Urinary Incontinence

Updated: May 26, 2023
Author: Sandip P Vasavada, MD; Chief Editor: Edward David Kim, MD, FACS 


Practice Essentials

Urinary incontinence is an underdiagnosed and underreported problem that increases with age, affecting 38-55% of women older than 60 years[1] and 50-84% of the elderly in long-term care facilities.[2]  At any age, urinary incontinence is more than twice as common in females than in males.[3]

Signs and symptoms

Types of urinary incontinence

  • Stress: Urine leakage associated with increased abdominal pressure from laughing, sneezing, coughing, climbing stairs, or other physical stressors on the abdominal cavity and, thus, the bladder[4, 5]

  • Urge: Involuntary leakage accompanied by or immediately preceded by urgency (often referred to as an overactive bladder)

  • Mixed: A combination of stress and urge incontinence, marked by involuntary leakage associated with urgency and also with exertion, effort, sneezing, or coughing

  • Functional: The inability to hold urine due to reasons other than neuro-urologic and lower urinary tract dysfunction (eg, delirium, psychiatric disorders, urinary infection, impaired mobility)

See Presentation for more detail.


Patients with urinary incontinence should undergo a basic evaluation that includes a history, physical examination, and urinalysis. In selected patients, the following may also be needed:

  • Voiding diary
  • Cotton swab test (optional)
  • Cough stress test
  • Measurement of postvoid residual (PVR) urine volume
  • Cystoscopy
  • Urodynamic studies (see the image below)
Urinary incontinence. Urodynamic study revealing d Urinary incontinence. Urodynamic study revealing detrusor instability in a 75-year-old man with urge incontinence. Note the presence of multiple uninhibited detrusor contractions (phasic contractions) that is generating 40- to 75-cm H2O pressure during the filling cystometrogram (CMG). He also has small bladder capacity (81 mL), which is indicative of poorly compliant bladder.

Videourodynamic studies are reserved to evaluate complex cases of stress urinary incontinence. Videourodynamic studies combine the radiographic findings of a voiding cystourethrogram and multichannel urodynamics.  Go to Urodynamic Studies for Urinary Incontinence for more information on this topic.

The following points regarding the clinical presentation should be sought when obtaining the history:

  • Severity and quantity of urine lost and frequency of incontinence episodes
  • Duration of the complaint and whether problems have been worsening
  • Triggering factors or events (eg, cough, sneeze, lifting, bending, feeling of urgency, sound of running water, sexual activity/orgasm)
  • Constant versus intermittent urine loss
  • Associated frequency, urgency, dysuria, pain with a full bladder
  • History of urinary tract infections (UTIs)
  • Concomitant fecal incontinence or pelvic organ prolapse
  • Coexistent complicating or exacerbating medical problems
  • Obstetrical history, including difficult deliveries, grand multiparity, forceps use, obstetrical lacerations, and large babies
  • History of pelvic surgery, especially prior incontinence procedures, hysterectomy, or pelvic floor reconstructive procedures
  • Other urologic procedures
  • Spinal and central nervous system surgery
  • Lifestyle issues, such as smoking, alcohol or caffeine abuse, and occupational and recreational factors causing severe or repetitive increases in intra-abdominal pressure
  • Medications

Relevant complicating or exacerbating medical problems may include the following:

  • Chronic cough
  • Chronic obstructive pulmonary disease (COPD)
  • Congestive heart failure
  • Diabetes mellitus
  • Obesity
  • Connective tissue disorders
  • Postmenopausal hypoestrogenism
  • CNS or spinal cord disorders
  • Chronic UTIs
  • Urinary tract stones
  • Benign prostatic hyperplasia
  • Cancer of pelvic organs

Medications that may be associated with urinary incontinence include the following:

  • Cholinergic or anticholinergic drugs
  • Alpha-blockers
  • Over-the-counter allergy medications
  • Estrogen replacement
  • Beta-mimetics
  • Sedatives
  • Muscle relaxants
  • Diuretics
  • Angiotensin-converting enzyme (ACE) inhibitors

See Workup for more detail.


Successful treatment of urinary incontinence must be tailored to the specific type of incontinence and its cause. The usual approaches are as follows:

  • Stress incontinence: Pelvic floor physiotherapy, anti-incontinence devices, and surgery
  • Urge incontinence: Changes in diet, behavioral modification, pelvic-floor exercises, medications, and/or therapies such as onabotulinum toxin injections and neuromodulation therapies.
  • Mixed incontinence: Pelvic floor physical therapy, anticholinergic drugs, and surgery
  • Overflow incontinence: Catheterization regimen or diversion
  • Functional incontinence: Treatment of the underlying cause

Absorbent products may be used temporarily until a definitive treatment has a chance to work, in patients awaiting surgery, or long-term under the following circumstances:

  • Persistent incontinence despite all appropriate treatments
  • Inability to participate in behavioral programs, due to illness or disability
  • Presence of an incontinence disorder that cannot be helped by medications
  • Presence of an incontinence disorder that cannot be corrected by surgery

In stress and urge urinary incontinence, the following medications may provide some benefit:

  • Anticholinergic agents
  • Antispasmodic drugs
  • Beta-adrenergic agonists
  • Tricyclic antidepressants
  • Estrogen
  • Botulinum toxin

Surgical care for stress incontinence involves procedures that increase urethral outlet resistance, including the following:

  • Bladder neck suspension
  • Periurethral bulking therapy
  • Midurethral slings
  • Artificial urinary sphincter

The transobturator male sling may be of particular benefit to men who experience stress incontinence after prostatectomy.[6] Transobturator vaginal tape (TVT-O) is widely used for stress incontinence in women[7] . Please realize this is not available, there are other commercial options.

Surgical care for urge incontinence involves procedures that improve bladder overactivity or bladder capacity, including the following:

  • Sacral nerve modulation
  • Tibial nerve stimulation
  • Injection of neurotoxins such as botulinum toxin
  • Bladder augmentation

See Treatment and Medication for more detail.

For patient education information, see Urinary Incontinence, Bladder Control Problems, and Understanding Bladder Control Medications, .


Urinary incontinence is defined by the International Continence Society as the involuntary loss of urine that represents a hygienic or social problem to the individual.[8] Urinary incontinence can be thought of as a symptom as reported by the patient, as a sign that is demonstrable on examination, and as a disorder.

Urinary incontinence should not be thought of as a disease, because no specific etiology exists; most individual cases are likely multifactorial in nature. The etiologies of urinary incontinence are diverse and, in many cases, incompletely understood.

Types of urinary incontinence

Four types of urinary incontinence are defined in the Clinical Practice Guideline issued by the Agency for Health Care Policy and Research: stress, urge, mixed, and overflow. Some authors include functional incontinence as a fifth type of incontinence.[9, 10, 5]

Stress incontinence is characterized by urine leakage associated with increased abdominal pressure from laughing, sneezing, coughing, climbing stairs, or other physical stressors on the abdominal cavity and, thus, the bladder.[4, 5] Urge urinary incontinence is involuntary leakage accompanied by or immediately preceded by urgency. Mixed urinary incontinence is a combination of stress and urge incontinence; it is marked by involuntary leakage associated with urgency and also with exertion, effort, sneezing or coughing.

Functional incontinence is the inability to hold urine due to reasons other than neuro-urologic and lower urinary tract dysfunction.

Other terms describing urinary incontinence are as follows:

  • Enuresis - Involuntary loss of urine
  • Nocturnal enuresis - Loss of urine occurring during sleep
  • Continuous urinary incontinence - Continuous leakage

Successful treatment of urinary incontinence must be tailored to the specific type of incontinence and its cause (see Treatment). The usual approaches are as follows:

  • Stress incontinence - Pelvic floor physiotherapy, anti-incontinence devices, and surgery
  • Urge incontinence - Changes in diet, behavioral modification, pelvic-floor exercises, and/or medications and new forms of procedural intervention
  • Mixed incontinence - Pelvic floor physical therapy, anticholinergic or beta-3 agonists drugs, and surgery
  • Overflow incontinence - Catheterization regimen or diversion
  • Functional incontinence - Treatment of the underlying cause

Historical context

Urinary incontinence in women is not a recent medical and social phenomenon, but the relative importance attributed to urinary incontinence as a medical problem is increasing. Several factors responsible for the increased attention to incontinence can be cited.

First, women are more willing to talk openly about this disorder. Women are realizing that, in most cases, urinary incontinence is a treatable condition. Consequently, less embarrassment and fewer social stigmas are associated with the diagnosis.

Second, as the population ages, incontinence becomes a more frequent concern. Urinary incontinence often is the chief reason for institutionalization of elderly people.

Third, interest in urinary incontinence disorders within the medical community is surging. This increased interest is arising among basic scientists, clinical researchers, and clinicians. The subspecialties of urogynecology and female urology are emerging, and structured fellowships are in the credentialing process. A Female Pelvic Medicine and Reconstructive Surgery fellowship is now accredited as a subspecialty by the American Board of Obstetrics and Gynecology (ABOG) and the American Board of Urology (ABU).

As a direct result of this increased interest, the public is becoming more aware of the problem and more active and educated about incontinence. Patient advocacy groups provide patients access to information, incontinence products, and physicians who have interest or special expertise in these disorders. In the last decade, funding opportunities for incontinence research have increased vastly. Subspecialty professional organizations and journals are now active.

Important contributions to the understanding of the structure and functioning of the lower urinary tract include an improved understanding of the anatomy and dynamic functioning of the pelvic floor and its contribution to continence. In addition, much study has been conducted to bolster the understanding of the neurophysiology of the bladder, urethra, and pelvic floor. Finally, interest in the diagnosis and treatment of incontinence is ongoing.

An estimated 50-70% of women with urinary incontinence fail to seek medical evaluation and treatment because of social stigma. Only 5% of individuals who are incontinent and 2% of nursing home residents who are incontinent receive appropriate medical evaluation and treatment. Patients who are incontinent often cope with this condition for 6-9 years before seeking medical therapy.

In a 1997 survey of primary care physicians, about 40% reported that they sometimes, rarely, or never ask patients about incontinence. More than 40% of internists and family practitioners routinely recommended absorbent pads to their patients as a solution to incontinence disorders.[11] Continued education of the public and medical professionals is needed to improve the care rendered to individuals with urinary incontinence.

In 1989, the National Institutes of Health Consensus Development Conference estimated the annual cost of urinary incontinence in the United States to be $12.4 billion. Some experts believe that this is a conservative estimate. True costs can be difficult to estimate because many individuals do not come to the attention of medical specialists.

A 2009 survey of women in a managed care population found that the prevalence of undiagnosed urinary incontinence was 53% in the preceding year.[12] Some individuals pay out of pocket for adult incontinence undergarments, absorbable pads, skin care products, deodorants, and increased laundry expenses.

The psychosocial costs and morbidities are even more difficult to quantify. Embarrassment and depression are common. The affected individual may experience a decrease in social interactions, excursions out of the home, and sexual activity.

The psychosocial impact on at-home caregivers, spouses, or family members rarely is considered. Kelleher et al developed a questionnaire to assess the quality of life of women with incontinence.[13] This questionnaire has proven to be easy to use, valid, and reliable. This tool may be a valuable adjunct to pretherapy and posttherapy assessment, as well as valuable in comparing the quality of life impact of different urodynamic diagnoses.

Several other questionnaires are available for urge incontinence, stress incontinence, and quality of life. Many have been validated in many languages, presurgery and postsurgery. The questionnaires most often used are the Urinary Distress Inventory (UDI)–6, Incontinence Quality of Life (IQoL) Questionnaire, Incontinence Impact Questionnaire (IIQ)–7, UDI, Overactive Bladder Symptom and Health-Related Questionnaire (OAB-Q), and King’s Health Questionnaire KHQ).[14]


For understanding urinary incontinence, the relevant anatomy of the lower urinary tract comprises the urethra and bladder. Go to Urinary Incontinence Relevant Anatomy for more information on this topic.


Micturition requires coordination of several physiological processes. Somatic and autonomic nerves carry bladder volume input to the spinal cord, and motor output innervating the detrusor, sphincter, and bladder musculature is adjusted accordingly. The cerebral cortex exerts a predominantly inhibitory influence, whereas the brainstem facilitates urination by coordinating urethral sphincter relaxation and detrusor muscle contraction.

As the bladder fills, sympathetic tone contributes to closure of the bladder neck and relaxation of the dome of the bladder and inhibits parasympathetic tone. At the same time, somatic innervation maintains tone in the pelvic floor musculature as well as the striated periurethral muscles.

When urination occurs, sympathetic and somatic tones in the bladder and periurethral muscles diminish, resulting in decreased urethral resistance. Cholinergic parasympathetic tone increases, resulting in bladder contraction. Urine flow results when bladder pressure exceeds urethral resistance. Normal bladder capacity is 300-500 mL, and the first urge to void generally occurs between bladder volumes of 150 and 300 mL.

Incontinence occurs when micturition physiology, functional toileting ability, or both have been disrupted.[10] The underlying pathology varies among the different types of incontinence (ie, stress, urge, mixed, reflex, overflow, and functional incontinence).

Stress incontinence pathophysiology

During episodes of stress incontinence, an increase in intra-abdominal pressure (eg, from laughing, sneezing, coughing, climbing stairs) raises pressure within the bladder to the point where it exceeds the urethra’s resistance to urinary flow.[4, 5] Leakage ceases when bladder pressure again falls below urethral pressure.

The major cause of stress incontinence is urethral hypermobility due to impaired support from pelvic floor. A less common cause is an intrinsic sphincter deficiency, usually secondary to pelvic surgeries. In either case, urethral sphincter function is impaired, resulting in urine loss at lower than usual abdominal pressures.

In women with stress urinary incontinence, either or both mechanisms may be present, although some authors hold that stress incontinence does not develop in patients with poor pelvic support unless intrinsic sphincter deficiency is also present. Intrinsic sphincter deficiency, resulting from loss of function of both the internal and the external sphincter mechanism, is the only cause of stress incontinence in males.

Urethral hypermobility

Urethral hypermobility is related to impaired neuromuscular functioning of the pelvic floor coupled with injury, both remote and ongoing, to the connective tissue supports of the urethra and bladder neck. When this occurs, the proximal urethra and the bladder neck descend to rotate away and out of the pelvis at times of increased intra-abdominal pressure.

Because the bladder neck and proximal urethra move out of the pelvis, more pressure is transmitted to the bladder. During this process, the posterior wall of the urethra shears off the anterior urethral wall to open the bladder neck when intrinsic sphincter deficiency is present.

In women without urethral hypermobility, the urethra is stabilized during stress by three interrelated mechanisms. One mechanism is reflex, or voluntary, closure of the pelvic floor. Contraction of the levator ani complex elevates the proximal urethra and bladder neck, tightens intact connective tissue supports, and elevates the perineal body, which may serve as a urethral backstop.

The second mechanism involves intact connective tissue support to the bladder neck and urethra. The pubocervicovesical or anterior endopelvic connective tissue in the area of the bladder neck is attached to the back of the pubic bone, the arcus tendineus fascia pelvis, and the perineal membrane. The pubourethral ligaments also suspend the middle portion of the urethra to the back of the pubic bone.

These connective-tissue components form the passive supports to the urethra and bladder neck. During times of increased intra-abdominal pressure, if these supports are intact, they augment the supportive effect of muscular closure of the pelvic floor.

The third mechanism involves 2 bundles of striated muscle, the urethrovaginal sphincter and the compressor urethrae, found at the distal aspect of the striated urethral sphincter. These muscles may aid in compressing the urethra shut during stress maneuvers. These muscles do not surround the urethra, as the striated sphincter does, but lie along the lateral and ventral aspects.

The exact function and importance of these muscles are controversial. Some authors suggest that the urethrovaginal sphincter and the compressor urethrae may provide compression and increased pressure in the distal urethra during times of stress.

Damage to the nerves, muscle, and connective tissue of the pelvic floor is important in the genesis of stress incontinence. Injury during childbirth probably is the most important mechanism. Aging, hypoestrogenism, chronic connective tissue strain due to primary loss of muscular support, activities or medical conditions resulting in long-term repetitive increases in intra-abdominal pressure, and other factors can contribute.

During childbirth, 3 types of lesions can occur: levator ani muscle tears, connective tissue breaks, and pudendal/pelvic nerve denervation. Any of these injuries can occur in isolation but 2 or more in combination are more likely to occur. The long-term result may be the loss of active and passive urethral support and loss of intrinsic urethral tone.

The loss of urethral and bladder neck support may impair urethral closure mechanisms during times of increased intra-abdominal pressure. This phenomenon can be viewed in several ways.

Some hypothesize that under normal circumstances, any increase in intra-abdominal pressure is transmitted equally to the bladder and proximal urethra. This is likely due to the retropubic location of the proximal and mid urethra within the sphere of intra-abdominal pressure. At rest, the urethra has a higher intrinsic pressure than the bladder. This pressure gradient relationship is preserved if acute increases in intra-abdominal pressure are transmitted equally to both organs.

When the urethra is hypermobile, pressure transmission to the walls of the urethra may be diminished as it descends and rotates under the pubic bone. Intraurethral pressure falls below bladder pressure, resulting in urine loss.

A related way of describing the mechanism of hypermobility-related stress incontinence is the hammock theory posited by DeLancey.[15] Normally, an acute increase in intra-abdominal pressure applies a downward force to the urethra. The urethra is then compressed shut against the firm support provided by the anterior vaginal wall and associated endopelvic connective tissue sheath. If the endopelvic connective tissue is detached from its normal lateral fixation points at the arcus tendineus fascia pelvis, optimal urethral compression does not take place.

A simple analogy is that of a garden hose (urethra) running over a pavement surface (anterior endopelvic connective tissue). A force is applied in a downward direction using the foot (increased intra-abdominal pressure). This force compresses the hose shut, occluding flow. If the same hose is run through a soft area of mud (damaged connective tissue), then the downward force does not occlude the hose but, rather, pushes the hose deeper into the mud.

An alternative theory of the mechanism of stress incontinence stems from research involving ultrasound visualization of the bladder neck and proximal urethra during stress maneuvers. This research found that 93% of patients with stress incontinence displayed funneling of the proximal urethra with straining, and half of those individuals also showed funneling at rest.[16] In addition, during stress maneuvers, the urethra did not rotate and descend as a single unit; rather, the posterior urethral wall moved farther than the anterior wall.

Although mobile, the anterior urethral wall has been observed to stop moving, as if tethered, while the posterior wall continued to rotate and descend. Possibly, the pubourethral ligaments arrest rotational movement of the anterior wall but not the posterior wall. The resulting separation of the anterior and posterior urethral walls might open the proximal urethral lumen, thus allowing or contributing to stress incontinence.

Intrinsic sphincter deficiency

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. (Although it should be noted estrogen therapy is controversial.)

Occult stress incontinence

Stress incontinence on prolapse reduction (previously termed latent stress incontinence) is a term used to describe stress incontinence observed only after reduction of pelvic prolapse. Some believe that kinking of the urethra caused by the prolapse itself provides for at least part of the continence mechanism. These patients may have a history of stress incontinence that improved and finally resolved as their prolapse worsened.

In diagnosing occult incontinence, the goal is to avoid new-onset incontinence following surgical correction of prolapse. This may be accomplished through the use of an incontinence procedure, such as a colposuspension or sling. The diagnosis can be made by stress testing with the prolapse reduced or by pessary placement and pad testing. No particular method of prolapse reduction has been proved superior.

In a study of continent women with severe pelvic organ prolapse, reduction of the prolapse with a pessary revealed occult incontinence in 58% of cases.[17] These patients were treated with a pubovaginal sling, anterior colporrhaphy, and other appropriate reparative operations. Eighty-six percent of the patients with potential incontinence so treated had no postoperative stress-related urine loss.

The group of patients with no demonstrable occult incontinence underwent anterior colporrhaphy and additional individualized procedures. Incontinence procedures, per se, were not performed in this group. No patients had postoperative stress incontinence. Mean follow-up was 40-50 months.

This study points out that bladder neck procedures need not be performed if potential incontinence has been ruled out, even if bladder neck hypermobility is present. Indeed, incontinence procedures are not without their own morbidities and should not be performed unless necessary.

Urge incontinence pathophysiology

Urge incontinence is involuntary urine loss associated with a feeling of urgency. The corresponding urodynamic term is detrusor overactivity, which is the observation of involuntary detrusor contractions during filling cystometry.[18, 19] These contractions may be voluntary or spontaneous and may or may not cause symptoms of urgency and/or urgency incontinence.

However, a study using a quality of life assessment of women with incontinence showed that women with urge incontinence from detrusor overactivity consistently had a worse quality of life than did women with other urodynamic diagnoses.

Urge incontinence may be a result of detrusor myopathy, neuropathy, or a combination of both. When the identifiable cause is unknown, it is termed idiopathic urge incontinence. When a definable causative neuropathic disorder exists, the coexisting urinary incontinence disorder is termed neurogenic detrusor overactivity. Symptoms of overactive bladder or urge incontinence in the absence of neurologic causes are known simply as detrusor overactivity.

The term overactive bladder describes a syndrome of urinary urgency, usually accompanied by frequency and nocturia, with or without urgency urinary incontinence, in the absence of urinary tract infection or other obvious pathology. Overactive bladder in adults is a disorder of unclear etiology and incompletely understood pathophysiology. For discussion of this topic, see the article Overactive Bladder.

