Urinary Incontinence:

Urinary incontinence affects more than 17 million Americans; it is most common in women and in elderly persons.¹ Although the prevalence of most forms of incontinence increases with age, incontinence is considered abnormal, regardless of age.

Urinary incontinence affects 10% to 30% of women between 30 and 60 years of age; the prevalence in women older than 60 years ranges from 15% to 43%.² The prevalence in men at all ages ranges from 1.6% to 24%.² Urinary incontinence affects more than 50% of patients in nursing homes and has been associated with dementia, fecal incontinence, and the inability to walk and transfer independently.³

In spite of the prevalence of urinary incontinence, this condition remains underdiagnosed, underreported, and undertreated.Only 32% of primary care physicians routinely ask all of their patients about incontinence, and 50% to 75% of incontinent community-dwelling patients never describe their symptoms to physicians.⁴ This is regrettable, because incontinence is highly treatable.

In this article, we review what to include in the evaluation to help you arrive at a working diagnosis, and we describe nonpharmacologic and pharmacologic management strategies for each type of urinary incontinence.

OVERVIEW

Urinary incontinence may be transient or persistent.

Risk factors for persistent incontinenceinclude impaired functional and mobility status, impaired cognition, multiparity, vaginal delivery,estrogen depletion, hysterectomy, obesity (body mass index greater than 30 kg/m²), stroke, Parkinson disease, diabetes, benign prostatic hypertrophy, and the use of certain medications (Table 1).³

Transient causes-such as delirium, infection, and urethritis-are reversible with treatment (Table 2).⁵ Transient incontinence affects one third of community-dwelling and half of hospitalized elderly persons.⁶ If a patient continues to have incontinence after transient causes have been ruled out, he or she may have persistent incontinence.

PATHOPHYSIOLOGY

Most of the detrusor muscle is innervated by the cholinergic nervous system via the sacral plexus (S2 through S4), which, when stimulated, causes the bladder to contract and empty.⁷ The bladder outlet has 2 components. The internal urethral sphincter is innervated by the α-adrenergic nervous system via the hypogastric plexus (T11 through L2), which, when stimulated, contracts the internal urethral sphincter to allow storage of urine. The distal component-the external urethral sphincter-is innervated by the somatic nervous system via the pudendal nerve, which also innervates pelvic floor muscles and is under voluntary control.

Urine is storedwhen thedetrusor muscle relaxes and the sphincters close. The normal bladder stores between 300 and 600 mL of urine; the first urge to void occurs between 150 and 300 mL. Emptying of the bladder occurs with detrusor contraction and the opening of the sphincters as true detrusor pressure increases and exceeds urethral resistance.

Estrogen also affects continence via receptors in the urethra and pelvic floor musculature. Estrogen deficiency can reduce the effectiveness of the sphincters and pelvic muscles and may exacerbate stress incontinence. Estrogen deficiency may also predispose women to urethritis, trigonitis/cystitis, and atrophic vaginitis, all of which may exacerbate urge incontinence.⁸

Changes that accompany aging may also affect continence. These include a decrease in bladder capacity, contractility, and the ability to postpone voiding; a reduction in urethral length and sphincter strength in women; and increased prostate size in men.

TYPES OF INCONTINENCE

Persistent incontinence includes urge, stress, overflow, mixed, and functional incontinence.

Urge incontinence-also known as detrusor instability (a urodynamic diagnosis), detrusor hyperreflexia, overactive bladder, and irritable bladder-is the most common cause of persistent incontinence, especially in persons older than 75 years. Patients complain of loss of urine, preceded by a strong urge to void, and frequency both during the day and at night. This form is usually idiopathic; however, it may also be caused by bacterial cystitis, bladder tumor, bladder stones, atrophic vaginitis, urethritis, stroke, Parkinson disease, and dementia.³

Stress incontinence is the second most common type of incontinence in elderly persons. In 85% of cases, urinary leakage results from increased abdominal pressure (stress) that causes the bladder neck and urethra to drop below the pelvic floor. This effect may be related to aging, hormonal changes, multiparity, hysterectomy, or pelvic surgery. In the remaining 15% of cases, incontinence is attributable to intrinsic sphincter deficiency, which results in incomplete closure of the internal sphincter and subsequent leakage. This disorder can be secondary to pelvic or incontinence surgery, pelvic radiation, trauma, or neurogenic disorders.⁹

Overflow incontinence may be related to overdistention of the bladder, which results in constant or frequent dribbling. Causes include bladder outlet obstruction as a result of benign prostatic hypertrophy, a stricture, a cystocele, or fecal impaction. Another type of overflow incontinence is acontractile bladder (also known as detrusor hypoactivity or atonic bladder), which can result from diabetes, multiple sclerosis, lower spinal cord damage, and/or medications.³

Mixed incontinence is a combination of any 2 or more of the above causes of persistent incontinence. The most common combination is urge and stress; typically, 1 type predominates.

