Bladder Dysfunction and Urinary Incontinence

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[edit] Bladder Dysfunction and Urinary Incontinence

Kathleen C. Kobashi

Gary E. Leach

Urinary incontinence affects an estimated 13 million adults in the United States.The prevalence varies with the profile of the group considered.Some 10% to 20% of women aged 15 to 64 years and 40% of women over 60 years of age have urinary incontinence.Some 56% of institutionalized patients of both sexes, or 1.06 million individuals, are incontinent of urine.In 1995, the cost of treatment of urinary incontinence in patients over 65 years of age was approximately $26 billion, amounting to $3565 per individual.Incontinence is a prevalent and costly problem that affects not only patients' physical health (infection and physical debility) but also their psychologic and social status.Incontinence can clearly have a devastating impact on quality of life.

The treatment modalities used for urinary incontinence can, in themselves, cause complications.Chronic indwelling catheters place a patient at risk for infection, stones, tumors, and urethral and meatal damage.Condom catheters and diapers lead to chronic infections, skin breakdown, and decubiti.

Since many patients find it humiliating and difficult to express the inconveniences associated with urinary incontinence, appropriate diagnosis and treatment are often not administered as readily as they should be.Patient, family, and caretaker education is one of the most important issues to be addressed when instituting proper treatment for urinary incontinence.Throughout this chapter incontinence refers to urinary incontinence.

[edit] NORMAL PHYSIOLOGY

An intricate control system regulates bladder function.Normal bladder physiology involves both a storage phase and an evacuation phase, which must be coordinated.Both these phases depend on interaction between the bladder and the sphincteric mechanism, which allows for low-pressure storage and the maintenance of continence.Subsequent voiding is accomplished by detrusor muscle contraction accompanied by essentially simultaneous relaxation of the sphincteric mechanism.

The detrusor is composed of smooth muscle.The sphincteric mechanism has two well-defined components in the male patient.The bladder neck and proximal prostatic urethra form the internal sphincteric mechanism, which is a smooth muscular structure.The external sphincter is formed by skeletal muscle contributions from the pelvic floor and a second component arising from the urethral wall.A third component of the distal mechanism is an intrinsic urethral, smooth muscular component.

In female patients the continence mechanism is formed predominantly by the bladder neck and proximal urethra.This mechanism is further augmented by the urethral submu cosal tissues, which create a “seal” effect in the urethra, thus potentiating continence.Estrogens enhance this seal by mechanisms that may involve the maintenance and proliferation of the urethral submucosal vascular plexus and by promotion of the function of the adrenergic receptor population that exists in this area and is crucial to urethral mucosal closure.Failure of this seal results in intrinsic sphincteric deficiency or type III urinary incontinence.

The motor nucleus controlling detrusor function is located in the sacral spinal cord between the S2 and S4 cord levels (spinal column levels T11 to L1) (Fig.151-1).Parasympathetic afferents from this motor nucleus course in the hypogastric nerve to synapse with ganglia located within the detrusor wall.Postganglionic afferents carry impulses that cause detrusor excitation and bladder contraction.Receptors in the detrusor muscle are predominantly parasympathetic in mediation, with primarily muscarinic and to a lesser extent cholinergic receptors being identified.These receptors mediate detrusor contraction.Also present within the detrusor muscle are adrenergic receptors that are responsible for muscular relaxation.Efferent fibers transmit impulses from the bladder back to the detrusor nucleus.These impulses convey information, including degree of bladder distention.In the bladder base and proximal urethra, the predominant type of neuroreceptor is α-adrenergic.These receptors mediate contraction and are intimately involved in the continence mechanism.The nucleus controlling external sphincteric function is also located in the sacral cord.Extensive neural interconnections between these two cell groupings provide continual interplay between these entities and allow coordination between them.

Figure 151-1 The bladder and urinary sphincter are controlled by an intricate neurologic system.

The sacral cord is tonically inhibited by descending impulses carried by the spinal cord that arise in the pontine mesencephalic reticular formation located in the midbrain.A specialized neural grouping that governs voiding is located in this area of the pons.This micturition center in turn receives descending input from the cerebral cortex, cerebellum, and limbic system.

When the detrusor reaches capacity, the higher centers cease to inhibit the sacral cord.Through descending paths, the pons potentiates the initiation of voiding and the coordination of detrusor contraction and sphincteric relaxation.Voiding is completed by a detrusor contraction, which is facilitated until emptying is complete.

[edit] PATHOPHYSIOLOGY

Dysfunction of any element of this mechanism produces some loss of regulation of voiding and may result in urinary incontinence or retention.Interruption by pathology above the midbrain center results in loss of inhibitory influences on the midbrain.This may be reflected in the appearance of uninhibited bladder contractile activity, causing urgency symptomatology and urgency incontinence.Two notable exceptions to this statement should be considered.Cerebrovascular accidents (CVAs) may rarely result in retention but only in the acute phase.Parkinson's disease often results in uninhibited and poorly sustained detrusor contractile activity.However, this activity is usually accompanied by sphincteric dysfunction, which results in poor coordination between detrusor and sphincter (sphincter bradykinesia).

