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Urinary Incontinence, Surgical 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; Farzeen Firoozi, MD, Clinical Fellow, Center for Female Urology and Pelvic Reconstructive Surgery, Glickman Urological and Kidney Institute of the Cleveland Clinic; Michael S Ingber, MD, Clinical Fellow, Glickman Urological and Kidney Institute of the Cleveland Clinic
Contributor Information and Disclosures

Updated: May 8, 2009

Introduction

Urinary incontinence is a medical condition that has significant negative effects on quality of life and may cause social stigma, financial hardship, and associated medical problems. Affected individuals often delay seeking treatment due to shame and embarrassment. Urinary incontinence is not a normal part of the aging process. This condition has multiple etiologic factors.

With recent advances in medical technology and better understanding of female anatomy and physiology, many innovative surgical methods are available for correcting stress incontinence. This article reviews these surgical options.

History of the Procedure

Described by Kelly in 1913, anterior vaginal repair is the oldest surgical procedure for correcting stress incontinence. Kelly believed the cause of stress incontinence was an incompetent urethra. Anterior vaginal repair was designed to correct this condition.

In 1949, the Marshall-Marchetti-Krantz (MMK) operation was described. The suspension sutures were placed within the urethral wall and tied to the periosteum of the pubic symphysis. The original MMK operation was complicated by urethral obstruction and erosion because the surgical sutures were placed directly into the urethral wall.

In 1961, Burch reported a modification of the MMK operation. The modifications involved placing the surgical sutures at the bladder neck and tying them to the Cooper ligament.

The original transvaginal bladder neck suspension was described by Pereyra in 1959. Many modifications of the Pereyra transvaginal bladder neck suspension exist today. They include Stamey (1975), Raz (1981), and Gittes (1987) bladder neck suspensions. Although initial success rates were quite promising, the long-term success rate with transvaginal bladder neck suspensions has been disappointing; they are now considered substandard treatment options.

In contrast, sling procedures, first introduced by Ulmsten (1995), are gaining in popularity for all types of female stress urinary incontinence (SUI). Various slings have been introduced to the market since the mid 1990s, offering both retropubic and transobturator approaches. Historically, the indication for a sling procedure was limited to women with severe intrinsic sphincter deficiency (ISD). However, it has been expanded to include all types of stress incontinence.

Problem

Stress urinary incontinence is defined as the involuntary loss of urine coincident with increased intra-abdominal pressure in the absence of uninhibited detrusor contraction. Currently, no accepted classification of stress urinary incontinence is used in clinical practice because stress urinary incontinence is caused by a continuum of intrinsic sphincter deficiency severity with or without significant urethral hypermobility. For historical purposes, the most widely accepted classification, by Blaivas and others, is as follows:

  • Type I stress urinary incontinence is defined as urine loss occurring in the absence of urethral hypermobility. This is the mildest form of stress urinary incontinence. Patients with type I stress urinary incontinence have a Valsalva cotton-swab angle less than 30° and an abdominal leak-point pressure (ALPP) of greater than 120 cm water.
  • Type II stress urinary incontinence is defined as stress incontinence due to urethral hypermobility. Patients with urethral hypermobility have a Valsalva cotton-swab angle greater than 30° and an ALPP of more than 90 cm water.
  • Type III stress urinary incontinence is defined as stress incontinence due to intrinsic sphincter deficiency. Patients with intrinsic sphincter deficiency have a Valsalva cotton-swab angle less than 30° and an ALPP of less than 60 cm water.

Frequency

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 home residents. Up to 60% of nursing home patients are incontinent, while 30% of elderly persons 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. Incontinent patients 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 persons. More than a quarter 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
  • 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).5

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).5

Etiology

The causes of intrinsic sphincteric deficiency that leads to stress urinary incontinence are complex and may include advancing age, multiparity, prolonged or difficult labor, and hysterectomy. Other factors that may increase the risk of stress urinary incontinence include obesity, straining at stool as a child or young adult, heavy manual labor, chronic obstructive pulmonary disease, and smoking. Previous pelvic surgery, radiation therapy, and sympathetic nerve dysfunction are all etiologic factors.

Pathophysiology

Intrinsic sphincter deficiency arises from a defect within the urethra proper.

Although urethral hypermobility results from weakened anatomic support of the urethra, stress urinary incontinence does not develop unless intrinsic sphincter deficiency is also present. When a loss of anatomic support 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.

The uneven pressure transmission and the opening of the bladder neck secondary to intrinsic sphincter deficiency results in involuntary urine loss due to excessive urethral hypermobility during periods of physical activity.