Functional incontinence does not involve the lower urinary tract and is usually the result of physical and/or cognitive impairment (eg, from arthritis or stroke) that prevents the patient from getting to the toilet.⁵

DIAGNOSIS

The evaluation of urinary incontinence in the office setting includes a focused history taking and physical examination, a postvoid residual (PVR) urine volume measurement, and urinalysis. These components usually suffice to provide a working diagnosis on which to base initial therapy.

A useful screening question to help identify patients with incontinence is, "In the past year, have you ever lost urine?" If the answer is yes, ask, "Have you lost urine on at least 6 different days?" Once a diagnosis of incontinence has been established, inquire about the onset and duration of symptoms, previous treatment, comorbid conditions, and medications. Obtain a genitourinary history (eg, previous incontinence surgery or prostate surgery). Determine whether the incontinence is transient or persistent and how it affects the patient's quality of life. Explore the patient's desire for treatment.

A bladder record is often a useful adjunct to the history.It logs the frequency, timing, and the number of continent and incontinent episodes over a 1- or 2-day period.³ It can be completed by the patient and reviewed at a subsequent office visit.

Physical examination. Assess the patient's mental status and mobility and determine whether there are signs of peripheral edema or congestive heart failure. Include a neurologic evaluation, with specific attention to the lumbosacral nerves and possible signs of peripheral neuropathy.³ A pelvic examination helps assess paravaginal muscle tone and the presence of atrophic vaginitis, cystocele, rectocele, tenderness, and mass.^3,9 The focus of a rectal examination is to assess sphincter tone (active and resting tone, which helps determine the integrity of the sacral plexus), and check for fecal impaction, the presence of a mass and, in a male patient, prostate consistency and symmetry.³

Diagnostic testing. A cough stress test is performed by having the patient cough forcefully in the standing position before voiding. Immediate leakage of urine is diagnostic for stress urinary incontinence with specificity greater than 90%.³ Within 5 minutes after the patient has voided, obtain a PVR value by catheterization or bladder ultrasonography. A PVR value of less than 50 mL (less than 100 mL in elderly persons) suggests adequate bladder emptying. A PVR value of more than 200 mL suggests detrusor weakness or obstruction; evaluation by a urologist is recommended in such cases.^3,5

Laboratory evaluations include measurement of calcium and glucose levels if polyuria is present and a blood urea nitrogen/creatinine test if the PVR value is more than 200 mL.³ An initial urinalysis is done to assess for heme, glucose, and leukocytes. Order a urine culture if infection is suspected; a urinary tract infection can cause urge incontinence.¹⁰ Simple cystometrics are useful if symptoms are ambiguous; testing can be done in the office.¹¹ Cystometric testing determines bladder capacity and stability and has a 70% to 91% positive predictive value for urge incontinence.¹¹ If the diagnosis remains unclear, refer the patient to a specialist for formal multichannel urodynamic testing.

BEHAVIORAL INTERVENTIONS

Patient-dependent behavioral interventions are always the first line of therapy; they have been shown to be as effective as pharmacologic therapies.¹² Simple recommendations include the following:

Reduce the amount of fluid intake after 7 PM.

Avoid bladder stimulants, such as caffeine.

Use diuretics judiciously and do not take before bedtime.

Elevate legs when sitting to relieve diuresis before bedtime (for patients with lower extremity edema).

Have easy access to a toilet (eg, a bedside commode, if necessary).

Bladder training or retraining. This method works equally well with urge or stress incontinence. It involves educating patients about the physiology of their type of incontinence and having them attempt a scheduled voiding trial, with an initial delay of 15 minutes. This intervention has a reported 20% dry rate, and 75% of patients experience at least a 50% reduction in the number of incontinent episodes.³

Pelvic floor muscle training (Kegel exercises) involves "drawing in" or "lifting up" the perivaginal (levator ani) muscles and anal sphincter for a 10-second contraction followed by a 10-second relaxation. Providing the patient with both written and verbal instructions increases the success rate of the intervention. The exercises should be performed 30 to 80 times a day for at least 6 weeks. An improvement rate of up to 95% has been reported.^3,13