Some researchers believe that detrusor overactivity represents the premature initiation of a normal micturition reflex. In vitro studies of bladder muscle strips from patients with detrusor overactivity have demonstrated an increase in response to electrical stimulation and an increased sensitivity to stimulation with acetylcholine.[20] These findings may indicate a higher sensitivity to efferent neurologic activity or a lower threshold of acetylcholine release needed to initiate a detrusor contraction.

A relative cholinergic denervation may explain some of these findings. This proposed mechanism is most plausible in cases of de novo detrusor overactivity, which follow hysterectomy or other pelvic surgery. The mechanism of denervation in idiopathic detrusor overactivity is less certain. Subtle obstruction and the effects of aging on smooth muscle and the autonomic nervous system are 2 possible contributors.

Another finding described in bladder muscle specimens from patients with detrusor overactivity is local loss of inhibitory medullary neurologic activity. Vasoactive intestinal peptide, a smooth muscle relaxant, is decreased markedly in the bladders of patients with detrusor overactivity. In addition, bladders of individuals with detrusor overactivity have been found deficient in smooth muscle–relaxing prostaglandins.

Mills and colleagues conducted a comparison study of bladder muscle strips from patients with severe idiopathic detrusor overactivity and from organ donors with no known urologic problems.[18] The following are some of the findings:

  • Patchy partial denervation of the detrusor with areas of normal innervation and areas of reduced innervation by fibers staining for acetylcholinesterase

  • A reduced force of contraction in response to electrical field stimulation: This finding is in contrast to a previous study showing an increased sensitivity to electrical field stimulation, but the authors believe that the muscle strips may have had increased sensitivity to direct electrical stimulation (non–nerve mediated).

  • Supersensitivity to potassium

  • Increased electrical coupling of cells via cell-to-cell junctions

  • Variability in the activity of muscle strips from the same bladder

The authors believe that the primary abnormality in detrusor overactivity is at the detrusor muscle level with an increased capacity for spontaneous myogenic contractile activity and spread of electrical activity from cell to cell, resulting in tetanic contractions. Epidemiological studies have shown an association between detrusor overactivity and irritable bowel syndrome.[21] Some authorities have proposed that a syndrome of smooth muscle dysfunction may underlie this association.

Another study demonstrated the presence of an increased ratio of abnormal-to-normal cell junctions in patients with bladder dysfunction. The increased ratio was demonstrated most markedly in patients with detrusor overactivity. To a lesser degree, these changes also were observed in patients with outlet obstruction combined with detrusor overactivity and with idiopathic sensory urgency alone.[22]

These authors concluded that idiopathic sensory urgency might represent a milder or less overt variant of detrusor overactivity. They suggested that, in the future, bladder biopsy with structural evaluation of cell junctions might become a useful clinical tool in the diagnostic evaluation of bladder dysfunction.[22]

One study proposed that urge incontinence, regardless of the triggering mechanism, may share a final common pathway of myogenic dysfunction of the detrusor.[23] Spread of contractile signals via cell-to-cell coupling was proposed as the likely mechanism.

Another possible explanation for detrusor overactivity in a subgroup of patients involves the triggering of the micturition reflex by leakage of urine into a funneled and partially incompetent proximal urethra. This theory is consistent with the findings of detrusor overactivity caused by coughing or changing position.

In males, early obstruction due to benign prostatic hyperplasia (BPH) may result in urge incontinence.[24] The pathophysiology of BPH is poorly understood. Relative obstruction develops because of mechanical factors, dynamic factors, and detrusor alterations.

Androgen-induced enlargement of nodules of glandular tissue comprises the mechanical portion of the disorder. The dynamic component is related to increased alpha tone in prostatic and urethral smooth muscle. Detrusor dysfunction may consist of impaired contractility, detrusor overactivity, or both. In severe cases of obstruction, retention and overflow incontinence may develop, and the upper urinary tract can become damaged.

The presence of inflammation in the bladder is believed to result in bladder muscle irritability and urge incontinence in some instances, as depicted in the image below. One study showed that approximately 8% of patients with bacterial urinary tract infections had nonneuropathic bladder instability. If bacterial infection and detrusor overactivity coexist, successful treatment of the infection results in resolution of the detrusor overactivity in about one half of the patients.

A cystoscopic view of the bladder mucosa reveals s A cystoscopic view of the bladder mucosa reveals shallow ulcerations and petechial hemorrhages, which are findings consistent with interstitial cystitis.

Nonbacterial inflammatory conditions of the bladder, including interstitial cystitis, have been associated with detrusor overactivity. Foreign bodies, including permanent sutures, bladder stones, and neoplasms, also have been linked to bladder irritability and instability.

Mixed incontinence pathophysiology

Mixed incontinence is urinary incontinence resulting from a combination of stress and urge incontinence.[10] Approximately 40-60% of females with incontinence have this combination. Although it is generally defined as detrusor overactivity and impaired urethral function, the actual pathophysiology of mixed urinary incontinence is still being investigated. While generally thought of as separate etiologies for incontinence, some indirect evidence may link these disorders in some instances. In order to effectively treat, it is important for clinicians to determine which subtype of incontinence is more dominant, if relevant.

In mixed incontinence, the bladder outlet is weak and the detrusor is overactive. A classic example of mixed incontinence is a patient with meningomyelocele and an incompetent bladder neck with a hyperreflexic detrusor; however, a combination of urethral hypermobility and detrusor instability is a more common scenario.

Mixed incontinence is a common finding in older patients with urinary incontinence disorders. Often, stress incontinence symptoms precede urge incontinence symptoms in these individuals. Urgency without actual urge-related urine loss also is a common complaint of patients with stress incontinence.

Some patients with stress incontinence have urine leakage into the proximal urethra that may, at first, trigger sensory urgency and/or bladder contractions, which initially are suppressible. Later, in a subgroup of these individuals, myopathic changes may occur in the bladder that make the spread of abnormally generated contractile signals more efficient and more difficult to suppress voluntarily.

Reflex incontinence pathophysiology

Reflex incontinence is due to neurologic impairment of the central nervous system. Common neurologic disorders associated with reflex incontinence include stroke, Parkinson disease, and brain tumors. Reflex incontinence also occurs in patients with spinal cord injuries and multiple sclerosis. Urge incontinence in patients with suprapontine or suprasacral spinal cord lesions, which was formerly known as detrusor hyperreflexia, is currently considered part of neurogenic detrusor overactivity.

Spinal cord injuries interrupt the sacral reflex arc from the suprasacral spinal cord, cerebral cortex, and higher centers. These pathways are crucial for voluntary and involuntary inhibition. In the initial phase of spinal cord injury, the bladder is areflexic and overflow incontinence results. Later, detrusor hyperreflexia usually is found upon urodynamic evaluation.

In multiple sclerosis (MS), demyelinating plaques in the frontal lobe or lateral columns can produce lower urinary tract disorders. Incontinence may be the presenting symptom of MS in about 5% of cases. Approximately 90% of individuals with MS experience urinary tract dysfunction during the course of the disease.

A summary of the published series of urodynamic findings in MS demonstrated that in patients with lower urinary tract dysfunction, the most common urodynamic diagnosis is detrusor hyperreflexia (62%). Detrusor-sphincter dyssynergia (25%) and detrusor hyporeflexia (20%) also are common. Obstructive findings are much more common in males. Of note, the urodynamic diagnosis may change over time as the disease progresses.[25]

Hemorrhage, infarction, or vascular compromise to certain areas of the brain can result in lower urinary tract dysfunction. The frontal lobe, internal capsule, brainstem, and cerebellum commonly are involved sites. Initially, urinary retention due to detrusor areflexia is observed. This may be followed by detrusor hyperreflexia.

Approximately 40-70% of patients with Parkinson disease have lower urinary tract dysfunction. Controversy exists as to whether specific neurologic problems in patients with Parkinson disease lead to bladder dysfunction or if bladder symptoms simply are related to aging. The extrapyramidal system is believed to have an inhibitory effect on the micturition center; theoretically, loss of dopaminergic activity in this area could result in loss of detrusor inhibition.

In patients with dementia, incontinence and urinary tract dysfunction may be due to specific involvement of the areas of the cerebral cortex involved in bladder control. Alternatively, incontinence may be related to global deterioration of memory, intellectual capacity, and behavior. Urodynamically, both detrusor hyperreflexia and areflexia have been found.

CNS neoplasms may result in incontinence. Tumors of the superior medial frontal lobe, spinal cord tumors above the conus medullaris, and cervical spondylosis can cause detrusor hyperreflexia.

Overflow incontinence pathophysiology

The major contributing factor to overflow incontinence is incomplete bladder emptying secondary to impaired detrusor contractility or bladder outlet obstruction.[10] Impaired detrusor contractility is typically neurogenic in nature; causes include diabetes mellitus, lumbosacral nerve disease from tumors, meningomyelocele, MS, prolapsed intravertebral disks, and high spinal cord injuries. Less common causes of overflow incontinence include AIDS, genital herpes affecting the perineal area, and neurosyphilis.

In most cases, both sensory and motor neuropathies are present. The maximal storage capacity of the bladder is reached, oftentimes without the individual realizing that this has occurred. Incontinence occurs off the top of a chronically over-filled bladder. Effective emptying is not possible because of an acontractile detrusor muscle.

Common causes of bladder outlet obstruction in men include benign prostatic hyperplasia (BPH), vesical neck contracture, and urethral strictures. In women, urethral obstruction after anti-incontinence surgery such as a sling or bladder neck suspension can result in iatrogenically induced overflow incontinence. Additionally, prolapse of the anterior vaginal wall can affect bladder emptying.

Functional incontinence

Functional incontinence is seen in patients with normal voiding systems but who have difficulty reaching the toilet because of physical or psychological impediments. In some cases, the cause is transient or reversible. In others, a permanent problem can be identified. The etiology of the incontinence may be iatrogenic, environmental, situational, or disease related. The following common mnemonic, DIAPPERS, is helpful in remembering the functional contributors to incontinence[26] :

  • D - Delirium
  • I - Infection, urinary
  • A - Atrophic urethritis or vaginitis
  • P - Pharmacologic agents
  • P - Psychiatric illness
  • E - Endocrine disorders
  • R - Reduced mobility or dexterity
  • S - Stool impaction

Integral theory

A unifying theory of the etiology of stress incontinence, urge incontinence, voiding dysfunction, and fecal incontinence in women has been proposed.[27] The basis of the theory is that these disorders are the result of overstretching of the vaginal connective tissue and supporting ligaments, which usually occurs during childbirth.

Laxity of the pubourethral ligaments (ie, anterior zone of damage), mid vagina (ie, middle zone), and uterosacral ligaments (ie, posterior zone) make the usual tridirectional support of the vagina ineffective. With the vagina no longer properly tethered to the pelvic girdle, the usual neuromuscular actions that occur during increases in intra-abdominal pressure or pelvic floor relaxation during voiding are not translated as effectively into urethral closure and opening, respectively.

Detrusor overactivity, according to this theory, occurs because of the premature firing of stretch receptors in the bladder base secondary to poor endopelvic connective tissue support to the filling bladder.

The integral theory is attractive from the standpoint of parsimony but is complex. The theory is best appreciated and understood with the help of illustrations and diagrams showing directional force vectors.

Continuous incontinence

This severe type of incontinence is characterized by constant or near constant leakage with no symptoms other than wetness. Generally, this represents a significant breech in the storage capabilities of the bladder or urethra. Urogenital fistulas are a classic example.

A nonfunctioning urethra can result in continuous leakage. Scarring and fibrosis from previous surgery, partial urethral resection for vulvar cancer, and urethral sphincter paralysis due to lower motor neuron disease can cause the urethra to fail.

Pelvic irradiation may not only cause urogenital fistula but in rare cases causes bladder noncompliance that results in continuous incontinence. Congenital malformations of the genitourinary tract, such as bladder exstrophy,[28] epispadias, and ectopic ureters, can result in total incontinence.

Pediatric urinary incontinence

Pediatric incontinence disorders are classified according to cause. Primary incontinence disorders generally are due to congenital structural disorders, including ectopic ureter, exstrophy, epispadias, and patent urachus. Secondary structural causes can result from obstruction from urethral valves, congenital urethral strictures, and large ectopic ureteroceles. In addition, trauma can result in secondary structural incontinence.

Neurogenic lesions make up the next category of pediatric incontinence disorders. These include spinal dysraphism, tethered spinal cord, and spinal cord tumors.

Nonstructural causes account for most cases of pediatric incontinence.[29] Infection and inflammation may be the source. Dysfunctional voiding habits can develop even at a young age. Some children may become so preoccupied with activities that voiding is delayed until capacity is reached and accidents result.

Some believe that certain children develop a pattern of not relaxing the pelvic floor while voiding. In some cases, this can be traced back to an infection or some other noxious stimuli. A vicious cycle of pelvic floor spasm, constipation, and urinary retention can develop.

So-called giggle incontinence has been thought to represent an underlying temporal lobe seizure. Other studies do not support this theory, however.

Vaginal voiding is a pseudoincontinence disorder, which may result from voiding with the legs held too tightly together. The impeded flow of urine may fill the vagina. The vagina empties when the child stands.

Nocturnal enuresis is the most common pediatric incontinence disorder. For discussion of this topic, see Enuresis.


Even in an individual patient, urinary incontinence may have multiple etiologies, with varying degrees of contribution to the overall disorder. Structural and functional disorders involving the bladder, urethra, ureters, and surrounding connective tissue can contribute. In addition, a disorder of the spinal cord or central nervous system (CNS) may be the major etiologic factor in some cases. Medical comorbidities also can be important. Finally, some cases of urinary incontinence may be pharmacologically induced.[30]

The most common cause of stress incontinence in women is urethral hypermobility secondary to poor anatomic pelvic support. Women may lose this pelvic support with postmenopausal estrogen loss, childbirth, surgery, or certain disease states that affect tissue strength. A less common cause of stress incontinence is intrinsic sphincter deficiency, which can result from the aging process, pelvic trauma, surgery (eg, hysterectomy,[31] urethropexy, pubovaginal sling), or neurologic dysfunction.

The most common cause of intrinsic sphincter deficiency in men is radical prostatectomy for prostate cancer or transurethral resection of the prostate for benign prostatic hyperplasia.[32] A less common cause of intrinsic sphincter deficiency is trauma to the bladder neck or prostate, resulting from pelvic fracture due to high-impact deceleration injuries.

Contributing factors with aging-related urinary incontinence include a weakening of connective tissue, genitourinary atrophy due to hypoestrogenism, increased incidence of contributing medical disorders, increased nocturnal diuresis, and impairments in mobility and cognitive functioning.[10, 33]  Vitamin D deficiency has been identified as a risk factor for urinary incontinence in older adults.[34]

Other factors that may increase the risk of developing incontinence include obesity, straining at stool as a child or young adult, heavy manual labor, chronic obstructive pulmonary disease, and smoking.[35, 36, 37] In many cases of incontinence that are due to detrusor overactivity, the problem is idiopathic in nature.

In a prospective cohort study of 5,391 young women from the Australian Longitudinal Study on Women's Health, depressive symptoms were associated with 37% higher odds of having urinary incontinence after adjustment for sociodemographic factors, body mass index, health behaviors, and reproductive factors. Having physician-diagnosed depression was associated with 42% higher odds.[38]

A review of women with type 1 diabetes mellitus who participated in the Diabetes Control and Complications Trial (DCCT) and its observational follow-up study, the Epidemiology of Diabetes Interventions and Complications (EDIC), found that incident urinary incontinence was associated with higher hemoglobin A1c levels, independent of other recognized risk factors. Thus, improved glycemic control might reduce the risk of urinary incontinence in such patients.[39]

Less frequent causes of urinary incontinence include complications of urologic procedures or pelvic radiation therapy. In the pediatric population, causes include enuresis and congenital abnormalities of the genitourinary system.

Transient causes

Transient urinary incontinence is often seen in both elderly and hospitalized patients. The mnemonic DIAPPERS is a good way to remember most of the reversible causes of incontinence, as follows[26] :

  • D - Delirium or acute confusion
  • I - Infection (symptomatic UTI)
  • A - Atrophic vaginitis or urethritis
  • P - Pharmaceutical agents
  • P - Psychological disorders (depression, behavioral disturbances)
  • E - Excess urine output (due to excess fluid intake, alcoholic or caffeinated beverages, diuretics, peripheral edema, congestive heart failure, or metabolic disorders such as hyperglycemia or hypercalcemia)
  • R - Restricted mobility (limits ability to reach a bathroom in time)
  • S - Stool impaction

In addition to urinary tract infection, conditions such as bladder cancer, bladder stones, and foreign bodies can irritate the bladder, resulting in involuntary bladder contractions and incontinence. Less common infectious causes of overflow incontinence include AIDS, genital herpes affecting the perineal area, and neurosyphilis. Stones or neoplasms may also result in incontinence due to obstruction.

Neurologic causes

Cortical lesions (eg, from strokes, tumors, aneurysms, or hemorrhages) can lead to inappropriate voiding secondary to depressed social awareness, decreased sensation, and/or inappropriate urethral sphincter relaxation.[26] Cerebrovascular disease doubles the risk for urinary incontinence in older women.

Spinal cord lesions can alter sympathetic and parasympathetic tone, resulting in urinary incontinence. Peripheral nerve disease such as diabetic peripheral neuropathy can cause urinary incontinence through a contractile dysfunction of the bladder.

Metastatic carcinoma can cause epidural spinal cord compression. Back pain is the initial symptom in most cases. Almost 20% of cases involve the lumbosacral spine. If the sacral cord is involved, urinary incontinence or retention can be expected. Urinary incontinence symptoms represent an unfavorable prognostic indicator in this patient population. Early diagnosis and treatment of spinal cord compression is extremely important. Paraplegia or quadriplegia can develop within hours or days after the first neurologic deficit appears.

S2-S5 nerve root injury (herniation) can cause bladder dysfunction. Cauda equina syndrome can develop in patients with a large centrally protruding disk. Symptoms include bilateral leg pain and weakness, saddle anesthesia, urinary retention or incontinence, and fecal retention or incontinence. It is important to recognize this syndrome early because there is a high risk for chronic neurologic deficits if treatment is delayed.

Hemi–cauda equina syndrome (from a herniated lumbar disk) can also manifest as urinary incontinence. It presents as unilateral leg pain, unilateral sensory deficit in the S1-S5 dermatomes, and urinary incontinence or urinary retention. These patients require urgent neurosurgical consultation for emergency surgery.

Multiple sclerosis should be considered in any patient without evidence of urinary tract infection who has episodic or rapid onset of urinary symptoms. Urinary incontinence may occur by itself or may be accompanied by other vague neurological symptoms.

Patients with a neurogenic disorder such as myelomeningocele may have an open bladder neck that results in severe intrinsic sphincter deficiency and urinary loss.

Pharmacologic causes

Many medications contribute to urinary incontinence, directly or indirectly. Medications must always be considered as the cause of new-onset urinary incontinence—especially in elderly persons, in whom polypharmacy is often encountered.[40, 26]

Medication may result in incontinence through the following mechanisms:

  • Drugs with anticholinergic properties or side effects (eg, antipsychotics, antidepressants) - Urinary retention and thus overflow incontinence

  • Alpha-adrenergic agonists - Urinary retention and thus overflow urinary incontinence

  • Alpha-antagonist - Urethral relaxation

  • Diuretics – Overwhelming of bladder capacity in elderly persons

  • Calcium channel blockers - Decreased smooth muscle contractility in the bladder, causing urinary retention with overflow incontinence

  • Sedative-hypnotics - Immobility secondary to sedation, leading to functional incontinence

  • Angiotensin-converting enzyme (ACE) inhibitors – Diuretic effect, as well as side effect of cough with relaxation of pelvic floor musculature, can exacerbate incontinence

  • Antiparkinson medications - Urinary urgency and constipation


The precise prevalence of urinary incontinence is difficult to estimate. Part of the difficulty has been in defining the degree, quantity, and frequency of urine loss necessary to qualify as pathologic, with varying definitions among studies. Consequently, the prevalence of urinary incontinence reported in the literature is varied.

In addition, urinary incontinence is underdiagnosed and underreported. An estimated 50-70% of women with urinary incontinence fail to seek medical evaluation and treatment because of social stigma. Only 5% of incontinent individuals in the community and 2% in nursing homes receive appropriate medical evaluation and treatment. People with incontinence often live with this condition for 6-9 years before seeking medical therapy.

In a Swedish study of 9197 nulliparous women aged 25-64 years, the rate of urinary incontinence increased from 9.7% in the youngest women with a body mass index < 25 kg/m2 to 48.4% among the oldest women with a body mass index ≥35 kg/m2.[41] In a Dutch study of 1257 adults, the prevalence of urinary incontinence was 49.0% in women versus 22.6% in men. In both men and women, the prevalence of urinary incontinence increased with aging.[42, 43]

Urinary incontinence has been estimated to affect 10-13 million people in the United States and 200 million people worldwide. The cost of treating urinary incontinence in United States alone is $16.3 billion, 75% of which is spent on treatment of women. Urinary incontinence can result in prolonged hospital admission, urinary tract infections, contact dermatitis, and falls. Urinary incontinence is a leading cause of admission to a nursing home when families find it too difficult to care for a relative with incontinence.

