ANATOMY AND PATHO-
PHYSIOLOGY 

DIAGNOSIS AND TREATMENT 
Classification of Incontinence 

Overactive Bladder

Stress Incontinence

Overflow Incontinence

Malignant Prostatic Disease

Mixed Incontinence

CONCLUSION

REFERENCES

The Pharmacologic Management 
of Urinary Incontinence

George A. DeMaagd, PharmD, BCPS

Dr. DeMaagd is Assistant Professor of Pharmacy Practice at Ferris State University in Big Rapids, MI; Clinical Instructor at Michigan State University College of Medicine; and Adjunct Faculty at Western Michigan University, College of Health and Human Services, in Kalamazoo, MI.

Introduction

Urinary incontinence can be defined as a group of symptoms resulting in the inability to experience normal micturition, and may include difficulty initiating and controlling urine loss. The symptoms of urinary incontinence may vary depending on the etiology and incontinence type. This disorder, which primarily affects the elderly population, is associated with significant inconveniences both for patients and their caregivers.^1,2 Urinary incontinence affects up to 30% of community-dwelling elderly, and a similar percentage of acute-care hospital patients. Approximately 60% of nursing home patients suffer from incontinence and are often admitted for this disorder.³ Many patients may be reluctant to disclose their urinary incontinence problem, so the actual incidence may be underestimated.^1,4  The costs, both direct and indirect, associated with urinary incontinence can have a significant impact on the health care system.⁵ In addition to the inconveniences and cost issues, urinary incontinence may be associated with other medical complications. Skin breakdown can occur as a secondary event and may lead to ulceration in those who are chronically wet; this in turn may predispose patients to infections or exacerbate existing pressure ulcers.^6-9

Causes of Urinary Incontinence

Urinary incontinence is usually associated with storage or emptying problems of the bladder. The causes of urinary incontinence are numerous. The overall incidence increases with age, primarily as a result of age-related problems or events. The

aging process is associated with declines in bladder capacity, increases in residual urine volumes, involuntary bladder contractions (in addition to restricted mobility), and sex-specific changes. Elderly women may experience a decline in bladder outlet and urethral resistance secondary to the effects of estrogen loss on the pelvic musculature. Estrogen deficiency may lead to atrophic vaginitis, which may contribute to urgency and urinary tract infections.^9-11 Elderly men commonly experience prostate enlargement, which may affect flow rates and detrusor instability, causing bladder overflow problems. Additional causes include irreversible functional deficits secondary to Alzheimer’s disease, cerebrovascular disease (stroke), spinal cord lesions, and diseases such as multiple sclerosis. Other contributing factors may include urinary tract infections, menopause, genitourinary surgery, lack of postpartum exercise, and chronic illness. Extrinsic problems are often referred to using the mnemonic DIAPPERS and are described in Table 1.^11-13 In addition, medications can also cause or exacerbate existing incontinence (Table 2).^15-17

Table 1. Causes of Urinary Incontinence ¹⁴

Table 2.  Medications That May Affect Incontinence ^15-17

The Anatomy and Pathophysiology of Bladder Control 

Certain features of the bladder (Figure 1) are important when describing the various types of incontinence and its basic pathophysiology. The neurological control of urination involves the central nervous system, spinal cord, and the peripheral nerves. The nervous systems involved include the somatic, parasympathetic, and sympathetic systems—each of which is important for proper bladder control.^18-20 

Figure 1.  Bladder Anatomy

The bladder is an organ innervated through the pelvic nerves and controlled by both spinal cord and higher cerebral centers. The detrusor muscle that controls the bladder is innervated by the parasympathetic nervous system and involves cholinergic receptors. The internal sphincter, which is extremely important in maintaining continence, is innervated by the sympathetic nervous system and involves alpha-adrenergic receptors. The external sphincter is innervated by the somatic nervous system, which also controls micturition and may prevent urine loss. The external sphincter does not play a major role in maintaining continence since it fatigues rapidly.^18,21

The normal process of micturition can be described as follows: as the bladder fills, inhibitory signals allow the detrusor muscle to relax and sympathetic stimulation causes the internal sphincter muscles to contract, allowing bladder relaxation and the storage of urine. In addition, the somatic system causes contraction of the external sphincter to assist in maintaining continence. The volume of urine stored in the bladder, before the brain recognizes a sense of fullness, may vary from one individual to the next, but is approximately 100 to 200 mL. At these volumes, sensory receptors located within the bladder wall respond to stretching of the detrusor muscle. This sensation of distention travels up the spinal cord via the spinothalamic tracts to cortical centers in the frontal lobe of the brain. When bladder emptying is necessary, excitatory signals for detrusor contraction via the parasympathetic nervous system occur in concert with relaxation of internal and external sphincters—and urination takes place. The process of micturition requires a coordinated nervous system effort, and any insult affecting this process may lead to various forms of incontinence.^18,21 

When treating urinary incontinence, the pathophysiology and innervation are important since problems with different bladder control systems will dictate the type of pharmacologic agents deployed for a particular form of this disorder.^18-25 

