Chapter 30. Urinary Incontinence

It is estimated that 45.2%, 10.7%, 8.2%, and 21.5% of the 2008 worldwide population (4.3 billion) was affected by at least one lower urinary tract symptoms (LUTS), overactive bladder (OAB), urinary incontinence, and LUTS/bladder outlet obstruction (BOO), respectively (Irwin et al, 2011). Urinary incontinence is a major health issue and the total direct and indirect cost in the United States alone was estimated at $19.5 billion in 2000, of which 75% is for the management of women with this condition. Incontinence also results in psychological and medical morbidity, significantly impacting health-related quality of life in a manner similar to other chronic medical conditions including osteoporosis, chronic obstructive pulmonary disease, and stroke. Overall prevalence of female incontinence is reported at 38%, increasing with age from 20–30% during young adult life to almost 50% in the elderly (Anger et al, 2006; Hawkins et al, 2010). Recent advances in the understanding of pathophysiology, as well as development of novel pharmacotherapy and surgical techniques for stress, mixed, and urge incontinence (UI), have redefined contemporary care of this patient group.

To facilitate comparisons of results and enable effective communication by investigators, the International Continence Society (ICS) has proposed standard terminology to be used to describe symptoms, signs, conditions, urodynamic findings, as well as treatment (Abrams et al, 2003). The ICS defines the symptom of urinary incontinence as “the complaint of any involuntary loss of urine.” It is also recommended, when describing incontinence, to specify relevant factors such as type, severity, precipitating factors, social impact, effect on hygiene and quality of life, measures used to contain the leakage, and whether or not the individual experiencing incontinence desires help.

Incontinence can be transient or chronic. Transient incontinence may occur after childbirth or during an acute lower urinary tract infection and usually resolved spontaneously. Chronic incontinence can result from a multitude of causes and is often persistent and progressive. From a functional and anatomic perspective, it is intuitive to consider the lower urinary tract as a two-part system: the urinary bladder as a reservoir and the bladder outlet as a sphincteric mechanism. Incontinence occurs when either part or both malfunction. Several common types of incontinence are discussed herein: stress urinary incontinence (SUI), urgency urinary incontinence, mixed urinary incontinence (MUI), neuropathic incontinence, and overflow incontinence (OI).

A step-wise management algorithm has been recommended for the management of male and female incontinence by the scientific committee of the 4th International Consultation on Incontinence (Abrams et al, 2010). In principle, the committee recommends an initial management and a specialized management algorithm for all types of incontinence. In initial assessment, one should identify the complicated incontinence group for specialized management. This includes recurrent or total incontinence, incontinence associated with pain, hematuria, recurrent infection, prostate irradiation, and radical pelvic surgery, suspected of fistula and significant postvoid residual. The following groups are suitable for initial management: stress incontinence, urgency incontinence, and incontinence with mixed symptoms. The initial clinical assessment should include general, urinary, pelvic floor, symptom scores, quality of life, desire for treatment, physical examination, urinalysis, and postvoid residual urine. The initial management consists of lifestyle intervention, bladder and pelvic floor muscle training, and incontinence products and medications. Specialized management is recommended for patients who failed the above-mentioned managements or those with specialized conditions. The assessment includes imaging of urinary tracts, urodynamics, and cystourethroscopy, and more invasive treatments including surgery, neuromodulation, and prosthetics are recommended for these patients.

The ICS defines it as involuntary urine leakage on effort or exertion, or on sneezing or coughing. In men, stress incontinence is mostly due to surgery (eg, after radical prostatectomy) or trauma to the bladder neck/urethral sphincter. The causes of stress incontinence in women are more complicated and somewhat controversial and therefore the following discussion is mostly related to female stress incontinence. The vast majority of stress incontinence occurs in women after middle age (with repeated vaginal deliveries and obstructed labor). It is usually a result of weakness/disruption of the pelvic floor muscle and ligaments leading to poor support of the vesicourethral sphincteric unit. An increase in urethral closure pressure is normally seen during bladder filling; when assuming an upright position; or in stressful events such as coughing, sneezing, or bearing down. During exertion, both passive pressure transmission from increased abdominal pressure and reflexic contraction of the sphincteric mechanism augment urethral resistance to prevent urine leakage.