Sex- and age-related patterns

Age is the single largest risk factor for urinary incontinence, although at any age, urinary incontinence is more than 2 times more common in females than in males. Urinary incontinence affects up to 7% of children older than 5 years, 10-35% of adults, and 50-84% of the elderly persons in long-term care facilities.[2]

In a cross-sectional analysis of women who participated in the 2005-2006 National Health and Nutrition Examination Survey (NHANES), Nygaard et al demonstrated that the prevalence of urinary incontinence increased with age, but reported a lower overall prevalence than other researchers. The prevalence was 6.9% in women aged 20-39 years, 17.2% in those aged 40-59 years, 23.3% in those aged 60-79 years, and 31.7% in women older than 80 years.[44]

An age-related pattern also appears in the predominant type of urinary incontinence experienced. In general, studies have shown that stress urinary incontinence tends to be more common in women younger than 65 years, while urge urinary incontinence and mixed urinary incontinence is more common in women older than 65 years.

Stress incontinence affects 15-60% of women—both young and old individuals. More than 25% of nulliparous young college athletes experience stress incontinence when participating in sports.

Race-related factors

Although data concerning urinary incontinence in people of different races are sparse, reports are emerging that race may play an important role in the prevalence and likelihood of reporting of incontinence. In addition, differences in anatomic morphology of the urinary sphincter mechanism in people of different races may affect the likelihood of developing incontinence.

Fultz et al found that 23.02% of white women reported incontinence, compared with 16.17% of black women.[45] In a study by Anger et al, based on the 1999-2000 NHANES data, the prevalence of urinary incontinence was higher in non-Hispanic white women (41%) than in non-Hispanic black (20%) or Mexican American women (36%).[46] In contrast, Freeman et al found that black women were significantly more likely than white women to report menopausal symptoms (46% vs 30%), urinary incontinence, and vaginal dryness.[47]

Howard et al described functional and morphologic differences in the urethral sphincteric and support system of nulliparous black and white women. Black women demonstrated a 29% higher average urethral closure pressure during a maximum pelvic muscle contraction. Paradoxically, a 36% greater bladder neck hypermobility was present as measured with the cotton-swab test (black women at 49° vs white women at 36°).[42]

Sears et al reported that, among patients with incontinence, urge incontinence was more common in black women (51.5%), whereas stress incontinence was statistically significantly more common in white women (66.2%).[48] Daneshgari et al found that Hispanic women reported stress incontinence and mixed incontinence more often than did non-Hispanic white women. However, the increased prevalence of incontinence in Hispanic women is likely due to higher prevalences of obesity, hysterectomy, and parity than in white women.[49]

Nygaard et al examined the prevalence of symptomatic pelvic floor disorders in women in the United States and found no difference among non-Hispanic whites (16%), Hispanics (15.9%), non-Hispanic blacks (13.8%), and other races (15%).[44] These authors did not differentiate urge from stress incontinence.


The prognosis of a patient with incontinence is excellent with current health care. With improvement in information technology, well-trained medical staff, and advances in modern medical knowledge, patients with incontinence should not experience the morbidity and mortality of the past. Although the ultimate well-being of a patient with urinary incontinence depends on the precipitating condition, urinary incontinence itself is easily treated and prevented by properly trained health care personnel.

In stress incontinence, the improvement rate with alpha-agonists is 19-74%; improvement rates with muscle exercise and surgery, improvement rates are 87% and 88%, respectively.[50] In urge incontinence, the improvement rate is higher with bladder training (75%) than with the use of anticholinergics (44%). Surgical options for urge incontinence are limited and have a high morbidity.

In mixed incontinence, bladder training and pelvic exercises result in higher improvement rate than the use of anticholinergic medications. In overflow incontinence, medications and surgery are very effective in improving symptoms.

Without effective treatment, urinary incontinence can have an unfavorable outcome. Prolonged contact of urine with the unprotected skin causes contact dermatitis and skin breakdown. If left untreated, these skin disorders may lead to pressure sores and ulcers, possibly resulting in secondary infections.

The medical morbidity includes includes the following:

  • Perineal candidal infections
  • Cellulitis
  • Pressure sores
  • Constant skin irritation and moisture
  • Falls and subsequent fractures from slipping on urine
  • Sleep deprivation from nocturia

Psychological morbidity includes the following:

  • Poor self-esteem
  • Social withdrawal
  • Depression
  • Sexual dysfunction from embarrassment
  • Curtailed social and recreational activities

For individuals with a decompensated bladder that does not empty well, the postvoid residual urine can lead to overgrowth of bacteria and subsequent urinary tract infection (UTI). Untreated UTIs may lead to urosepsis and death.

Patients whose urinary incontinence is treated with catheterization also face risks. Both indwelling catheters and intermittent catheterization have a range of potential complications (see Treatment).

Urinary incontinence is a leading cause of admission to a nursing home when families find it too difficult to care for a relative with incontinence.

A study by Foley et al looked at the connection between urinary symptoms, poor quality of life, and physical limitations and falls among elderly individuals. These authors found that urinary incontinence and falling had an impact on quality of life and were, in fact, associated with physical limitations.[51]

Patient Education




A thorough history is essential to the evaluation of urinary incontinence. The clinical presentation of urinary incontinence, based on severity, frequency, and amount of debilitation varies from patient to patient.

Patients may be reluctant to initiate discussions about incontinence; therefore, all patients, especially those older than 65 years, should be asked focused questions about voiding problems. In wording these questions, it is best to avoid nonspecific terms such as urge or nocturia, as they may have different meanings for different patients.

The Women's Preventive Services Initiative (WPSI), a national coalition of women's health professional organizations and patient representatives, recommends screening women for urinary incontinence annually. Screening ideally should assess whether women experience urinary incontinence and whether it affects their activities and quality of life. The WPSI recommends referring women for further evaluation and treatment if indicated.[52]

The clinical presentation of urinary incontinence can be varied in many respects. Patient complaints may be minor and situational or severe, constant, and debilitating. When obtaining a clinical history, determining whether the problem is a social and/or hygienic problem and the degree of disability attributable to the incontinence also is important. In addition, the following points regarding the clinical presentation should be sought when obtaining the history:

  • Severity and quantity of urine lost and frequency of incontinence episodes

  • Duration of the complaint and whether problems have been worsening

  • Triggering factors or events (eg, cough, sneeze, lifting, bending, feeling of urgency, sound of running water, sexual activity/orgasm)

  • Constant versus intermittent urine loss and provocation by minimal increases in intra-abdominal pressure, such as movement, changes in position, and incontinence with an empty bladder

  • Associated frequency, urgency, dysuria, pain with a full bladder, and history of urinary tract infections (UTIs)

  • Concomitant symptoms of fecal incontinence or pelvic organ prolapse

  • Coexistent complicating or exacerbating medical problems

  • Obstetrical history, including difficult deliveries, grand multiparity, forceps use, obstetrical lacerations, and large babies

  • History of pelvic surgery, especially prior incontinence procedures, hysterectomy, or pelvic floor reconstructive procedures

  • Other urologic procedures

  • Spinal and CNS surgery

  • Lifestyle issues, such as smoking, alcohol or caffeine abuse, and occupational and recreational factors causing severe or repetitive increases in intra-abdominal pressure

  • Medications

Patients with coexisting pelvic organ prolapse may report dyspareunia, vaginal pain upon ambulation, and a bulging sensation in the vagina. Patients with severe pelvic organ prolapse may experience herniation of pelvic organs out of the vaginal introitus, necessitating manual reduction of the uterine cervix or vaginal splinting during bowel movements.

Patients with symptomatic rectoceles report severe constipation, often necessitating digital disimpaction. Severe cystoceles may drag both ureters through the true pelvis as the bladder herniates out of the vagina, causing renal azotemia. Bilateral hydroureteronephrosis is due to compression of the ureters against the bony pelvic inlet, resulting in ureteral obstruction.

Relevant complicating or exacerbating medical problems may include the following:

  • Chronic cough
  • Chronic obstructive pulmonary disease (COPD)
  • Congestive heart failure
  • Diabetes mellitus
  • Obesity [35]
  • Connective tissue disorders
  • Postmenopausal hypoestrogenism
  • CNS or spinal cord disorders
  • Chronic UTIs
  • Urinary tract stones
  • Cancer of pelvic organs

Medications that may be associated with urinary incontinence include the following:

  • Cholinergic or anticholinergic drugs
  • Alpha-blockers
  • Over-the-counter allergy medications
  • Estrogen replacement
  • Beta-mimetics
  • Sedatives
  • Muscle relaxants
  • Diuretics
  • Angiotensin-converting enzyme (ACE) inhibitors

Incontinence histories can be very complex and time consuming. Most centers use some form of incontinence questionnaire as an aid. Sending the questionnaire to patients in advance so that they can give appropriate time and thought to their answers may be helpful. Part of the questionnaire should deal with the patient's quality of life, sexual and lifestyle issues, and the relationship of these factors to the incontinence disorder.

Voiding diary

The patient also should be instructed to fill out a voiding diary and to write down any questions. A voiding diary is a daily record of the patient's bladder activity and is a useful supplement to the medical history of the patient.

Voiding diaries should record the volume and type of fluid intake and the frequency and volume of voids. Episodes of nocturia should be noted. Finally, episodes of incontinence should be recorded, including an estimate of the volume; associated activities such as coughing, straining, and dishwashing; and associated symptoms such as urgency.

Voiding diaries are helpful as a pretherapy diagnostic tool, but they have also been used to measure posttherapy outcomes. Estimates of voiding frequency and amounts obtained by history alone can be unreliable.

Voiding diaries are reproducible in the setting of stress incontinence. One study found that in patients with stress incontinence, a representative and reproducible measure of incontinence episodes and mean daily voids can be obtained with a 3-day diary.[53] A 1-day diary is probably too short. Fewer data exist regarding the reliability of voiding diaries in patients with urge incontinence; further research is needed.

Pace of onset

Many cases of urinary incontinence present as a gradually progressive disorder. Progression from very mild symptoms to more severe and debilitating urine loss may take many years. The patient may come to medical attention only after experiencing a progressive worsening of symptoms.

In other patients, symptoms may appear suddenly and may or may not be associated with a specific inciting event, such as pelvic/urinary tract surgery, trauma, and genitourinary tract infection. In these instances especially, associated symptoms such as pelvic pain, urgency, frequency, dysuria, and hematuria may point to a specific etiology.


Classification of urinary incontinence into types allows the clinician to make an educated guess at a particular anatomic abnormality that warrants further investigation. The major types of urinary incontinence are as follows:

  • Stress incontinence
  • Urge incontinence
  • Mixed incontinence
  • Overflow incontinence

Stress incontinence

Episodes of stress incontinence occur during periods of increased intra-abdominal pressure. Triggers of stress incontinence are predictable: typically, patients report involuntary urine loss during coughing, laughing, and sneezing. Incontinence worsens during high-impact sports activities such as golf, tennis, or aerobics. Leakage is more common while standing than while lying down (eg, at night).

Little urine is lost, unless the condition is severe. Typically, affected patients use thin to medium-thickness pads. The number of pads used ranges from 1-3 per day.

Irritative voiding symptoms, such as urinary frequency, urgency, and nocturia, are typically absent. The presence of irritative voiding symptoms should raise an index of suspicion for overactive bladder. Irritative voiding symptoms in combination with hematuria (gross or microscopic) warrant a complete bladder tumor workup.

Stress urinary incontinence due to severe intrinsic sphincter deficiency produces much more severe symptoms than cases due principally to urethral hypermobility. Involuntary urine loss occurs not only with coughing, laughing, and sneezing but also with standing up from a sitting position. Patients describe continuous dribbling of urine and typically require a high volume of pad use.

This degree of urine loss is similar that seen with vesicovaginal or ureterovaginal fistula. These patients complain of being wet all the time and use large amounts of thick pads to stay dry. If suspecting a fistula, be sure to ask about previous surgical history, including a hysterectomy. Although uncommon, consider ectopic ureter/ureterocele in the differential diagnoses.

Urge incontinence

Urge incontinence or symptoms of an overactive bladder are uncontrolled urine loss associated with a strong desire to void, which is often a very sudden and rapid event that occurs without any warning. Urge incontinence is a type of uncontrolled urine loss that cannot be prevented. In this situation, the entire contents of the bladder are lost rather than a few drops of urine.

Patients with symptoms of an overactive bladder are aware of the intense need to void but are unable to hold back urine. Symptoms also include urinary frequency and nocturia.

Examples of situations that may precipitate urge incontinence include turning a key in the door, washing dishes, or hearing running water. Urge incontinence may also be triggered by drinking too much water or drinking coffee, tea, or alcohol.

Mixed incontinence

Patients with mixed incontinence exhibit symptoms of both stress incontinence and urge incontinence. Affected patients experience mild-to-moderate urine loss with physical activities (stress incontinence). At other times, they experience acute urine loss without any antecedent warning (urge incontinence). Urinary frequency, urgency, and nocturia complement urge incontinence symptom complex.

Most of the time, patients are not able to distinguish these 2 different symptom complexes. The symptoms of urge incontinence may unwittingly be confused with the symptoms of stress incontinence and vice versa. In this situation, the symptom complex most unbearable to the patient is treated first.

Overflow incontinence

Overflow incontinence occurs when the bladder is overdistended and reaches its limit of compliance. At this point, the intravesical pressure exceeds the resting urethral closure pressure and urine overflows despite the absence of detrusor contraction. Patients experience a sense of incomplete emptying, slow-flowing urine, and urinary dribbling.

Symptoms of overflow incontinence may mimic those of mixed incontinence. Patients lose a small amount of urine when intra-abdominal pressure is increased. Patients who are affected often experience symptoms of frequency and urgency as the detrusor attempts to expel urine.

The history in these patients may suggest a cause of bladder outlet obstruction, such as benign prostatic hyperplasia, anti-incontinence surgery (eg, a pubovaginal sling operation), or use of anticholinergic or antispasmodic drugs. Alternatively, the history may identify a possible neurologic cause of a nonfunctioning detrusor, such as diabetic neuropathy.

Physical Examination

A focused physical examination should be performed. The examination is tailored somewhat in each case, based on the specifics of the patient's incontinence complaint and pertinent medical and surgical history. Each patient should have height, weight, blood pressure, and pulse recorded. Obesity is an important contributor to stress incontinence, and the presence of obesity may influence management decisions.

The patient should provide a urine sample for urinalysis and culture. Some practitioners have the patient arrive with a full bladder, measure the volume voided, and then catheterize the patient to obtain a postvoid residual measurement. Others incorporate this step into the urodynamics portion of the evaluation if that is to be performed.

Medical illnesses and comorbidities that may be contributing to the overall incontinence disorder should be sought. Cardiac and pulmonary evaluation can be important. The abdomen should be examined for surgical scars, hernias, masses, organomegaly, and distended bladder after voiding. The presence of hernias may indicate inherent connective tissue weakness, a possible contributor to incontinence. Masses may contribute to stress incontinence and, occasionally, may cause obstructed voiding with resultant overflow incontinence.

The back should be inspected for deformity, dimpling, or hair tuft and the flank and costovertebral angles should be palpated. Tenderness, deformity, or the presence of surgical scars should prompt further investigation.

Neurologic examination

Because neurologic disorders can cause or exacerbate urinary incontinence, a focused neurologic examination should be a part of every incontinence evaluation.

Much information can be gained from simple conversation with the patient (eg, mental status) and observation of gait (eg, CNS, spinal cord, peripheral nervous system disease). Any abnormalities should prompt more in-depth investigations. Strength, sensation, and deep tendon reflexes of the lower extremities should be tested.

Sensation of the perineum and perianal area should be tested with a soft touch and light prick. Using a cotton swab, the anal wink pelvic floor reflex can be elicited by stroking laterally to the anal canal. The bulbocavernosus reflex can be elicited by gently tapping the clitoris with a cotton swab in the female patient.

The presence of these perineal reflexes ensures that a significant pudendal neuropathy does not exist. The absence of these reflexes does not diagnose neuropathy but merely raises suspicion. These reflexes may be extinguished if the patient is anxious during the examination.

Pelvic floor examination

The pelvic floor examination is an integral part of the incontinence evaluation. In female patients, in particular, incontinence disorders often coexist with pelvic floor relaxation. If a surgical approach to the incontinence is chosen, other pelvic floor defects of significance can be treated simultaneously.

The examination begins with inspection of the external genitalia and urethral meatus. Evidence of atrophy, such as pallor and thinness of tissue, may indicate estrogen deficiency. A red, fleshy lesion of the posterior urethra, a caruncle, may be another indicator of urogenital hypoestrogenism. The suburethral area should be inspected and palpated. A suburethral mass should raise suspicion for a urethral diverticulum.

Other signs of a diverticulum might include tenderness and purulent or watery discharge upon compression. Urethral and trigonal tenderness also may indicate urethritis, urethral syndrome, or interstitial cystitis. The vaginal mucosa should be inspected for pallor, thinning, loss of rugae, and other signs of hypoestrogenism. If clinically suspected, a fistula opening may be discovered during vaginal examination. At times, pooling of fluid, exudate, or granulation tissue may indicate a nearby fistula tract.

A detailed pelvic floor examination should be performed for signs of pelvic organ prolapse. A systematic examination is conducted for cystocele, rectocele, uterine or vaginal prolapse, enterocele, and perineal laxity. A bivalve speculum should be used to visualize the cervix or vaginal apex. With the patient straining maximally, the speculum is withdrawn slowly, and any descent of the cervix or vaginal cuff is noted.

The speculum is then disarticulated, and a single blade examination is performed, inspecting the anterior vaginal wall during straining with the posterior wall retracted. If a cystocele is observed, then a ring forceps or similar instrument is inserted over the speculum blade and opened to support the lateral vagina. The tips of the ring forceps should be against the bilateral ischial spines. If the cystocele is present with the patient straining and the lateral vagina supported, then a midline defect exists either in isolation or with a paravaginal defect.

Another clue to a midline defect is the loss of rugae with straining. If the cystocele is no longer present with lateral support, then a pure paravaginal defect is present.

Another clue to paravaginal defects is collapsing side walls during bivalve speculum examination. If anterior wall prolapse is present with lateral support, then the next maneuver is to use the closed ring forceps to provide midline anterior vaginal support while the patient is straining again. If some cystocele is still noted, then a combined central and paravaginal cystocele is present. If no bulge is noted, then the defect is purely central.

Next, attention is turned to the posterior vaginal wall. The half speculum is used to retract the anterior wall of the vagina, while the posterior wall is examined during Valsalva maneuver. The presence or absence of a rectocele should be noted. If a double bump is observed when the patient strains, an enterocele may be present in addition to the rectocele.

Next, the perineal body is inspected. The height and thickness of the tissue is noted. A badly compromised perineal body may be short and consist of mostly skin with little or no underlying muscle. The levator muscles are palpated, and the resting tone is noted. Then, the patient is instructed to squeeze the examining fingers, and the levator strength can be appreciated. A rectovaginal examination is performed to determine the thickness of the rectovaginal septum.

The patient then is asked to strain. Tissue felt sliding through the examining fingers may indicate an enterocele. Resting and squeezing rectal sphincter tone is noted. As the rectal finger is withdrawn, the external anal sphincter should be palpated between this finger and the thumb. The absence or attenuation of this body of muscle indicates a sphincter laceration.

If any doubt remains about pelvic organ prolapse, examine the patient in the standing position. Instruct the patient to stand with legs apart and one foot resting on a step stool. When the patient performs the Valsalva maneuver, the force of gravity helps the pelvic organs (eg, uterus, bladder) slide down the vagina and helps enhance diagnostic capability.

In the male patient, levator ani muscle tone and strength can be tested during a rectal examination. The prostate should be palpated for tenderness, enlargement, and nodularity.

Cotton Swab Test

The cotton swab test is used to assess urethral mobility in women. To perform the test, place the patient in a dorsal lithotomy position. Make sure the examining table is parallel to the floor. Insert a lubricated sterile cotton swab through the urethra until the cotton portion is completely in the bladder. Then, gently pull back on the cotton swab until the cotton is snug against the bladder neck. The swab is pulled back until increased resistance is met, indicating that the cotton tip is entering the urethra.

Women with normal pelvic anatomy should have a resting cotton-swab angle of 0° with respect to the floor. The patient then is instructed to perform a Valsalva maneuver or to contract the abdominal muscles. Having the patient put forth a maximal effort is important. The examiner should not use a posterior vaginal retractor. Part the labia if the tissue is touching the wooden shaft of the swab because this may impair movement during straining.

The change in angle when the swab is deflected upward with maximal strain, indicated by the arc of the wooden end of the swab, is measured with a goniometer or estimated visually. A change of greater than 30° indicates urethral hypermobility. (See the images below.)

A positive finding does not confer a specific diagnosis, and older women have a high false-negative rate.[54] However, hypermobility is present in most cases of stress incontinence. If hypermobility is not present and stress incontinence is diagnosed, intrinsic sphincter deficiency should be suspected.

A cotton swab angle greater than 30° denotes ureth A cotton swab angle greater than 30° denotes urethral hypermobility. Figure 1 shows that the cotton swab at rest is zero with respect to the floor. Figure 2 shows that the cotton swab at stress is 45° with respect to the floor.

A study that used receiver-operating characteristic analysis of the swab test found that the optimal cut-off point for the change in angle from resting to straining was 30° or more, which had a sensitivity of 82% and a specificity of 54%. The very best discriminator was an absolute straining angle of 40° or more, which had a sensitivity of 83% and specificity of 64%.[55] No resting angle value had sufficient discriminatory power to be useful.