Injury or disease of the midbrain or descending spinal pathways results in loss of coordination between the bladder and the urinary sphincter, as well as loss of descending inhibitory input on the detrusor nucleus.The resulting clinical picture is that of uninhibited detrusor contractile activity associated with a nonrelaxing urinary sphincter.The result of this process is a high-pressure, poorly emptying bladder that is prone to decompensation.This high pressure is subsequently transmitted to the kidneys, resulting in hydronephrosis and eventual azotemia.The most common setting for this scenario is a spinal cord injury (trauma or infection), tumor, or vascular event.

Injury or disease of the sacral cord, or peripheral neural projections from this level, results in ablation of detrusor and sphincteric nuclei function.Initially, this is manifested by an areflexic (noncontractile) detrusor.Low-pressure, large-volume urinary retention results.With chronicity, however, the characteristics of the bladder wall that produce a low pressure, high-capacity reservoir (compliance) are altered.This alteration results in part from the loss of innervation and also from changes in the composition (increasing fibrosis) of the bladder wall.Higher pressures ensue, which may be deleterious to renal function and may also produce spontaneous urine loss.

In the discussion of any pathologic process involving the nervous system, it is important to note that the resultant clinical picture infrequently reflects a “complete” lesion.More often, an incomplete neural lesion results.Frequently, some function is preserved in the absence of other functions, which cannot be predicted by the level or degree of injury.Another aspect of importance that further obfuscates the clinical presentation is that neural lesions also may be present at multiple levels.

[edit] EVALUATION

Data regarding an individual's bladder dysfunction should be gathered in an orderly manner so as to delineate all appropriate historic and physical examination elements crucial to establishing a diagnosis and treatment plan.These elements are supplemented by urinary evaluation and further urologic tests as indicated.

[edit] History

The patient history should include a notation of the duration of symptoms.Whether the patient has experienced symptoms since childhood or only relatively recently yields information regarding the potential for congenital disorders.Symptoms noted only recently may indicate a potentially reversible cause of bladder dysfunction or incontinence.The presence of irritative symptoms, including nocturia and frequency, is recorded.Dysuria or pain with bladder filling may indicate infectious or inflammatory conditions.Obstructive symptoms include hesitancy, straining to void, intermittency of stream, and incomplete emptying.These symptoms may further complicate overflow incontinence.The presence of intercurrent urinary tract infection or gross hematuria is established.Diurnal and nocturnal frequency should be recorded.The volume of fluid ingested also should be evaluated.If necessary, patient home logs of intake and output should be kept to evaluate the appropriateness of fluid ingestion.

Incontinence should be classified to better define possible etiologies.The failure to store urine or the failure to empty provides an easily reproducible method by which to categorize bladder function.This system conceptualizes lower urinary tract function as depending on the interaction of the bladder and bladder outlet (sphincter) for normal urine storage and expulsion.A defect in either bladder or sphincteric function can result in either failure to store or failure to empty.Mixed bladder and sphincteric dysfunction may also be responsible for the clinical scenario (Box 151-1).

Incontinence may be considered as fixed or transient.Transient incontinence usually has a definable, sudden onset and often has a discrete cause.A simple mnemonic summarizes the differential diagnosis of transient incontinence (Box 151-2).%Fixed or established causes of incontinence may be subdivided into several broad headings with differential considerations on the basis of patient sex.These etiologic possibilities may affect storage, emptying, or both functions of the lower urinary tract (Box 151-3).

Urge incontinence is characterized by the patient experiencing a strong desire to void and doing so precipitously without the ability to suppress the urinary loss.This type of incontinence results from overactivity of the detrusor, resulting in uncontrollable bladder contractions.The patient may experience this loss related to a particular activity or exposure or may note no inciting etiology.This is the most common type of incontinence noted in elderly populations.Urge incontinence frequently complicates central disorders such as Parkinson's disease, Alzheimer's disease, CVA, and brain tumor.Urge incontinence is also noted with local bladder disorders such as outlet obstruction, carcinoma in situ, and infection.

Reflex incontinence is another category of incontinence related to urge incontinence.This type of incontinence is manifested by the precipitous loss of urine with no sense of urgency.This category is most often noted in patients with suprasacral spinal cord lesions, in whom midbrain inhibitory influences are ablated.Failure of the storage component of bladder function ensues.

Overflow incontinence is caused by the chronic retention of urine, with small volumes being frequently voided.Overflow incontinence may result from detrusor hypocontractility, as seen in tabes dorsalis, diabetes mellitus, or vitamin B₁₂deficiency.Overflow incontinence may alsoresult from bladder outlet obstruction, which is caused by prostatic or urethral pathology, with subsequent bladder decompensation.

