Urinary incontinence is the involuntary loss of urine. Stress urinary incontinence (SUI) is characterized by leakage during activities that increase abdominal pressure, such as coughing or exercising. Intrinsic Sphincter Deficiency (ISD) is a severe form of SUI resulting from damage or weakness to the muscle structure responsible for urethral closure. ISD is defined by the failure of the urethral sphincter to generate sufficient resistance to hold urine, even when surrounding anatomical support is adequate. This profound structural problem often requires different and more advanced treatment strategies than milder forms of SUI.
The Mechanism of Intrinsic Sphincter Deficiency
Normal urinary continence depends on sufficient support from pelvic floor tissues and the intrinsic function of the urethral sphincter muscle. The urethral sphincter is a complex structure of muscle, submucosal tissue, and vascular cushions that act as a seal to keep the urethra closed. Intrinsic Sphincter Deficiency occurs when this muscular component is functionally compromised, meaning the sphincter cannot close tightly enough to prevent leakage.
ISD is distinct from urethral hypermobility, a form of SUI caused by poor structural support that allows the urethra to descend. In hypermobility, the sphincter muscle may be strong, but its position prevents correct function under pressure. With ISD, the failure is inherent to the muscle and surrounding tissue, creating a failing seal regardless of the urethra’s position.
The urethra’s ability to maintain a seal relies on the health of the striated sphincter muscle, its nerve supply, and surrounding soft tissue. When these elements are damaged, the urethra offers low resistance to pressure increases from the abdomen. This results in severe urine leakage with minimal physical strain because the final closing mechanism is weakened.
Key Factors That Increase Risk
Damage to the urethral sphincter can result from several factors, often involving mechanical trauma or neurological insult. A significant cause in men is radical prostatectomy, where surgery to remove the prostate can damage the external urethral sphincter and its surrounding nerves. In women, previous anti-incontinence surgeries, especially those involving the urethra, can lead to scarring or direct injury to the sphincter mechanism.
Severe pelvic trauma, such as that sustained in an accident, can also directly injure the urethral sphincter or the nerves supplying it. Neurological conditions affecting the lower spinal cord, such as diabetic neuropathy, can impair the sphincter’s innervation, leading to muscle weakness.
Age-related changes also contribute to risk, particularly in women, due to tissue degradation and loss of hormonal support. A decline in estrogen levels can negatively affect the urethral mucosa and submucosal cushions, which are components of the intrinsic closing mechanism.
Confirming the Diagnosis
Clinical history and physical examination alone are often insufficient to definitively diagnose ISD, making specialized testing necessary to confirm structural weakness. The gold standard for diagnosis involves Urodynamic Studies, which are functional tests that measure pressures within the bladder and urethra during filling and voiding. These studies help distinguish between ISD and other causes of SUI, such as urethral hypermobility.
A specific measurement within this testing is the Valsalva Leak Point Pressure (VLPP). This test measures the lowest pressure exerted on the abdomen—through a cough or Valsalva maneuver—that causes urine to leak from the urethra. A low VLPP indicates a weak sphincter that cannot withstand modest pressure increases.
ISD is commonly diagnosed when the VLPP is less than 60 cm of water (H2O). Another important urodynamic measurement is the Maximum Urethral Closure Pressure (MUCP). This measures the highest pressure the urethra can generate to resist the flow of urine. A MUCP reading below 20 cm H2O is highly suggestive of intrinsic sphincter failure.
Treatment Options Tailored for Deficiency
Treating ISD requires interventions that directly address the weakened sphincter muscle by providing a new closing mechanism or increasing urethral resistance. Unlike procedures for hypermobility, which focus on support and repositioning the urethra, ISD treatments must actively compress or bulk the urethral tissue. Surgical options are generally considered more effective than conservative treatments for severe ISD.
One common surgical approach involves using specific types of slings designed to provide higher tension or compression to the mid-urethra. Retropubic mid-urethral slings may be favored over transobturator slings in women with ISD, as they offer more effective compression to the sphincter mechanism.
For cases involving extreme or recurrent ISD, the Artificial Urinary Sphincter (AUS) is often considered the gold standard treatment, particularly in men. The AUS is a mechanical device implanted around the urethra that the patient manually controls to open for urination and keep closed for continence.
For less severe cases or for patients who prefer a minimally invasive option, urethral bulking agents can be injected into the tissue surrounding the urethra. These agents work by adding volume and stiffness to the urethral walls, narrowing the channel and improving the sealing effect. Bulking agents are often performed in an outpatient setting but may require repeat injections over time as the material can resorb or shift.
Conservative treatments, such as Pelvic Floor Muscle Training (PFMT), are generally recommended as a first-line approach for all forms of SUI. However, in patients with severe, confirmed ISD, PFMT often has limited success because the muscle structure is significantly damaged. Specialized devices like pessaries, which are inserted vaginally to provide targeted urethral compression, can be a non-surgical alternative for managing symptoms.