The authors cautioned that the cotton swab test does not have sufficient discriminatory power to make urodynamics unnecessary. They do believe that the test has a role in conjunction with urodynamics and may be used as a screening test in situations where urodynamic testing is not readily available.

Pad Test

A pad test is a useful adjunct to the patient's history and physical examination. The pad test is an objective test that determines whether the fluid loss the patient is experiencing is in fact urine. Intravesical methylene blue, oral phenazopyridine (Pyridium), or oral Urised (methenamine, methylene blue, phenyl salicylate, benzoic acid, atropine sulfate, hyoscyamine) may be used as a coloring agent. Methylene blue and Urised turn the urine blue; phenazopyridine turns the urine orange.

Pad tests may be short term or long term. Short-term tests have the advantage of convenience and assured compliance. Long-term tests may be more representative of daily incontinence.

Short-term tests generally involve the subject drinking a known volume of liquid or undergoing retrograde filling of the bladder. A preweighed sanitary pad is applied. The individual is instructed to perform specific activities such as coughing, running in place, bending and lifting, and hand washing. The testing interval can range from 15 minutes to 2 hours. At the end of the test period, the pad is removed and weighed.

Long-term tests are conducted under normal living conditions for 24-48 hours. Each pad is preweighed and then weighed again after use by the patient at home, or, alternatively, the pad is placed in an airtight plastic bag and weighed later by the clinician.

Every 1 g increase in weight is equivalent to 1 mL of urine. The International Continence Society considers the finding of a weight change of less than 1 g during its standardized 1-hour test to be a negative result. Vaginal discharge and sweat can be other physiologic sources of pad weight gain. Testing should not be conducted during menstruation, for obvious reasons.

Paper Towel Test

A paper towel test provides a quick estimate of the degree of stress urine loss.[56] The patient is asked to cough repetitively and forcefully with a paper towel held a short distance from the urethra.

Standardization is accomplished by dripping known volumes of liquid onto the same type of paper towel to be used in the test. The area of the visible spread of the liquid on the towel is calculated for each known volume. The area of staining on the paper towel used by the patient with incontinence can be measured and the volume of the loss estimated.

Stress Testing

A critical part of the pelvic examination is direct observation of urine loss using the cough stress test. This test evaluates stress-induced leakage when the bladder is full. This test is very sensitive but can be misleading in inhibited patients and in those with low bladder volume.[54]

The cough stress test is performed by filling the bladder with sterile fluid at least halfway (eg, 200-250 mL). Have the patient in the lithotomy position or standing. While directly visualizing the urethra, instruct the patient to bear down (Valsalva) or cough. Observation of leakage during Valsalva maneuver or cough denotes a positive test result.

Urine loss directly observed from the urethral meatus at the peak of the increase in intra-abdominal pressure is strongly suggestive of stress incontinence (see the image below). Characteristically, patients with stress incontinence display immediate loss of a few drops to a brief squirt of urine. Delayed loss or prolonged loss raises the question of stress-induced detrusor instability.

A squirt of urine is observed at the peak of an in A squirt of urine is observed at the peak of an increase in intra-abdominal pressure in a supine patient

If no urine loss is observed, the test can be repeated with the patient in another position or repeated at another date. If more than mild pelvic organ prolapse is present, reduction of the prolapse should be performed with a half speculum, a pessary, or the examining fingers during the stress test. Care must be taken not to compress the urethra, regardless of which reduction method is used.

A small study showed that when the diagnosis of stress urinary incontinence was made on the basis of a negative finding on cystometrogram and a positive result on cough stress test, the reproducibility of a positive stress test result 1-4 weeks later was 100%.[57] If the initial diagnosis was mixed incontinence, stress leakage was demonstrated on a second cough stress test 80% of the time. Conversely, if the initial diagnosis was detrusor instability with a negative result on cough stress test, the repeat cough stress test result was negative 86% of the time.

The authors point out that in the setting of pure stress incontinence, the cough stress test may be more useful than complex urodynamic cough profiles. Some believe that, in some cases, the presence of catheters may be sufficiently obstructive to cause a small number of false-negative test results. If mixed incontinence is diagnosed by a cystometrogram and cough stress test, more complex testing may be required to confirm the diagnosis. False-positive stress test results due to cough-induced detrusor overactivity may occur in this situation.

Positive stress test findings in the supine position with a relatively empty bladder and with position change or other minimal increases in intra-abdominal pressure raise the question of intrinsic sphincter deficiency. Complex urodynamic testing would be indicated in such cases. Pad testing can be used if the history strongly suggests stress incontinence, stress test findings are negative, and detrusor instability is ruled out.

Standing cough stress test

If the cough leak test is initially performed with the patient in the lithotomy position and leakage is not observed, repeat this test with the patient in the standing position.

The patient stands upright with feet shoulder-width apart. Place a large towel under patient's feet. If pelvic prolapse is present, the prolapsed organ should be pushed up either with a pessary or gauze. Instruct patient to perform the Valsalva maneuver and cough in gradients (ie, mild, moderate, strong). Observable urine leakage in this position constitutes a positive test.

Marshall test

If the cough stress test is positive, a Marshall test (also known as the Marshall-Bonney test) may determine if the urine loss is caused by urethral hypermobility. This test consists of stress testing with support provided for the proximal urethra.

The Marshall test is performed by placing an index finger and the second finger on either side of the bladder neck, to support the proximal urethra. With the bladder relatively full, the patient is instructed to perform Valsalva or cough. The absence of leakage with bladder neck elevation and the presence of leakage without of bladder neck support confirms stress urinary incontinence due to urethral hypermobility.

In addition to examiners’ fingers, a number of other ways to provide elevation and support of the urethrovesical junction for this test have been described, including ring forceps, large cotton-tipped swabs, and specialized instruments. Data do not exist to recommend one method over another definitively.

The Marshall test has been criticized for susceptibility to examiner error. If one is not careful, the supporting fingers may accidentally occlude the urethra (ie, rather than supporting the bladder neck) and cause a false-positive result. A negative result (ie, incontinence persists despite support to the hypermobile urethra) may also be useful, however, in that it might dictate a more aggressive surgical approach, such as performing a sling procedure rather than a Burch retropubic urethropexy.

Nevertheless, the Marshall test is neither sensitive nor specific enough to diagnose stress urinary incontinence by current standards. Thus, this test is no longer widely used.



Diagnostic Considerations

The differential diagnoses of urinary incontinence are broad, with multiple causes. Sometimes, more than one contributing factor exists, further complicating diagnosis and therapy. Distinguishing these different etiologies is imperative because each condition warrants a different, but often overlapping, therapeutic approach.

Differential Diagnoses



Approach Considerations

Patients with urinary incontinence should undergo a basic evaluation that includes a history, physical examination, and urinalysis. Additional information from a patient's voiding diary, cotton-swab test, cough stress test, measurement of postvoid residual (PVR) urine volume, cystoscopy, and urodynamic studies may be needed in selected patients. Videourodynamic studies are the criterion standard for the evaluation of an incontinent patient but are typically reserved for the evaluation of complex cases of stress urinary incontinence.

Most authorities agree that diagnosis from the history alone is not an adequate basis for surgical therapy.[58] A review of the role of patient history in the diagnosis of urinary incontinence showed that a history of stress incontinence carries a sensitivity of about 0.91, but specificity is only 0.51. Positive predictive values in the range of 0.75-0.87 have been reported for a history of stress incontinence.[59]

Sensitivity and specificity are worse if the history is indicative of urge or mixed incontinence. Because some believe that many failed stress incontinence procedures are the result of incorrect or incomplete diagnoses, improving on the positive predictive value of history alone seems worthwhile.

The more difficult question to answer is which battery of tests and examinations produces a high positive predictive value at the lowest cost and inconvenience to the patient. One study demonstrated the benefit of combining the following 4 factors to improve diagnostic accuracy:

  • Predominant stress incontinence history
  • Postvoid residual (PVR) volume of no more than 50 mL
  • Positive cough stress test
  • Functional bladder capacity of at least 400 mL

Complex urodynamic testing in patients with these factors confirmed the diagnosis of stress incontinence 97% of the time; however, 15% of these patients also had coexisting detrusor instability. The positive predictive value, if one considers mixed incontinence as a separate disorder, is 82%.

The VALUE study concluded that for women with uncomplicated, demonstrable stress incontinence, urodynamic studies offered no superiority when compared with office evaluation alone for outcomes at one year.[60]  

Emergency Department Workup

Urinary incontinence is not a common presenting complaint in the emergency department (ED); however, its presence is always abnormal. The role of the emergency physician is to rule out some of the serious causes such as cauda equina syndrome, cord compression, and paraspinal abscess, as well as, most commonly, overflow incontinence and infections. If life-threatening conditions exist, the patient needs to be admitted for a complete workup of the disease entity.

Depending on the clinical presentation, the following basic tests may be useful[26] :

  • Obtain a urinalysis and urine culture, as necessary
  • Hematuria should be evaluated as per American Urological Association hematuria guidelines
  • Check serum electrolytes and calcium levels
  • Check blood urea nitrogen (BUN)/creatinine levels; decreased muscle mass in elderly patients may affect kidney function measurement
  • Check glucose level, especially in diabetic patients or patients with polyuria or polydipsia

In addition, specialists consulted on cases of urinary incontinence may request a variety of urodynamic studies for diagnosing the underlying cause. Such studies will be conducted on an outpatient basis.[54, 61]

Imaging studies

In the ED setting, the following imaging studies are helpful for delineating serious causes of urinary incontinence, when appropriate[33, 54, 26] :

  • Spinal MRI should be performed for ruling out cord compression, cauda equina, or spinal abscess if symptoms support the diagnosis

  • Ultrasonography allows for evaluation of hydronephrosis, hydroureter, and urinary tract stones. Ultrasonography is noninvasive, widely available, and cost-effective

  • CT scans with or without contrast for nephrolithiasis or pyelonephritis

Additional imaging studies that can aid in delineating the characteristics of urinary incontinence but are usually not ordered from an emergency perspective include the following:

  • Fluoroscopy and video urodynamics determines bladder, intra-abdominal, and urethral pressures. It is often a valuable tool in the evaluation of complex stress incontinence

  • Cystourethrography is a useful diagnostic adjunct in suspected cases of urinary tract fistulas

Urinalysis and Urine Culture

Urinary tract infection (UTI) can cause irritative voiding symptoms and urge incontinence. UTI can cause or contribute to urinary incontinence disorders in several ways. Local inflammation can serve as a bladder irritant, causing uninhibited bladder contractions. Endotoxins produced by some bacterial strains can have an alpha-blocking effect on the urethral sphincter, thereby lowering intraurethral pressures.

Postmenopausal women are especially susceptible to these effects on the urethra and bladder. Hypoestrogenism may enhance the effects. Postmenopausal women with UTI may present without the classic symptoms of irritation and pain. The predominant symptom in some patients may be the onset or the worsening of urge urinary incontinence.

A screening urinalysis is generally recommended as part of the testing of women for urinary incontinence. In postmenopausal women, a urine culture should also be done. Cultures may show bacterial growth in patients whose urinalysis shows little or no evidence of inflammation. Colony counts of less than 105/mL may be of significance in postmenopausal women and merit treatment.

Urine Cytology

Patients with carcinoma in situ of the urinary bladder experience urinary frequency and urgency and show evidence of microscopic hematuria. Irritative voiding symptoms disproportionate to the overall clinical picture and/or persistent unexplained hematuria warrant urine cytology and cystoscopy. Other potential indications for this testing include bladder lesions and masses visible on cystourethroscopy.

Kidney Function Studies

BUN and creatinine levels should be checked when poor kidney function, obstructed ureters, or urinary retention is suggested. This is especially important in the case of a stage III or stage IV cystocele.

In stage III cystocele, the bladder protrudes out of the vaginal introitus to greater than 1 cm outside of the hymenal ring upon abdominal strain; in stage IV cystocele, the bladder protrudes out of the vagina to greater than 3 cm from the hymen with the patient at rest (see the image below). When the bladder herniates out of the vagina, it may drag ureters with it. Both ureters can become trapped and obstructed at the bony pelvis, causing hydroureteronephrosis. This results in elevated BUN and azotemia.

This photo illustrates a variety of pelvic organ p This photo illustrates a variety of pelvic organ prolapses, including grade-IV cystocele, uterine descensus, enterocele, and rectocele alone or in combination. In situations where a significant prolapse (eg, uterus, bladder) has occurred, evaluate for possible ureteral obstruction at the level of the pelvic inlet.

Diabetes Testing

Testing for diabetes mellitus is not routine in the setting of urinary incontinence. However, it should be considered if polyuria and polydipsia are a part of the clinical picture or if diabetes risk factors are present and poor bladder emptying is found.

Urodynamic Studies

Urodynamics are a means of evaluating the pressure-flow relationship between the bladder and the urethra for the purpose of defining the functional status of the lower urinary tract. The ultimate goal of urodynamics is to aid in the correct diagnosis based on pathophysiology.

Simple urodynamic tests involve performing a noninvasive uroflow study, obtaining a postvoid residual (PVR) urine sample, and performing single-channel cystometrography (CMG). A single-channel CMG (ie, simple CMG) is used to assess the first sensation of filling, fullness, and urge. Bladder compliance and the presence of uninhibited detrusor contractions (eg, phasic contractions) can be noted during this filling CMG. A simple CMG may be performed using water or gas (carbon dioxide). Water is the most common filling medium.

Multichannel urodynamic studies are more complex than simple urodynamics and can be used to obtain additional information, including a noninvasive uroflow, PVR urine, filling CMG, abdominal leak-point pressure (ALPP), voiding CMG (pressure-flow), and electromyography (EMG). Water is the fluid medium used for multichannel urodynamics.

The most sophisticated study is videourodynamics, the criterion standard in the evaluation of a patient with incontinence. In this study, the following are obtained: noninvasive uroflow, PVR urine, filling CMG, ALPP, voiding CMG (pressure-flow), EMG, static cystography, and VCUG. The fluid medium used for videourodynamics is radiographic contrast.

Go to Urodynamic Studies for Urinary Incontinence for more information on this topic.

Chain-Bead Cystography

The significance of this test is largely historical. Chain-bead cystography involves the passage of a radiopaque chain transurethrally, with a portion of the chain piled just within the bladder at the urethrovesical junction. Urethra and bladder neck mobility, the presence or absence of urethral funneling, and the posterior urethrovesical angle can be determined with this test.

Incontinence experts no longer use this test. Instead, less invasive techniques, including the cotton swab test, bladder neck ultrasound, video urodynamics, and dynamic pelvic floor magnetic resonance imaging (MRI), now are used to study bladder neck anatomy and function.

Postvoid Residual Volume

Measurement of postvoid residual urine volume, using either a bladder ultrasonography or urethral catheter, may be a part of the evaluation for urinary incontinence of patients with apparent failure to empty the bladder completely. If the PVR urine volume is high, the bladder may be acontractile or the bladder outlet may be obstructed. Both of these conditions cause urinary retention from overflow incontinence. Go to Urodynamic Studies for Urinary Incontinence for more information on this topic.

Cystoscopy and Urethroscopy

Cystourethroscopy allows an anatomical assessment of the bladder and the urethra. The precise role of cystourethroscopy in the evaluation of female urinary incontinence is controversial.

The general agreement is that cystoscopy is indicated for patients with persistent irritative voiding symptoms or hematuria, persistent postoperative incontinence, voiding dysfunction, and findings suggestive of a diverticulum or fistula. Obvious causes of bladder overactivity, such as cystitis, stone, and tumor, can be easily diagnosed. This information is important in determining the etiology of the incontinence and may influence treatment decisions.

Go to Cystoscopy and Urethroscopy in the Assessment of Urinary Incontinence for more information on this topic.

Pessary Trial

A pessary trial may be useful in the preoperative evaluation of female patients who have severe pelvic organ prolapse but no complaints of urinary incontinence. After being fitted with a pessary, which effectively reduces her prolapse, the patient is asked to wear the pessary for a few days during usual activities. The patient may also obtain commercially available incontinence pessaries for treating stress predominant incontinence.

In some instances, the patient may experience stress incontinence while using the pessary. Some experts consider this to be evidence of so-called occult or potential stress incontinence—in other words, that stress incontinence may develop after surgical correction of the prolapse in these patients, because kinking of the urethra and/or limitation of urethral mobility secondary to the large prolapse may contribute to their continence.

The preoperative diagnosis of potential stress incontinence prompts the surgeon to add an anti-incontinence procedure to the overall surgical management scheme.


MRI and Ultrasonography

MRI remains investigational in the assessment of urinary incontinence. It is not used in clinical practice.

Ultrasonography (US) is a readily available and versatile tool that has many potential uses in urology and urogynecology.[62] However, it has only recently begun to be used in the evaluation of urinary incontinence, such as post-void residual urine volume determinations.



Approach Considerations

Treatment is keyed to the type of incontinence. The usual approaches are as follows:

  • Stress incontinence - Surgery, pelvic floor physiotherapy, anti-incontinence devices, and medication
  • Urge incontinence - Changes in diet, behavioral modification, pelvic-floor exercises, and/or medications and new forms of surgical intervention
  • Mixed incontinence - Anticholinergic drugs and surgery
  • Overflow incontinence - Catheterization regimen or diversion
  • Functional incontinence - Treatment of the underlying cause

Some experts recommend a trial of medical therapy before considering surgical treatment. Others believe that if the incontinence is severe and correctable by surgical means, a trial of medical therapy is not mandatory and need not be performed if the informed patient chooses to proceed directly to surgery.

Treatment of comorbid disease may minimize incontinence episodes. Measures such as smoking cessation, control of asthma, and relief of chronic constipation may be beneficial.

A network meta-analysis of 84 randomized trials of urinary incontinence concluded that behavioral therapies are generally more effective than pharmacologic interventions for stress or urge urinary incontinence,[63] Findings included the following:

  • Except for hormones and periurethral bulking agents, all treatments were more effective than no treatment in achieving at least one favorable outcome

  • For urgency incontinence, behavioral therapy was statistically significantly more effective than anticholinergics in achieving cure or improvement; onabotulinum toxin A may be more effective than neuromodulation in achieving cure, but both interventions were more effective than no treatment. 

  • Second-line interventions (eg, alpha-agonists, anticholinergics) were associated with adverse effects, such as dry mouth.

Absorbent Products

Absorbent products are pads or garments designed to absorb urine to protect the skin and clothing. Both disposable and reusable forms are available. By reducing wetness and odor, these products help to keep patients comfortable and allow them to function in usual activities.

Do not consider anti-incontinence products to be a cure-all for urinary incontinence; however, judicious use of pads and devices to contain urine loss and maintain skin integrity are extremely useful in selected cases. Absorbent pads and internal and external collecting devices have an important role in the management of chronic incontinence.

The criteria for use of these products are fairly clear-cut, and these products are beneficial for patients who meet the following conditions:

  • Persistent incontinence despite all appropriate treatments
  • Inability to participate in behavioral programs, due to illness or disability
  • Presence of an incontinence disorder that cannot be helped by medications
  • Presence of an incontinence disorder that cannot be corrected by surgery

Absorbent products may also be used temporarily until a definitive treatment has a chance to work, in patients awaiting surgery, or long-term if treatment has yielded less-than-perfect results. Absorbent products are helpful during the initial assessment and workup of urinary incontinence. As an adjunct to behavioral and pharmacologic therapies, they play an important role in the care of persons with intractable incontinence.

More than 50% of the members of the National Association for Continence (NAFC), a national support group for incontinent patients, use some form of protective garment to remain dry. In addition, 47% of all elderly men and women use some type of absorbent products. In nursing homes, disposable diapers or reusable pad and pant systems are used.

Do not use absorbent products in place of definitive interventions to decrease or eliminate urinary incontinence. Early dependency on absorbent pads may be a deterrent to achieving continence, providing the wearer a false sense of security. Long-term use of absorbent products may lead to inevitable acceptance of the incontinence condition, which removes the motivation to seek evaluation and treatment.

In addition, improper use of absorbent products may contribute to skin breakdown and urinary tract infections (UTIs). Thus, appropriate use, meticulous care, and frequent pad or garment changes are needed when absorbent products are used.

Different types of products with varying degrees of absorbency exist. Unlike sanitary napkins, these absorbent products are specially designed to trap urine, minimize odor, and keep the patient dry. These products may absorb 20-300 mL, depending on the brand and the absorbent material of the product. Absorbent products used include underpads, panty shields, pant guards, adult diapers (briefs), various washable pants and disposable pad systems, or combinations of these products.

For occasional minimal urine loss, panty shields (small absorbent inserts) may be used. For light incontinence, guards (close-fitting pads) may be more appropriate. Absorbent guards are attached to the underwear and can be worn under usual clothing.

Adult undergarments (full-length pads) are bulkier and more absorbent than guards. They may be held in place by waist straps or snug underwear.

Adult briefs are the bulkiest type of protection, they offer the highest level of absorbency, and they are secured in place with self-adhesive tape. Absorbent bed pads also are available to protect the bed sheets and mattresses at night. They are available in different sizes and absorbencies.

Urethral Occlusion

Urethral occlusive devices are artificial devices that may be inserted into the urethra or placed over the urethral meatus to prevent urinary leakage. These devices are palliative measures to prevent involuntary urine loss. Urethral occlusive devices are more attractive than absorbent pads because they tend to keep the patient drier; however, they may be more difficult and expensive to use than pads.