Diagnosis and Treatment

Although the evaluation and diagnosis of urinary incontinence are not the focus of this review, an overview of some of the common tests and procedures may be useful. Patients being evaluated for urinary incontinence require a complete physical evaluation and medical history, including past drug use. A urinalysis is an important component of any objective evaluation to rule out infection, stones, or other obstruction. Additional tests may include a postvoid residual bladder volume measurement, which can be utilized to assess adequate emptying, and may be useful when evaluating urge and overflow incontinence types. Another common test that is useful in female patients is the provocative stress testing—to determine if there is leakage with stimulus (eg, cough when the bladder is full). This test may be useful when evaluating for stress incontinence. Numerous other supplemental assessments are available and can be performed by qualified specialists, if necessary.⁹ The diagnosis and treatment of urinary incontinence can be performed by general practitioners familiar with this disorder or, in some cases, may require a specialist. An excellent clinical practice guideline is available from the Agency for Health Care Policy and Research (AHCPR), Public Health Service, Department of Health and Human Services.⁹ This guideline, which was developed by a multidisciplinary team of health practitioners, addresses evaluation, diagnosis, and the management of urinary incontinence. 

Once the correct diagnosis is made, a number of pharmacologic and nonpharmacologic treatments are available. The importance of a correct diagnosis cannot be over-emphasized since drug therapies utilized for some forms of incontinence can exacerbate other forms of this disorder. Since the majority of patients diagnosed with urinary incontinence are elderly, concerns with pharmacologic management and increased drug adverse effects should always be a concern. Some general advice for practitioners should be to always start low and slow when utilizing pharmacologic therapies in the elderly.^1,9,26

Classification of Incontinence 

Incontinence is classified in a variety of ways, but for the purpose of this article, the most common types will be described. The five major types are described in Table 3, and most patients will fit into one of these classifications. It is important to remember that many patients suffer from mixed forms of incontinence, which may require a more complete evaluation to provide appropriate management.^27,28

Table 3. Overview of Common Incontinence Types^9,26,29-32

Overactive Bladder 

Overactive bladder, which may also be referred to as urge incontinence or detrusor instability, can best be described as a bladder detrusor muscle experiencing uncontrolled or uninhibited contractions. Other mechanisms that may be involved include inappropriate contraction of the external sphincter or detrusor hyperactivity with impaired bladder contractility (DHIC). Overactive bladder is the most common cause of urinary incontinence in the elderly, occurring in approximately 60% of the cases in this age group.^2,9 

The causes of urge incontinence are varied but are often secondary to neurologic disorders or insults, including stroke, trauma, Parkinson’s disease, or Alzheimer’s dementia. Additional causes include diabetes, drugs, infections, bladder stones, tumors, and atrophic vaginitis. A sudden episode of urge incontinence may be secondary to a urinary tract infection and is rapidly reversible with proper treatment. The clinical signs and symptoms are described as urgency and frequency, with patients reporting symptoms throughout the day and several times each night. The urgency can be intense and may result in a sudden leakage of large amounts of urine. In addition to the urgency, patients often experience a sensation of incomplete emptying.^24,33,34

The treatment of overactive bladder should include trials of nonpharmacologic therapies (ie, behavioral bladder training). This training involves timed voidings and the subsequent gradual increases of the time intervals between voids. Usually voiding is started at 1- to 2-hour intervals and increased from that point. Behavioral treatment should be considered prior to drug therapy; it may be more effective and may be a safer alternative in some patients.³⁵ Pelvic floor exercises may also improve detrusor instability and relieve the symptoms of urge incontinence. Other efforts may include biofeedback, pads for temporary support, and, in serious cases of urge incontinence, surgery may be necessary.^36,37 Drug therapy is usually considered second line but is often necessary in patients with overactive bladders.³⁵ Anticholinergic drugs, which decrease detrusor contractions and promote storage of urine (Table 4), are the drugs used most frequently.

Table 4. Anticholinergic Agents Employed 
in the Treatment of Overactive Bladder^40,41,44

 Since many patients with overactive bladder are elderly, the use of such drug therapy may be problematic due to adverse effects (Table 5).^1,38-40 

Table 5. Adverse Effects of Anticholinergic Drugs^17,39

The mechanism of action of anticholinergic drugs is to inhibit parasympathetic (cholinergic)-induced bladder contractions and reduce the urge to urinate. Although effective at reducing urgency, anticholinergic drugs can cause a number of adverse effects both peripheral and central (Table 5).^41,42 The two agents used most often in clinical practice include oxybutynin chloride (Ditropan) and tolterodine (Detrol). Oxybutynin is dosed three to four times daily, although recent release of a long-acting product allows once-daily dosing. Oxybutynin, which has anticholinergic effects in addition to smooth-muscle-relaxing properties, is the most common agent used; the muscle-relaxing properties of oxybutynin may offer some additional benefits.¹⁷ Tolterodine is the newest agent to enter the market (1998) and at standard doses may be more selective for the bladder.⁴³ Tolterodine, because of its increased selectivity for the bladder at therapeutic doses, may be associated with less systemic adverse effects compared with oxybutynin chloride, especially dry mouth.^44-46 Elderly patients may still experience anticholinergic adverse effects from tolterodine, especially at higher doses, and should be monitored carefully.⁴⁷ Tolterodine is metabolized by the cytochrome P-450 system, specifically by the 2D6 and 3A4 enzyme systems. Numerous drugs may inhibit its metabolism and may potentially lead to increases in adverse effects. Drugs such as cimetidine, fluconazole, erythromycin, nefazodone, and fluoxetine can interact with tolterodine, although the clinical significance is not known at this time. Monitoring for drug interactions is important when tolterodine is prescribed with other agents.²⁹ The decision to use oxybutynin versus tolterodine must take into account cost issues and tolerability with oxybutynin. A recent population analysis suggests that adherence to therapy was greater with tolterodine versus oxybutynin, although more pharmacoeconomic analyses are needed to define tolterodine’s role in the treatment of urinary incontinence.⁴⁸ If patients respond to and can tolerate low doses of oxybutynin, it may be the more cost- effective choice—with tolterodine as the more costly but better-tolerated second-line agent.