Continuous incontinence implies total and unabated leakage of urine, unrelated to activity.This situation is identified when a fistula of the urinary tract is present.The most common etiology for urinary tract fistula in a woman is prior hysterectomy.

Stress incontinence is manifested by urinary loss with physical activity or sudden increases in abdominal pressure, as encountered with coughing or lifting.This type of incontinence arises from a deficiency of the bladder outlet resulting either from hypermobility of the urethra and bladder neck in women or from intrinsic damage in either sex.

A mixed category of incontinence also should be considered because in many cases, especially those noted in elderly persons, more than one type of incontinence is present (see Box 151-3).An example of this situation arises in women with stress urinary incontinence.In this group, a significant incidence of coexistent urge incontinence is identified, which may confuse the presenting symptomatic complaints.The need for and use of protective garments should be established.

Symptomatic history, although important in establishing the magnitude and extent of the condition, is often inaccurate in predicting the ultimate bladder or sphincter dysfunction defined by more involved testing.However, in institutionalized elderly patients, simple algorithms based on patient symptoms and bedside assessment have been reported to have a diagnostic accuracy of greater than 80% when verified by urodynamic testing.

Significant neurologic symptoms are also important in the evaluation of urinary tract dysfunction.Prior cranial or spinal surgical procedures should be ascertained.Symptoms of lower extremity motor or sensory deficit are significant.Diplopia, vertigo, and gait disturbance indicate central neurologic pathology, including multiple sclerosis and neoplasm.Voiding dysfunction associated with neurologic abnormalities noted on a screening examination may be thefirst indication of multiple sclerosis.Perineal or genital anesthesia associated with impotence indicates involvement of the cauda equina and interruption of the sacral nerves (S2 to S4) or their roots.Fecal incontinence or chronic constipation further indicates neural pathology, related either to specific nervous system lesions or to more global systemic processes such as diabetes mellitus.Any recent or chronic change in mentation or sensorium could indicate dementia, CVA, or other demyelinating disease.All have an impact on bladder dysfunction.

Other components of the medical history are also essential.The presence of systemic diseases such as diabetes mellitus or autonomic neuropathy should be noted.A history of cancer and therapies rendered for malignancy, including radiotherapy and chemotherapy, can give important diagnostic clues regarding metastases or injury resulting from therapy.Renal disorders may lead to neuropathy or bladder dysfunction related to increased urine production resulting from concentration defects.In women, a prior gynecologic and obstetric history is crucial.Hysterectomy can cause detrusor denervation when performed for uterine or cervical carcinoma.Prior therapy for endometriosis indicates the potential for recurrent disease and associated symptoms.If the patient is perimenopausal or postmenopausal, relative lack of estrogenic supple mentation can lead to vaginal atrophy and susceptibility to urinary tract infection and incontinence.

Previous surgical history is extremely important.As noted, prior neurosurgical procedures involving the back or cranium can directly contribute to bladder dysfunction.Any prior urologic or gynecologic procedure may also contribute to current symptoms.

Elucidation of the patient's current drug regimen is extremely important.Medications in many categories affect the bladder and voiding function.Antihypertensive agents, including sympatholytics, ganglionic blocking agents, and calcium channel blockers, affect bladder physiology.α Adrenergic antagonists may worsen preexisting stress urinary incontinence in women.Tranquilizing agents and psychotropic drugs can result in retention because of decreased appreciation of bladder filling or parasympatholytic effects.Similarly, many medications used in the therapy of Parkinson's disease can worsen bladder function as a result of anticholinergic side effects.Decongestants, as a result of sympathomimetic side effects, can exacerbate borderline voiding in men with bladder outlet obstruction caused by benign prostatic hyperplasia.The recent addition or change of diuretic medication can result in substantial urinary volume increases and decompensation of a borderline obstructive situation.Opiates, including antidiarrheal agents, may inhibit detrusor contraction.Antiarrhythmic agents, such as disopyramide, may also have a negative impact on detrusor contraction.The physician should note not only the drug and dose but also any possible relationship to the onset of the current symptoms.

[edit] Physical Examination

Physical examination includes a general examination with special attention to the genitourinary system.Blood pressure evaluation should be included.

Inspection of the back should be performed to identify an overt spinal deformity such as scoliosis.Attention to the base of the spine should exclude the identification of sacral skin discoloration or tufts of hair as well as an overt skin deformity such as a pit.These stigmata indicate the presence of spinal dysraphism and the possibility of a coexistent neurogenic bladder.The sacrum should be palpated to ensure bony integrity.

Abdominal examination should include palpation of the flanks for a mass or tenderness.The suprapubic area is evaluated for pain, and an attempt to palpate and percuss the bladder is made to identify distention.

Examination of the genitalia often indicates the presence of longstanding incontinence, with skin irritation and fungal infestation easily identifiable.Rectal examination reveals not only mucosal evaluation but also the presence and degree of resting and augmented sphincter tone.The size and consistency of the prostate gland are evaluated at this time.The covert presence of prostatic carcinoma can be manifested by symptomatic voiding dysfunction.