Urethral occlusive devices must be removed after several hours or after each voiding. Unlike pads, these devices may be more difficult to change. With device manipulation, patients may soil their hands. In addition, there is always a risk that a urethral plug may fall into the bladder or fall off the urethra. Urethral occlusive devices may be best suited for an active incontinent woman who does not desire surgery.

The Impress Softpatch (UroMed Corporation, Needham, MA) is an adhesive foam patch designed for a single use. A hydrogel adhesive anchors the patch over the urethral meatus. In one study, 52% of women with mild-to-moderate stress incontinence were dry, and 82% were improved with the use of this device.

The Reliance Urinary Control Insert (UroMed Corporation, Needham, MA) is a small catheterlike device that is inserted into the urethra. The balloon is inflated with air. The single-use device is removed before voiding by pulling on an attached thread. Approximately 80% of patients are dry with the use of this insert, with an additional 12% greatly improved. Complications such as migration into the bladder and UTI have been reported.

The FemAssist (Insight Medical Corporation, Boston, Mass.) and CapSure Shield (Bard Urological, Covington, GA) are silicon devices that seal the urethral meatus with an action similar to a suction cup. These devices can decrease significantly the urine loss in short-term pad test studies.

In a more extended study of the device, only 2 of 31 women finished a 6-month trial. Reasons cited for dropout were lack of efficacy, poor adhesion, discomfort, and difficulty placing the device. This study points out that short-term results in highly motivated individuals may not be generalized to longer-term use under real-life circumstances.

The Introl Bladder Neck Support Prosthesis (UroMed Corporation, Needham, MA) is an insertable vaginal device with arms that provide support on each side of the bladder neck. If properly fitted, the prosthesis can achieve cure rates of approximately 80% for stress incontinence.

Incontinence pessaries also are available for use in mild stress incontinence. These ring- or dish-shaped devices usually are reinforced in the area that sits under the bladder neck/proximal urethra. A modicum of success has been achieved with these specially designed pessaries.

Various penile-compression devices are available to men with incontinence who have undergone radical prostatectomy. In a very small study (12 men), Moore et al showed that the Cunningham clamp provided better urinary leakage control and overall patient satisfaction than the C3 and U-Tex. However, the Cunningham clamp did cause reduced systolic velocity in the penis. In many cases, these devices do not eliminate leakage but may be suitable for men who wish to avoid surgery.[64]

For patients undergoing robot-assisted radical prostatectomy (RARP), a study by Lee et al found that the bladder plication stitch is an effective technical modification for lessening the period of recovery of urinary continence.[65]


Urinary diversion, using various catheters, has been one of the mainstays of severe anti-incontinence therapy. The use of catheters for bladder drainage has withstood the test of time. Bladder catheterization may be a temporary measure or a permanent solution for overflow incontinence. The use of a urethral catheter is contraindicated in the treatment of urge incontinence.

Catheterization is the only way to treat overflow incontinence. This is true whether the bladder has become decompensated as a result of a neurologic insult (areflexic detrusor) or from a mechanical source (atonic detrusor).

Self-catheterization is the preferred approach if the patient is able to perform it. Indwelling Foley catheters or a suprapubic tube is considered if a patient is not able to perform self-catheterization.

Some patients with overflow incontinence respond well to temporary continuous catheter drainage: their bladder capacity returns to normal, and voluntary detrusor pressure improves. Return of spontaneous voiding is more likely for patients without neurologic injury. This usually takes at least 1 week of catheter drainage, depending on the degree of bladder muscle injury. If overflow incontinence has not resolved after 4 weeks, then the bladder is unlikely to recover with catheter drainage alone.

If the underlying cause of the overflow problem can be treated or eliminated, these patients may be able to return to normal voiding. If this is unsuccessful, intermittent catheterization is usually preferred for long-term therapy if logistically possible. Otherwise, a permanent catheter may need to be considered.

Some patients respond well to temporary continuous Foley catheter drainage. Their bladder capacity returns to normal, and voluntary detrusor pressure improves. Return of spontaneous voiding is more likely for patients without neurologic injury. This usually takes at least 1 week of catheter drainage, depending on the degree of bladder muscle injury. If it has not resolved after 4 weeks, then the bladder is unlikely to recover using catheter drainage alone.

If the underlying cause of the overflow problem is bladder outlet obstruction, these patients may be able to return to normal voiding after relief of obstruction. If this is unsuccessful or not feasible, intermittent catheterization is usually preferred for long-term therapy if logistically possible. Otherwise, a permanent catheter may need to be considered.

Different types of bladder catheterization include indwelling urethral catheters, suprapubic tubes, and intermittent self-catheterization.

Indwelling urethral catheters

Commonly known as Foley catheters, indwelling urethral catheters historically have been the mainstay of treatment for bladder dysfunction. If urethral catheters are being used for a long-term condition, they need to be changed monthly. These catheters may be changed at an office, a clinic, or at home by a visiting nurse. Indwelling use of a Foley catheter in individuals who are homebound requires close supervision by a visiting nurse and additional personal hygiene care.

The standard catheter size for treating urinary retention is 16F or 18F, with a 5-mL balloon filled with 5-10 mL of sterile water. Larger catheters (eg, 22F, 24F) with bigger balloons are used for treating grossly bloody urine found in other urologic conditions or diseases.

Increasing the balloon size to treat a catheter that leaks is not appropriate. Treat leakage around a catheter by eliminating the cause of the leakage. Change or irrigate the catheter if it is blocked. Empty the drainage bag if it is full. Treat any bladder spasms or uninhibited contractions with appropriate anticholinergic medications.

Proper management of indwelling urethral catheters varies somewhat per individual patient. Some type of catheter bag tubing support usually is recommended to prevent inadvertent pressure on the Foley catheter balloon and bladder neck tissue. Adequate slack should be afforded to allow reasonable unimpeded leg motion without stretching the Foley catheter.

The authors also recommend the routine use of a water-soluble surgical lubricant on the catheter where it exits the urethra, especially in males because of the soreness that can be produced there. The lubricant affords significant symptomatic relief.

The usual practice is to change indwelling catheters once every month. The catheter and bag are replaced on a monthly basis; however, catheters that develop encrustations and problems with urine drainage need to be changed more frequently. After more than 2 weeks in the urinary bladder, all indwelling catheters become colonized with bacteria. Bacterial colonization does not mean the patient has a clinical bladder infection.

Symptoms of bladder infection include foul odor, purulent urine, and hematuria. Fever with flank pain often is present if upper tracts are involved. If a bladder infection occurs, change the catheter and the entire drainage system.

The urinary drainage bag does not need to be disinfected routinely to prevent infection. A dilute vinegar solution can be used to dissolve the encrustations that tend to form in the drainage bags.

Routine irrigation of catheters is not required. However, some authors favor the use of 0.25% acetic acid irrigation because it is bacteriostatic, minimizes catheter encrustation, and reduces odor. When used, 30 mL is instilled into the bladder and allowed to freely drain twice per day.

Similarly, 30 mL of hydrogen peroxide can be added to the drainage bags immediately before connecting them to the Foley catheter. This supposedly reduces odor and bacterial growth by using a safe, nontoxic, and inexpensive agent.

Patients do not have to be taking continuous antibiotics while using the catheter. In fact, continuous use of antibiotics while a catheter is used is contraindicated. Prolonged use of antibiotics to prevent infection actually may cause paradoxical generation of bacteria that are resistant to common antibiotics.

In spite of its seeming advantages, the use of a Foley catheter for a prolonged period of time (eg, months or years) is strongly discouraged. Long-term dependence on these catheters poses significant health hazards.

Indwelling urethral catheters are a significant cause of UTIs that involve the urethra, bladder, and kidneys. Within 2-4 weeks after catheter insertion, bacteria are present in the bladders of most women. Asymptomatic bacterial colonization is common and does not pose a health hazard. However, untreated symptomatic UTIs may lead to urosepsis and death. The death rate of nursing home residents with urethral catheters has been found to be 3 times higher than for residents without catheters.

Other problems associated with indwelling urethral catheters include encrustation of the catheter, bladder spasms resulting in urinary leakage, hematuria, and urethritis. More severe complications include formation of bladder stones, development of periurethral abscess, kidney damage, and urethral erosion.

Another problem of long-term catheterization is bladder contracture, which occurs with urethral catheters as well as suprapubic tubes. Anticholinergic therapy and intermittent clamping of the catheter in combination have been reported to be beneficial for preserving the bladder integrity with long-term catheter use. Individuals who did not use the medication and daily clamping regimen experienced a decrease in bladder capacity and vesicoureteral reflux. For this reason, some physicians recommend using anticholinergic medications with intermittent clamping of the catheter if lower urinary tract reconstruction is anticipated in the future.

Foley catheter clamping is not a benign procedure. Potential risks include cystitis, pyelonephritis, urosepsis, and bladder perforation. Thus, Foley catheter clamping is not commonly employed except in those rare occasions where bladder reconstruction is being contemplated. The clamping should be performed under strict supervision, with monitoring of patient comfort and bladder capacity. Coexisting UTIs must be eradicated prior to proceeding with this endeavor.

The maximum time limit for Foley clamping to expand the bladder capacity should be tailored to the individual but should not exceed 3-4 hours. Patients with small-capacity bladders do not tolerate Foley clamping for more than 1 hour. The Foley catheter should be unclamped immediately if fever, suprapubic pain, obvious bladder distention, leakage around the Foley catheter, or changes in hemodynamics are noted.

Suprapubic catheters

When long-term catheterization is anticipated, a suprapubic catheter is an attractive alternative to a urethral catheter. Restrict the use of indwelling catheters to the following situations:

  • As comfort measures for terminally ill patients
  • To avoid contamination or to promote healing of severe pressure sores
  • In case of inoperable urethral obstruction that prevents bladder emptying
  • In individuals who are severely impaired for whom alternative interventions are not an option
  • When an individual lives alone and a caregiver is unavailable to provide other supportive measures
  • For acutely ill persons in whom accurate fluid balance must be monitored
  • For severely impaired persons for whom bed and clothing changes are painful or disruptive

The most common use of a suprapubic catheter is in individuals with spinal cord injuries and a malfunctioning bladder. It also can be used in patients with intractable decompensated bladders or complicated urethral strictures. Both paraplegic and quadriplegic patients have benefited from this form of urinary diversion.

Other indications for suprapubic catheters include short-term use following gynecologic, urologic, and other types of surgery. Suprapubic catheters may be used whenever the clinical situation requires the use of a bladder drainage device.

Suprapubic catheters are contraindicated in persons with chronic unstable bladders or intrinsic sphincter deficiency because involuntary urine loss is not prevented. A suprapubic tube does not prevent bladder spasms from occurring in unstable bladders nor does it improve the urethral closure mechanism in an incompetent urethra.

When suprapubic tubes are needed, usually smaller (eg, 14F, 16F) catheters can be placed, although some practitioners prefer a larger tube (eg, 24F-28F), especially if they are concerned about the catheter becoming clogged. As with urethral catheters, the suprapubic tubes should be changed at least once a month on a regular basis.

Suprapubic catheters have many advantages, as follows:

  • The risk of urethral damage is eliminated
  • Multiple voiding trials may be performed without having to remove the catheter
  • Because the catheter comes out of the lower abdomen rather than the vaginal area, a suprapubic tube is more patient-friendly
  • Bladder spasms occur less often because the suprapubic catheter does not irritate the trigone as the urethral catheter does
  • Suprapubic tubes are more sanitary for the individual; bladder infections are minimized because the tube is away from the perineum

Suprapubic catheters are changed easily by either a nurse or a doctor. Unlike the urethral catheter, a suprapubic tube is less likely to become dislodged because the exit site is so small. When the tube is removed, the hole in the abdomen quickly seals itself within 1-2 days.

Some of the potential complications with long-term suprapubic catheterization are similar to those associated with indwelling urethral catheters, including leakage around the catheter, bladder stone formation, UTI, and catheter obstruction. Potential problems unique to suprapubic catheters include cellulitis around the tube site, hematoma, bowel injury, and difficulties with catheter reinsertion.

The potential for bowel injury exists during the initial placement of a suprapubic tube. Although uncommon, bowel perforation is known to occur in this circumstance.

If the suprapubic tube falls out inadvertently, the exit hole of the tube seals up and closes quickly within 24 hours if the tube is not replaced with a new one. If tube dislodgment is recognized promptly, a new tube can be reinserted quickly and painlessly as long as the tube site remains patent.

Long-term management of a suprapubic tube also may be problematic if the health care provider lacks the knowledge and expertise of suprapubic catheters or if the homebound individual lacks quick access to a medical center in case of an emergency. Nevertheless, in the right hands, the suprapubic catheter affords many advantages over long-term urethral catheters.

Intermittent catheterization

Intermittent catheterization, or self-catheterization, is a mode of draining the bladder at timed intervals, as opposed to continuous bladder drainage. Of all 3 possible options (ie, urethral catheter, suprapubic tube, intermittent catheterization), intermittent catheterization is the best solution for bladder decompression of a motivated individual who is not physically handicapped or mentally impaired.

Intermittent catheterization is most appropriate for patients with detrusor hyperreflexia and functional obstruction. Many of these patients have detrusor-sphincter dyssynergia and are at risk for pyelonephritis and upper tract injury.

Some patients with urge incontinence and coexisting hypofunctioning detrusors may benefit from self-catheterization. For example, some diabetic patients with bladder neuropathy may have instability requiring bladder-relaxing pharmacotherapy but, at the same time, may have intermittent detrusor hypofunctioning with poor emptying. The addition of bladder-relaxing drugs may worsen the baseline poor detrusor function, resulting in retention and overflow incontinence. In some cases, the solution may be to combine bladder-relaxing medical therapy with intermittent self-catheterization.

The ability of patients to use their hands and arms is usually a prerequisite for self-catheterization. However, in a situation in which the patient is physically or mentally impaired, a caregiver or health professional can perform intermittent catheterization for the impaired individual.

Many studies of young persons (both male and female) with spinal cord injuries have shown that intermittent catheterization is preferable to indwelling catheters (ie, urethral catheter, suprapubic tube). Intermittent catheterization has become a valuable alternative to indwelling catheters for individuals with chronic urinary retention due to an obstructed, weak, or nonfunctioning bladder.

Young children with myelomeningocele have benefited from the use of intermittent catheterization. In addition, self-catheterization is recommended by some surgeons for women during the acute healing process after anti-incontinence surgery.

Intermittent catheterization may be performed using a short rigid plastic catheter or a soft red rubber catheter. Plastic catheters are preferable to red rubber catheters because they are easier to clean and last longer.

The bladder must be drained on a regular basis, either based on a timed interval (eg, on awakening, every 3-6 hours during the day, and before bed) or based on bladder volume. The average adult bladder holds approximately 400-500 mL of urine, and ideally, the amount drained each time should not exceed 400-500 mL.

This drainage limit may require decreasing the fluid intake or increasing the frequency of catheterizations. For example, if catheterization is being performed every 6 hours and the amount drained is 700 mL, increase the frequency of catheterization to, perhaps, every 4 hours to maintain the volume drained at 400-500 mL.

The idea is to simulate normal voiding. Usually, the average adult empties the bladder 4-5 times a day. Thus, catheterization should occur 4 or 5 times a day; however, individual catheterization schedules may vary, depending on the amount of fluid taken in during the day.

Candidates for self-catheterization must have motivation and intact physical and cognitive abilities. Anyone who has good use of the hands and arms can perform self-catheterization. Young children and older people have proved capable of doing this every day without any problems. For individuals who are impaired, a home caregiver or a visiting nurse can be instructed to perform intermittent catheterization.

Self-catheterization may be performed at home, at work, or other sites. In young, immunocompetent patients, intermittent catheterization may be performed using either a sterile catheter or a nonsterile clean catheter. Patients should wash their hands with soap and water. Sterile gloves are not necessary. Clean intermittent catheterization results in lower rates of infection than the rates noted with indwelling catheters.

Studies show that in patients with spinal cord injuries, the incidence of bacteria in the bladder is 1-3% per catheterization and 1-4 episodes of bacteriuria occur per 100 days of intermittent catheterization (when drainage is performed 4 times daily). Furthermore, the infections that do occur usually are managed without complications.

In general, routine use of long-term suppressive therapy with antibiotics in patients with long-term clean intermittent catheterization is not recommended. The use of long-term suppressive antibiotic therapy in people regularly using clean intermittent catheterization is undesirable because it may result in the emergence of resistant bacterial strains.

In high-risk populations, such as patients with an internal prosthesis (eg, artificial heart valve, artificial hip) or patients who are immunosuppressed because of age or disease, whether to use antibiotic therapy for asymptomatic bacteriuria depends on individual merits.

For the older population and individuals with an impaired immune system, the sterile technique of intermittent catheterization has been recommended. Older persons are at higher risk than younger people for developing bacteriuria and other complications caused by intermittent catheterization because they do not have a strong defense system against infection. Although the incidence of infection and other complications with sterile versus clean intermittent catheterization is not well established for older patients, sterile intermittent catheterization appears to be the safest method for this high-risk population.

Potential advantages of performing intermittent catheterization include patient autonomy, freedom from indwelling catheter and bags, and unimpeded sexual relations. Potential complications of intermittent catheterization include bladder infection, urethral trauma, urethral inflammation, and stricture.

Concurrent use of anticholinergic therapy maintains acceptable intravesical pressures and also prevents bladder contracture. Studies have demonstrated that long-term use of intermittent catheterization appears to be preferable to indwelling catheterization (ie, urethral catheter, suprapubic tube), with respect to UTIs, kidney failure, and the development of stones within the bladder or kidneys.

Medicated and silver-coated catheters

The type of urinary catheter used may affect the likelihood of catheter-related UTIs. Urinary catheters impregnated with medications (eg, nitrofurazone or minocycline and rifampin) or coated with a silver alloy-hydrogel significantly reduce the risk of catheter-related UTI for catheterizations not exceeding 2-3 weeks.

In trials of silver-coated urinary catheters, silver alloy catheters appear to be significantly more effective than silver oxide catheters in preventing UTIs.[66] Although silver alloy catheters cost about $6 more than conventional urinary catheters, they may be worth the extra cost to prevent symptomatic UTIs and urosepsis. This type of catheter especially may be apropos in immunocompromised patients at high risk for infection.

Pharmacologic Therapy

Medication may have some benefit in stress and urge urinary incontinence. These agents are not uniformly effective, and adverse effects may limit their long-term use. Medications used for treatment of urinary incontinence include the following:

  • Anticholinergic agents
  • Antispasmodic drugs
  • Beta-adrenergic agonists
  • Tricyclic antidepressants (TCAs)
  • Estrogen
  • Botulinum toxin

Tricyclic antidepressants

TCAs have historically been used to treat major depression, but their pharmacologic effects also make these drugs good choices for mixed incontinence, nocturia, and nocturnal enuresis. TCAs have also been used in the treatment of stress incontinence.

TCAs have complicated direct and indirect effects on the lower genitourinary tract. They possess both a central and peripheral anticholinergic effect, as well as being alpha-adrenergic agonists and central sedatives. The resultant clinical effect is bladder muscle relaxation and increased urethral sphincter tone. High pretreatment urethral closure pressure has served as a predictor of success.

Imipramine (Tofranil) is the most widely used TCA for urologic indications. It facilitates urine storage by decreasing bladder contractility and increasing outlet resistance. It has an alpha-adrenergic effect on the bladder neck, an antispasmodic effect on the detrusor muscle, and a local anesthetic effect on the bladder mucosa. (Note the black box warning: In short-term studies, antidepressants increased the risk of suicidal thinking and behavior in children, adolescents, and young adults (< 24 y) taking antidepressants for major depressive disorders and other psychiatric illnesses.)

Adult dosing is 10-50 mg 1 to 3 times daily, with a range of 25-100 mg qd. Pediatric dosing is not established. Imipramine is a pregnancy category D drug.

The combination of imipramine and oxybutynin (Ditropan) produces a synergistic effect to relax the unstable bladder, allowing it to better hold urine and preventing urge incontinence.

Amitriptyline (Elavil) is a TCA with sedative properties that increases circulating levels of norepinephrine and serotonin by blocking their reuptake at nerve endings. It is ineffective for use in urge incontinence but extremely effective in decreasing symptoms of urinary frequency in women with pelvic floor muscle dysfunction. It restores serotonin levels and helps break the cycle of pelvic floor muscle spasms.

Amitriptyline is well tolerated and effective in most women with urinary frequency. Adult dosing is 10 mg qd; titrate if necessary by 10 mg/wk until a maximum dose of 150 mg is reached, urinary symptoms disappear, or adverse effects become intolerable. Pediatric dosing is not established. Amitriptyline is also a pregnancy category D drug.

In addition to anticholinergic adverse effects, serious allergic reactions have been reported with TCAs, although rarely. Cardiotoxicity rarely is problematic at the low doses used for treatment of urinary incontinence. Central effects, such as sedation and tremor, may be troublesome to some patients. On occasion, prescribing imipramine at bedtime and a musculotropic agent in the daytime may be helpful.

These products are no longer commonly used in the treatment of incontinence. 


The serotonin/norepinephrine reuptake inhibitor duloxetine is the first drug developed and marketed specifically for stress urinary incontinence. Duloxetine has been approved for the treatment of stress incontinence in Europe, but is not approved for this indication by the US Food and Drug Administration (FDA).