Biofeedback therapy is done with a single measurement (vaginal or anal probe) using electromyelographic or manometric methods with simultaneous measurement of pelvic, abdominal, and detrusor muscle activity. With the guidance of a physical therapist, the patient learns how to isolate and strengthen the pelvic floor muscles. This modality is associated with a 54% to 87% improvement rate and is useful in managing urge, stress, and mixed incontinence.^3,12

Caregiver-dependent interventions for urge and functional incontinence include scheduled toileting on a fixed schedule at regular intervals every 2 to 4 hours, day and night. In uncontrolled studies, the rate of improvement is 29% to 85%.³Habit training is a toileting schedule that matches the patient's voiding habits; the improvement rate is 86%.³Prompted voiding involves monitoring the patient, encouraging him to use the toilet, and praising him for maintaining continence. This technique is most useful in the nursing home setting and reduces incontinent episodes by an average of 1 or 2per day.³

PHARMACOLOGIC AND SURGICAL MANAGEMENT

Although most patients experience relief of symptoms with behavioral therapies, many will likely require the addition of pharmacologic agents for optimal control.

Urge incontinence. A number of approved pharmacologic therapies are available for urge incontinence (Table 3). However, caution is advised in prescribing these agents for patients who have a pretreatment PVR volume of more than 100 mL because of the risk of urinary retention.

The antispasmodics oxybutynin and tolterodine are the most commonly used agents; they inhibit the effects of acetylcholine on the detrusor muscle. Oxybutynin is available in immediate-release, extended-release, and transdermal formulations. Tolterodine is available in immediate-release and extended-release formulations. Both immediate-release preparations reduce incontinence by about 45% to 50%.^14,15 Extended-release tolterodine reduces incontinence by 71%; extended-release oxybutynin, by 83%.¹⁶

In a double-blind study that compared extended-release preparations of oxybutynin and tolterodine in women, the agents were equally effective in reducing weekly urge incontinence and total incontinence episodes. However, the percentage of women who reported no urinary incontinence episodes was significantly higher in the oxybutynin group than in the tolterodine group (23% vs 16%; P = .03).¹⁶

Anticholinergic side effects, especially dry mouth, are more common with oxybutynin. A meta-analysis comparing the 2 agents found that tolterodine caused less dry mouth than oxybutynin.¹⁷ The transdermal preparation of oxybutynin appears to cause less dry mouth than either immediate- release or extended-release formulations. In a double-blind trial, the transdermal formulation was associated with fewer anticholinergic side effects than extended-release tolterodine.¹⁸

Other agents are used for urge incontinence, but they have not shown consistent efficacy in randomized controlled trials. Propantheline reduces incontinence by up to 53% but is not well tolerated in older patients.³Hyoscy- amine is rapid and short-acting and can be taken sublingually. Dicyclomine is thought to improve incontinence, but there are few studies of its effectiveness.³ It is not well tolerated in older patients, and treatment of urinary incontinence is an unlabeled use. Flavoxate has no benefits.³

Newer treatments. These include vanilloids, botulinum toxin, and the sacral nerve stimulation system for urinary control (InterStim).The vanilloids capsaicin and resiniferatoxin can be instilled directly into the bladder; they selectively inhibit reflex bladder contractions. These agents are considered experimental; they may be effective for urge incontinence resulting from spinal cord lesions, multiple sclerosis, or Parkinson disease.¹⁹

Botulinum toxin can be injected directly into the urethral and bladder skeletal and smooth muscle, which results in reversible chemical denervation. It can be used to treat detrusor-sphincter dyssynergia and detrusor hyperreflexia attributable to spinal cord injury. Clinical trials are current-ly under way to test its effectiveness in patients with recalcitrant overactive bladders. The effects of botulinum toxin are seen within 5 to 7 days and can last up to 3 to 6 months.¹⁹

The InterStim system can be likened to a pacemaker for the bladder. It involves the surgical placement of a lead into the S3 nerve root that is attached to a neurostimulator implant- ed under the skin on the back and controlled by a handheld programmer that can be adjusted to increase or decrease bladder contractions. This device may be effective in the management of intractable symptoms of urge incontinence, urgency-frequency, or nonobstructive urinary retention.²⁰

Stress incontinence. There are no FDA-approved drugs for stress or overflow incontinence. The α-adrenergic agonist pseudoephedrine has been shown to reduce incontinence by 20% to 60%.^4,21 However, most of the studies that demonstrated this effect used phenylpropanolamine, which is no longer available.