Pelvic examination must be performed to evaluate the adnexal structures for mass or tenderness.Speculum examination of the vaginal vault may reveal vulvar or cervical malignancy.Atrophy of the epithelial lining of the vagina is often present in postmenopausal women.Also, the presence of significant pelvic prolapse (cystocele, rectocele, uterine prolapse, vault descent) should be identified.Pelvic examination should be performed with the patient in both the supine and the standing positions to better elucidate the degree of uterine prolapse.This prolapse may be significantly underestimated if the examination is performed only while the female patient is supine.Significant bladder prolapse may result in hydronephrosis because of traction on the bladder base.Speculum examination of the vagina documents other forms of vaginal prolapse.A cystocele can be identified as a protrusion of the anterior vaginal wall that is accentuated when the patient strains.The coexistence of urinary loss associated with Valsalva's maneuvers or coughing should also be identified.A cystocele represents prolapse of the bladder base and proximal urethra and is frequently seen as a component of the hypermobility associated with uncomplicated stress urinary incontinence (Fig.151-2).This defect arises from weakness of the supporting (pubocervical) fascia of the bladder base.

Figure 151-2 A cystocele appears as a large bulge in the anterior vaginal wall that may be exacerbated when the patient strains. (From Webster GD, et al, editors:Reconstructive urology, Cambridge, Mass, 1993, Blackwell.)

A rectocele can be identified as a posterior vaginal wall protrusion composed of the rectum, which can also be accentuated by Valsalva's maneuver (Fig.151-3).This form of prolapse arises from a defect in the pelvic floor (pubococcygeus muscles) allowing anterior “herniation” of the rectum.

Figure 151-3 Rectoceles are confirmed by placing a finger in the rectum and applying anterior pressure.Any weakness of the posterior vaginal wall is demonstrated. (From Foote JE, Zimmerman PE, Leach GE: Vaginal reconstruction for pelvic floor laxity.In Webster GD, et al, editors:Reconstructive urology, Cambridge, Mass, 1993, Blackwell.)

An enterocele represents a defect at the vaginal apex usually seen after hysterectomy (Fig.151-4).This entity contains peritoneal contents.If a woman has previously undergone hysterectomy, the entire vaginal vault may prolapse to or through the introitus as a result of surgical damage to the supporting structures of the upper vagina (uterosacral ligaments).

Figure 151-4 An enterocele can be differentiated from vaginal vault prolapse by assessing the length of the posterior vaginal wall.The posterior wall is shortened in vault prolapse but retains its length with an enterocele. (From Webster GD, et al, editors:Reconstructive urology, Cambridge, Mass, 1993, Blackwell.)

Evaluation of the sacral cord can be enhanced further by eliciting the bulbocavernosus reflex, which reflects the integrity of the S2 to S4 levels of the cord.Compression of the glans penis (male) or mons pubis clitoris (female) produces anal sphincter contraction if the sacral cord is intact.Approximately thirty percent of neurologically normal women and five percent of normal men do not exhibit this reflex.^[1] The sacral dermatomes in the perianal area (S2, S3) should be tested for anesthesia or diminished sensation.

Neurologic examination is crucial to the initial patientevaluation.Mental status should be documented.Gait and balance are observed.Gross abnormalities of the cranial nerves and upper extremity function can yield information regarding systemic neurologic disease.Reflex testing of the knee (L2, L3) and ankle (L5, S1) is performed.The presence of Babinski's reflexes and clonus indicating upper motor neuron disease is also identified.Sensory evaluation of the lower extremities for fine touch, pinprick, vibratory, and positional sensation is performed.Gross motor weakness of the lower extremities is documented.

The initial examination includes an assessment of postvoiding residual urine volume.Difficulty in passing a small urethral catheter for this purpose may indicate the presence of urethral stricture, prostatic enlargement, or another abnormality.The presence of overflow incontinence or large volumes of retained urine can be a significant and often overlooked etiology to the presenting symptom complex, especially in the patient with urge incontinence.

[edit] Laboratory Evaluation

Urinary examination includes urinalysis, culture, and voided cytology.Microscopic inspection of the urine reveals hematuria, pyuria, or bacteriuria, which may coexist with pathology of the urinary system.Urinary tract infection may present with urgency or urge incontinence as the primary symptom.A voided urine cytology identifies malignant cells reflective of transitional carcinoma, which symptomatically can cause urgency and frequency.

Hematologic evaluation includes a serum creatinine analysis to estimate renal function.Evaluation of serum glucose and calcium may be indicated in patients with large urine volumes.Other testing is determined on the basis of any specific disease entity that is identified.