Contraindications to the use of anticholinergic agents include tasks requiring mental alertness, angle-closure glaucoma, myasthenia gravis, or gastrointestinal obstruction disorders. Anticholinergic agents should be used with caution in patients with a history of cardiac disease (including arrhythmias and coronary heart disease). Patients who are prescribed anticholinergic drugs should be counseled on potential adverse effects (ie, sedation, cognitive effects, and the common peripheral effects).^7,39,42,49 

Imipramine, a tricyclic antidepressant, is also utilized in the treatment of overactive bladder, and in addition to its anticholinergic effects has agonist effects on alpha receptors. Its effects on alpha receptors at the internal sphincter may benefit a patient with stress incontinence mixed with features of overactive bladder.³⁹ 

Stress Incontinence

Stress incontinence, the second most common cause of urinary incontinence, occurs most commonly in women, and is relatively rare in men. Stress incontinence is often seen in elderly women who have had multiple childbirths. The pathophysiology can be described as problems with urethra support or weakened sphincter function resulting in insufficient bladder outlet resistance. The results are a urethra that cannot maintain the pressure gradient required for urinary control, and involuntary voiding may occur. Additional pathologic causes may be the result of hypermobility of the bladder neck, resulting in significant displacement and anatomic defects where the urethra is out of alignment with the bladder neck.^7,12,13,50 

The major clinical symptom of stress incontinence is small amounts of urine leakage—usually secondary to any stimulus that causes an increase in intra-abdominal pressure. Stimulus (ie, coughing, sneezing, laughing, or rising from a chair) may trigger urine release. The leakage that results from this disorder may be quite bothersome and create significant hygiene problems. The social stigma from concerns of urine odor may keep patients from social activities. The clinical presentation of stress incontinence differs from urge incontinence, primarily in lacking urgency symptoms and nocturia. Patients with pure stress incontinence are usually dry at night and do not complain of frequent trips to the bathroom.^2,23,50,51

The causes of sphincter weakness and subsequent stress incontinence include a history of multiple vaginal childbirths, trauma, post-surgery effects, neurogenic insults such as sacral cord lesions, obesity, and radiation.^2,9 Pharmacologic causes include alpha-adrenergic blockers and angiotensin-converting enzyme inhibitors (Table 2).^50,51 In addition to the causes described above, estrogen deficiency with advancing age can result in atrophy of the sphincter area, leading to the stress incontinence. There is also some data suggesting a genetic component to the development of stress incontinence.^2,23 

Treatment of stress incontinence includes both nonpharmacologic and pharmacologic therapies. Nonpharmacologic therapies include timed voiding practices and pelvic floor (or Kegel) exercises. Recent data suggest that pelvic muscle exercises may be an effective nonpharmacologic therapy, although these exercises require a serious commitment by the patient and compliance may be a problem.⁵² Surgery is considered very effective, and success has been reported to be as high as 75% to 85%.⁵³ Incontinence pads are often used by patients and provide a temporary security when the patients are away from home and involved in various activities.^36,37,54

The pharmacologic management of stress incontinence is limited to alpha-adrenergic agonists and/or estrogen therapy. The goals of therapy with pharmacologic agents are to improve bladder sphincter tone and eliminate or reduce leakage.^1,7,19 The outlet system of the female bladder consists of the internal and external sphincters, which are innervated by the sympathetic and somatic nervous systems, respectively. As women reach their postmenopausal years, the ability of the sphincter muscle to prevent leakage is weakened, secondary to aging changes or atrophy that occurs in this anatomic area. The atrophy that occurs results in a lack of alpha receptor functionality and is the basis or rationale for using alpha-adrenergic agonists in this disorder^.9,50,51 Alpha agonists act on the receptors of the internal sphincter muscle, resulting in improvement in sphincter tone, which results in a reduction in urine leakage. Alpha agonists utilized may include over-the-counter (OTC) decongestant agents including phenylpropanolamine 50 to 75 mg bid or the long-acting formulations once daily, or pseudoephedrine 30 to 60 mg tid to qid.^55,56 Although effective in relieving the symptoms of stress incontinence, these agents are nonselective and may affect alpha receptors in other body systems. The prolonged vasoconstricting action of these agents on other alpha-adrenergic receptors may be a relative contraindication for their use in some patients. A patient with a history of cardiac arrhythmias, uncontrolled hypertension, or severe coronary artery disease should use these agents with caution and be monitored carefully.^9,19,57 Patients requesting OTC alpha agonists for their stress symptoms should be asked about their medical history. Although hypertension is a relative contraindication for the use of alpha agonists, their use may exacerbate blood pressure in some patients. Patients with a history of hypertension should be instructed to monitor their blood pressure periodically and should be instructed to communicate their use of these agents to their physicians or other practitioners. Other adverse effects that may be bothersome in some patients include nausea, itching, restlessness, and insomnia. Avoiding nighttime dosing can reduce the insomnia that may occur with these agents.^57,58 

