Etiology and Pathogenesis of Urinary Incontinence

Urinary incontinence (UI) is defined as the involuntary loss of urine that constitutes a social or hygienic problem and can be objectively demonstrated. The term UI commonly refers to four main types: stress urinary incontinence (SUI), urge urinary incontinence (UUI), mixed urinary incontinence (MUI), and overflow urinary incontinence. Among these, SUI is the most common, accounting for approximately 40%–50% of cases.

1. Stress Urinary Incontinence (SUI)

Stress urinary incontinence refers to the involuntary leakage of urine during activities that increase intra-abdominal pressure, such as coughing, sneezing, postural changes, or heavy physical exertion. It occurs when a sudden increase in intra-abdominal pressure is transmitted to the bladder, raising intravesical pressure above the resistance generated by the bladder neck and urethral sphincter, resulting in urine leakage. Common etiologies include intrinsic sphincter deficiency (ISD), laxity of pelvic floor muscles, fascia, and ligaments, and urethral hypermobility.

1.1 Intrinsic Sphincter Deficiency (ISD)

ISD may present with or without urethral hypermobility. The internal urethral sphincter is primarily composed of smooth muscle. The principal causes of ISD include:

① Neurological disorders: The sympathetic nerves originating from the thoracic and lumbar spinal cord are the main nerves innervating the internal sphincter. Congenital conditions, spinal cord tumors, peripheral neuropathy, and diseases causing systemic muscle atrophy in this neural region can all lead to ISD.
② Childbirth, urogenital surgery, and trauma may damage the internal sphincter and its sympathetic innervation, resulting in ISD.
③ Advanced age and estrogen deficiency can lead to a reduction in the number of urethral smooth muscle and striated muscle fibers, causing atrophy of the urethral mucosa and submucosal connective tissue, which results in ISD.
④ Other causes such as radiation therapy can also contribute to ISD.

1.2 Abnormalities of Pelvic Floor Support Structures

The pelvic floor muscles, connective tissue, and nerves form a balanced system that plays a vital role in maintaining pelvic floor function. UI occurs when these support structures are damaged or defective. The pelvic floor support system is divided into an active support system (composed of pelvic floor muscles), a passive support system (composed of fascial tissue), and a mixed support system (composed of bones and ligaments), which together maintain coordinated function in both resting and active states.

When the active support system (e.g., the levator ani muscle) contracts, the pelvic floor and organs move upward and forward. When the pubovaginalis muscle is activated, it pulls the vaginal wall and urethra upward, closing the urethra or counteracting the downward pressure exerted on the urethra by intra-abdominal forces.

Causes of pelvic floor support structure damage or deficiency include:

① Aging: Declining ovarian function and reduced estrogen levels lead to laxity of the periurethral sphincter and ligaments.
② Pregnancy: During pregnancy, the lumbar spine protrudes forward and the abdomen bulges forward and downward, pushing the uterus toward the vagina. Pelvic floor muscles are displaced downward or contract under pressure. Over time, sustained stress leads to increased muscle fiber fatigue and gradual decline in the contractile capacity of different muscle fiber types, eventually resulting in pelvic floor dysfunction. Multiparity, prolonged labor, difficult delivery, polyhydramnios, and macrosomia are all risk factors.
③ Childbirth and surgical procedures can damage pelvic muscles, sphincters, and ligamentous structures, leading to dysfunction. Injury to the pubourethral ligament is the most significant factor in SUI.
④ Other factors: Chronic obesity, heavy physical labor, chronic obstructive pulmonary disease, smoking, and constipation, if persistent, can also cause pelvic floor support dysfunction and lead to UI.

1.3 Urethral Hypermobility

The hammock theory proposes that the urethra is supported by the underlying fascia, which is connected to muscle fibers and connective tissue within the vaginal wall, maintaining urethral closure. These structures work together with the internal urethral sphincter to effectively close the urethra and prevent involuntary urine loss even when intravesical pressure increases. Obesity, chronic cough, constipation, childbirth, advanced age, and prolonged excessive physical load can damage the aponeurosis, fascia, or paravaginal tissue, thereby reducing the anatomical support for the bladder neck and urethra. This loss of support leads to urethral hypermobility, where the urethra — which should remain closed when intra-abdominal pressure increases — moves downward instead, causing intraurethral pressure to fall below intravesical pressure and resulting in urine leakage.

2. Urge Urinary Incontinence (UUI)

Urge urinary incontinence refers to urine leakage that follows a sudden and intense urge to void. Triggers such as pain, lower abdominal discomfort, or the sound of running water can provoke the sensation of needing to urinate in these patients. There are three main etiologies: detrusor overactivity, poor detrusor compliance, and bladder hypersensitivity.

Many patients with UUI exhibit spontaneous, uninhibited detrusor contractions during bladder filling, a condition known as detrusor overactivity. These contractions may correspond to the sensation of urgency. If the pressure generated by these contractions overcomes urethral sphincter resistance, UI results.