[edit] Radiographic Evaluation

Radiographic evaluation should be tailored according to symptomatology.Plain films of the abdomen (kidneys, ureters, and bladder) give information regarding soft tissues and any radiopaque urinary tract calculous disease.These radiographs are useful if the patient has a history of prior stones and or symptoms suggestive of this diagnosis.Ultrasound of the kidneys and abdomen is particularly useful in identifying hydronephrosis, calculous disease, and soft tissue pathology of the kidneys (tumor, abscess, medical renal disease).Renal ultrasound is indicated in the presence of azotemia to rule out any obstructive component.It is also indicated in the evaluation of neurogenic dysfunction of the bladder as a baseline study for longitudinal follow-up of ongoing therapy.

Further testing is predicated on diagnostic suspicions and often occurs after urologic referral.Criteria for referral have been established.This simplified system uses six categories to delineate factors that may indicate the presence of complicated urologic disease.These criteria arise from data easily obtainable from the history, physical examination, and simple diagnostic tests (Box 151-4).

Further radiographic imaging of the urinary tract may include an intravenous urogram to define urinary tract anatomy or to evaluate hematuria.Voiding cystourethrography (VCUG) is selectively performed to identify vesicoureteral reflux, the presence and degree of cystocele in the standing position, postvoiding residual, and any urethral abnormality.

[edit] Urodynamic Evaluation

Bladder storage function is evaluated by cystometrogram.Cystometry may be modified in several ways.The bedside cystometrogram is the most basic form of cystometry.This involves the insertion of a 12 or 14 Fr urinary catheter into the bladder.A 50-ml syringe, without the piston, is then attached to the end of the catheter.Sterile water is poured into the syringe in 50-ml aliquots while the syringe is held 15 cm above the symphysis pubis.Filling is continued until the column of water in the syringe rises, indicating a bladder contraction.The study is also terminated in the presence of patient discomfort or an infused volume greater than 500 ml.

More formal cystometry involves multichannel recording of bladder and rectal pressures.This study identifies the compliance (volume-related pressure changes) of the bladder.Fluid is instilled through a urethral catheter at a constant rate with continuous pressure monitoring.During recording, the patient's first urgency to urinate is identified, as is the sensation of bladder fullness.Failure to store urine appropriately is identified during this stage of the study.The presence of detrusor contractions that occur involuntarily during filling is noted.If this type of activity is noted, the contractions are referred to as detrusor instability(in the absence of overt neurogenic disease) or detrusor hyperreflexia(in the presence of nervous system pathology).Carbon dioxide has also been used as the infusant for cystometry.However, gas cystometry is difficult to interpret and prone to artifact.Findings are also not as reproducible as with water cystometry.

Failure to store urine on the basis of outlet dysfunction is also evaluated.During this phase of the study, the patient is asked to perform Valsalva's and stress maneuvers, which may identify stress incontinence.Failure to store urine as a result of combined defects in bladder storage and outlet resistance is elucidated by this simultaneous monitoring of bladder and bladder outlet events.

When the characteristics of the individual's voiding are to be determined, the patient is asked to void, and pressure and flow monitoring is continued.This simultaneous evaluation gives additive information to that obtained by uroflowmetry, which is usually performed at the same session.Failure to empty because of poor bladder contraction is identified during this segment of the evaluation.High-pressure, low flow voiding identifies outlet obstruction as the cause of failure to empty resulting from outlet obstruction.

Infusion with radiographic contrast allows the study to be monitored fluoroscopically, and real-time evaluation of bladder events may be made.Videourodynamics represents the most complex form of urodynamic evaluation.This type of evaluation is used to document the presence of bladder outlet dysfunction.It also identifies continuous loss of urine across the sphincteric mechanism in the absence of bladder contraction, which is seen in intrinsic sphincteric deficiency.

[edit] Cystourethroscopy

Outpatient urologic evaluation also includes cystoscopy.This reveals any overt pathology of the urethra or bladder, such as tumor, stone, stricture, or foreign body.

[edit] THERAPEUTIC INTERVENTIONS

Therapeutic options for voiding dysfunction include medical, surgical, and biofeedback and behavioral therapy.The primary goals of the treatment of bladder dysfunction are preservation of renal function, alleviation of urinary tract infection, and improved quality of life.

[edit] Failure to Store

Failure of the bladder to store urine at low pressures is treated according to whether the cause is secondary to a problem with the bladder, a problem with the bladder outlet, or a combination thereof.Incontinence may be caused by transient or chronic factors, and it is important to determine all potential etiologies to provide proper management.Remediable etiologies for incontinence include urinary tract infection, drug interactions, bladder tumors or stones, and problems related to changes in mental status.If the incontinence persists once these issues have been addressed, therapy for more chronic etiologies can be administered as indicated.

[edit] Secondary to Problems With the Bladder.

The true incidence of bladder overactivity in the general population has been estimated to be approximately 8%.^[2] In the geriatric patient population, failure to store urine is due to detrusor overactivity in more than 70% of patients.Treatment is optimally nonsurgical, with surgical therapy used only as a last resort.Therapeutic options include various medications, behavioral therapy, biofeedback, neuromodulation, and acupuncture, the last of which is not routinely used in the United States.