Estrogen replacement in postmenopausal women may improve the tone and alpha-adrenergic responsiveness of urethral muscle and reduce the symptoms of stress incontinence.^51,59-61 Estrogen both in topical and oral formulations has demonstrated benefits in some patients with stress incontinence. Some data suggest that the combination of oral and topical formulations should also be considered.⁶² The estrogens most often used are oral conjugated forms in doses of 0.3 to 1.25 mg daily, or topical doses of 0.5 to 2 grams daily. The onset of clinical benefits is usually seen in 4 to 6 weeks. Estrogen alone and in combination with alpha-adrenergic agonists have demonstrated benefits in the treatment of stress incontinence. Studies evaluating the use of estrogen formulations with concurrent alpha-adrenergic agonists report an additive response.^63,64 Risks associated with estrogen use include coagulation disorders and a small risk of breast and endometrial cancer.^65,66 Patients receiving estrogen should be counseled regarding the risks and potential adverse effects of estrogen, including return 
of periods (vaginal bleeding), breast tenderness, and mild fluid retention.^60-64,67-71 

Overflow Incontinence

Overflow incontinence is best described as an overfilled bladder or an overdistention of the bladder secondary to improper emptying; this type of incontinence is primarily seen in males with benign prostatic hyperplasia (BPH), an enlargement of the prostate that occurs with the natural process of aging.^19,72 Other causes of overflow incontinence include fecal impaction, abnormal relaxation as a result of detrusor inadequacy seen in some patients with diabetes, or a condition defined as dyssynergia where the sphincter muscle contracts when the detrusor contracts, resulting in inhibition of bladder outflow. Women may develop an obstructive incontinence secondary to pelvic prolapse, cystocele, urethral stricture, or other conditions that result in alignment problems between bladder and urethra.⁷³ 

The clinical presentation of overflow incontinence can be described as frequent or constant dribbling of urine along with urgency symptoms. In males with prostatic hypertrophy, the presentation is usually hesitancy or difficulty starting a urine stream and/or a sense of incomplete emptying. Patients will often report that they are up numerous times each night, and, in approximately two thirds of patients, urge symptoms coexist. On physical examination, an enlarged prostate is noted and biopsy may be performed if the prostate-specific antigen is elevated (to rule out malignancy). Other testing may include renal ultrasounds (to rule out hydronephrosis and other obstructions).^{9,10,19,25,34} The underlying cause of overflow incontinence is an important part of the evaluation process since it may dictate or provide guidance for treatment decisions. If significant obstruction is present, surgeries including transurethral resection of the prostate (TURP) in males or repair of cystocele in women may be utilized. In males with BPH with mild symptoms, watchful waiting may be the initial course, followed by the use of low-dose pharmacologic therapies, as described below.^36,72 Drugs with anticholinergic adverse effects may exacerbate overflow incontinence and should be avoided in these patients.^10,39,42

If the decision is made to initiate drug therapy in males with BPH, the drug therapy options are quite limited. The peripheral alpha-adrenergic blockers are most often utilized and are excellent choices in patients with concurrent hypertension (Table 6).⁷⁴ The agents that are most often used within the class are those with longer half-lives, allowing once-daily dosing. In addition, the longer-acting agents have a more gradual onset resulting in less postural hypotension, which can be an advantage in the elderly who are at greater risk for this event. The mechanism of action of these agents in overflow incontinence is through alpha-adrenergic blocking at the prostate level, resulting in less alpha-induced constriction in this area; this allows for improved urine flow and a reduction in symptoms. One drawback to these agents is their nonselective alpha blockage of vascular alpha receptors, resulting in a reduction in blood pressure.⁷⁵ Although this lowering of blood pressure is an advantage in the patient with current hypertension, it may be problematic in the nonhypertensive.⁷⁴ The potential to cause orthostatic hypotension exists, especially in the elderly patient. Proper monitoring of blood pressures is important, especially during initial dose titration. As is recommended in the dosing of drugs in all elderly patients, starting low and slow is the proper method of initiating these agents. The most convenient dosing schedule for these agents is once daily at bedtime.⁷⁵ The newest alpha-1 blocker, tamsulosin, appears to be more selective for prostate alpha1A receptors. This alpha-receptor subtype is reported to be found in 70% of alpha receptors in the prostate tissue—a tissue that selectively offers the benefits of reducing obstruction but also minimizing effects on peripheral blood pressure. Other adverse effects associated with alpha blockers include dizziness, lightheadedness, edema, palpitations, sedation, headaches, and gastrointestinal effects. These agents should be avoided in patients with stress incontinence since they can exacerbate the condition.^75-77 Counseling of patients who are dispensed alpha blockers should include reminders regarding the central nervous system adverse affects (including sedation) in addition to educating them on the potential for these agents to affect blood pressure. 