2.1 Detrusor Overactivity

Early pathophysiological research on detrusor overactivity focused on anatomical mechanisms — the so-called neurogenic hypothesis — which proposed loss of central or peripheral neural inhibition, increased afferent input from the lower urinary tract, and activation of excitatory pathways in the bladder reflex that override central inhibition. Since the early 21st century, much research has shifted to the detrusor muscle itself — the myogenic hypothesis — which emphasizes changes in detrusor muscle properties leading to hyperexcitability and enhanced intercellular excitation transmission, producing coordinated myogenic contractions. Myogenic and neurogenic mechanisms can coexist. These patients often have concomitant urinary or central nervous system conditions such as urethritis, tumors, stones, diverticula, cystitis, stroke, Parkinson's disease, or spinal cord injury.

2.2 Poor Detrusor Compliance

In patients who have undergone radiation therapy or have chronic infections or long-term indwelling catheterization, urgency or pain often results from bladder fibrosis, stiffening of the bladder wall, and reduced compliance, so that the bladder cannot accommodate progressively increasing urine volumes, leading to UI.

2.3 Bladder Hypersensitivity

The urothelium of the lower urinary tract not only provides a barrier function but is also a sensitive structure capable of perceiving temperature, mechanical forces, and chemical stimuli. Afferent bladder sensory signaling is considered a key factor in overactive bladder. Urethral or bladder hypersensitivity causes a strong urge to void even when the bladder contains a relatively small volume of urine, sometimes with a persistent sensation of needing to urinate. This sensation may or may not resolve after voiding. Conditions that can increase bladder sensitivity include urethritis, acute and chronic cystitis, interstitial cystitis, and bladder stones or tumors.

3. Mixed Urinary Incontinence (MUI)

MUI refers to the simultaneous presence of both SUI and UUI symptoms, which tend to interact and exacerbate each other. It is a combined result of bladder and urethral dysfunction and accounts for approximately 42.1% of UI cases in women. MUI is one of the most common types of UI among newly diagnosed patients.

MUI is considerably more complex than either pure SUI or pure UUI. In most patients, successful treatment of the SUI component can significantly improve UUI symptoms. However, in some severe MUI patients, surgical intervention may cause bladder outlet obstruction, which paradoxically worsens postoperative UUI symptoms; these may resolve after a period of conservative management.

4. Overflow Urinary Incontinence

Overflow urinary incontinence occurs when the bladder becomes overdistended, intravesical pressure steadily rises and exceeds the maximum urethral pressure, resulting in involuntary leakage. It is associated with impaired bladder contractility and may present with incomplete voiding, excessive bladder distension, and urinary retention. Overflow incontinence results from decreased detrusor muscle elasticity, weakened contractility, lack of adequate sensitivity to filling, and impaired voiding.

Lower spinal cord injury, peripheral neuropathy of the bladder, multiple sclerosis, use of antipsychotic medications, and radical pelvic tumor surgery can all cause varying degrees of pathological damage to the bladder nerves. Local scar contracture following urethral or vaginal surgery, and urinary outlet obstruction caused by stones can all lead to voiding difficulty and urinary retention, subsequently causing overflow incontinence. Overflow incontinence is classified into acute and chronic types.

4.1 Acute Overflow Incontinence

This type often occurs after central nervous system injury or damage. Nervous system injury can cause paralysis of the micturition reflex or spasm of the external urethral sphincter, leading to acute urinary retention. Pelvic surgery (especially perineal or pubic surgery) and impaired micturition reflex after childbirth can also cause acute urinary retention. When the bladder is severely overdistended, intravesical pressure steadily rises, and blood circulation in the bladder wall becomes impaired, potentially causing degenerative changes in intramural nerves and neural receptors, as well as degeneration and rupture of detrusor muscle fibers. These changes are mostly reversible once the underlying cause is addressed.

4.2 Chronic Overflow Incontinence

Common conditions include:

① Urethral obstruction and bladder outlet obstruction: commonly seen in urethral stricture, external urethral meatus stenosis, urethral and bladder neck tumors, etc.
② Neurogenic bladder with urethral dysfunction: commonly seen in disruption of the reflex arc at the sacral detrusor nucleus, with decreased or absent detrusor reflex.
③ Bladder contracture: common causes include tuberculous bladder contracture, radiation cystitis, and interstitial cystitis. Inflammatory processes cause varying degrees of detrusor fibrosis. As the bladder contracts, detrusor muscle fiber contractility simultaneously weakens or disappears, and the bladder gradually transforms into a fibrous sac with almost no contractile function.

In summary, UI is a common condition in women, with multiple subtypes and complex etiology. The pathogenesis of some forms of UI remains unclear. Clinical management should be individualized based on the type, etiology, and pathogenesis of the UI.

Disclaimer

Some of the content in this article comes from online sources. If there is any infringement, please contact us for removal.

The medical information provided here is for reference only and should not be used as a basis for clinical diagnosis or treatment.