Oral estrogen cannot be recommended as a first-line treatment for stress and/or urge incontinence. Clinical trial data from the Women's Health Initiative and secondary data analysis from the Heart and Estrogen/Progestin Replacement Study showed a worsening of incontinence (urge, stress, or mixed) in the women who took estrogen plus medroxyprogesterone acetate.^22,23 However, a systematic review of randomized trials found that unopposed estrogen therapy is effective in treating incontinence: approximately 50% of women treated with estrogen were cured or showed improvement, compared with 25% of patients who received placebo.²⁴

A trial with local vaginal estrogen may be undertaken to improve stress incontinence and urgency symptoms; however, definitive data on its effectiveness are lacking. Topical forms of estrogen include vaginal cream and an impregnated estrogen ring that is changed every 3 months.

The tricyclic antidepressant imipramine has dual α-agonist and anticholinergic activity and can be useful for nocturnal incontinence and mixed incontinence.³Duloxetine, a selective serotonin/norepinephrine reuptake inhibitor in phase 3 trials, increases pudendal nerve activity and appears to have a strengthening effect on the external urethral sphincter.²⁵

For stress incontinence resulting from urethral hypermobility, surgical techniques include open retropubic suspension (Marshall-Marchetti-Krantz procedure or Burch colposuspension) and bladder neck needle suspension. For intrinsic sphincter deficiency, the Sling procedure is recommended.Surgery can cure incontinence in 4 of 5 cases, but the long-term success rate drops to 50% after 10 years.⁹

Overflow incontinence caused by an anatomic obstruction (eg, an enlarged prostate) can be treated with an α-blocker, such as doxazosin, terazosin, tamsulosin, or afluzosin, or surgically.^3,26 For overflow incontinence resulting from an acontractile detrusor (atonic bladder), intermittent catheterization is the treatment of choice. Bethanechol is rarely effective, except perhaps for patients with overflow incontinence who must continue to take anticholinergic medications.²⁷

OTHER THERAPIES

Pessaries are indicated as a temporary measure for women who are awaiting surgery for pelvic prolapse or as a treatment for women who are unable, for medical reasons, or unwilling to undergo correction of their prolapse. Complications can include erosion or ulceration of vaginal epithelium and/or a rectovaginal and vesicovaginal fistula.^3,28

Periurethral bulking agents. Polytetrafluoroethylene, collagen, or autologous fat is injected under cystoscopic guidance into an incompetent periurethral area. This procedure may be useful for women with stress incontinence resulting from an incompetent internal sphincter in whom general anesthesia is contraindicated. Data from randomized studies suggest short-term improvement in symptoms.²⁹Urinary tract infections and transient urethral irritation are the most common side effects. Other complications include urgency, incontinence, and urinary retention.

Absorbent products (diapers, pads) are a last resort for many patients. An indwelling catheter is indicated only for significant, irreversible urinary retention; skin disorders, such as perineal groin rash or stage III or IV pressure sores;or patient comfort or preference.

WHEN TO REFER

Further evaluation by a urologist or urogynecologist is recommended when:

Office-based interventions fail.

The diagnosis is uncertain.

The patient's incontinence is associated with recurrent symptomatic urinary tract infections, a symptomatic pelvic prolapse, an abnormal PVR volume, and/or hematuria without a coexisting infection. n

References:

REFERENCES:

1. Appell RA, Sand P, Dmochowski R, et al. Prospective randomized controlled trial of extended-release oxybutynin chloride and tolterodine tartrate in the treatment of overactive bladder: results of the OBJECT Study. Mayo Clin Proc. 2001;76:358-363.

2. Hampel C, Wienhold D, Benken N, et al. Definition of overactive bladder and epidemiology of urinary incontinence. Urology. 1999;50(suppl 6A): 30-40.

3. Fantl JA, Newman DK, Coiling J, et al. Clinical Practice Guidelines Number 2, 1996 Update: Urinary Incontinence in Adults: Acute and Chronic Management. Rockville, Md: Agency for Health Care Policy and Research, US Dept of Health and Human Services. Public Health Service; 1996:3-90. AHCPR publication 92-0682.

4. Chutka DS, Fleming KC, Evans MP, et al. Urinary incontinence in the elderly population. Mayo Clin Proc. 1996;71:93-101.

5. Resnick NM, Yalla SV. Management of urinary incontinence in the elderly. N Engl J Med. 1985;313: 800-805.

6. DuBeau CE. Urinary incontinence. Clin Geriatr. 2001;9:31-47.

7. Kane RL, Ouslander JG, Abrams IB, eds. Essentials of Clinical Geriatrics. 3rd ed. San Francisco: McGraw-Hill; 1994:145-196.

