eMedicine Specialties > Urology > Incontinence

Urinary Incontinence, Nonsurgical Therapies

Author: Raymond Rackley, MD, Professor of Surgery, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University; Staff Physician, Center for Pelvic Medicine and Pelvic Reconstruction, Glickman Urological Institute, Cleveland Clinic Foundation
Coauthor(s): Sandip P Vasavada, MD, Physician, Center for Female Pelvic Medicine and Genitourinary Reconstructive Surgery, The Glickman Urological and Kidney Institute; Joint Appointment with Women's Institute, Cleveland Clinic; Michael S Ingber, MD, Clinical Fellow, Glickman Urological and Kidney Institute of the Cleveland Clinic; Farzeen Firoozi, MD, Clinical Fellow, Center for Female Urology and Pelvic Reconstructive Surgery, Glickman Urological and Kidney Institute of the Cleveland Clinic
Contributor Information and Disclosures

Updated: May 6, 2009

Introduction

Background

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. The different types of incontinence include stress incontinence, urge incontinence, mixed incontinence, overflow incontinence, and functional incontinence. Successful treatment of urinary incontinence must be tailored to the specific cause of incontinence.

Stress incontinence may be treated with surgery, pelvic floor physiotherapy, and anti-incontinent devices. Urge incontinence may be treated with changes in diet, behavioral modification, pelvic-floor exercises, and/or medications and new forms of surgical intervention. Mixed incontinence often requires anticholinergics and surgery. Overflow incontinence is usually treated with some type of catheter or diversion regimen. Functional incontinence is self-limited when the underlying cause is identified and treated in an appropriate fashion.

In general, the first choice for treatment is the least invasive, with the least number of potential complications for the patient. Examples of noninvasive treatments include medications or exercises; however, the least invasive treatment may not afford the best outcome in certain situations. In specific situations, minimally invasive surgery may be the most effective form of managing urinary incontinence.

Pathophysiology

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.

Stress incontinence is urinary incontinence coincident with increased intra-abdominal pressure in the absence of uninhibited detrusor contraction. In stress incontinence, the bladder outlet has poor resistance to urinary flow. The most common cause of stress incontinence is urethral hypermobility secondary to poor anatomic pelvic support. A less common cause of stress incontinence is an inherent defect in the urethra known as intrinsic sphincter deficiency.

Urge incontinence is involuntary urine loss due to detrusor overactivity. 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. Symptoms of overactive bladder or urge incontinence in the absence of neurologic causes are known as detrusor instability.

Mixed incontinence is urinary incontinence resulting from a combination of stress and urge incontinence. 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.

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. When patients with suprapontine or suprasacral spinal cord lesions present with symptoms of urge incontinence, this is known as detrusor hyperreflexia.

Overflow incontinence is due to overdistention of the detrusor muscle. Overflow incontinence may occur as a result of bladder outlet obstruction, detrusor atony, or neurologic impairment of the urinary bladder. 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.

Some common neurologic causes of overflow incontinence include herniated lumbar disc, diabetic cystopathy, and peripheral neuropathy. Less common causes of overflow incontinence include AIDS, genital herpes affecting the perineal area, and neurosyphilis. A decompensated detrusor resulting from a neurologic disorder is known as an areflexic detrusor.

Frequency

United States

Urinary incontinence affects approximately 13 million people in the United States, predominantly women. This includes 10%-35% of adults and 50% of the 1.5 million nursing homes residents. Up to 60% of nursing home patients are incontinent, while 30% of elderly people living at home are incontinent.

Urinary incontinence is an underdiagnosed and underreported medical problem. 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.

Stress incontinence affects 15%-60% of women. Stress incontinence is a disorder of young and old people alike. More than one fourth of nulliparous young college athletes experience stress incontinence when participating in sports.

Mortality/Morbidity

Chronic urinary incontinence is a major problem in the older population, particularly in patients in nursing homes. Chronic urinary incontinence is a health hazard that affects 10%-35% of adults and 50% of the 1.5 million residents in nursing homes.

Urinary incontinence–related morbidities include prolonged hospital admission (35%), urinary tract infections (UTIs; 2%), contact dermatitis (1.6%), and falls (1%). Costs incurred for treating incontinence-related complications approach $2.8 billion, in contrast to $35 million for diagnostic and treatment costs.

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. Of nursing home patients, 60% have been reported to be incontinent, while as many as 30% of the older population living at home are incontinent. Individuals with incontinence may experience the sudden involuntary loss of urine several times a day.

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. For individuals with a decompensated bladder that does not empty well, the elevated postvoid residual (PVR) urine can lead to overgrowth of bacteria and subsequent UTI.

The treatment of urinary incontinence with catheters also poses potential problems. Indwelling catheters left in the bladder for more than 2 weeks become colonized with bacteria. While asymptomatic bacterial colonization does not cause health hazards, unrecognized bacterial colonization can produce symptomatic bladder infections that can manifest as purulent urine, fever, bladder spasms, and hematuria.