In animal models, duloxetine seems to increase pudendal motor nerve output via increased levels of serotonin and norepinephrine in the pudendal motor nucleus of the sacral spinal segments. As a result, urethral muscular tone and closure pressure is augmented. Similarly, studies in humans suggest that duloxetine enhances urethral closure through neuromodulation of the external urethral sphincter.[67]

A number of clinical trials have demonstrated the efficacy of duloxetine compared with placebo in the treatment of mild and moderate stress incontinence. A small, prospective, double-blind, randomized, placebo-controlled trial demonstrated modest efficacy in patients with severe stress urinary incontinence.[68]

In this study, patients with pure, urodynamically confirmed stress incontinence who were awaiting surgery were treated with duloxetine for 8 weeks. All participants had, on average, 14 or more episodes of stress incontinence per week. Significant improvement was observed in the quality of life indices and in frequency of incontinence episodes and use of protective pads in the patients treated with duloxetine compared with placebo. All positive clinical responses were observed within 2 weeks after initiation of therapy–some as early as 5 days.

The most common side effect was nausea, which tended to decrease with continued use. Discontinuation of therapy was significantly more common in the treatment group, with equal numbers of patients withdrawing because of nausea, vomiting, worsening of hypertension, and headache. Other common side effects included constipation and dry mouth. At the end of the 8-week trial, 20% of the treatment group patients were no longer interested in surgical therapy, versus 0% in the placebo arm.

Another small study demonstrated similar results, with 24% of the patients who received duloxetine declining their planned surgical therapy. Of note, 48% of the patients stopped the medication due to side effects at the 40 mg twice-daily dose schedule used in this study.[69]

A multicenter, double-blind, randomized, placebo-controlled study in 2,758 women with predominant stress incontinence found that after 6 weeks, the decrease in weekly incontinence episode frequency was significantly greater with duloxetine compared with placebo (-50 vs -29.9%). In an uncontrolled, open-label, 72-week extension of the study in 2,290 patients, 21.5% of patients discontinued the drug because of adverse effects. However, the efficacy of duloxetine was maintained in those women who remained on therapy.[70]

Anticholinergic agents

The clinical and urodynamic effects of blocking cholinergic receptors in the bladder are as follows:

  • Increased bladder capacity
  • Increased volume threshold for initiation of an involuntary contraction
  • Decreased strength of involuntary contractions

Propantheline bromide

Propantheline bromide is an anticholinergic agent that has been used to treat detrusor overactivity. Propantheline commonly is prescribed in dosages of 15-30 mg every 4-6 hours. In one study, propantheline bromide decreased the rate of urge incontinence by 13-17% when 30 mg were used qid. When higher doses were used, 60 mg qid, the cure rate was reported to be over 90%. Because gastrointestinal (GI) absorption is poor, it is often recommended that propantheline be taken on an empty stomach.

Typical anticholinergic adverse effects can be expected, including dry mouth, constipation, dry eyes, blurred vision, orthostatic hypotension, and increased heart rate. This agent probably should be avoided by patients with heart disease and closed-angle glaucoma. Improvement rates in various studies generally have been approximately 50%. Propantheline is no longer considered a first-line drug for detrusor instability due to relatively poor efficacy and a high incidence of adverse effects.


Tolterodine (Detrol) is a potent antimuscarinic agent for treating detrusor overactivity. In animal models, the drug has shown selectivity for the urinary tract over the salivary glands. Tolterodine has performed well in clinical trials, showing comparable efficacy to oxybutynin with lower discontinuance rates. The dosage range is 1-2 mg twice daily.

In clinical studies, the mean decrease in urge incontinence episodes was 50% and the mean decrease in urinary frequency was 17%. The mean decrease in urge incontinence episodes per week was 53% for long-acting tolterodine (Detrol LA) 4 mg qd.


Oxybutynin (Ditropan XL), which has both antimuscarinic and antispasmodic effects, reduces incontinence episodes by 83-90%. The total continence rate has been reported to be 41-50%. Mean reduction in urinary frequency was 23%. In clinical trials, only 1% stopped taking the drug because of dry mouth and less than 1% stopped taking it due to central nervous system adverse effects.

In the Overactive Bladder: Judging Effective Control and Treatment (OBJECT) trial, extended-release oxybutynin 10 mg was statistically superior to tolterodine 2 mg bid in controlling urge incontinence, total incontinence, and micturition frequency. Both drugs had similar adverse-effect profiles.[71] OBJECT was a large double-blind, multicenter, prospective, randomized controlled study in 276 women and 56 men with symptoms of overactive bladder.


Trospium (Sanctura) elicits antispasmodic and antimuscarinic effects and is indicated to treat urinary incontinence, urgency, and frequency. It acts by antagonizing acetylcholine effect on muscarinic receptors. Parasympathetic effect reduces smooth muscle tone in the bladder. The typical trospium dosage is 20 mg bid taken on an empty stomach at least 1 h before meals. The dose is reduced to 20 mg hs in patients with kidney insufficiency (ie, creatinine clearance [CrCl] < 30 mL/min). Elderly individuals (ie, > 75 y) may require a similar dose reduction to avoid adverse effects. Mild anticholinergic effects (eg, dry mouth, constipation, dry eyes, blurred vision) may occur.


Solifenacin (VESIcare) is a competitive muscarinic receptor antagonist that causes anticholinergic effects and inhibits bladder smooth muscle contraction. The initial dosage is 5 mg qd, which may be increased to 10 mg/d if tolerated and warranted.[72] The tablet must be swallowed whole (not crushed) with liquid.

Precautions include the following:

  • Kidney or liver impairment (do not exceed 5 mg in patients with creatinine clearance < 30 mL/min or moderate liver impairment [Child-Pugh class B])
  • Controlled narrow-angle glaucoma
  • History of prolonged QT interval
  • Bladder outflow obstruction
  • Decreased GI motility


Darifenacin (Enablex) is an extended-release anticholinergic agent. It has high affinity for M3 receptors involved in bladder and GI smooth muscle contraction, saliva production, and iris sphincter function. A prospective, randomized, placebo-controlled, double-blind study demonstrated the efficacy of extended-release darifenacin with regard to reductions in incontinence episodes, decreases in frequency and urgency, and improved bladder capacity.[73]

The initial dose is 7.5 mg PO qd. After 2 weeks, the dose may be increased to 15 mg/d based on response.[73] Do not exceed 7.5 mg/d if moderate hepatic impairment (Child-Pugh class B) is present or the patient is also taking potent CYP-450 3A4 inhibitors. Darifenacin must be swallowed whole; do not chew, divide, or crush.

Additive toxicity may occur if darifenacin is taken with other anticholinergics (eg, antihistamines). Coadministration with CYP-2D6 substrates that have a narrow therapeutic index (eg, flecainide, thioridazine, TCAs) may cause toxicity of these other 2D6 substrates. Coadministration may also increase midazolam or digoxin levels.


Fesoterodine (Toviaz) has been FDA approved for symptoms of overactive bladder (eg, urinary urge incontinence, urgency, frequency). It is a competitive muscarinic receptor antagonist and administered once daily.

Adverse effects of antimuscarinic therapy

Increasingly, prolongation of the QT interval has been recognized as a potential problem with antimuscarinic drugs as well as medications of many different classes. Individuals with pharmacologic prolongation of the QT interval may be at increased risk for potentially fatal polymorphic ventricular tachyarrhythmia. Additional risk factors include female sex, advanced age, hypokalemia, and polypharmacy.

No direct studies compare the incidence of prolonged QT intervals or clinically concerning tachyarrhythmias among commonly prescribed antimuscarinic agents. However, in a study of 188 healthy volunteers receiving therapeutic (15 mg) and supratherapeutic doses of darifenacin, no prolongation of the corrected QT interval could be documented.[74]

More commonly observed adverse effects include dry mouth, constipation, and blurred vision.

Rule out narrow-angle glaucoma prior to prescribing an anticholinergic agent. Experienced ophthalmologists can convert narrow-angle glaucoma to open-angle glaucoma. Patients who are taking an anticholinergic agent should be monitored to prevent pharmacologically induced urinary retention.

Calcium channel blockers

In a small study, verapamil was no more effective than placebo and less effective than oxybutynin. However, verapamil combined with oxybutynin was more effective than oxybutynin alone. Terodiline was once a very popular drug for the treatment of detrusor overactivity in Europe but has since been withdrawn from the market due to a potential for serious adverse cardiac effects.

A small study showed magnesium hydroxide to be beneficial for some patients with sensory urgency and detrusor overactivity.[75] The presumed mechanism of action is through calcium antagonism. More work is needed before this treatment is recommended.

Beta-adrenergic agonists

These agents relax beta-adrenergic receptors that are contained in smooth muscle, such as the bladder. Studies of terbutaline and clenbuterol have yielded mixed results. The role of these drugs as adjuncts to other pharmacologic therapies has not been explored.

Mirabegron (Myrbetriq), a beta-3 adrenergic receptor agonist, causes relaxation of the detrusor muscle and increases bladder capacity. It is indicated for overactive bladder with symptoms of urge urinary incontinence, urgency, and urinary frequency. A guideline from the American Urological Association recommends beta-3-adrenergic receptor agonists as second-line therapy in patients with an inadequate response to behavioral therapy.[76]

The agent 1-desamino-8-D-arginine vasopressin (DDAVP) has been used in children with nocturnal enuresis, with good results. The hormone causes water to be reabsorbed from the renal collecting system. Reduction in nighttime urine production may be beneficial in patients with detrusor overactivity and a significant degree of nocturia. Caution is needed when using this drug in elderly patients. Do not use in patients with significant heart failure or in children younger than 5 years (eg, water intoxication). 

Vibegron (Gemtesa) is another beta-3 adrenergic agonist that is indicated for adults with overactive bladder who have symptoms of urge urinary incontinence, urgency, and urinary frequency. Approval was based on the EMPOWUR phase 3 clinical trial, which compared vibegron with tolterodine and placebo. Of 1518 randomized patients, 90.4% completed the trial. At 12 weeks, micturition episodes decreased by an adjusted mean of 1.8 episodes per day for vibegron compared with 1.3 for placebo (P < 0.001) and 1.6 for tolterodine. Among incontinent patients, urge incontinence episodes decreased by an adjusted mean 2 episodes per day for vibegron compared with 1.4 for placebo (P < 0.0001) and 1.8 for tolterodine.[77]  

In a 52-week continuation study of EMPOWUR, vibegron demonstrated favorable long-term safety, tolerability, and efficacy. For this study, patients who had completed 12 weeks of once-daily vibegron 75 mg or tolterodine 4 mg extended release continued double-blind treatment, while patients who had completed 12 weeks of placebo were randomly assigned to receive double-blind vibegron or tolterodine. Of the 506 participants, 430 (85%) completed the study; only 12 (2.4%) discontinued owing to adverse events. Patients receiving vibegron maintained improvements in efficacy endpoints.[78]  


Estrogen therapy may have several positive effects in women with stress incontinence who are estrogen deficient. Estrogen may increase the density of alpha-receptors in the urethra. In addition, it increases the vascularity of the urethral mucosa and may augment the coaptive abilities of the urethral mucosa. In theory, those effects should translate into improved continence; however, several studies stand in opposition of those assumptions.

A number of small studies show oral estrogen therapy to be of no clinical benefit to women with stress incontinence or detrusor overactivity. In a subgroup analysis of postmenopausal women enrolled in the Heart and Estrogen/Progestin Replacement Study (HERS), worsening of incontinence occurred in 39% of patients in the hormone treatment group, compared with 27% of patients in the placebo group.[79]

In the Women's Health Initiative Study, women with baseline incontinence being treated with combined or unopposed estrogen oral therapy also showed exacerbation of symptoms significantly more often than women in the placebo group. In addition, women in the hormone-exposed groups with no baseline incontinence developed symptoms more often than those in the placebo group.[80]

Both of these trials present level 1 evidence against oral hormone therapy to treat incontinence. No adequate studies of local estrogen therapy exist. A meta-analysis found some evidence that local estrogen may improve incontinence, but there was little evidence on post-treatment results and none on long-term effects.[81] Local urogenital treatment provides more rapid and reliable effects in treating genitourinary atrophy and deserves study as a preoperative adjunct.

Pharmacologic therapy using estrogen derivatives results in few cures (0-14%) but may cause subjective improvement in 29-66% of women. It may be useful in postmenopausal women with atrophic vaginitis or intrinsic sphincter deficiency.

Botulinum toxin

A neurotoxin produced by Clostridium botulinum, onabotulinumtoxinA (Botox) prevents acetylcholine release from presynaptic membrane. Therapy for urinary incontinence consists of 30 intradetrusor injections via cystoscopy.

In 2011, onabotulinumtoxinA was approved by the FDA for urinary incontinence in patients with neurologic conditions (eg, spinal cord injury, multiple sclerosis) who have overactive bladder. Placebo-controlled trials have shown significant reduction in urinary incontinence episodes and improved urodynamics at 12 weeks in patients who received onabotulinumtoxinA.[82, 83, 84]  

In 2013, the FDA expanded the approved use of onabotulinumtoxinA to treatment of adults with overactive bladder who cannot use or do not adequately respond to anticholinergic drugs. The new indication was based on results of two placebo-controlled clinical trials in 1105 patients with symptoms of overactive bladder. After 12 weeks, patients who received injections of 100 units of onabotulinumtoxinA (20 injections of 5 units each) experienced urinary incontinence an average of 1.6 to 1.9 times less per day than patients treated with placebo. Treatment with onabotulinumtoxinA can be repeated if necessary, but at least 12 weeks should elapse between treatments.[85]

The ABC trial (Anticholinergic therapy vs onabotulinum toxinA for urgency incontinence) shed some light on the utility of 100 units of onabotulinumtoxinA in the setting of overactive bladder. The data have shown comparable efficacy of 100 units of onabotulinumtoxinA to anticholinergic medications with reduced systemic side effects in the onabotulinumtoxinA-injected group, yet higher rates of retention and urinary tract infections. Patients receiving onabotulinumtoxinA were more likely to be dry, however. Patients who received anticholinergic drugs were more likely to suffer from dry mouth and other systemic side effects.[86]

In a study that compared sacral neuromodulation and onabotulinumtoxinA in 364 women with refractory urge urinary incontinence, treatment with onabotulinumtoxinA resulted in a greater reduction in the 6-month mean number of daily episodes of urge incontinence. However, the authors note that although the difference was statistically significant, it is of uncertain clinical importance. In addition, treatment with onabotulinumtoxinA resulted in a higher risk of urinary tract infection (UTI) and need for transient self-catheterizations.[87]

A comparative study shows neuromodulation and botulinum toxin to have fairly equivalent success rates at 200 units.[88]

Other intravesical pharmacotherapy

Intravesical instillation of oxybutynin chloride has been used in patients who are nonresponsive to oral oxybutynin or have severe adverse effects from it. Intravesical oxybutynin has proved effective for treatment of neurogenic bladder dysfunction, although the effects are often transient.. Honda et al reported that intravesical oxybutynin chloride solution supplemented with hydroxypropylcellulose (HPC), a mucosal adhesive substance, provided long-term improvement in bladder compliance in three of four children (ages 1 to 3 years) with neurogenic bladder.[89]

In older patients, intravesical oxybutynin can be self-administered following clean catheterization and has been shown to be safe and efficacious. Studies have shown that tissue and plasma concentration of the drug are higher after intravesical administration than after oral administration.[90] Despite higher plasma levels, adverse effects appear to be minimal. This finding suggests that a hepatic metabolite may be responsible for many of the adverse effects observed after oral administration.

Intravesical capsaicin, the main pungent ingredient of hot peppers, has shown benefit for the treatment of detrusor overactivity and neurogenic detrusor overactivity.[91, 92]  Similarly, resiniferatoxin, a naturally occurring pungent substance from the Euphorbia resinifera plant that has very potent capsaicinlike activity, has been used successfully to treat detrusor overactivity and neurogenic detrusor overactivity. However, intravesical capsaicin has not been approved for use in neurogenic detrusor overactivity, and resiniferatoxin was found to adhere to the plastic bags it was dispensed in; both agents have largely been superseded by onabotulinumtoxinA.[93]

Investigational agents

Potassium channel openers relax smooth muscle by increasing potassium efflux, with resultant membrane depolarization. Supersensitivity of the detrusor muscle to depolarizing stimuli, such as potassium, in individuals with urge incontinence is the theoretical basis for the use of these agents in patients with detrusor overactivity. One problem in the development of potassium channel openers for use in bladder disorders has been the lack of organ specificity. Overall progress toward the development of a viable clinical formulation has been disappointing.

Prostaglandin may have an excitatory role in bladder contractility, and prostaglandin inhibitors, in theory, may block bladder contractility. Clinical trials (eg, with indomethacin) have shown mixed and generally not impressive results. One research group reported evidence of the role of a relative prostacyclin deficiency in the promotion of bladder contractions. Pharmacotherapy to increase the ratio of prostacyclin to other prostaglandins has not been investigated to date.

A pilot study by Kuismanen et al suggested that urethral injection of a combination of patient-derived adipose stem cells (ASCs) and collagen can improve the symptoms of stress urinary incontinence in women, possibly providing a nonsurgical alternative to sling procedures for this condition. All five women in the study, each of whom received ASCs and collagen for stress urinary incontinence, demonstrated subjective improvement. In addition, three women passed the cough stress test at 1-year follow-up, and two women considered themselves cured.[94]

Treatment of Nocturnal Enuresis

While nocturnal enuresis—defined as involuntary loss of urine during sleep that occurs at least twice a week in children older than 5 years of age for at least 3 months—is the most common urologic complaint in pediatric patients, it also affects a significant number of adults. Nocturnal enuresis in adults may have multiple underlying pathologies, and treatment should first target identifiable etiologies, although a generalized approach can then be followed, utilizing behavioral and lifestyle modifications followed by medical therapy.[95, 96]

Such basic measures as evening fluid restriction and daytime bladder training can be beneficial.[97]  Desmopressin (DDAVP) decreases nighttime urine production; it is administered orally for primary nocturnal enuresis and intranasally or sublingually for nocturnal polyuria. Imipramine (2 mg/kg/d) has been one of the most common pharmacologic therapies. Oxybutynin and other anticholinergics have been used.

Although pharmacologic treatment can help, the underlying disorder often returns after discontinuation. Conditioning therapy with moisture-sensitive alarms are effective. Positive results usually persist even after the device is removed.

Nighttime voiding and incontinence

Nighttime voiding and incontinence are major problems in the older population. Women who have nocturia more than twice a night or experience nighttime bed-wetting may benefit from fluid restriction and the elimination of caffeine-containing beverages from their diet in the evening. Patients should restrict fluids after dinnertime so they can sleep uninterrupted through the night. In some cases, DDAVP can be used to decrease nighttime urine production and help reduce nocturia; however use caution regarding the risk of hyponatremia, especially in elderly patients.

Finally, individuals who develop edema of the lower extremities during the day experience nighttime voiding because excess fluid from lower extremities returns to the heart when the person is in a recumbent position. This problem may be handled with a behavior technique, support hose, and/or medications.

Advise these individuals to elevate their lower extremities several hours during the late afternoon or evening to stimulate a natural diuresis and limit the amount of edema present at bedtime. Support hose (Jobst) or intermittent sequential compression devices (SCDs) used briefly at the end of the day can reduce lower extremity edema and minimize night time diuresis, thus improving sleep.

Lastly, the judicious use of diuretics has been associated with a decrease in lower-extremity edema and lower nighttime urine volumes. If patients are already taking diuretics, altering the administration time of the diuretics may decrease nighttime voiding and incontinence. Depending on other medical conditions, changing the time of diuretic administration to the morning may prevent large nighttime urinary volumes.

Pelvic Floor Rehabilitation

A level A guideline from the American Congress of Obstetricians and Gynecologists (ACOG) recommends pelvic floor training as an apparently effective noninvasive treatment for adult women with stress and mixed incontinence.[98] In women with mild stress urinary incontinence without vaginal prolapse, a success (ie, cure, improvement) rate of 75-80% may be attained by properly performed pelvic floor exercises.

A systematic review and meta-analysis of 31 studies concluded that pelvic floor muscle exercises can cure, or relieve symptoms, of stress urinary incontinence, mixed urinary incontinence, and urgency urinary incontinence in women. The authors recommended that although further research into long-term effectiveness and cost-effectiveness is needed, pelvic floor exercise therapy could be included in first-line conservative management programs for women with urinary incontinence.[99]

Pelvic floor exercises (ie, Kegel exercises) work best in mild cases of stress incontinence associated with urethral hypermobility but not intrinsic sphincter deficiency. They also benefit men who develop urinary incontinence following prostate surgery.[100]

Kegel exercises have been shown to improve the strength and tone of the muscles of the pelvic floor (ie, the levator ani, and particularly the pubococcygeus). During times of increased intra-abdominal pressure, tensing of these muscles tightens the connective tissue that supports the urethra. Thus, pressure transmission to the urethra may increase, and the urethra compresses shut during times of increased stress.

The exercises consist of voluntary contractions of the muscles of the pelvic floor. Because both fast-twitch and slow-twitch muscle fibers are found in the levator ani complex, both rapid contractions and slow contractions held for maximal duration should be performed to achieve the best possible results.

Patients can perform pelvic floor muscle exercises by drawing in or lifting up the levator ani muscles, as if to control urination or defecation with minimal contraction of abdominal, buttock, or inner-thigh muscles. The patient can confirm that she is using the correct muscles at home by periodically performing the contractions during voiding with the goal of interrupting the urinary stream.