Table 6. Alpha-1 Adrenergic Blockers^75-77

An alternative to the alpha blockers in the treatment of overflow incontinence secondary to BPH is the use of finasteride (Proscar). Finasteride is a 5-alpha-reductase inhibitor that blocks the formation of dihydrotestosterone (DHT) from testosterone. This results in a decrease in DHT and lack of support for gland growth or involution of hyperplastic prostatic tissue.⁷⁸ A clinical study comparing the efficacy of finasteride and the alpha-adrenergic blocker terazosin was conducted in patients with BPH. This comparative study demonstrated that terazosin was more effective than finasteride in end points including improved clinical response. It also demonstrated that the combination of finasteride and terazosin was no more effective than terazosin used alone.⁷⁹ Finasteride remains an alternative therapy for the treatment of males with BPH.^80,81 

The berries of the saw palmetto plant contain a lipidosterolic extract that has some inhibitor action on 5-alpha-reductase. Clinical studies have demonstrated mixed results using saw palmetto in the treatment of BPH. Some studies have reported similar efficacy in subjective measures (eg, International Prostate Symptom Score [IPSS], urinary flow rates) with finasteride. In addition, saw palmetto was reported to be better tolerated than finasteride.^82,83 When recommending herbal supplements to patients, it is important to instruct them regarding the disparity in content between herbal products, because of the lack of regulation. A trial of saw palmetto may be warranted for some patients with BPH under the medical supervision of their physicians and pharmacists. 

Another agent that has been used for overflow incontinence is bethanechol, a cholinergic agonist. This agent may be used to stimulate bladder contractions, thus leading to some improvement in overflow symptoms. In patients with poorly contractile bladders (eg, following surgery), clinicians may utilize this agent for 2 to 3 weeks along with a Foley catheter.² This agent has numerous adverse effects, including flushing, hypotension, and gastrointestinal problems, that limit its clinical utility. Use of this agent in patients with detrusor instability (urge incontinence) will exacerbate the urgency symptoms and should be avoided.^19,39 

Surgical treatment described as a TURP is performed in patients with severe symptoms unresponsive to medication management. Newer therapies including laser ablation and thermotherapy are future options that may offer a less invasive alternative.^72,81,84,85

Malignant Prostatic Disease

In malignant prostatic disease (nonbenign prostatic hyperplasia) nonpharmacologic treatments include prostatectomy, radiation therapy, and cryosurgical ablation. Drug and hormonal treatments are also utilized. Hormonal downstaging is the use of androgen ablation for 2 to 6 weeks before radical prostatectomy to downstage the tumor and improve surgical outcomes. Although surgical castration is one method to decrease the testosterone support of the prostate cancer, androgen deprivation can also be accomplished with drug therapies. The luteinizing-hormone-releasing hormone agonists may result in castrate testosterone serum levels in 3 to 4 weeks (Table 7). Because these agents cause an initial surge in testosterone by increasing luteinizing hormone after which a downregulation occurs, concurrent antiandrogen treatment is recommended. Antiandrogens are rarely effective as monotherapy, since they fail to completely block androgen action. An emerging concept in the treatment of prostate cancer is intermittent androgen withdrawal. Although the exact mechanism is not clear, patients who develop resistant disease while on an antiandrogen appear to develop symptomatic and biochemical improvement when the antiandrogen is withdrawn. Other pharmacologic treatments for malignant prostatic disease include the use of growth factor inhibitors (eg, suramin, paclitaxel, estramustine phosphate, retinoids, strontium 89 chloride).⁸⁵

Table 7. Agents Used in the Management 
of Malignant Prostatic Disease⁸⁵

In addition to the major types of incontinence, there are a few other types referred to in the medical literature. Functional incontinence is a form of incontinence secondary to external causes, resulting in an inability to reach the bathroom. Causes of functional incontinence include arthritis, weakness, stool impaction, urinary tract infections, medications, or changes in mental status. The treatment of this form of reversible incontinence is to eliminate the cause; pharmacologic management is rarely necessary. 

Atonic bladder is at times referred to in patients who have lost total innervation of the bladder, resulting in detrusor underactivity or complete lack of detrusor activity. These patients often require intermittent catheterizations to remove urine. Atonic bladder is a condition seen as a complication of diabetes, spinal cord injuries, or in patients with a history of severe alcoholism.^1,2 

Mixed Incontinence 

An important concept in the evaluation of incontinence is that the types of incontinence described above may not occur alone. Patients may present with more than one type of incontinence and may need a more complete evaluation from their primary care practitioner. In elderly males, detrusor hyperactivity or instability may occur with impaired bladder contractility. Fifty percent of elderly males with outlet obstruction, usually caused by BPH, may also have detrusor instability. Elderly women with stress incontinence may also have concurrent detrusor instability.^28,86-88 Achieving the most beneficial therapy requires appropriate evaluation and management, often focusing on treating the symptoms that predominate.^9,88

Conclusion

The pharmacologic management of urinary incontinence requires appropriate evaluation by qualified clinicians, but requires a multidisciplinary approach. Many patients are reluctant to discuss their incontinence problems, thus denying themselves benefit from the many new nonpharmacologic and pharmacologic therapies. Taking the time to get to know your patients may allow the pharmacist the opportunity to provide valuable education, intervention, and recommendations to improve patient care outcomes in the management of urinary incontinence. 

Acknowledgment

Special thanks to Anne Westra and Wendy Huff for their technical assistance.

References

1. Chutka DS, Takalhashi PY. Urinary incontinence in the elderly Drugs 1998;56(4):587-595. 

2. Rosenthal AJ, McMurtry CT, Urinary Incontinence in the Elderly. PostGrad Med
1995;97(5):109-121. 

3. Ouslander J, Schnelle J, Simmons S, et al. The dark side of incontinence: nighttime incontinence in nursing home residents. J Am Geriatr Soc 1993;41(4):371-6.