Detrusor instability or hyperreflexia may coexist with impaired contractility (DHIC) in up to 33% of cases.^[3] Despite overactivity of the bladder, the patient is unable to sustain a contraction sufficient for complete bladder emptying.DHIC may be suspected when instability is identified in the presence of significant postvoiding residual urine volumes.Anticholinergic medications to control the symptoms of urgency and clean intermittent catheterization to ensure complete bladder emptying are indicated in the treatment of DHIC.Regular catheterization not only helps avoid the complication of urinary tract infection that may be seen as a result of poor emptying but also contributes to alleviation of the symptoms of urgency associated with higher vesical volumes.

[edit] Medications.

Agents that inhibit bladder contractility can thereby increase bladder capacity and may also decrease intravesical pressures.Sustained elevation of intravesical pressures above 40 cm H₂O, seen especially in patients with myelodysplasia, puts the patient at risk for upper tract damage.Renal ultrasound should be performed to rule out the presence of hydronephrosis in these patients.

Anticholinergic medications competitively inhibit acetylcholine at the postganglionic autonomic (muscarinic) receptors. Musculotropics act directly on smooth muscle contractility by a papaverine-like action and also have varying anesthetic properties.Medications and their respective dosages are listed in Table 151-1.

Table 151-1 Anticholinergics and Musculotropics

The adverse effects of these medications vary with the systemic absorption and tend to be the most pronounced with oxybutynin (Ditropan).Effects include dry mouth, constipation, blurred vision, tachycardia, drowsiness, precipitation of urinary retention, and confusion.Narrow-angle glaucoma is an absolute contraindication to the use of this group of medications.The adverse effects often result in poor compliance by patients.The hepatic metabolites of oxybutynin are responsible for the severity of its side effects.Once-a-day slow-release oxybutynin (Ditropan XL) recently became available.Although the efficacy of immediate-release oxybutynin appears to be equivalent to that of Ditropan XL, the incidence of dry mouth is significantly lower for the latter.The incidence of other anticholinergic adverse effects was similar in both groups.Patients who are unable to tolerate the adverse effects of oral oxybutynin, patients in whom other oral therapies have failed, and patients who are willing to undergo catheterization are all candidates for intravesical oxybutynin.Intravesical instillation of oxybutynin bypasses the liver, and therefore the tolerance of this route of administration is better.^[4] Tolterodine (Detrol) is a competitive muscarinic antagonist that was released for use in the United States in mid-1998; it is administered at 2 mg twice a day.Because of its higher specificity for bladder muscarinic receptors (as compared to the salivary gland muscarinic receptors), its systemic and central side effects are significantly decreased and it is far better tolerated than oxybutynin.^[5]

Tricyclic antidepressants (TCAs) have both anticholinergic and local anesthetic effects, which make them a good choice for the treatment of detrusor instability.In addition, the increase in norepinephrine increases α-stimulation at the bladder neck to increase bladder outlet resistance.The primary agent in this category is imipramine (Tofranil), which is administered at 10 to 25 mg two or three times a day and may be increased up to 150 mg/day.Higher doses are used for the treatment of depression.

The adverse effects of TCAs can be divided into α-adrenergic and anticholinergic effects.The medication is generally well tolerated but is contraindicated in patients with cardiac arrhythmias or heart block.α-Adrenergic side effects include tachycardia, restlessness, blood pressure elevation, and exacerbation of heart block.Anticholinergic effects include orthostatic hypotension, dry mouth, ataxia, tachycardia, restlessness, hallucinations, and mental status changes.The latter effects are typically only seen at the higher doses used for antidepressive therapy.

The administration of an agent such as 1-desaminocystine-8-d-arginine vasopressin (DDAVP), a synthetic analog of the antidiuretic hormone, vasopressin, decreases urine production.In this manner, the problem of bladder instability may be eluded altogether, although it is not treated.This drug is used primarily in patients with nocturnal enuresis and diabetes insipidus and is not routinely administered in the therapy of detrusor instability.Adverse effects are rare and usually occur within the first few weeks of therapy.^[6] The main risk includes water intoxication and hyponatremia, and therefore the drug must be used with caution in the elderly, particularly in patients with a history of congestive heart failure.

[edit] Behavioral Modification, Bladder Training, and Biofeedback.

All patients deemed to be mentally and physically fit for active participation are candidates for behavioral modification.Patients must also be dedicated to compliance to the program to benefit maximally from it.Instructional teaching materials to assist patient education, such as those from H elpfor Incontinent People, or HIP, are available.Fluid restriction to 30 to 40 oz/day with avoidance of caffeine and alcohol is imperative.Fluid restriction is particularly important in patients who experience urgency and urge incontinence only at higher bladder volumes.Often, patients increase fluid intake in response to the dry mouth they experience when on anticholinergic medications and must be counseled strongly to avoid drinking more fluid.Candy, gum, artificial saliva, or small sips of fluid can be used to overcome the dry mouth.In addition, the constipation experienced by many patients can be treated with polycarbophil (Mitrolan), a wafer laxative that does not require the intake of the large amounts of fluid required by some fiber supplements.