If instructions for Kegel exercises are provided verbally or in written form alone, a significant percentage of individuals perform repetitive Valsalva maneuvers or gluteal contractions rather than pelvic muscle contractions. Therefore, instructing the patient in the examining room by having her squeeze the examiner's intravaginal or intrarectal finger is important.

Initially, patients are instructed to perform the squeezing exercise 5 times, holding each contraction for a count of 5. Five contractions equal 1 set. Patients should do 1 set every hour while they are awake, during such activities as driving, reading, or watching television. An alternate program requires 1 set of exercises every time the patient uses a bathroom. Soon after starting the exercises, the patient may be able to hold each contraction for at least 10 seconds, followed by an equal period of relaxation.

Another regimen is to perform the exercises for 10 minutes twice a day using an audiocassette tape. The audiocassette coaches the patient to contract the levator ani muscles for a count of 10 seconds and then to relax for a count of 10 seconds, performing 25 repetitions in a row. Twenty-five contractions equal 1 set. Perform the first set slowly, followed by a second set performed rapidly.

Approximately 6-12 weeks of exercises are required before improvement is noted, and 3-6 months are needed before maximal benefit is reached. The key to success with pelvic floor exercises is a commitment on the patient’s part to performing them for a long period of time. Patients who do not tend to revert back to pretherapy levels of incontinence.

Individuals who benefit most tend to be young healthy women who can identify the levator ani muscles (specifically, the pubococcygeus portion) accurately. Older adults with weak pelvic muscle tone or women who have difficulty recognizing the correct muscles need adjunctive therapy such as biofeedback or electrical stimulation. Patients with severe neuromuscular damage to the pelvic floor may not be able to perform Kegel exercises, even with proper instruction.

Internet and mail-based treatment programs based on pelvic floor muscle training significantly improved symptoms and condition-related quality of life in a study of 250 community-dwelling women (aged 18-70 years) with stress urinary incontinence. At 1-year follow-up, 69.8% (60/86) of patients in the Internet treatment group and 60.5% (46/76) of patients in the postal treatment group reported continued satisfaction with their treatment result. At 2-year follow-up, these proportions were 64.9% (48/74) and 58.2% (46/79), respectively.[101]

However, the addition of pelvic muscle floor muscle exercises to incontinence surgery may not result in clinically important improvement. The Effects of Surgical Treatment Enhanced With Exercise for Mixed Urinary Incontinence (ESTEEM) trial compared outcomes in 207 patients who underwent midurethral sling surgery and 209 patients who received surgery combined with behavioral and pelvic muscle floor therapy (1 preoperative and 5 postoperative sessions through 6 months). Incontinence symptoms, measured by the Urogenital Distress Inventory (UDI) long form, fell from 178.0 points at baseline to 30.7 at 12 months in the combined group, and fell from 176.8 to 34.5 points in the surgery-only group. The model-estimated between-group difference did not meet the minimal clinically important difference threshold.[102]

Pelvic muscle exercises may be used alone, augmented with vaginal cones, reinforced with biofeedback therapy, or enhanced with electrical stimulation.

Vaginal cones

Vaginal cones are weighted devices designed to increase the strength of the pelvic floor muscles. The cones are available in sets of 5, with identical shape and volume but increasing weights (ie, 20 g, 32.5 g, 45 g, 60 g, 75 g). As part of a progressive resistive exercise program, a single cone is inserted into the vagina and held in place by tightening the levator ani muscles for as long as 15 minutes. As the levator ani muscles become stronger, the exercise duration may be increased to 30 minutes.

This exercise is performed twice daily. The intravaginal weight provides the sensory feedback for the desired pelvic muscle contraction. The sustained contraction required to retain the weight within the vagina increases the strength of the pelvic floor muscles. The best results are achieved when standard pelvic muscle exercises (ie, Kegel exercises) are performed with intravaginal weights.

In premenopausal women with stress incontinence, the subjective cure or improved continence status is approximately 70-80% after 4-6 weeks of treatment. Vaginal cones also may be useful for postmenopausal women with stress incontinence; however, the cones are not effective in the treatment of pelvic organ prolapse.


Biofeedback therapy is a form of pelvic floor muscle rehabilitation using an electronic device for individuals having difficulty identifying levator ani muscles. Biofeedback therapy is recommended for treatment of stress incontinence, urge incontinence, and mixed incontinence.

Biofeedback therapy uses a computer and electronic instruments to relay auditory or visual information to the patient about the status of pelvic muscle activity. These devices allow the patient to receive immediate visual feedback on the activity of the pelvic floor muscles, thereby providing incentive and confirmation of proper performance of the muscle contractions.

Biofeedback is intensive therapy, with weekly sessions performed in an office or a hospital by a trained professional, and it often is followed by a regimen of pelvic floor muscle exercises at home. During biofeedback therapy, a special tampon-shaped sensor is inserted in the patient's vagina or rectum and a second sensor is placed on her abdomen. These sensors detect electrical signals from the pelvic floor muscles. The patient then is instructed to contract and relax the pelvic floor muscles upon command.

When the exercises are performed properly, the electric signals from the pelvic floor muscles are registered on a computer screen. Biofeedback, using multimeasurement recording, displays the simultaneous measurement of pelvic and abdominal muscle activity on the computer monitor.

Biofeedback allows the patient to correctly identify the pelvic muscles that need rehabilitation. The benefit of biofeedback therapy is that it provides the patient with minute-by-minute feedback on the quality and intensity of her pelvic floor contraction. Combining bladder and urinary sphincter biofeedback allows the patient to regulate the pelvic muscle contraction in response to increasing bladder volumes and to monitor the bladder activity. Biofeedback is best used in conjunction with pelvic floor muscle exercises and bladder training.

Studies on biofeedback combined with pelvic floor exercises show a 54-87% improvement with incontinence. The best biofeedback protocol is the one that reinforces levator ani muscle contraction with inhibition of abdominal and bladder contraction. Reports using this method show a 76-82% reduction in urinary incontinence. Biofeedback also has been used successfully in the treatment of men with urge incontinence and intermittent stress incontinence after prostate surgery.

Studies have demonstrated significant improvement in urinary incontinence in women with neurologic disease and in the frail older population when a combination of biofeedback and bladder training is used. Biofeedback provides a specific reinforcement for pelvic muscle contraction that is isolated from the counterproductive abdominal contraction. Therefore, awareness of levator ani muscle contraction can be achieved more efficiently using biofeedback than vaginal palpation alone.

Biofeedback produces a greater reduction in female urinary incontinence, compared with pelvic muscle exercises alone. Overall, the medical literature indicates that pelvic muscle exercises and other behavioral strategies, with or without biofeedback, can cure or reduce incontinence. However, the maximum benefit is derived from any pelvic muscle rehabilitation and education program when ongoing reinforcement and guidance, such as biofeedback therapy, are provided.

Electrical stimulation

Electrical stimulation is a more sophisticated form of biofeedback used for pelvic floor muscle rehabilitation. This treatment involves stimulation of levator ani muscles using painless electric currents.

Electrical stimulation of pelvic floor muscles produces a contraction of the levator ani muscles and external urethral sphincter while inhibiting bladder contraction. This therapy depends on a preserved reflex arc through the intact sacral micturition center. Similar to biofeedback, electrical stimulation can be performed at the office or at home. Electrical stimulation can be used in conjunction with biofeedback or pelvic floor muscle exercises.

Electrical stimulation therapy requires a similar type of probe and equipment as those used for biofeedback. This form of muscle rehabilitation is similar to the biofeedback therapy, except small electric currents are used. Nonimplantable pelvic floor electrical stimulation uses vaginal sensors, anal sensors, or surface electrodes. Adverse reactions are minimal.

Like biofeedback, pelvic floor muscle electrical stimulation has proved effective in treating female stress incontinence. It may be effective in men and women with urge or mixed incontinence. Urge incontinence secondary to neurologic diseases may be decreased with this therapy. Unfortunately, this treatment does not appear to benefit patients who are cognitively impaired.

Electrical stimulation may be the most beneficial when stress incontinence and very weak or damaged pelvic floor muscles coexist. A regimented program of electrical stimulation helps these weakened pelvic muscles contract so they can become stronger. For women with urge incontinence, electrical stimulation may help the bladder relax and prevent it from contracting involuntarily.

Electrical stimulation appears to be the most effective when augmented with pelvic floor exercises. In order to derive significant benefit, stimulation must be performed for a minimum of 4 weeks, and patients must continue pelvic floor exercises after the treatment.

The 2 main modes of electrical stimulation therapy are long-term stimulation and short-term maximal stimulation. Long-term therapy requires the use of an intravaginal or intra-anal probe for several hours a day. Low intensity, subthreshold stimulation is used. Patient acceptance can be low due to the discomfort of wearing the probe for several hours each day.

Short-term maximal stimulation therapy was developed because it is more practical, and high intensity stimulation may produce a better inhibitory effect. Maximal inhibition of involuntary bladder contractions takes place at stimulation intensity levels that are 2-3 times sensory threshold levels. The closer the proximity of the stimulating device to the selected nerve, the lower the intensity can be and remain effective. In practical terms, maximal tolerance levels usually are approximately 1.5-2 times the sensory perception threshold.

Short-term maximal therapy uses high-intensity stimulation for 15-30 minutes once or twice a day. Treatment generally is continued over several weeks. Improvement rates of 52-77% have been documented. Carryover effects of 31-92% have been shown for as long as 1 year after therapy.

Transcutaneous electrical nerve stimulation (TENS) has been tried in patients with detrusor overactivity, using several different methods. Applying a positive electrode applied to the area of the anal sphincter and a negative electrode to the posterior tibial nerve has yielded mixed results in 2 studies. TENS of the S2-S3 dermatomes has been tried with some success.

An interesting method of alternating stimulation of the hamstring and quadriceps muscle groups has been reported. In this study, which included patients with detrusor overactivity, 20 minutes of stimulation per day was given for 14 consecutive days and clinical improvement was observed in 68% of subjects. The mechanism of detrusor inhibition by this method of TENS is unclear but may involve increases in segmental inhibitory tone due to manipulation of peripheral neural input.

Interferential therapy is a type of TENS in which external electrodes are positioned over the pelvis, and the interference produced by the competing electrical fields produces low-level nerve stimulation in the area of interference. A small study showed a 90% improvement rate in 20 patients with detrusor instability that was unresponsive to pharmacotherapy. In 18 months of observation, no complications were reported, and no recurrences were observed.


Acupuncture is a promising alternative therapy. A 2013 review of four randomized controlled trials of of acupuncture or acupressure in the treatment of urinary incontinence found no statistically significant improvement in urinary incontinence, but did note favorable effects on overactive bladder symptoms and quality of life.[103] A more recent randomized clinical trial by Liu et al in 504 women with stress urinary incontinence, treatment with electroacupuncture involving the lumbosacral region (18 sessions over 6 weeks) resulted in less urine leakage compared with sham electroacupuncture.[104]

Extracorporeal magnetic resonance therapy

Extracorporeal magnetic resonance therapy has been introduced as a therapy for stress incontinence. The NeoControl unit (Neotonus, Marietta, Ga.) was approved by the Food and Drug Administration (FDA) for this purpose in 2000. Resonating magnetic flux within a magnetic field induces electrical depolarization of targeted nerves and muscles. No probes are required. The patient simply sits on a chair containing the magnetic device.

A small study achieved an improvement rate of 77% after 8 weeks of therapy, with 56% of patients being completely dry. However, a 3-year follow-up study found that the benefits tend to be temporary: at 6 months, the recurrence rate was 53%.[105]

Weight Loss

Given that obesity has been identified as a risk factor for development of urinary incontinence, it is not surprising that interventions to address obesity can result in improved continence. Researchers who followed a prospective cohort of women who were morbidly obese found that prevalence of urinary incontinence decreased after bariatric surgery. The magnitude of weight loss was associated with reduction in urinary incontinence prevalence.[106]

Another group demonstrated that a behavioral intervention targeting weight loss reduced urinary incontinence in women who were overweight and obese compared with a control group.[107]

The benefits of weight loss in patients who are overweight or obese are numerous and encompass improvements in type 2 diabetes mellitus, hypertension, dyslipidemia, and mood. The results above should encourage patients to consider weight loss as a first-line treatment for reducing urinary incontinence before embarking on more invasive medical and surgical therapies.

A study by Phelan et al found that moderate weight loss reduced the incidence of urinary incontinence among overweight/obese women with type 2 diabetes; however, it did not improve the resolution rates.[108]

Behavioral Approaches

A level A guideline from the ACOG recommends behavioral therapy, including bladder training and prompted voiding, as a noninvasive method for improving symptoms of urge and mixed incontinence in women.[98] Timed, frequent voiding can be used to minimize incontinence, especially if the bladder is kept empty before incontinence-producing activities.

Bladder training is most useful in young women. It may not be successful in frail older women. It is difficult to implement in cognitively impaired persons.

Bladder training involves relearning how to urinate. This method of rehabilitation most often is used for active women with urge incontinence and sensory urge symptoms; however, it also may be used for stress and mixed incontinence. Often, these patients find that when they respond to symptoms of urge and return to the bathroom soon after they have voided, they do not urinate much. In other words, although their bladder is not full, it is signaling for them to void.

Bladder training generally consists of self-education, scheduled voiding with conscious delay of voiding, and positive reinforcement. Bladder training requires the patient to resist or inhibit the sensation of urgency and postpone voiding. Patients urinate according to a scheduled timetable rather than the symptoms of urge.

Bladder training also uses dietary tactics such as adjustment in fluid intake and avoidance of dietary stimulants. In addition, distraction and relaxation techniques allow delayed voiding to help distend the urinary bladder. By using these strategies, patients can induce the bladder to accommodate progressively larger voiding volumes.

Initially, the interval goal is determined by the patient's current voiding habits and is not enforced at night. The interval goal between each void usually is set at 2-3 hours, but may be set further apart if desired.

As the bladder becomes accustomed to this delay in voiding, the interval between mandatory voids is increased progressively, in 15- to 30-minute increments, with simultaneous distraction or relaxation techniques and dietary modification. Typically, the interval is increased by 15 minutes per week until the patient reaches a voiding interval of approximately 3-4 hours.

Another method of bladder training is to maintain the prearranged schedule and disregard the unscheduled voids. However, patients need to continue to maintain the prearranged voiding times. They need to continue this program for several months.

Bladder training can be conducted with or without simultaneous pharmacotherapy. Subjective response rates of 85% and objective response rates of 50% have been achieved with short-term observation.

Symptoms of urgency and frequency can develop over time with this strategy due to decreased bladder capacity. Anticipatory pelvic floor contractions can be taught to patients to cut down on incontinence episodes. The patient is taught to perform a strong pelvic floor contraction just before anticipated episodes of increased intra-abdominal pressure, such as a cough or a sneeze.

Alternatively, bladder ultrasound may be employed. If patients need an objective demonstration that their bladder is relatively empty, a portable bladder scanner may be used.

A bladder scanner is a portable ultrasound machine that measures the amount of urine present in a patient's bladder. With this device, patients can void when their bladder fills to a certain volume visible on ultrasound rather than responding to the sensation of needing to go to the bathroom. When patients feel the urge to void, they can check the bladder using the scanner to visualize how much urine is present. If the bladder is empty, they should ignore that sensation.

Clearly, behavioral therapies can be successful in the highly motivated patient in the short-term. Long-term efficacy is much less certain, and relapse rates, when reported, have been high. In addition to a highly motivated patient, this type of therapy requires a dedicated team to provide support and reinforcement to the patient.

Modification of activity occasionally can be a solution to incontinence-related specific activities. For example, if a woman experiences incontinence only during high-impact aerobics, substitution of another fitness activity, such as swimming, may solve the incontinence problem.

Surgical Treatment

Patients with urinary incontinence that is refractory to medical therapy may be offered surgical treatment. The procedures used vary, depending on whether the patient has stress or urge incontinence.

Stress incontinence

Surgical care for stress incontinence involves procedures that increase urethral outlet resistance. In women, recommended procedures include the following[109] :

  • Midurethral sling (synthetic)
  • Autologous fascia pubovaginal sling
  • Bladder neck suspension (Burch colposuspension)

In a randomized study of 460 women with moderate to severe stress urinary incontinence, 90.8% of those who underwent midurethral sling surgery reported improvement at 1-year follow-up, compared with 64.4% of those who underwent physiotherapy training.[110] The rate of objective cure was 76.5% in the surgery group and 58.8% in the physiotherapy group.

Midurethral slings may be transobturator or retropubic.[109] Transobturator vaginal tape (TVT-O) is widely used for stress incontinence in women. In an Italian study of 181 consecutive cases of TVT-O surgery, Serati et al found no significant difference between older women (70 years or older) and younger women in terms of cure rate, voiding dysfunction, vaginal erosion, persistent groin pain, or onset of de novo overactive bladder.[7]  The cure rate was 88.3% for the older group and 92.5% for the younger group.

In a study specifically focusing on the use of TVT-O in women with urodynamically proven, pure stress incontinence, Serati et al found TVT-O implantation to be a highly effective treatment option in this population, with a very high cure rate and a low complication rate.[111] The 5-year subjective cure rate was 90.3%, and the 5-year objective cure rate was 90.8%. The incidence of de novo overactive bladder was 24.3% at 5 years; no factor predictive of this condition was identified.

A review of long-term outcome in over 95,000 English women who had a first-ever midurethral mesh sling insertion for stress urinary incontinence estimated that the rate of mesh sling removal at 9 years is 3.3%. The removal risk after transobturator insertion was lower than the risk after retropubic insertion (2.7% versus 3.6%, respectively).[112]

For more information, see Vaginal Sling Procedures.

The use of bulking agents has had some resurgence, due to concerns about the use of mesh for sling surgeries. At present, this has happened less in the United States than in other countries. Nevertheless, encouraging data from around the world and an office-based approach to bulking agents make it a viable option for many women with stress incontinence. The use in males is not as well established, with poor success rates reported. Failure in male patients may result from the injectables themselves or, in the common setting of post-prostatectomy incontinence, from the host factors of local scarring or radiation changes.

Therapy for stress urinary incontinence using mesenchymal stem cells has proved safe and effective. However, the underlying mechanisms of action remain nebulous, so further clinical trials are warranted.[113]

Updated guidelines on the treatment of female stress incontinence, from the American Urological Society and the Society of Urodynamics, Female Pelvic Medicine & Urogenital Reconstruction, include a treatment algorithm and associated data.[109] The algorithm is as follows:

  • Initial evaluation includes history, physical examination including a pelvic examination, demonstration of stress incontinence, postvoid residual assessment, and urinalysis. Additional evaulation should be performed in situations such as inability to demonstrate stress incontinence, abnormal urinalysis, or lack of definitive diagnosis. Cystoscopy can be performed if there is concern for lower urinary tract abnormalities. Urodynamics can be omitted if stress incontinence is clearly demonstrated. 
  • Treatment can be either surgical or nonsurgical. Nonsurgical treatment includes continence pessary, vaginal inserts, and pelvic floor muscle exercises with or without biofeedback.
  • Surgical options include midurethral sling (retropubic, transobturator, or single-incision sling), autologous fascia pubovaginal sling, Burch colposuspension, and bulking agents
  • There are also specific recommendations on special cases clearly outlined in the literature.

Male stress incontinence

The transobturator male sling may be of particular benefit to men who experience stress incontinence after prostatectomy.[6]  Artificial sphincter placement is also effective in this population.[114]

The AMS 800 (American Medical Systems, Minnetonka, Minn) artificial urinary sphincter is a standard option for the surgical management of male stress urinary incontinence. A retrospective review by Yafi et al of 27,096 cases of AMS 800 primary implantation determined that 21.1% of cases required either revision or explantation. Younger patient age and penoscrotal surgical approach were associated with higher rates of device explantation and revision, while use of a tandem cuff was associated with higher explantation rates.[115]

For more information, see Artificial Urinary Sphincter Placement.

Urge incontinence

Surgical care for urge incontinence involves procedures that improve bladder compliance, bladder capacity, or both. Surgical treatment is considered after the urilization of behavioral therapy, pharmacologic therapy, and onobotulinum toxin/neuromodulin respectively.[116] Acceptable operations that include the following:

Dietary Modification

Certain foods in a daily diet can worsen symptoms of urinary frequency and urge incontinence. If a patient's diet contains dietary stimulants, changes in the diet may help in ameliorating incontinence symptoms.

Dietary stimulants are substances contained within the food or drink that either cause or exacerbate irritative voiding symptoms. By eliminating or minimizing the intake of dietary stimulants, unwanted bladder symptoms can be improved or possibly cured.

Avoidance of dietary stimulants begins with consumer awareness through careful label reading and maintaining a daily diet diary. Experimenting with dietary changes is not appropriate for everyone and should be carried out on an individual basis.

A placebo-controlled pilot study in 56 postmenopausal women 50 years or older with urgency urinary incontinence and vitamin D insufficiency (serum vitamin 25-hydroxyvitamin D level 30 ng/mL or less) found that vitamin D supplementation significantly reduced incontinence episodes in Black women only, although a beneficial trend was evident overall. The authors recommend further study of vitamin D3 supplementation, particularly in women at high risk.[118] Another randomized trial, in 90 postmenopausal women with urgency urinary incontinence or nocturia, found that weekly use of vitamin D 50,000 IU tablets for 8 weeks can reduce the severity of urgency incontinence and the frequency of nocturia, and reduce their impact on disruption in daily life.[119]


Spicy foods may contribute to urge incontinence. Some examples of hot spices include curry, chili pepper, cayenne pepper, and dry mustard. A few medical reports have indicated that the avoidance of spicy foods may have a beneficial effect on urinary incontinence.