4. Wyman JF, Harkins SW, Choi SC, et al. Psychosocial impact of urinary incontinence in women. Obstet Gynecol Soc 1987;70:378-81. 

5. Hu TW. Impact of urinary incontinence on health-care costs. J Am Geriatr Soc 1990;38(3):292-5.

6. Resnick NM, Yalla SV. Management of urinary incontinence in the elderly. N Engl J Med 1985;313(13):800-5. 

7. Fourcroy JL. Urogynecology Update: Incontinence. Hospital Practice. 1998;(May 15)
63-81. 

8. Elving LB, Foldspang A, Lam GW, et al. Descriptive epidemiology of urinary incontinence in 3100 women age 30-59. Scand J Urol Nephrol Suppl 1989;125:37-43. 

9. US Agency for Health Care Policy and Research. Urinary incontinence in adults:
Clinical practice guidelines Number 2, Rockville, Md:Dept of Health and Human Services, Public Health Service, Agency for Health Care Policy and Research, 1996;DHHS publication No.AHCPR 96-0682.

10. Williams ME, Pannill FC III. Urinary incontinence in the elderly:pathsiology, pathophysiology, diagnosis and treatment. Ann Intern Med 1982;97:895-907.

11. Barrett DM, Wein AJ. Voiding dysfunction: diagnosis, classification, and management. In: Gillenwater JY, Grayhack JT, Howards SS, et al, eds Adult and pediatric urology. 2d ed, vol I.St. Louis:Mosby-Year Book, 1991:1001-99.

12. Thom DH, van den Eeden SK, Brown JS. Evaluation of parturition and other reproductive variables as risk factors for urinary incontinence in later life. Obstet Gynecol 1997;90(6):983-9.
13. Thom DH, Brown JS. Reproductive and hormonal risk factors for urinary incontinence in later life: a review of the clinical and epidemiologic literature. J Am Geriatri Soc 1998;46(11):1411-7.

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

15.Resnick NM in Current Medical Diagnosis and Treatment, LT Tierney et al (eds), Norwalk, Appleton & Lange, 1993.

16. Fuller MA, Borovicka MC, Jaskiw GE, et al. Clozapine-induced urinary incontinence: incidence and treatment with ephedrine. J Clin Psychiatry 1996;57(11):514-8.

17. Rondorf-Klyn LM, Colling J, Simonson W. Medication use by community-dwelling elderly with urinary incontinence. Urol Nurs 1998;18(3):201-6. 

18. Gosing JA: The structure of the female lower urinary tract and pelvic floor
Urol Clin North Am 1985;12:207.

19.Thompson JF. Geriatric Urological Disorders. In: Koda Kimble MA, Young LL, eds. Applied Therapeutics: The Clinical Use of Drugs. 6th ed.Vancouver, WA:Applied Therapeutics, Inc, 1995;103-1-103-25.

20. DeGroat WC. A neurological basis for the overactive bladder. Urology 1997;50(suppl 6a):36-52.

21. Bradley WE, Innervation of the male urinary bladder. Urol Clin North Am 1978;5:279-93.

22. Sourander LB. Treatment of urinary incontinence: the place of drugs. Gerontology 1990;36(suppl 2):19-26.

23. Campbell SC, Siegel SW. Female urinary incontinence, current evaluation and management. Consultant 1992 Sep Sep;32 (10):45-52.

24. Resnick NM. Urinary incontinence in older adults. Hosp Pract 1992 Oct 15;27 (10):552-66.

25. Sier HC. Urinary incontinence. Ann Intern Med 1988;108:720-4.

26. Ouslander JG, Bruskewski R. Disorders of micturition in the aging patient. Adv Intern Med 1989;34:165-90.


27. Resnick NM, Yalla SV, & Laurino. The pathophysiology of urinary incontinence among institutionalized elderly persons. N Engl J Med 1989;320(1):1-7.

28. Ouslander JG, Hepps K, Raz S, & Su HL. Genitourinary dysfunction in a a geriatric outpatient population. J of Amer Ger Soc 1986;(34(7):507-514.

29. Ruscin MJ, Morgenstern NE. Tolterodine use for symptoms of overactive bladder. Ann Pharmcother 1999;33:1073-82.

30. Ouslander JG. Asymptomatic bacteriuria and incontinence (Letter) J of Amer
Ger Soc 1989;37(2):197-198.

31. Andersson KE, Current concepts in the treatment of disorders of micturition. Drugs 1988;35(4):477-494.

32. Ouslander JG. Geriatric incontinence a review. Dis A Mon 1992;38:65-149.

33.Yim PS, Peterson AS. Urinary incontinence. Postgrad Med 1996;99(5):137-50.

34. Resnick NM, Blaivas JG, Ostergard DR. Practical pointers on urinary incontinence. Patient Care 1995;29:103-31.

35.Burgio KL, Locker JL, Goode PS, et al. Behavioral vs drug treatment for urge incontinence in older women: a randomized controlled trial. JAMA 1998;280(23):2034-5

36.Wyman JE, Fantl JA. Bladder training in ambulatory care management of urinary incontinence. Urol Nurs 1991;11(3):11-7.