Biofeedback is a method that uses monitoring equipment to facilitate the development of conscious control of various body functions of which the patient is unaware.It allows patients to take an active role in the management of their own health care.In combination with behavioral modification, biofeedback is used to train patients to postpone urination and void according to the clock rather than according to the urge to void.Using biofeedback, they are taught to inhibit or resist the sensation of urgency.Initially, the goal is set for urination every 1 to 2 hours; then it is gradually increased to 3 to 4 hours.For patients with instability only at high volumes, timed voiding every 2 to 3 hours may be helpful in avoiding the uninhibited contractions that result in the symptoms of urgency.

[edit] Electrical Stimulation.

Sacral nerve stimulation is currently increasing in use in the United States.^[7] The postulated mechanism of action is via activation of spinal or β-adrenergic nerves.A success rate of 60% to 70% is being reported in the initial studies.

[edit] Augmentation Cystoplasty and Urinary Diversion.

Surgery is the last resort for the treatment of urge incontinence.It may be offered to patients who have poor results with medications or are unable to continue medications because of the adverse effects.A patch of ileum or colon may be used to augment the bladder to decrease intravesical pressure and instability and increase bladder capacity.The authors counsel their patients that lifelong intermittent catheterization may be expected in 100% of patients after surgery.Urinary diversion or augmentation cystoplasty with creation of an abdominal stoma is a logical consideration for patients who may have difficulty accessing the urethra for catheterization.

[edit] Secondary to Problems With the Bladder Outlet.

When counseling patients about treatment alternatives for stress urinary incontinence, all options must be considered.Most patients wish to try noninvasive therapy before surgery.The goal, regardless of treatment choice, is to improve the patient's quality of life.Standard nonsurgical treatments include medications, biofeedback and behavioral therapy, and periurethral collagen injection.

Continuous incontinence or leakage of urine from the vagina may result from urinary-vaginal fistula.Fistulas tend to occur in patients who have had recent pelvic surgery or have a history of pelvic radiation.If a fistula is suspected, referral to a urologist should be obtained.

[edit] Medications.

α-Agonists stimulate the α-receptors at the bladder neck and proximal urethra, resulting in smooth muscle stimulation and increased bladder neck and proximal urethral resistance.α-Stimulators are useful in the treatment of mild to moderate stress incontinence but are usually not sufficient for treating this condition when it is severe.For maximal results, α-agonists should be used in conjunction with pelvic floor exercises and estrogens (see later paragraphs).

α-Stimulants should be used with caution in the elderly population, especially in patients with cardiac disease, hypertension, or hyperthyroidism.α-Agonists can cause drowsiness, anxiety, weakness, insomnia, headache, tremor, palpitations, cardiac arrhythmias, respiratory difficulty, and blood pressure elevation.Tachyphylaxis may be seen.Ephedrine and pseudoephedrine stimulate both α- andalpha;-and β-receptors and induce the release of norepinephrine.Phenylpropanolamine is a pure α-agonist with less central stimulation than ephedrine and pseudoephedrine; therefore the adverse effects of anxiety, insomnia, and headache tend to be minimized.

Because TCAs increase bladder outlet resistance and have anticholinergic and musculotropic effects and a strong direct inhibitory effect on the detrusor, they are ideal for treatment of mild stress incontinence, urge incontinence, and mixed stress and urge incontinence (see TCA discussion in previous section).

Estrogen supplementation plays an important role in the therapy of incontinence in women by enhancing the mucosal seal effect in the urethra.Intravaginal administration of ⅓ applicator three times a week amplifies the local effect of the estrogen over the effect of oral estrogen on the urethral and vaginal epithelium.^[8] Estrogen is usually used with other medications, pelvic floor exercises, and behavioral modification to get maximal benefit.

[edit] Behavioral Therapy and Biofeedback.

Patients who appear to benefit the most from behavioral therapy alone are those who suffer from only mild stress urinary incontinence.Concomitant use of biofeedback is an excellent treatment option for patients who would benefit from nonsurgical therapy based on either individual preference or clinical situation.A vaginal probe measures the activity of the levator ani musculature, and surface electrodes detect contractions of the abdominal or gluteal muscles, which might otherwise be mistaken by the patient as contraction of the pelvic floor musculature.Patients are taught to tighten the sphincter muscle without increasing abdominal pressure, and the biofeedback equipment relays auditory or visual feedback to patients regarding the physiologic activity.

[edit] Injection Therapy.

Various materials have been used in periurethral injection therapy for the treatment of ISD.Only collagen and fat are approved for use in the United States.The theory behind injection therapy is to bulk up the urethra to create a degree of outlet obstruction to facilitate continence.

[edit] Surgical Options.