Intrinsic sphincter deficiency is a condition in which the urethral sphincter is unable to coapt and generate enough urethral closing pressure to retain urine in the bladder at rest or when urethral hypermobility is induced with physical stress on the urethral and bladder neck support mechanisms. When the anatomic support is normal but the urethra cannot remain closed because of sphincteric incompetence, severe incontinence may result, even when the bladder and urethral support are not under physical stress. In the past, this was referred to as type III stress urinary incontinence.

Presentation

Stress incontinence occurs during periods of increased intra-abdominal pressure. Typically, patients report involuntary urine loss during coughing, laughing, and sneezing. Incontinence worsens during high-impact sports activities such as golf, tennis, or aerobics.

In general, women with stress incontinence experience less urine loss than women with overactive bladder. Stress incontinence occurs at predictable times. Irritative voiding symptoms, such as urinary frequency, urgency, and nocturia, are typically absent. Urethral hypermobility results in a smaller amount of urine loss and fewer pads needed compared to intrinsic sphincteric deficiency.

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 to evaluate complex cases of stress urinary incontinence.

Indications

The type of surgery required depends on the severity of intrinsic sphincter deficiency present that causes stress urinary incontinence. Individuals often have more than one cause for stress incontinence.

According to the treatment guidelines released by American Urologic Association (1997), surgery offers good long-term results as either initial or second-line treatment. Surgery may be offered as an initial form of treatment for selected women with stress urinary incontinence.

Surgery must be individualized for each patient, and it must follow standard recommendations for appropriate surgery. The option selected depends on the surgeon's training and expertise in a vaginal or abdominal approach.

The most important factor in choosing a surgical procedure is the specific nature of the patient's incontinence problem and any coexisting vaginal pathology. Patient preference, surgical complications, and comorbid medical conditions also play roles in the decision-making process.

The surgical management of stress incontinence can be divided into procedures designed to restore the active mechanism of continence (artificial urinary sphincter), to restore poor anatomic support that unmasks mild-to-moderate intrinsic sphincter deficiency (bladder neck suspensions, sling procedures), or to manage severe intrinsic sphincter deficiency in the setting of adequate anatomic support (pubovaginal sling, periurethral bulking agent, artificial urinary sphincter).

The surgical objective for mild-to-moderate intrinsic sphincter deficiency that worsens with excessive urethral hypermobility is to improve the support of the sphincter unit by preventing the descent of the bladder neck without causing significant outflow obstruction during urination. The goal of surgery for severe intrinsic sphincter deficiency with or without excessive urethral hypermobility is to increase urethral coaptation and resistance in order to compensate for the sphincteric incompetence. All procedures compensate for the intrinsic sphincter deficiency that leads to stress urinary incontinence by increasing urethral outlet resistance. No surgical intervention designed to support the bladder neck or mid urethra cures intrinsic sphincter deficiency, but rather compensates for intrinsic sphincter deficiency that worsens with excessive urethral movement or is present with minimal or no urethral support defects.

Relevant Anatomy

The female urethra is a 4-cm, elongated tube composed of an inner epithelial lining, a spongy submucosa, a middle smooth muscle layer, and outer fibroelastic connective tissue. The spongy submucosa contains a rich vascular plexus that is responsible for providing adequate urethral occlusive pressure to create the "washer effect," an important female continence mechanism. Urethral smooth muscle and fibroelastic connective tissues serve to circumferentially augment the occlusive pressure generated by the submucosa.

All parts of the female urethra are influenced by estrogen. The lack of estrogen at menopause leads to atrophy and replacement of the submucosa (vascular plexus) by fibrous tissue. Lack of estrogen is one of the risk factors for intrinsic sphincter deficiency; replacement of estrogen may reverse the effects of intrinsic sphincter deficiency. When estrogen is administered to a postmenopausal woman with atrophic vaginitis, the mucosa regains its turgor, with simultaneous up-regulation of alpha receptors and angiogenesis of the vascular plexus. Previous bladder neck operations, radiation, and neurogenic disease can also affect the ability to achieve a perfect seal.

Internal sphincter

Women do not have an anatomic internal sphincter like males, but women have a functional internal sphincter. The female internal sphincter is composed of a bladder neck and proximal urethra. Under normal circumstances, the pressure of the internal sphincter is much higher than that in the bladder.

External sphincter

The female external sphincter is known as the rhabdosphincter and is composed of 2 types of striated muscle fibers, fast-twitch and slow-twitch. Fast-twitch fibers cause sudden stopping of the urinary stream to provide the voluntary guarding reflex. Slow-twitch fibers maintain the constant tone of the external sphincter to provide involuntary passive continence called the involuntary guarding reflex.