Anatomy

Stress incontinence is thought to be caused by two major anatomical deficits: hypermobility of the sphincteric unit and intrinsic sphincter deficiency. In hypermobility, the assumption is that the intrinsic structure of the sphincter itself is intact. It loses closing efficiency because of excessive mobility and loss of support. Thus, the anatomic feature of stress incontinence is hypermobility or a lowering of the position of the vesicourethral segment (or a combination of the two factors) (Figure 30–1). On the other hand, some women who have undergone multiple retropubic or urethral operations have a deficient intrinsic sphincteric mechanism characterized by an open bladder neck and proximal urethra at rest with minimal or no urethral descent during stress. Nevertheless, many women maintain normal continence with hypermobility, and a recent dynamic magnetic resonance imaging (MRI) study finds no correlation between perineal descent and patients' symptoms of urinary incontinence (Broekhuis et al, 2010). Therefore, contemporary opinion suggests that all women with stress incontinence have some degree of intrinsic sphincter deficiency.

The relationships between the urethra, the bladder base, and various bony points have been the object of much study. For many years, the posterior vesicourethral angle has been considered a key factor indicating the presence of anatomic stress incontinence. Some authors, however, have emphasized the axis of inclination, that is, the angle between the urethral line and the vertical plane. Other investigators stress bony landmarks in the pelvis in their descriptions of the relationship of the bladder base and the vesicourethral junction to the sacrococcygeal inferior pubic point (Figure 30–2).

These descriptions illustrate that abnormal anatomic position and excessive mobility are essential elements in the diagnosis of stress incontinence due to hypermobility. To evaluate this aspect of incontinence, a simplified cystographic study (a lateral cystogram with a urethral catheter in place) is recommended. With the patient lying on the flat x-ray table, a lateral film is obtained, first at rest to determine the position of the vesicourethral segment in relation to the pubic bone and then with straining to ascertain its degree of mobility (Figures 30–3 and 30–4). Normally, the vesicourethral junction is opposite the lower third of the pubic bone and moves 0.5–1.5 cm with straining. This demonstration of abnormal position or excessive mobility of the vesicourethral segment is helpful in identifying the cause of existing urinary incontinence.

The urethral pressure profile is a measure of the activity of the external sphincter. A static profile demonstrates the resting tonus of both components of the sphincteric mechanism (see Figure 30–5); a dynamic profile gives the responses of these sphincteric elements to various activities, such as an increase in bladder volume, assumption of the upright position (Figure 30–6), the prolonged stress of bearing down, or the sudden stress of coughing and sneezing (Figure 30–7). Normally, the urethral closure pressure—the net difference between the intraurethral and intravesical pressures—is maintained or augmented during stress.

Detailed research of the role of smooth and striated components of the bladder and urethra were performed in animal experiments in the 1980's. Electrical stimulation of the pelvic nerve induces contraction of the smooth muscle of the bladder and urethra (Figure 30–8) while stimulation of the sacral nerve contracts smooth muscle of the bladder and urethra as well as striated muscle of the external sphincter (Figure 30–9). The contribution of smooth and striated muscle to urethral opening/closure pressure is further demonstrated in Figures 30–10, 30–11, and 30–12.

The high rate of success from midurethral sling surgery led some to believe that the midurethral support is the key element in preventing stress incontinence and raise doubts about the relevance of the cystographic study. Petros and Ulmstem (1990) proposed that support of the anterior vaginal wall is provided by three separate but synergistic mechanisms: the anterior pubococcygeus muscle; the bladder neck; and the pelvic floor musculature, which acts like a hammock to help close the bladder neck during stress. Laxity of the anterior vaginal wall causes dissipation of all of three forces, resulting in stress incontinence. Delancey (1994) proposes that the stability of the supporting layer rather than the position of the urethra determines stress continence. During rises in intra-abdominal pressure, the urethra is compressed against the supporting structures, which act like a backboard and prevent loss of urine. The fact that both bladder neck and midurethral slings have been shown to be successful in treating stress incontinence supports the above-mentioned theories (Novara et al, 2010; Ulmsten et al, 1998).