37. Wyman JF, Fantl JA, McClish DK, Bump RC. Comparative efficacy of behavioral interventions in the management of female urinary incontinence. Continence Program for Women Research Group. Am J Obstet Gynecol 1998;179(4):999-1007.

38. Goode PS, Burgio KL. Pharmacological treatment of lower urinary tract dysfunction in geriatric patients. Am J Med Sci 1997;314;14(4):262-7.

39. Brown JH, Palmer T. Muscarinic receptor agonist and antagonists. In. Goodman & Gilman's A. eds. The Pharmacolgical basis of therapeutics: 9th ed. New York:McCraw-Hill, 1996;Pp 141-160.

40. Wein AJ. Pharmacologic treatment of incontinence: National Institutes of Health Consensus Development Conference on Urinary Incontinence in adults, Bethesda MD, October 3-5, 1988 J of Amer Ger Soc 1990;38(3):317-325.

41. Holmes DM, Montz FJ & Stanton SL. Oxybutynin versus propantheline in the management of detrusor instability. A patient regulated variable dose trial.
Bri J Obst Gyn 1989;96(5):607-612.
42. Feinberg M. The problems of anticholinergic adverse effects in older patients. Drugs Aging 1993;3:335-48.

43. Eglen RM, Watson RH, Challis RAJ. Muscarinic acetylcholine receptor subtypes in smooth muscle. Trends Pharmacol Sci 1994;15:114-9.

44.Abrams P, Freeman R, Anderstrom C, et al. Tolterodine, a new antimuscarinic agent: as effective but better tolerated than oxybutynin in patients with an overactive bladder. Br J Urol 1998;81:801-10.

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

46. Millard R et al. Clinical efficacy and safety of tolterodine compared to placebo in detrusor overactivity. J Urol 1999;161:1551-5.

47. Abrams P et al. Tolterodine, a new antimuscarinic agent: as effective but better tolerated than oxybutynin in patients with overactive bladder. Br J Urol 1998;81:801-810.

48. Lawrence M, Guay DRP, Benson RS et al. Immediate-release oxybutynin versus tolterodine in detursor overactivity: A population Analysis. Pharmacotherapy 2000;20(4):470-475.

49. Karram MM, Partoll L, Rahe J. Efficacy of nonsurgical therapy for urinary incontinence. J Reprod Med 1996;41:215-219.

50. Mushkat Y, Bukovsky I, Lanfer. Female urinary stress incontinence, does it have familial prevalence. Am J Obstet Gynecol 1996;174:617-9.

51. Brown JS, Grady D, Ouslander JG, et al. Prevalence of urinary incontinence and associated risk factors in postmenopausal women. Heart & Estrogen/Progestin Replacement Study(HERS) Research Group. Obstet Gynecol 1999;94(1):66-70.

52. Bo K et al. Single blind, randomized controlled trial of pelvic floor exercises, electrical stimulations, vaginal cones and no treatment in management of genuine stress incontinence in women. BMJ 1999;318:487-93.

53. Houston KA. Incontinence and the older woman. Clin Geriatr Med 1993;9(1):157-71.

54. Weinberger MW, Goodman BM, Carnes M. Long-term efficacy of nonsurgical urinary incontinence treatment in elderly women. J Gerontol A Biol Sci Med Sci 1999;54(3):M117-21.

55. Collset L & Lindskog M. Phenylpropanolamine in the treatment of female stress urinary incontinence: double-blind placebo controlled study in 24 patients. Urology 1987;30(4):398-403.

56. Fossberg E, Bersland HO & Lundgren RA. Stress incontinence in females: treatment with phenylpropanolamine: A urodynamic and pharmacological evaluation. Urologia Internationalis 1983;38(5):293-299.

57. Hoffman BB, Lefkowitz RJ. Catecholamines, Sympathomimetic Drugs and Adrenergic Receptor Antagonists. In. Goodman & Gilman's, eds. The Pharmacological Basis of Therapeutics. 9th ed. New York: McGraw Hill, 1996:199-248.

58. Serels S, Stein M. Prospective study comparing hyoscyamine, doxazosin and combination therapy for the treatment of urgency and frequency in women. Neurour Urodyn 1998;17(1):31-6.

59. Pandit L, Ouslander JG. Postmenopausal vaginal atrophy and atrophic vaginitis. Am J Med Sci 1997;314(4):228-31.

60. Maloney C. Estrogen in urinary incontinence treatment: an anatomic and physiologic approach. Urol Nurs 1997;17(3):88-91.

61. Bernier F, Jenkins P. The role of vaginal estrogen in the treatment of urogenital
dysfunction in postmenopausal women. Urol Nurs 1997;17(3):92-5.

62. Makinen JI, Pitkanen YA, Salmi TA, et al. Transdermal estrogens for female stress urinary incontinence in postmenopause. Maturitas 1995;22(3):233-8.

63. Walter S, Kjaergaard B, Lose G, et al. Stress urinary incontinence in postmenopausal women treated with oral estrogen (estriol) and an alpha-adrenoceptor-stimulating agent (phenylpropanolamine): A randomized double-blind placebo-controlled study. J Int Urogynec 1990;1:74-79

64. Ahlstrom K, Sandahl B, Sjoberg B, et al. Effect of combined treatment with phenylpropanolamine and estriol, compared with estriol treatment alone, in postmenopausal women with stress incontinence. Gynecol Obstet Invest 1990;30(1):37-43.