The rhabdosphincter has its most prominent effect on the female urethra at the urogenital triangle. Located approximately 1.8 cm distal to the bladder neck, it exerts its influence for a distance of approximately 1.5 cm of urethral length.

Pelvic diaphragm

The pelvic diaphragm lines the floor of the bony pelvis and is composed of 4 sheets of muscles, including pubococcygeus, iliococcygeus, ischiococcygeus, and coccygeus.

The pelvic diaphragm is often referred to as the levator ani. The levator ani musculature is attached to the inner sides of the bony pelvis by a condensation of pelvic fascia called the arcus tendineus. The levator ani is the most important component of the pelvic diaphragm, and the integrity of the pelvic floor depends on its function. When the levator ani is damaged, stress urinary incontinence and/or herniation of pelvic organs through the vagina may occur.

Supporting ligaments and fascia

The urethropelvic ligament is a fibrous band of connective tissue that lines the undersurface of the bladder neck and attaches laterally to the arcus tendineus. It provides the major support to the bladder neck and proximal urethra. Laxity of the urethropelvic ligament results in stress urinary incontinence.

The pubocervical fascia is a fibrous sheet of connective tissue that lines the base of the urinary bladder and inserts laterally into the arcus tendineus. An intact pubocervical fascia prevents herniation of the bladder and proximal urethra into the vagina. Damage to the pubocervical fascia may cause the bladder to herniate through the vagina, resulting in cystocele formation.

The cardinal ligaments arise from the arcus tendineus and anchor to the uterine cervix. The cardinal ligaments stabilize and support the uterus, vagina, and bladder. Weakening of the cardinal ligaments may cause cystocele and uterine descensus.

The uterosacral ligaments originate from a condensation of fibrous connective tissue overlying the sacral promontory and insert into the uterine cervix. Uterosacral ligaments stabilize the uterus in the bony pelvis. Weakening of the uterosacral ligaments may result in uterine or vaginal vault prolapse.

Contraindications

Severe intrinsic sphincter deficiency is a contraindication to bladder neck suspension of all types (ie, transvaginal, retropubic, laparoscopic). Performing bladder neck suspension for severe intrinsic sphincter deficiency leads to persistent stress urinary incontinence.

Performing a bladder neck suspension alone is contraindicated in the presence of moderate or severe cystocele because urethral obstruction may occur or the cystocele may worsen. In this situation, bladder neck suspension must be accompanied by a formal cystocele repair at the time of surgery.

The presence of atrophic vaginitis and intrinsic sphincter deficiency are contraindications for an in situ vaginal wall sling.

Severe urge incontinence is a contraindication to any type of anti-incontinence surgery. Preoperative urge symptoms should be controlled with anticholinergic therapy prior to anti-incontinence surgery.

The absolute contraindications for a female artificial urinary sphincter include uncontrolled detrusor overactivity and high-grade vesicoureteral reflux. Relative contraindications include the presence of urinary tract infections (UTIs) and a lack of manual dexterity to manipulate the pump. Patient motivation is the foremost consideration because the potential exists for surgical revision for mechanical problems.

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References
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Further Reading

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Keywords

incontinence, urinary incontinence, stress incontinence, stress urinary incontinence, SUI, urge incontinence, overflow incontinence, mixed incontinence, reflex incontinence, Foley catheter, decompensated bladder, detrusor instability, Q-tip test, cotton swab test, cotton-swab test, cough stress test, CST, Marshall test, Kegel exercises, detrusor hyperreflexia, detrusor hyper-reflexia, overactive bladder, urethral hypermobility, intrinsic sphincter deficiency, intrinsic sphincteric dysfunction, ISD, anterior vaginal repair, MMK procedure, MMK operation, Marshall-Marchetti-Krantz procedure, Marshall-Marchetti-Krantz operation, urethral obstruction, bladder neck suspension, pubovaginal sling, pubo-vaginal sling, retropubic urethropexy, urethral hypermobility, involuntary urine loss, artificial urinary sphincter, periurethral bulking agent, artificial urinary sphincter, sling procedure, sling operation

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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

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.

Michael S Ingber, MD, Clinical Fellow, Glickman Urological and Kidney Institute of the Cleveland Clinic
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

Shlomo Raz, MD, Professor, Department of Surgery, Division of Urology, University of California at Los Angeles School of Medicine
Shlomo Raz, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Urological Association, and California Medical Association
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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