A recent report of a clinical study concludes that low urethral closure pressure is the best predictor of SUI in women (DeLancey et al, 2008). An MRI study also revealed that the striated urogenital sphincter in women with stress incontinence was 12.5% smaller than that in asymptomatic continent women (Morgen et al, 2009). A study on duloxetine, a serotonin and norepinephrine reuptake inhibitor, showed that it elevates both baseline urethral pressure (adrenergic innervation on the smooth muscle) and active pressure rise with sneezing (Onuf' nucleus activated striated muscle contraction (Miyazato et al, 2008). These observations reaffirm the original observation by Tanagho that smooth muscle, striated muscle, and mucosa and submucosal vessels each contribute about one-third of the urethral closure pressure and all are important in sphincter function.

Diagnosis

A detailed history is important, including the degree of leakage; its relation to activity, position, and state of bladder fullness; the timing of its onset; and the course of its progression. Knowledge of past surgical and obstetric history, medications taken, dietary habits, and systemic diseases (eg, diabetes) can be helpful in the diagnosis. A micturition diary that records the time of micturition, voided volume, and type of incontinence is recommended by the ICS as a useful supplement (Abrams et al, 2010). A pad test over 1 hour or 24 hours has also been recommended. In addition, history should also include the degree of bother and effect on quality of life. Many questionnaires and diaries are available for clinical and research use.

Physical examination is essential especially if urine leakage is witnessed by the examiner. In women, the pelvic examination demonstrates laxity of pelvic support, presence of any degree of prolapse, cystocele, rectocele, and mobility of the anterior vaginal wall. A neurologic examination should be done if neuropathy is suspected. Cystographic study for demonstration of the anatomic abnormality is helpful, as is urodynamic study to confirm the classic features of urinary incontinence and determine its cause. The goals of cystographic and urodynamic study are, first, to demonstrate the anatomic abnormality and its extent and, second, to assess the activity of the sphincteric mechanism and hence the potential for improvement by correcting the anatomic abnormality. The degree of hypermobility in women can also be assessed by a simple Q-tip test (Swift et al, 2010). This is done by inserting a well-lubricated sterile cotton-tipped applicator gently through the urethra into the bladder and then pulling it back to the level of the bladder neck. The angle from the horizontal at rest and after straining is recorded. Hypermobility is defined as a resting or straining angle >30° from the horizontal.

Urodynamic Characteristics of Stress Incontinence

Urethral Pressure Profile

The ICS defines urodynamic stress incontinence as the involuntary leakage of urine during increased abdominal pressure, in the absence of a detrusor contraction (Abrams et al, 2003). As would be expected, most patients with stress incontinence have a low urethral pressure profile with reduced closure pressure. This factor varies with the severity of the sphincteric impairment. Not infrequently, this weakness of the pressure profile is not demonstrable when the bladder is relatively empty. It becomes more significant when the bladder has been distended (Figure 30–13). Also, the pressure profile may appear normal when the patient is in the resting (sitting) position; when he or she assumes the upright position in the dynamic pressure profile, the weakness becomes apparent (Figure 30–14).

Functional Urethral Length

The anatomic length of the urethra is usually maintained, yet the functional length is shorter due to loss in the proximal urethral segment (Figure 30–15). Although it might not appear funneled on the cystogram, this segment has very low closure efficiency and its pressure is almost equal to intravesical pressure. The functional shortening might be minimal or it might involve more than one-half of the length of the urethra. It is important to note that the functional length, like the pressure profile, might appear normal when the bladder is not filled or the patient is in the sitting position.

Response to Stress

With the sustained stress of bearing down or the sudden stress of coughing or sneezing, the net urethral closure pressure is reduced, depending on the degree of sphincteric weakness. In severe urinary stress incontinence, any strain or increase in intravesical pressure leads to urinary leakage (Figure 30–16).

Voluntary Increase in Urethral Closure Pressure

Patients with mild stress incontinence might be capable of activating their external sphincter maximally and generating a high urethral closure pressure. However, with progression of the anatomic problem and hypermobility, this voluntary increase progressively diminishes.