8. Batra SC, Iosif CS. The female urethra: target for estrogen action. J Urol. 1983;129:418-421.

9. Rackley RR, Appell RA. Evaluation and medical management of female urinary incontinence. Cleve Clin J Med. 1997;64:83-92.

10. Bhatia NN, Bergman A. Cystometry: unstable bladder and urinary tract infection. Br J Urol. 1986; 58:134-137.

11. Ouslander JG, Leach GE, Staskin DR. Simplified tests of lower urinary tract function in the evaluation of geriatric urinary incontinence. J Am Geriatr Soc. 1989;37:706-714.

12. Burgio KL, Locher JL, Goode PS, et al. Behavioral vs drug treatment for urge urinary incontinence in older women: a randomized controlled trial. JAMA. 1998;280:1995-2000.

13. Elia G, Bergman A. Pelvic muscle exercises: when do they work? Obstet Gynecol. 1993;81: 283-286.

14. Anderson RU, Mobley D, Blank B, et al. Once

daily controlled versus immediate release oxybu-tynin chloride for urge urinary incontinence. OROS

Oxybutynin Study Group. J Urol. 1999;161:1809-1812.

15. Appell RA. Clinical efficacy and safety of tolterodine in the treatment of overactive bladder: a pooled analysis. Urology. 1997;50(suppl 6A):90-96.

16. Diokno AC, Appell RA, Sand PK, et al, for the OPERA Study Group. Prospective, randomized, double-blind study of the efficacy and tolerability of extended-release formulations of oxybutynin and tolterodine for overactive bladder: results of the OPERA Trial. Mayo Clin Proc. 2003;78:687-669.

17. Harvey MA, Baker K, Wells GA. Tolterodine versus oxybutynin in the treatment of urge urinary incontinence: a meta-analysis. Am J Obstet Gynecol. 2001;185:56-61.

18. Dmochowski RR, Davila GW, Zinner NR, et al, for the Transdermal Oxybutynin Study Group. Efficacy and safety of transdermal oxybutynin in patients with urge and mixed urinary incontinence. J Urol. 2002;168:580-586.

19. Yoshimura N, Chancellor MB. Current and future pharmacological treatments for overactive bladder. J Urol. 2002;168:1897-1913.

20. Siegel SW, Catanzaro F, Dijkema HE, et al. Long-term results of a multicenter study on sacral nerve stimulation for the treatment of urge urinary incontinence, urgency-frequency, and retention. Urology. 2000;56(suppl 6A):87-91.

21. Alhasso A, Glazener CM, Pickard R, N'Dow J. Adrenergic drugs for urinary incontinence in adults. Cochrane Database Syst Rev. 2003;(2): CD001842.

22. Writing Group for the Women's Health Initiative Investigators. Risks and benefits of estrogen plus progesterone in healthy postmenopausal women: principle results from the Women's Health

Initiative randomized controlled trial. JAMA. 2002;

288:321-333.

23. Grady D, Brown JS, Vittinghoff E, et al. Post-

menopausal hormones and incontinence: the Heart and Estrogen/Progestin Replacement Study. Obstet Gynecol. 2001;97:116-120.

24. Moehrer B, Hextall A, Jackson S. Oestrogens for urinary incontinence in women. Cochrane Database Syst Rev. 2003;(2):CD001405.

25. Norton P, Zinner N, Yalcin I, et al. Duloxetine versus placebo in the treatment of stress urinary incontinence. Am J Obstet Gynecol. 2002;187:40-48.

26. McConnell JD, Barry MJ, Bruskewitz RC, et al. Clinical Practice Guideline Number 8:Benign Prostatic Hyperplasia: Diagnosis and Treatment. Rockville, Md: Agency for Health Care Policy and Research Public Health Service, US Dept of Health and Human Services; 1994. AHCPR publication 94-0582.

27. Finkbeiner A. Is bethanechol chloride clinically effective in promoting bladder emptying? A literature review. J Urol. 1985;134:443-449.

28. Bash KL. Review of vaginal pessaries. Obstet Gynecol Surv. 2000;55:455-460.

29. Pickard R, Reaper J, Wyness L, et al. Periurethral injection therapy for urinary incontinence in women. Cochrane Database Syst Rev. 2003;(2): CD003881.

30. Resnick NM. Urinary incontinence in the elderly. Med Grand Rounds. 1984;3:281-290.

FOR MORE INFORMATION:

m Holroyd-Leduc JM, Straus SE. Management of urinary incontinence in women. Scientific review. JAMA. 2004;291:986-995.

m Holroyd-Leduc JM, Straus SE. Management of urinary incontinence in women. Clinical applications. JAMA. 2004;291:996-999.