Thus, long-term use of indwelling catheters may cause recurrent bladder infections, bladder stones, ascending pyelonephritis, and urethral erosions. Intermittent catheterization may result in bladder infections or urethral injury. Long-term use of suprapubic tubes may cause bladder spasms, bladder stone formation, and bladder infections. Urinary incontinence will continue to be a significant health care problem if left ignored.

Treatment of bladder infections in catheterized patients involves a combination of catheter changes, irrigation with bacteriostatic/bacteriocidal agents, or use of an antibiotic. To minimize symptomatic bladder infections, change long-term indwelling catheters every 3-4 weeks or when drainage is obstructed by debris or encrustations. Long-term prophylactic antibiotic use is discouraged because of the risk of preferentially selecting resistant organisms.

Catheter-associated UTI is the most common nosocomial infection. The type of urinary catheter used may affect the likelihood of catheter-related UTIs. The literature suggests that the risk with short-term catheterization is 5% per day. However, new 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.

Among trials of silver-coated urinary catheters, silver alloy catheters appear to be significantly more effective than silver oxide catheters in preventing UTIs. 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.

Race

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.

  • Older black women report a lower prevalence of urinary incontinence than white women. Fultz et al (1999) reported that 23.02% of white women reported incontinence, compared with 16.17% of black women.1
  • Freeman et al (2001) reported that black women were significantly more likely than white women to report that they experienced menopausal symptoms (46% vs 30%; P <0.001), urinary incontinence, and vaginal dryness.2
  • Howard et al (2000) reported that functional and morphologic differences exist 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°; P = 0.02).3
  • Sears et al (2008) 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%; P <0.05).4
  • Daneshgari et al (2008) reported that Hispanic women reported stress incontinence (odds ratio, 1.7; P = 0.005) and mixed incontinence (odds ratio, 1.8; P = 0.005) 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.5
  • Nygaard et al (2008) examined the prevalence of symptomatic pelvic floor disorders in women in the United States. Although they did not differentiate urge from stress incontinence, there was no difference among non-Hispanic whites (16%), Hispanics (15.9%), non-Hispanic blacks (13.8%), and other (15%) races (P = 0.83).6

Age

In a cross-sectional analysis of women who participated in the 2005-2006 National Health and Nutrition Examination Survey, Nygaard et al (2008) demonstrated that the prevalence of urinary incontinence increased with age. 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 (P <0.001).6

Clinical

History

One popular way to classify urinary incontinence is to define it according to symptom presentation. Although symptom classification is helpful in describing bladder and urethra function, the symptoms of urinary incontinence are not always clear markers for a proper diagnosis. Furthermore, the symptom complex alone does not allow accurate localization of the problem site, such as the bladder, urethra, or both.

Classification of urinary incontinence into types allows the clinician to make an educated guess at a particular anatomic abnormality that warrants further investigation. The 5 major types of urinary incontinence are as follows:

  • Stress incontinence: In stress incontinence, a variable amount of urine escapes suddenly with an increase in intra-abdominal pressure. Little urine is lost, unless the condition is severe.
    • This type of urinary loss is very predictable.
    • Irritative voiding symptoms and nocturia are typically absent.
  • 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. Patients have symptoms of urinary frequency, urgency, nocturia, and urge incontinence.
    • Some examples of situations that 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: In this type of incontinence, the symptoms of stress incontinence and urge incontinence coexist. With mixed incontinence, the problem is that the bladder is overactive and the urethra is underactive.
    • 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: As the term implies, the urine overflows from the bladder. Overflow incontinence is a condition that occurs when the bladder is overdistended and has reached its limit of compliance. At this point, the intravesical pressure is greater than the resting urethral closure pressure. Because the intravesical pressure exceeds the resting urethral closure pressure (when the bladder is overdistended), urinary incontinence occurs despite the absence of detrusor contraction.
    • Overflow incontinence may occur in the setting of infravesical bladder outlet obstruction or nonfunctioning detrusor. Causes of bladder outlet obstruction include benign BPH, urethral stricture, posterior urethral valve obstruction, or urethral obstruction after a pubovaginal sling. Causes of nonfunctioning detrusor include detrusor areflexia (ie, sensory or motor paralytic bladder due to underlying neurologic disease) or atonic bladder that has lost its muscular tone (ie, chronic overdistension resulting in decompensated detrusor) in the absence of a neurologic cause. 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.
    • Unfortunately, no medications effectively treat this condition. The only way to treat overflow incontinence is with a catheter. 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).
    • 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 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.

Physical

See Pathophysiology for discussion of physical signs of urinary incontinence.

Causes

The differential diagnosis of urinary incontinence has multiple causes. Sometimes, more than one contributing factor exists; distinguishing these different etiologies is imperative because each condition requires a different, but often overlapping, therapeutic approach.