Response to Bladder Distention and Change in Position

It must be emphasized that, although the features described might be normal in the resting position with minimal bladder filling, all of them can become aggravated with a full bladder or the upright position (Figures 30–14 and 30–17).

Abdominal Leak Point Pressure

Abdominal leak point pressure (ALPP) is defined as the intravesical pressure at which urine leakage occurs because of increased abdominal pressure in the absence of a detrusor contraction (Abrams et al, 2003). This test assesses the intrinsic urethral function, and thus the lower the ALPP, the weaker the sphincter.

Treatment

In mild and moderate cases, the ICS recommends lifestyle interventions, such as weight loss, caffeine reduction, pelvic floor muscle training, or duloxetine, a serotonin and norepinephrine reuptake inhibitor that has been approved in many countries but not in the United States. Electrical stimulation, vaginal devices, and urethral inserts may also help some women.

If the initial management fails, the principal surgical treatment of female urinary stress incontinence is to provide proper support of the vesicourethral segment or the midurethra.

There are numerous approaches to restoring the normal position and providing adequate support—some vaginal, others suprapubic. The suprapubic approach was popularized by the classic Marshall-Marchetti-Krantz (MMK) retropubic suspension described in 1949, in which periurethral tissue is attached to the back of the pubic symphysis. A modification was introduced by Burch in 1961, in which the anterior vaginal wall is fixed to Cooper's ligament. Many urologic surgeons today have found that the latter technique, with modifications, provides the most lasting results (Drouin et al, 1999; Kulseng-Hanssen and Berild, 2002) (Figures 30–18 and 30–19).

The other approach is to suspend the bladder neck or support the midurethra with an abdominal or transobturator sling. Numerous sling materials are being used: for example, cadaveric fascia lata and various synthetic materials. Tension-free vaginal tape (TVT) has been gaining popularity. Early results for TVT with follow-up to 11 years demonstrate comparable or improved versus traditional surgical approaches (suburethral slings, urethropexy, colposuspension, or injectable bulking agents) and reported success rates of up to 77% (Fong and Netti, 2010; Novara et al, 2010). Potential complications include bladder injury, infection, urinary retention, hemorrhage or hematoma, erosion (vaginal or urethral), and dyspareunia.

In patients with significant intrinsic sphincteric damage, local injection of bulking material, such as hyaluronic acid/dextranomer gel, polydimethylsiloxane (Macroplastique), pyrolytic carbon-coated beads suspended in a water-based carrier gel (Durasphere®), and collagen, is used to increase the bladder outlet resistance for patients in whom vesicourethral mobility is not excessive and whose primary problem is intrinsic sphincteric weakness (Ghoniem et al, 2010; Lightner et al, 2009). Recently, myoblast, fibroblast, and adult stem cells have been injected into periurethral tissue with very promising results (Carr et al, 1988; Mitterberger et al, 2007, 2008; Yamamoto et al, 2010). Besides the bulking effect, the injected stem cells seem to be able to stimulate local tissue proliferation (smooth muscle, collagen and elastic fibers) and thus improve the competence of the sphincter (Lin et al, 2010).

UI is defined as involuntary loss of urine, accompanied or immediately preceded by urgency. The basic feature of UI is detrusor overactivity or low bladder compliance and the loss of urine while attempting to inhibit micturition. Sphincteric instability is less common. The focus of this section is restricted to UI; OAB, which has replaced the term unstable bladder, and is clinically defined by symptoms of urgency, frequency, and nocturia with or without UI, is addressed only in the context of UI.

Neurogenic, myogenic, or urothelial bladder dysfunction can lead to UI or the constellation of symptoms that define OAB. OAB, with or without UI, is common in both men and women and can result from neuropathic injuries (brain or spinal cord deficit), obstruction, inflammation (interstitial cystitis), diabetes, benign prostatic hyperplasia (BPH), and so on, or be iatrogenic. Bladder overactivity may originate from the urothelium, detrusor muscle, or altered neural activation.