65. Ross RK et al. Effect of hormone replacement therapy on breast cancer risk:estrogen
versus estrogen plus progestin. J Natl Cancer Inst 2000;92:328-32. 

66. Schairer C et al. Menopausal estrogen and estrogen-progestin replacement therapy and breast cancer risk. JAMA 2000;283:485-91.

67. Hilton P, Tweddell AL, Mayne C. Estrogens alone and in combination with alpha-adrenergic stimulation in genuine stress incontinence. J Int Urogynec 1990:1;80-86.

68. Fantl JA, Cardozo L, McClish DK. Estrogen therapy in the management of urinary incontinence in postmenopausal women: a meta-analysis. First report of the hormones and urogenital therapy committee 1994;83(1):12-8.

69. Fantl JA, Bump RC, Robinson D, et al. Efficacy of estrogen supplementation in the treatment of urinary incontinence. The Continence Program for Women Research Group. Obstet Gynecol 1996;88(5):745-9.

70. Sartori MG, Baracat EC, Girao MJ, et al. Menopausal genuine stress incontinence treated with conjugated estrogens plus progestogens. Int J gynaecol Obstet 1995;49(2):165-9.

71. Griebling TL, Nygaard IE. The role of estrogen replacement therapy in the management of urinary incontinence and urinary tract infection in postmenopausal women. Endocrinol Metab Clin North Am 1997;26(2):347-60.

72. Harris JL. Treatment of postprostatectomy urinary incontinence with behavioral methods. Clin Nurse Spec 1997;11(4):159-166.

73. Zimmern PE, Hadley HR, Leach GE, et al. Female urethral obstruction after Marshall-Marchetti-Krantz operation. J of Urology 1987;138:517-520. 

74. American Society of Health Systems Pharmacists: Therapeutic position statement of optimizing the treatment of hypertension. Am J Health Syst Pharm 2000;57(2):162-73. 

75. Hawkins DW, Bussey HI, Prisant ML. Hypertension. In. Dipiro JT. Pharmacotherapy: A pathophysiologic approach, 3rd ed. Connecticut: Appeton & Lange, 1997;195-218.

76. Lepor H, Knapp-Maloney G, Wozniak-Petrofsky J. The safety and efficacy of terazosin for the treatment of benign prostate hyperplasia. Int J Clin Pharmacol Ther Toxicol 1989;27:392-7.

77. Noble AJ, Chess-Williams R, Couldwell C, et al. The effects of tamsulosin, a high affinity antagonist at functional alpha 1A and alpha 1D-adrenoceptor subtypes. Br J Pharmacol 1997;120:231-8. 

78. Marks LS, Partin AW, Gormley GL, et al Prostate tissue composition and response to finasteride in men with symptomatic benign prostatic hyperplasmia. J Urol 1997;157:2171-8.

79. Lepor H, Willford WO, Barry MJ, et al. The efficacy terazosin, finasteride, or both in beign prostate hyperplasia. N Engl J Med 1996;335;533-40. 

80. Walsh PC. Treatment of beign prostate hyperplasia. N Engl J Med 1996;335;586-7.

81. Anderson JT, Nickel JC, Marshall VR, et al. Finasteride significantly reduces acute urinary retention and need for surgery in patients with symptomatic benign prostatic hyperplasia. Urology 1997;49:839-45.

82. Wilt TJ, Ishani A, Stark G, et al. Saw palmetto extracts for treatment of benign prostatic hyperplasia. JAMA 1998;280(18):1604-9. 

83. Gerber GS, Zagaja GP, Bales GT et al. Saw palmetto (serenoa repens) in men with
lower urinary tract symptoms: effects on urodynamic parameters and voiding symptoms. 
Urology 1998;51(6):1003-07.

84. Ball AJ & Smith PJ, The long-term effects of prostatectomy: a uroflowmetric analysis. J of Urol 1982;128(3):538-540. 

85. Goldspiel BR, Kolesar JM, Kuhn JG. Prostate Cancer. In. Dipiro JT. Pharmacotherapy: A pathophysiologic approach, 3rd ed. Connecticut: Appeton & Lange, 1997;2539-2557.

86. Resnick NM, Yalla SV. Detrusor hyperactivity with impaired contractile function: an unrecognized but common cause of incontinence in elderly patients. JAMA 1987;257(22):3076-81. 

87. McGuire EJ. Neuromuscular dysfunction of the lower urinary tract. In: Walsh PC, Gittes RF, Perlmutter AD, et al, eds. Campbell's urology 5th ed, vol 1. Philadelphia: Saunders, 1986:616-38. 

88. Ouslander JG, Leach GE, & Staskin DR. Simplified tests of lower urinary tract function in the evaluation of geriatric urinary incontinence. J of Amer Ger Soc 1989;37(8)706-714.

Introduction  |  References

Temple University School of Pharmacy is approved by the American Council on Pharmaceutical Education (ACPE) as a provider of continuing pharmaceutical education. Its CE programs are developed in accordance with the “Criteria for Quality and Interpretive Guidelines” of ACPE. This program is acceptable for 2.0 hours of Continuing Education Credits (0.2 CEU) through July 31, 2003.
ACPE Program I.D.  057-999-00-058-H01