A second food group that may worsen irritative voiding symptoms is citrus fruit. Fruits and juices that have an acidic pH worsen preexisting urge incontinence. Examples of fruits that have significant acidity include grapefruits, oranges, limes, and lemons.

A third food group that may worsen urinary bladder incontinence is chocolate-containing sweets. Chocolate snacks and treats contain caffeine, which is a bladder-irritating agent. Excessive intake of chocolate confectioneries worsens irritative bladder symptoms.


The quantity and types of fluids consumed influences urinary voiding symptoms. Fluids refer to all the beverages a person consumes in a day, which include water, soda, and milk. The human body receives fluids from beverages consumed, water contained in the food ingested, and water metabolized from food eaten.

The recommended amount of fluids consumed (all types) in 24 hours totals 6-8 glasses. The benefits of adequate fluid intake include prevention of dehydration, constipation, UTI, and kidney stone formation.

Some patients tend to drink water to excess. They may simply enjoy the taste, they may be on medication that makes their mouths dry, or they may be on a weight-loss diet that requires consuming abundant amounts of water. Drinking water to excess actually worsens irritative bladder symptoms.

In contrast, some older women do not drink enough fluid to keep themselves well hydrated. They minimize their fluid intake to unacceptable levels, thinking that if they drink less, they will experience less incontinence. Trying to prevent incontinence by restricting fluids to excess may lead to bladder irritation and actually worsen urge incontinence.

In addition, dehydration contributes to constipation. If a patient has a problem with constipation, recommend eating a high-fiber diet, receiving adequate hydration, and administering laxatives.

The exact amount of fluid needed per day is calculated based on the patient's lean body mass. Thus, the amount of fluid requirement varies per individual. For an average adult woman with symptomatic urinary incontinence, drinking approximately 6 glasses of liquid per day is generally recommended.

Many beverages contain caffeine. Caffeine is a natural diuretic and has a direct excitatory effect on bladder smooth muscle. Thus, caffeine-containing products produce excessive urine and exacerbate symptoms of urinary frequency and urgency.

Caffeine-containing products include coffee, tea, hot chocolate, and colas. Even chocolate milk and many over-the-counter medications contain caffeine. Of these products, coffee contains the most amount of caffeine. Drip coffee contains the most caffeine, followed by percolated coffee and then instant coffee. Even decaffeinated coffee contains a small amount of caffeine, approximately the same amount found in chocolate milk.

Persons who consume a large amount of caffeine should slowly decrease the amount of caffeine consumed to avoid significant withdrawal responses, such as headache and depression.

Studies have shown that drinking carbonated beverages, citrus fruit drinks, and acidic juices may worsen irritative voiding or urge symptoms. Consumption of artificial sweeteners also has been theorized to contribute to urge incontinence.


All suspected cases of cauda equina syndrome, spinal cord compression, or paraspinal abscess warrant admission and neurology and neurosurgery consultation.[26] The following conditions warrant a urology consultation, although for ED patients, this can be obtained in the outpatient setting[26] :

  • Suspected bladder neoplasm, unexplained hematuria, and recent voiding symptoms
  • History of prior radical pelvic surgery or pelvic radiation
  • Prior pelvic incontinence surgery
  • Gross pelvic prolapse


Medication Summary

The goal of therapy is to improve the symptoms of frequency, nocturia, urgency, and urge incontinence.  Pharmacologic treatment options include anticholinergics, antispasmodic agents, tricyclic antidepressants (TCAs), and beta-3-adrenergic receptor agonists.

In patients with stress incontinence, alpha agonist treatment results in contraction of the internal urethral sphincter and increases the urethral resistance to urinary flow. Sympathomimetic drugs, estrogen, and tricyclic agents increase bladder outlet resistance to improve symptoms of stress urinary incontinence.

Pharmacologic therapy for stress incontinence and an overactive bladder may be most effective when combined with a pelvic exercise regimen. The 3 main categories of drugs used to treat urge incontinence include anticholinergic drugs, antispasmodics, and TCAs.

When a single drug treatment does not work, a combination therapy such as oxybutynin (Ditropan) and imipramine (Tofranil) may be used. Although their mechanism of action differs, oxybutynin and imipramine work together to improve urge incontinence.

Oxybutynin causes direct smooth muscle relaxation of the urinary bladder and has local anesthetic properties. Imipramine has a direct inhibitory and local anesthetic effect on the bladder smooth muscle, similar to oxybutynin; however, imipramine also increases the bladder outlet resistance at the level of the bladder neck. Thus, the combination of these drugs produces a synergistic effect to relax the unstable bladder and to hold in urine and prevent urge incontinence. Potential anticholinergic adverse effects may be additive because both drugs have similar adverse reactions.

Beta-3 adrenergic receptor agonists (eg, mirabegron, vibegron) cause relaxation of the detrusor muscle and increased bladder capacity. These agents are indicated for overactive bladder with symptoms of urge urinary incontinence, urgency, and urinary frequency.

Alpha-Adrenergic Agonists

Class Summary

The bladder neck contains a high concentration of receptors that are sensitive to alpha-agonists. Alpha-agonists increase bladder outlet resistance by contracting the bladder neck. These agents are beneficial in the treatment of mild to moderately severe stress incontinence in women.


The active metabolite of midodrine, desglymidodrine, is an alpha1-agonist that may increase bladder outlet resistance.

Pseudoephedrine hydrochloride (Sudafed, Genaphed, SudoGest)

Pseudoephedrine helps stress incontinence. The subjective improvement and cure rates are similar to that of phenylpropanolamine, which was recalled from the US market. Pseudoephedrine stimulates vasoconstriction by directly activating alpha-adrenergic receptors.

Anticholinergic Agents

Class Summary

These agents represent first-line medicinal therapy in women with urge incontinence. These agents are useful in treating urinary incontinence associated with urinary frequency, urgency, and nocturnal enuresis.

Anticholinergic agents inhibit the binding of acetylcholine to the cholinergic receptor, thereby suppressing involuntary bladder contraction of any etiology. In addition, they increase the urine volume at which first involuntary bladder contraction occurs, decrease the amplitude of the involuntary bladder contraction, and may increase bladder capacity.

All anticholinergic drugs have a similar performance profile and toxicity. Potential adverse effects of all anticholinergic agents include blurred vision, dry mouth, heart palpitations, drowsiness, and facial flushing. When anticholinergic drugs are used in excess, the bladder may go into acute urinary retention.

All drugs with anticholinergic effects or side effects are contraindicated if patients have documented narrow-angle glaucoma. Wide-angle glaucoma is not a contraindication to their use.

Other contraindications to anticholinergic use are urinary retention, bowel obstruction, ulcerative colitis, myasthenia gravis, and severe heart diseases. Because of the potential for drowsiness—especially when combined with alcohol, sedatives, or hypnotic drugs—these agents may impair the patient's ability to perform hazardous activities, such as driving or operating heavy machinery.

Dicyclomine hydrochloride (Bentyl)

An anticholinergic agent with smooth muscle relaxant properties, dicyclomine blocks the action of acetylcholine at parasympathetic sites in secretory glands and smooth muscle.

Darifenacin (Enablex)

Darifenacin is an extended-release product eliciting competitive muscarinic receptor antagonistic activity. It reduces bladder smooth muscle contractions. Darifenacin has high affinity for M3 receptors involved in bladder and GI smooth muscle contraction, saliva production, and iris sphincter function. It is indicated for overactive bladder with symptoms of urge incontinence, urgency, and frequency. Swallow whole; do not chew, divide, or crush.

Solifenacin succinate (VESIcare)

Solifenacin elicits competitive muscarinic receptor antagonist activity, which results in anticholinergic effects and inhibition of bladder smooth muscle contraction. This agent is indicated for overactive bladder with symptoms of urgency, frequency, and urge incontinence. It must be swallowed whole; do not crush or chew.

Hyoscyamine sulfate (Levsin/SL, Levsin, Levsinex, Cystospaz-M, Levbid)

Hyoscyamine blocks the action of acetylcholine at parasympathetic sites in smooth muscle, secretory glands, and the CNS, which in turn has antispasmodic effects. Hyoscyamine is absorbed well by the GI tract. Food does not affect absorption of this drug. Hyoscyamine is available in sublingual form (Levsin SL, Symax SL), conventional tablets (Levsin), and extended-release tablets (Levbid).

Propantheline (Pro-Banthine)

A prototypical anticholinergic agent, propantheline blocks action of acetylcholine at postganglionic parasympathetic receptor sites.

Tolterodine (Detrol and Detrol LA)

Competitive muscarinic receptor antagonist for overactive bladder. However, it differs from other anticholinergic types in that it has selectivity for urinary bladder over salivary glands. Exhibits a high specificity for muscarinic receptors, has minimal activity or affinity for other neurotransmitter receptors and other potential targets such as calcium channels. In clinical studies, the mean decrease in urge incontinence episodes was 50% and the mean decrease in urinary frequency was 17%. The mean decrease in urge incontinence episodes per wk was 53% for Detrol LA 4 mg qd.

Trospium (Sanctura)

Quaternary ammonium compound that elicits antispasmodic and antimuscarinic effects. Antagonizes acetylcholine effect on muscarinic receptors. Parasympathetic effect reduces smooth muscle tone in the bladder. Indicated to treat symptoms of overactive bladder (eg, urinary incontinence, urgency, frequency).

Fesoterodine (Toviaz)

Competitive muscarinic receptor antagonist. Antagonistic effect results in decreased bladder smooth muscle contractions. Indicated for symptoms of overactive bladder (eg, urinary urge incontinence, urgency, and frequency). Available as 4- or 8-mg extended-release tab.

Antispasmodic Drugs

Class Summary

These agents relax the smooth muscles of the urinary bladder. By exerting a direct spasmolytic action on the smooth muscle of the bladder, these medications have been reported to increase bladder capacity and effectively decrease or eliminate urge incontinence.

The adverse effect profile of antispasmodic drugs is similar to that of anticholinergic agents. These drugs may impair the ability to perform activities requiring mental alertness and physical coordination. Drinking alcohol and using sedatives in combination with these antispasmodic drugs is contraindicated.

Oxybutynin chloride (Ditropan IR, Ditropan XL, Gelnique)

Both the immediate-release and the extended-release forms of oxybutynin have both an anticholinergic and a direct smooth muscle relaxant effect on the urinary bladder. In addition, oxybutynin provides a local anesthetic effect on the irritable bladder.

The human detrusor has M2 and M3 muscarinic receptors. The M3 receptor mediates contractile response of human detrusor. Oxybutynin has greater affinity for the M3 receptor. Urodynamic studies have shown oxybutynin increases bladder size, decreases frequency of symptoms, and delays initial desire to void.

Ditropan XL has an innovative drug delivery system: oral osmotic delivery system (OROS). The Ditropan XL tablet has a bilayer core that contains a drug layer and a "push layer" that contains osmotic components. The outer tablet is composed of a semipermeable membrane with a precision laser-drilled hole that allows the drug to be released at a constant rate.

When the drug is ingested, the aqueous environment in the gastrointestinal tract causes water to enter the tablet via semipermeable membrane at a constant rate. The introduction of water inside the tablet liquefies drug and causes the push layer to swell osmotically. As the push layer swells, it forces the drug suspension out the hole at a constant rate over a 24-h period.

Ditropan XL achieves steady-state levels over a 24-h period. It avoids first pass metabolism in liver and upper gastrointestinal tract to avoid cytochrome P450 enzymes. It has excellent efficacy, with minimal adverse effects.

Flavoxate (Urispas)

Flavoxate is used for symptomatic relief of dysuria, urgency, nocturia, and incontinence, as may occur in cystitis, prostatitis, urethritis, and urethrocystitis/urethrotrigonitis. It exerts a direct relaxant effect on smooth muscles via phosphodiesterase inhibition. It provides relief for a variety of smooth muscle spasms.

Tricyclic Antidepressants

Class Summary

Historically, these drugs were used to treat major depression; however, TCAs have an additional use in the treatment of bladder dysfunction. They function to increase norepinephrine and serotonin levels. In addition, they exhibit an anticholinergic and direct muscle relaxant effect on the urinary bladder. Due to their black box warnings, the use of TCAs are often avoided.

Imipramine hydrochloride (Tofranil)

A typical TCA, imipramine facilitates urine storage by decreasing bladder contractility and increasing outlet resistance. It has an alpha-adrenergic effect on the bladder neck and an antispasmodic effect on the detrusor muscle. Imipramine also has a local anesthetic effect on bladder mucosa.

Amitriptyline hydrochloride (Elavil)

A TCA with sedative properties, amitriptyline increases the circulating levels of norepinephrine and serotonin by blocking their reuptake at nerve endings. It ineffective for use in urge incontinence but is extremely effective in decreasing symptoms of urinary frequency in women with pelvic floor muscle dysfunction. Amitriptyline restores serotonin levels and helps break the cycle of pelvic floor muscle spasms. It is well tolerated and effective in the majority of women with urinary frequency.

Beta3 Agonists

Class Summary

Cause relaxation of the detrusor smooth muscle of the urinary bladder and increased bladder capacity.

Mirabegron (Myrbetriq)

Indicated for overactive bladder (OAB) with symptoms of urge urinary incontinence, urgency, and urinary frequency

Vibegron (Gemtesa)

Indicated for adults with OAB who have symptoms of urge urinary incontinence, urgency, and urinary frequency. 


Class Summary

Conjugated estrogens increase the tone of urethral muscle by up-regulating the alpha-adrenergic receptors in the surrounding area, and they enhance alpha-adrenergic contractile response to strengthen the pelvic muscles, which is important in urethral support (ie, prevents urethral hypermobility). Mucosal turgor of periurethral tissue from proper nourishment enhances urethral mucosal coaptation.

The result is an improved mucosal seal effect, which is important in urethral function (ie, it prevents intrinsic sphincter deficiency). Estrogen supplementation appears to be the most effective in postmenopausal women with mild-to-moderate incontinence. Both types of stress incontinence improve with estrogen fortification. There is also evidence however, estrogen use can exacerbate incontinence.

Conjugated estrogen (Premarin)

Conjugated estrogen may be used as an adjunctive pharmacologic agent for postmenopausal women with stress or mixed incontinence. Oral or vaginal form of estrogen may be used. The usual oral dose is 0.3-1.25 mg taken daily in a cyclic regimen.

When oral estrogens are needed, prescribe 0.625-mg pills. To prevent overstimulation of the uterus, conjugate estrogen is taken once a day for 21 consecutive days, followed by 7 days without the drug (eg, 3 wk on and 1 wk off). This regimen is repeated as necessary and tapered or discontinued at 3- to 6-month intervals.

Conjugated estrogen vaginal cream is available in a package with a plastic applicator and a tube that contains 42.5 grams of conjugated estrogens. Each gram contains 0.625 mg of conjugated estrogens. When vaginal cream is used, 2-4 g (0.5-1 applicator) of the cream may be administered intravaginally daily in the usual cyclic regimen.

Estrogen cream is readily absorbed through the skin and mucous membranes. When this cream is used for treatment of atrophic vaginitis, it may be placed intravaginally or applied topically around the vaginal tissues.

When estrogen is used long term in women with an intact uterus, the addition of progestin therapy is recommended to prevent endometrial hyperplasia. Medroxyprogesterone 2.5-10 mg/d is needed for 10-13 days to provide maximum maturation of endometrium and to eliminate any hyperplastic changes. Medroxyprogesterone may be administered continuously or intermittently.

Treatment with estrogen derivatives results in few cures (0-14%) but may cause subjective improvement in 29-66% of women. Limited evidence suggests that oral or vaginal estrogen therapy may benefit some women with stress and mixed urinary incontinence. Other potential beneficial effects of estrogen use include decreased bone loss and resolution of hot flashes during menopause.

Routinely prescribing conjugated estrogens to premenopausal women is not recommended. Use this medication in postmenopausal women who are incontinent and who have had a hysterectomy. For postmenopausal women with an intact uterus, cautiously recommend a short-term low-dose of conjugated estrogen and monitor frequently.

Antidepressants, Serotonin/Norepinephrine Reuptake Inhibitors

Class Summary

Some agents in this class may improve stress incontinence

Duloxetine (Cymbalta)

Duloxetine is a potent inhibitor of neuronal serotonin and norepinephrine reuptake. Its antidepressive action is theorized to be due to serotonergic and noradrenergic potentiation in the CNS.

Alpha-Adrenergic Blockers

Class Summary

These agents have been used to decrease bladder overactivity. They have shown some success in patients who have decentralized or autonomous bladders as the result of myelodysplasia, spinal cord injury, or radical pelvic surgery.

Phenoxybenzamine (Dibenzyline)

This agent decreases bladder contractions through long-lasting, noncompetitive, alpha-adrenergic blockade of postganglionic synapses at smooth muscle and exocrine glands.

Prazosin (Minipress)

Prazosin decreases internal sphincter tone and can improve the flow of urine, improving emptying of bladder. Although doses greater than 20 mg/d usually do not increase efficacy, a few patients may benefit from dose as high as 40 mg/d. If an increase in dose is needed, give first dose of each increment at bedtime to reduce syncopal episodes.

Botulinum Toxins

Class Summary

Intradetrusor injections with botulinum toxin are a novel treatment modality that has been shown to decrease episodes of urinary leakage in patients who have failed pharmacological therapy.

OnabotulinumtoxinA (BOTOX)

Neurotoxin from Clostridium botulinum; prevents ACh release from presynaptic membrane. Indicated for urinary incontinence in patients with neurologic conditions (eg, spinal cord injury, multiple sclerosis) in adults who have an inadequate response to or are intolerant of an anticholinergic medication.


Questions & Answers


How common is urinary incontinence?

What are the types of urinary incontinence?

How is urinary incontinence diagnosed?

What is the focus of clinical history for the evaluation of urinary incontinence?

Which medical problems may complicate or exacerbate urinary incontinence?

Which medications are associated with urinary incontinence?

Which therapies are used to treat urinary incontinence?

When are absorbent products indicated in the treatment of urinary incontinence treatment?

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What is the role of detrusor overactivity in urge urinary incontinence pathophysiology?

What is the pathophysiology of urge urinary incontinence in men?

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Which medications are associated with urinary incontinence?

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When is a standing cough stress test indicated in the evaluation of urinary incontinence?

What is the role of the Marshall test in the evaluation of urinary incontinence?


Which conditions are included in the differential diagnoses of urinary incontinence?

What are the differential diagnoses for Urinary Incontinence?


How is urinary incontinence diagnosed?

Which factors improve diagnostic accuracy of urinary incontinence?

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How is urinary incontinence treated?

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What how frequently should the bladder be drained with intermittent catheterization for urinary incontinence?

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Which medications are used for urinary incontinence treatment?

What is the role of alpha agonists in urinary incontinence treatment?

What is the role of tricyclic antidepressants (TCAs) in urinary incontinence treatment?

What is the role of duloxetine in urinary incontinence treatment?

What is the role of anticholinergic agents in urinary incontinence treatment?

Which precautions should be taken when using anticholinergic agents in urinary incontinence treatment?

What is the role of darifenacin (Enablex) in urinary incontinence treatment?

What is the role of fesoterodine (Toviaz) in urinary incontinence treatment?

What is the role of antispasmodic drugs in urinary incontinence treatment?

What is the role of calcium channel blockers in urinary incontinence treatment?

What is the role of beta-adrenergic agonists in urinary incontinence treatment?

What is the role of estrogen therapy in urinary incontinence treatment?

What is the role of botulinum toxin in urinary incontinence treatment?

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How is nocturnal enuresis treated in urinary incontinence?

How is nighttime voiding treated in urinary incontinence?

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Which patients benefit from pelvic floor muscle training for urinary incontinence?

Which treatments may be combined with pelvic floor muscle training for urinary incontinence?

What is the role of vaginal cones in urinary incontinence treatment?

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When is surgery indicated to treat urinary incontinence?

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What is the role of surgery in the treatment of stress urinary incontinence in men?

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Which dietary modifications are used in the treatment of urinary incontinence?

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Which specialist consultations are beneficial to patients with urinary incontinence?

When is emergency department (ED) care indicated in urinary incontinence treatment?


What is the role of medications in urinary incontinence treatment?

Which medications in the drug class Botulinum Toxins are used in the treatment of Urinary Incontinence?

Which medications in the drug class Alpha-Adrenergic Blockers are used in the treatment of Urinary Incontinence?

Which medications in the drug class Antidepressants, Serotonin/Norepinephrine Reuptake Inhibitors are used in the treatment of Urinary Incontinence?

Which medications in the drug class Estrogens are used in the treatment of Urinary Incontinence?

Which medications in the drug class Beta3 Agonists are used in the treatment of Urinary Incontinence?

Which medications in the drug class Tricyclic Antidepressants are used in the treatment of Urinary Incontinence?

Which medications in the drug class Antispasmodic Drugs are used in the treatment of Urinary Incontinence?

Which medications in the drug class Anticholinergic Agents are used in the treatment of Urinary Incontinence?

Which medications in the drug class Alpha-Adrenergic Agonists are used in the treatment of Urinary Incontinence?