Diagnosis

Assessment of patients with symptoms of UI, or OAB, should include detailed history, including an assessment of the impact of the disorder on daily life; physical examination; urinalysis; and identification of modifiable causes such as impaired mobility. A sudden urge with uncontrolled loss of urine not associated with physical activity and leak of urine prior to reaching the bathroom are common patient complaints. Because cough-induced urinary leakage may be symptomatic of urgency and stress urinary incontinence, this simple stress incontinence test should be performed in the office setting to rule out mixed incontinence (Dmochowski, 2006). Most women with uncomplicated urinary incontinence can be given a preliminary diagnosis at this point and treatment is initiated. Should initial management fail (usually after 8–12 weeks trial), or if complex conditions are present (eg, pelvic organ prolapse, significant postvoid residual), urodynamics or other specialized investigations are recommended (Abrams et al, 2010).

Treatment

The treatment of UI often progresses from lifestyle change, behavioral techniques (bladder training) to anticholinergic pharmacotherapy. Options for nonresponders to drug therapy may include implanted sacral nerve stimulation (SNS). More invasive surgical procedures, including bladder augmentation or urinary diversion for persistent severe UI, are rarely indicated.

Lifestyle modification includes fluid management, as large volumes can exacerbate urinary incontinence, and bladder training to correct voiding patterns, improve the ability to suppress urge, and increase bladder capacity. Maneuvers included pelvic muscle training, scheduled voiding, and relaxation techniques. The International Consultation on Continence recommends an initial voiding interval of 1 hour during waking hours, with weekly increases of 15–30 minutes until a 2–3-hour interval is achieved (Norton and Brubaker, 2006).

Anticholinergic agents, such as oxybutynin (Ditropan), tolterodine (Detrol), fesoterodine (Toviaz), propiverine, and trospium (Sanctura), suppress involuntary bladder contractions and thus reduce the symptoms of OAB and are considered first-line therapy for UI (Andersson et al, 2009). Controlled clinical trials have demonstrated improvements in micturition frequency and episodes of incontinence, although side effects of dry mouth and constipation can lead to discontinuation of treatment. Extended release formulations of oxybutynin (Ditropan XL) and tolterodine (Detrol LA) can be dosed once daily, increasing patient compliance. More selective M3 receptor antagonists, solifenacin (Vesicare) darifenacin (Enablex), have also demonstrated good efficacy, safety, and patient tolerance (Dmochowski, 2006). A new oxybutynin 10% gel (Gelnique) has also been available with similar effect but has less incidence of dry mouth and constipation.

Intravesical botulinum toxin A has shown significant benefits for UI, OAB, prostatic enlargement, and neurogenic detrusor overactivity, and it may offer an important alternative to long-term oral pharmacotherapy or more invasive treatments. Quality of life, urgency, frequency, and bladder capacity improvements have been impressive to date (Chancellor, 2010; Kuo and Liu, 2009). Resiniferatoxin and capsaicin are two other agents currently under investigation but are not recommended by the International Consultation on Incontinence (Andersson et al, 2009). Others have proposed beta-3 adrenoceptor agonist as a potential agent for OAB (Igawa et al, 2010).

The results of randomized control trials provide evidence of SNS in decreasing episodes of incontinence, pad use, voiding frequency, and improvement of bladder capacity and voided volume (Tanagho and Schmidt, 1988; Thompson et al, 2010). Although surgical revision was required for one-third of cases, no major irreversible complications were reported and benefits of SNS were reported to persist at follow-up of 3–5 years.

MUI refers to the complaint of an involuntary leakage of urine associated with urgency and also with exertion, effort, sneezing, or coughing. This disorder comprises an element of detrusor dysfunction (motor or sensory) and is associated with urethral sphincter underactivity. About one-third of incontinent patients have both UI linked to idiopathic overactivity and genuine SUI. Some experts believe that MUI is now the predominant symptom grouping, with rates >50% reported in large population studies (Dmochowski, 2006). The relative incidence increases with advancing age and occurs most commonly in women older than 60 years.