  • 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 age, childbirth, surgery, or certain disease states that affect tissue strength. A less common cause of stress incontinence is an inherent defect in the urethra known as intrinsic sphincter deficiency.
  • Men who have undergone radical prostatectomy may have damage to their continence mechanism. Similarly, men who undergo transurethral resection of the prostate may also develop stress incontinence due to injury to the external urethral sphincter.
  • Urge incontinence may be a result of detrusor myopathy, neuropathy, or a combination of both.
  • Mixed incontinence is urinary incontinence resulting from a combination of stress and urge incontinence. The bladder outlet is weak, and the detrusor is overactive.
  • Bladder obstruction may result in urinary incontinence due to overflow of urine. Alternatively, urge incontinence may result from an obstructed outlet, both in men and in women. Common causes of bladder outlet obstruction in men include BPH, vesical neck contracture, and urethral strictures. In women, urethral obstruction may be due to severe pelvic organ prolapse. It rarely occurs after anti-incontinence surgery, such as a sling or bladder neck suspension. Some common neurologic causes of overflow incontinence include herniated lumbar disc, diabetic cystopathy, and peripheral neuropathy. Less common causes of overflow incontinence include AIDS, genital herpes affecting the perineal area, and neurosyphilis.

More on Urinary Incontinence, Nonsurgical Therapies

Overview: Urinary Incontinence, Nonsurgical Therapies
Differential Diagnoses & Workup: Urinary Incontinence, Nonsurgical Therapies
Treatment & Medication: Urinary Incontinence, Nonsurgical Therapies
Follow-up: Urinary Incontinence, Nonsurgical Therapies
Multimedia: Urinary Incontinence, Nonsurgical Therapies
References

References

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Further Reading

Keywords

incontinence, urinary incontinence, functional incontinence, stress incontinence, urge incontinence, overflow incontinence, mixed incontinence, reflex incontinence, Foley catheter, decompensated bladder, detrusor instability, Marshall test, Kegel exercises, detrusor hyperreflexia, overactive bladder, urinary tract infections, UTI, underpads, pant liners, shields and guards, adult diapers, disposable pad systems, urethral occlusive devices, indwelling urethral catheters, suprapubic catheters, intermittent catheterization

Contributor Information and Disclosures

Author

Raymond Rackley, MD, Professor of Surgery, Cleveland Clinic Lerner College of Medicine at Case Western Reserve University; Staff Physician, Center for Pelvic Medicine and Pelvic Reconstruction, Glickman Urological Institute, Cleveland Clinic Foundation
Raymond Rackley, MD is a member of the following medical societies: American Urological Association
Disclosure: Pfizer, Novartis, Proctor & Gamble, Allergan Honoraria None; Pfizer, Novartis, Proctor & Gamble, Allergan Consulting fee Other

Coauthor(s)

Sandip P Vasavada, MD, Physician, Center for Female Pelvic Medicine and Genitourinary Reconstructive Surgery, The Glickman Urological and Kidney Institute; Joint Appointment with Women's Institute, Cleveland Clinic
Sandip P Vasavada, MD is a member of the following medical societies: American Urogynecologic Society, American Urological Association, International Continence Society, and Society for Urology and Engineering
Disclosure: pfizer Honoraria Speaking and teaching; allergan Consulting fee Consulting; ndi medical, LLC Ownership interest Review panel membership; novartis Honoraria Speaking and teaching

Michael S Ingber, MD, Clinical Fellow, Glickman Urological and Kidney Institute of the Cleveland Clinic
Disclosure: Nothing to disclose.

Farzeen Firoozi, MD, Clinical Fellow, Center for Female Urology and Pelvic Reconstructive Surgery, Glickman Urological and Kidney Institute of the Cleveland Clinic
Farzeen Firoozi, MD is a member of the following medical societies: American Medical Association and American Urological Association
Disclosure: Nothing to disclose.

Medical Editor

Martha K Terris, MD, FACS, Professor, Department of Surgery, Medical College of Georgia
Martha K Terris, MD, FACS is a member of the following medical societies: American Cancer Society, American College of Surgeons, American Institute of Ultrasound in Medicine, American Urological Association, New York Academy of Sciences, and Society of University Urologists
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Mark Jeffrey Noble, MD, Consulting Staff, Urologic Institute, Cleveland Clinic Foundation
Mark Jeffrey Noble, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Urological Association, Kansas Medical Society, Sigma Xi, Society of University Urologists, and Southwest Oncology Group
Disclosure: Nothing to disclose.

CME Editor

J Stuart Wolf Jr, MD, FACS, David A Bloom Professor of Urology, Director of Division of Minimally Invasive Urology, Department of Urology, University of Michigan
J Stuart Wolf Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, Society of University Urologists, and Society of Urologic Oncology
Disclosure: Terumo Corporation Consulting fee Consulting; Omeros Corporation Consulting fee Consulting

Chief Editor

Edward David Kim, MD, FACS, Professor of Surgery, Division of Urology, University of Tennessee Graduate School of Medicine; Consulting Staff, University of Tennessee Medical Center
Edward David Kim, MD, FACS is a member of the following medical societies: American College of Surgeons, American Society for Reproductive Medicine, American Society of Andrology, American Urological Association, and Tennessee Medical Association
Disclosure: Lilly Consulting fee Consulting; Astellas Consulting fee Speaking and teaching; Indevus Consulting fee Speaking and teaching

 
 
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