damage occurs, leading to urinary retention or incontinence. The urethral sphincter is a series of muscles that surround the urethra and controls the release of urine from the urethra and bladder by relaxing to open or constricting to close.
When a person wants to urinate, the sphincter relaxes and the bladder pushes urine out of the urethra. When finished, the sphincter closes.
When the nerves and muscles to the bladder or urethra are damaged, the symptoms might be urinary leakage, urinary retention, or overflow incontinence.
Urethral sphincter damage is caused by trauma to the pelvic floor, bladder, and urethra. This can happen due to childbirth, surgery, radiation therapy, spinal cord injuries, etc. Some forms of damage are temporary, and some are permanent.
Intrinsic sphincter deficiency is a condition in which the urethral sphincter is unable to close enough to retain urine in the bladder. The anatomic support of the urethra may be normal.
Intrinsic sphincter deficiency (ISD) is due to reduced blood or nerve supply bladder neck and proximal urethra. The urethral sphincter may become weak after pelvic surgery (eg, failed bladder suspension surgery and hysterectomy) because of nearby nerve damage or excessive scarring of the urethra and surrounding tissues. Childbirth can cause damage to any of these structures. Additional causes of urethral dysfunction include pelvic radiation or neurologic injury.
Women with severe intrinsic sphincter deficiency do not always have the usual urethral excessive movement during the bearing-down process. The urethra remains open at rest. Whenever intra-abdominal pressure exceeds urethral pressure, involuntary urine loss ensues. Because the urethra cannot remain closed, the patient experiences almost continuous urinary loss.
Estrogen influences the function of the female urethra. The lack of estrogen at menopause leads to thinning of the vaginal and urethral tissue with reduced blood supply. Lack of estrogen is a risk factor for developing intrinsic sphincter deficiency, but estrogen replacement may reverse its effects.
Surgical options include attaching the neck of the bladder to the pubic bone or ligaments, needle suspensions, various types of suburethral slings and the artificial urinary sphincter, whereas nonsurgical options include urethral bulking agents. No standardized treatment for ISD exists and catheters to keep the bladder empty may be the best option.
In the case of a lack of urethral mobility, the artificial urinary sphincter (AUS) remains the gold standard. Adjustable continence therapy (ACT®) can be proposed as an alternative option.
Uromedica, Inc. (Plymouth, MN) developed Adjustable Continence Therapy. The device compresses the urethra to keep urine from leaking by inflating two silicone balloons on each side of the urethra near the bladder.
The efficacy and safety of muscle-derived cell therapy in ISD needs more studies.
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CompactCath® is designed at Stanford d.school. It is FDA-cleared in 2014, holds six patents, covered by CNN Money, won two grants (BioDesign Spectrum grant, LPCH Pediatric Innovation grant) and two iF product design awards (2016, 2017).