Diagnosis

The definition of MUI by the ICS emphasizes the presence of SUI and components of OAB (frequency and urgency) with or without UI, in the absence of known instigating factors. Urodynamically, detrusor overactivity is often noted. However, it should be emphasized that the underlying source of MUI may be a reflex response initiated by urine released into the proximal urethra during stress events. In this way, some individuals with SUI may mimic MUI due to a significant urge component associated with spontaneous urine loss. The diagnostic steps for MUI are the same as for SUI and are described in Section “Stress Urinary Incontinence.” In those individuals with equal bother (UI and SUI), or difficulty defining their symptoms, urodynamics may help define dysfunction and therapy.

Treatment

The presenting symptoms serve as a guide to initial therapeutic approach. The most bothersome aspect, SUI versus UI, is usually addressed first. If both types of incontinence are equally bothersome, treatment of the urge component is preferred in most cases.

Initial approaches include behavioral therapy, biofeedback, and treatment with anticholinergics, with approximately 70% of patients experiencing symptomatic improvement with this class of medications; the notable exception is the patient with severe stress incontinence. In men, antimuscarinics for treatment of storage LUTS and prostate enlargement have also been shown to be effective with <3% chance of developing urinary retention (Kaplan et al, 2011). Once the initial treatment response is determined, further therapies can be initiated for persistent or secondary symptoms as outlined in Sections “Stress Urinary Incontinence” and “Urge Incontinence,” respectively.

Surgical outcomes for MUI have been reviewed for various sling techniques. Correction of a low-pressure outlet may benefit at least some patients with detrusor overactivity, although results for pure SUI remain superior. MUI symptom resolution has been demonstrated for upward of 70% of patients in some series, including a 4-year cure rate of 85% reported for the TVT approach (Dmochowski and Staskin, 2005; Lleberia, 2011). Current data support the use of either midurethral or pubovaginal slings for MUI.

OI is defined as the involuntary loss of urine associated with bladder overdistension. Two primary processes are involved: urinary retention caused by BOO or inadequate bladder contractions. Outflow obstruction may be secondary to BPH, bladder neck contracture or urethral stricture, or, less commonly, prostate cancer in men and due to cystocele, pelvic organ prolapse, or previous incontinence surgery in women. Impaired bladder emptying caused by decreased detrusor contractility may be the result of medications, spinal or peripheral nerve injuries, or due to long-standing overdistension. Diabetic cystopathy can result in OI, as both sensory and contractile functions may be compromised. OI may also occur following transurethral prostatectomy (TURP), as urine flow is impeded by stricture, contracture, or residual adenoma.

Diagnosis

A similar approach is followed as outlined previously for the other incontinence subtypes. Reversible causes can usually be identified by patient history. Specific to OI, overflow bladder is detected by measuring postvoid residual urine volume with ultrasonography (preferred) or urethral catheterization immediately after the patient urinates. Normally, <50 mL of urine remains in the bladder immediately following voiding and residual volumes of >200 mL indicate overflow bladder. Urodynamic testing and cystourethroscopy are used to determine the underlying cause or differentiate OI from other incontinence states.

Treatment

Initial treatment of OI focuses on addressing reversible causes identified during patient evaluation such as cystocele, pelvic organ prolapse, impaired mobility, and so on.

Should such precipitating elements not be found, outlet obstruction may be treated conservatively, with adjustment of fluid intake and timed voiding. However, male patients will often require further intervention, including pharmacotherapy with alpha-adrenergic antagonists or 5α-reductase (finasteride)/dual 5α-reductase (dutasteride) inhibitors. If stricture or prostatic obstruction is present, surgical intervention (transurethral resection of prostate, incision of the bladder neck, visual internal urethrotomy) may offer definitive treatment.

For OI secondary to nonobstructive underactive detrusor, the first step is to decompress the bladder with an indwelling catheter or clean intermittent catheterization (CIC) for 7–14 days, while addressing potential reversible causes such as medications, infection, or constipation. An alpha-blocker may be initiated during this time period. Should voiding trials fail repeatedly in the patient with an acontractile detrusor, CIC is the treatment of choice versus a permanent indwelling catheter (if feasible).