Innumerable surgical techniques have been described for the treatment of stress urinary incontinence in the female patient, including pubovaginal slings, retropubic suspensions (e.g., Marshall-Marchetti-Krantz, Burch), needle suspensions (e.g., Raz, Stamey, Pereyra), anterior colporrhaphy, and variations thereof.For male patients, surgical treatment involves the placement of an artificial urinary sphincter.

The authors prefer to use pubovaginal slings for all female patients with stress urinary incontinence who opt for surgical therapy.Slings are placed beneath the proximal urethra andbladder to provide a “hammock” for support and direct urethral compression.The sling serves as a “backstop” to prevent urethral descensus and opening when increased intraabdominal pressure occurs.Slings and retropubic suspensions maintain an 83%-84% success rate beyond 48 months as compared to that for the needle suspensions, which decreases to 67% at that point.Overall, slings appear to be the most efficacious treatment over time.

Pubovaginal slings have been created from a variety of materials, including synthetic, autologous, allogenic, and xenogenic tissues.The authors use cadaveric fascia lata, placed via a transvaginal approach (Cadaveric Transvaginal Sling, or CaTS), which achieves better cosmesis and affords a significantly shorter operative time, hospital stay, and recovery period than the combined transvaginal/transabdominal approach or when harvesting of fascia is necessary.CaTS also results in less postoperative pain, typically requiring only acetaminophen for adequate analgesia in the experience of the authors.

In male patients, the artificial urinary sphincter is a successful therapeutic option.The device involves a fluid-filled cuff placed around the bulbous urethra to provide occlusion.When the patient wishes to void, a pump located in the dependent portion of the scrotum is pumped to move the fluid from the cuff to a pressurized suprapubic reservoir.Deflation of the cuff temporarily relieves the obstruction of the urethra, allowing the urine to pass.The cuff automatically refills in 3 to 5 minutes.

[edit] Failure to Empty

Failure to empty the bladder is also treated according to whether the pathology is due to the bladder, the outlet, or a combination.First, the patient's medication profile is reviewed for the possibility of urinary retention secondary to the anticholinergic or α-adrenergic side effects of medications.When possible, any medications that could be contributing to the problem is discontinued.

When there is persistent retention or when discontinuation of contributing medications is not feasible, the patient should be placed on intermittent catheterization.

[edit] Secondary to Problems With the Bladder.

In theory, medications that increase detrusor contractility, such as bethanechol (Urecholine), should promote bladder emptying if there is no concomitant outlet obstruction.However, there is no evidence to support that any medication this satisfactorily accomplishes this action.^[9]

Clean intermittent catheterization is the treatment of choice for incomplete bladder emptying with or without overflow incontinence.However, this option requires compliant patients (or caretakers) with the mental capacity and manual dexterity to perform catheterization.Indwelling catheters are a last resort because of the risks of complications from long-term catheterization.Complications include urethral damage, infections, stones, and tumor.If a long-term indwelling catheter is necessary despite these risks, a suprapubic cystostomy is preferred to avoid urethral damage.Catheters should be changed monthly.

Surgical therapy for the treatment of the acontractile bladder, including continent urinary diversion or the creation of a conduit with an external drainage device, is infrequently performed.Indications include patients who are unable to perform catheterization because of problems with manual dexterity or difficulty accessing the urethra.

[edit] Secondary to Problems With the Outlet.

Bladder outlet obstruction secondary to prostatism is commonly encountered in male patients.First-line therapy is α-blockers such as terazosin (Hytrin), doxazosin (Cardura), prazosin (Minipress), and tamsulosin (Flomax).Tamsulosin is more specific for the α_1a-receptors found in the prostate and therefore theoretically causes fewer side effects, such as dizziness and headache, than the other nonspecific α₁-antagonists.Anticholinergic medications may be added to control the urgency at the discretion of the clinician.Obviously, in patients with outlet obstruction, the addition of medications to relax the bladder may exacerbate urinary retention.In patients in whom medical therapy fails and who demonstrate a low flow rate despite adequate bladder function, prostate surgery is an option.Transurethral incision of the prostate is highly successful in small glands with minimal risk of incontinence, erectile dysfunction, or retrograde ejaculation.Larger glands may require resection (transurethral resection of the prostate) or open simple prostatectomy.Other therapies, such as microwave treatment or laser ablation of the prostate, are also widely used.

Bladder outlet obstruction is rarely seen in female patients and is most commonly due to periurethral scarring or suture “kinking” the urethra after antiincontinence surgery.Other causes include pelvic prolapse and very rarely, urethral malignancy.Release of the sutures and the scar tissue around the urethra or prolapse repair may be performed as indicated to relieve the obstruction.

[edit] SUMMARY

Bladder dysfunction and urinary incontinence are common and affect patients of all ages.Only about 2% of patients with incontinence actually receive treatment; therefore physicians should educate patients and other practitioners about the successful treatment options that are available.Incontinence is a problem with which no individual should live.A systematic approach to evaluation can lead to successful treatment and significant improvement in a patient's continence and quality of life.

[edit] REFERENCES