Many diseases or conditions involving the brain, spinal cord, and peripheral nerve can affect the function and structure of the bladder and sphincter as well as the synergic action of the two structures. Although complete lesions at different levels of the nervous system may produce typical urodynamic findings, the symptoms of patients suffering from the same lesion may vary due to nerve plasticity, secondary changes from infection, fibrosis, etc. Many diseases can also involve both peripheral and central nervous system to varying degrees. Incontinence can also be due to patient's inability to respond to sensory cue from bladder or having no perception of bladder fullness at all.

Failure of Bladder Storage Function

Loss of reservoir function in a contracted bladder can be caused by poor compliance in the detrusor muscle. Intravesical pressure rises with minimal bladder filling, exceeding the outlet resistance and causing urinary leakage. Failure of reservoir function may be found in patients who have meningomyelocele or exhibit other upper motor neuron lesions. Although these patients may have partial lesions with significant striated sphincteric activity offering some degree of resistance, early loss of bladder compliance increases intravesical pressure with minimal bladder filling and overcomes remaining outlet resistance (Figure 30–20). These patients, once recognized, must be managed aggressively because they often have a significant risk to the upper urinary tract, which can lead to possible vesicoureteral reflux, early renal deterioration, or lower ureteral obstruction.

Failure of Sphincter Function

Complete lesions of the sacral segment or the cauda equina result in a total loss of smooth and striated sphincteric activity. The external sphincter offers minimal resistance. Most patients experiencing such failure can retain some volume, because the bladder musculature becomes atonic and intravesical pressure remains low, but any increase in intravesical pressure can cause leakage and the bladder never reaches full capacity. Consequently, the integrity of the upper urinary tract is not endangered, as in cases of reservoir failure.

Diagnosis

Diagnostic evaluation of neuropathic urinary incontinence determines whether the condition arises from detrusor or sphincteric dysfunction, or from a combination of the two. In many patients with multiple sclerosis, spinal stenosis, herniated disk, or partial traumatic damage to the spinal cord, the contribution of neural deficit to urinary incontinence can be difficult to determine.

A complete urologic and neurologic history, physical examination, and urodynamics (cystometry, urethral pressure recordings, uroflowmetry) should be performed. Ultrasound evaluation, which can accurately measure renal size and identify scarring, calculi, and hydronephrosis (obstruction or vesicoureteral reflux), is an appropriate baseline study for all patients with neuropathic lesions. Other radiologic studies (voiding cystourethrography, excretory urography, computed tomography scanning, MRI) and neurologic studies (electromyography, evoked potentials) are performed as indicated. Cystourethroscopy is not recommended as part of the routine screening evaluation; if clinically indicated, it is used to assess the integrity of the urethra and identify stricture sites, diverticula, calculi, or other anatomic abnormalities.

The following are valuable in determining the underlying cause of incontinence:

1. Bladder responses to progressive filling.

2. Sphincteric pressure profile and its response to progressive filling and the initiation of voiding.

3. The presence of detrusor overactivity.

4. Electromyographic studies of the striated urinary sphincter.

5. In selected patients, response to neurostimulation of the sacral roots and pudendal nerve and measurement of latencies.

Differentiation among incontinence caused by neurogenic detrusor overactivity and poor bladder compliance is a straightforward process. Significant findings include sphincteric weakness, precipitous sphincteric relaxation, and decrease in pressure, as well as a lack of electromyographic activity of the pelvic floor musculature and external sphincter.

The proper diagnosis can be achieved by establishing the integrity of the sacral root reflex arc by neurostimulation of the sacral roots, with simultaneous recording of intravesical and intraurethral pressures at the levels of the internal and the external sphincter. The extent of one cause relative to another (eg, sphincteric weakness versus detrusor overactivity) should be taken into consideration, and management should be directed toward the predominating cause of incontinence.

Treatment

The management of neurogenic urinary incontinence can be challenging. The rehabilitation of the neuropathic condition and the alleviation of potentially damaging sequelae must be the guiding principles of management (see also Chapter 28—Neuropathic Bladder Disorders). Choices must be made according to the severity and potential progression of the lesion and the integrity of the system, with great care taken to prevent deterioration of the upper tracts. In patients with spinal cord injury and meningomyelocele, early treatment provides the best chance of preserving the integrity of the entire urinary system.

Failure of Storage Function

Anticholinergic agents are commonly used to treat detrusor overactivity. These medications inhibit the binding of acetylcholine to muscarinic receptors in the detrusor muscle, increasing bladder capacity and inhibiting involuntary contractions. Treatment with oxybutynin chloride (Ditropan) 5 mg three times daily, tolterodine tartrate (Detrol) 2 mg twice daily, and single-dose extended release daily formulations (Ditropan XL 10 mg and Detrol ER 4 mg) has proven to be highly effective and well tolerated. Fesoterodine fumarate (Toviaz), propiverine hydrochloride (Detrunorm), trospium chloride (Sanctura), and the more selective M3 receptor antagonists (darifenacin hydrochloride [Enablex] and solifenacin succinate [Vesicare]) are newer anticholinergic options (Andersson et al, 2009). Dosages can be increased above these levels in some patients, dependent on tolerance of adverse effects and treatment response. Common side effects include dry mouth, palpitations, constipation, nausea, or drowsiness, although newer extended-release formulations provide a reduced incidence versus immediate-release anticholinergics.

Propantheline bromide (Pro-Banthine) and imipramine hydrochloride (Tofranil) are considered second-line treatments for some patients, while the efficacy of flavoxate hydrochloride (Urispas) is unclear (Corcos et al, 2006).

Injection of botulinum-A toxin into the detrusor muscle for both children and adults who have failure of reservoir function is a promising new treatment that has demonstrated a significant increase in bladder capacity and compliance as well as symptomatic improvement for several weeks after cystoscopic injection (Chancellor, 2010). This neurotoxin binds to the presynaptic nerve endings of cholinergic neurons and leads to a temporary chemodenervation and the reduction of neural activity, as well as changes the muscarinic receptors in the bladder (Datta et al, 2010).

Failure of Sphincter Mechanism

CIC is the first line of conservative management in this group. Although such patients have very low outlet resistance, atonic bladder function may result in some retention. Most of the time, CIC every 4–6 hours avoids leakage. When CIC is not possible and the increase in intravesical pressure becomes excessive, the patient can wear pads or diapers. Pharmacotherapy has proven unsuccessful to date.

Surgical Management

Sphincterotomy

For spastic hyperreflexive male patients, this procedure can eliminate outlet resistance so that, with an external appliance or condom catheter, the bladder will remain empty (Perkash, 2007). Although many consider this procedure the easiest way to preserve the upper urinary tract, it is clearly not rehabilitative and might interfere with other treatments.

Bladder Augmentation

In patients with poor compliance owing to bladder wall hypertrophy or fibrosis, augmentation improves reservoir function. If the sphincteric mechanism is adequate, detubularized bowel segments can be used to expand a small contracted bladder. Usually, patients will be required to perform CIC to empty the bladder postoperatively.

Artificial Urinary Sphincter (AUS)

For patients with severe sphincteric damage and a low-pressure, large-capacity bladder, the AUS is a useful option. In males, it is applied around the bulbous urethra. When the device is deflated, the patient can void either by detrusor contraction (if some capability is preserved) or by straining and the Valsalva maneuver. A complete sphincterotomy can be performed first.

Continent Urinary Diversion

This method should be considered only with progressively deteriorating upper urinary tract function, and even then, a simple conduit is often preferable.

Neurostimulation

In selected patients with detrusor overactivity, stimulation of the sacral roots can be used to suppress the overactive detrusor. If such patients with spinal cord injury, meningomyelocele, multiple sclerosis, and other neuropathies show significant improvement after temporary testing, a permanent electrode can be placed over the most responsive root, usually S3.

Dorsal Rhizotomy

Complete dorsal rhizotomy of S2–S4 extra- or intradurally effectively eliminates detrusor hyperreflexia and increases bladder capacity. Increases have been seen from a capacity of 150 or 200 mL to 600–800 mL. In patients with suprasegmental lesions and spastic upper motor neuron lesions, sacral root electrode (bladder pacemaker) implantation promotes detrusor contraction and bladder evacuation.