DEFINITION AND PREVALENCE

The term mixed urinary incontinence (MUI) has been defined by the International Continence Society as a condition characterized by symptoms of both stress and urge incontinence, or a combination of leakage associated with urgency as well as with exertion.¹ However, this is a term that can apply both to a combination of incontinence symptoms and to a combination of urodynamic findings in the same individual.

Studies have reported variable prevalence estimates for MUI symptomatology, ranging historically from 30% to 50%.² According to the more recent National Overactive Bladder Evaluation (NOBLE) study, which relied on census data from the year 2000, approximately one third (34.4%) of the 14.8 million women with urinary incontinence were defined as having MUI.³ Mixed symptoms appear to be more prevalent in clinical-based than in population-based epidemiologic studies.⁴ Sandvik and colleagues⁵ summarized eight articles and demonstrated that as many as 61% of incontinent women reported MUI. In contrast, Hampel and associates⁶ reported that 29% of women with incontinence had MUI, based on the average prevalence from 21 epidemiologic studies.

It is well recognized that incontinence symptoms poorly predict the true etiology of an individual patient’s incontinence. Several studies have demonstrated that mixed symptoms are much more common than mixed conditions.⁷ Cardozo and Stanton⁸ reported that, of those patients presenting with MUI symptoms, more than 50% had only stress urinary incontinence (SUI) and approximately 40% had only detrusor instability as seen on urodynamics. Sandvik and colleagues⁵ found that, of the 46% of patients presenting with MUI symptoms, only 44% were diagnosed with a mixed condition. This trend was also demonstrated by a sample of 950 incontinent women evaluated at Duke University: 52% presented with mixed symptoms, but only 14% had mixed conditions.⁹

Several studies have attempted to define MUI using findings seen on urodynamics, namely the coexistence of SUI and detrusor overactivity. Prevalence of MUI in urodynamic studies ranges from 36% to 56% of patients. However, the characteristics of these groups have often not been clearly defined, and therefore these studies have comprised patients with many different pathologic processes, most likely including those with abnormal compliance.¹⁰ Furthermore, 50% of patients with motor urge incontinence can have a normal cystometrogram (CMG),^11,12 whereas normal patients can exhibit uninhibited bladder contractions of unknown significance on CMG. Therefore, the true prevalence of MUI as defined by urodynamics is difficult to estimate.

The condition known as MUI has historically lacked a unified definition. The symptom complex itself has not been well defined. Specifically, there are those with both urge and stress incontinence, often referred to as overactive bladder (OAB) or wet OAB, and those with stress incontinence plus urge symptoms but without urge incontinence, called dry OAB.¹³ Furthermore, because some studies have been based on symptoms and others have been based on urodynamic findings, meaningful comparison of the results of different studies is often difficult. Given the lack of a strict universal definition, as well as the limitations of any urodynamic study, the quoted prevalence of MUI is probably inaccurate, and the true prevalence is almost impossible to determine.

IMPLICATIONS OF MIXED URINARY INCONTINENCE

Several studies have shown that women with MUI symptoms typically report more severe incontinence than do women with either SUI or urinary urge incontinence (UUI) alone. In the Norwegian Epidemiology of Incontinence in the County of Nord-Trondelag (EPINCONT) study,¹⁴ “severe incontinence,” as defined by validated instruments, was seen in 38% of women with MUI, compared with 28% of those with UUI and 17% of those with SUI. Furthermore, more women with MUI (47%) were bothered by their incontinence, compared to women with UUI (36%) or SUI (24%). Bump and coworkers⁴ conducted a secondary analysis of data from the duloxetine study group and found that the 171 women (31%) with baseline MUI complained of more severe urinary incontinence than did those with SUI.

The negative personal impact of MUI on patients with this condition appears to be significant. Coyne and associates¹⁵ sought to examine the impact of urinary incontinence on health-related quality of life (HRQOL). A case-control study of 171 incontinent women showed that respondents with UUI or MUI reported not only significantly greater ratings of urinary urge intensity and more incontinence episodes, but also significantly worse HRQOL, compared to patients with isolated SUI.

ETIOLOGY

Before being able to critically evaluate the theories proposed to explain the etiology of MUI, it is important to note the following facts, some of which may seem counterintuitive. First, of those women with SUI who also complain of urgency, frequency, and/or urge incontinence, 50% to 75% of them are cured of their urge symptomatology by surgery for SUI.^16–23 Furthermore, overall cure rates are poor for those patients with MUI treated with anticholinergics alone.^19,24 Several theories have addressed the potential causes of mixed symptomatology, although not all of them can reconcile these facts.

One theory is that MUI is the result of a patient’s having two separate conditions. The greater perceived severity of MUI is attributed to the additive effects of the two conditions being more severe and bothersome than the effect of a single condition.⁴ However, this would not explain the poor response rates of anticholinergics in these patients or the fact that surgery may cure most of these symptoms.

An alternative explanation is that mixed symptoms are a result of more severe incontinence rather than the presence of two conditions.⁴ As stated previously, women with more severe incontinence are more likely to report mixed symptoms. In the study by Bump and associates,⁴ as the severity of incontinence improved during treatment, mixed symptoms resolved. Furthermore, in patients with severe SUI, the bladder may never completely fill, thereby leading to an essentially defunctionalized bladder and concomitant urge symptomatology. Severity of incontinence causing a mixed symptom complex is perhaps a reason for resolution of these symptoms once a successful anti-incontinence surgery is completed.

Others suggest that these symptoms may be the result of a behavioral adaptation in the woman with SUI. For instance, the patient may empty her bladder more frequently in an attempt to reduce stress-induced leakage and therefore induce symptoms of frequency and urgency.²⁵ These symptoms may represent a false interpretation of impending stress-induced leakage. The patient rushes to the toilet to protect herself from stress-induced leakage at the perception of the first or normal desire, which may result in a learned behavior that the patient develops and reinforces over time. These patients are seen as having SUI with “pseudourgency syndrome.”²⁶

Other theories have lent support to an actual link between SUI and detrusor overactivity. One such theory is that, in patients with SUI, traction on or stretching of the pelvic nerves as a result of poor pelvic floor support and severe urethral hypermobility causes this symptom complex.¹⁹ When the bladder neck is stabilized to prevent this stretching, both SUI and UUI are corrected. A solid experimental background has suggested a link between the pelvic floor, pudendal innervation, and detrusor inhibition. Artibani²⁷ suggested that decreased inhibition from the pelvic floor or the urethra, caused by pelvic floor or urethral deficiency, can lead to increased efferent activity and subsequent detrusor overactivity. In his opinion, the best support for this hypothesis is given by the positive clinical results of pelvic floor electrical stimulation and rehabilitation.

Mahoney and colleagues²⁸ proposed that “micturition reflex instability” may result from malfunction of the detrusor reflex or instability of the pudendal nucleus, which innervates the pelvic floor muscles and external sphincter. He proposed that detrusor instability is the result of hyperexcitability of the sacral micturition reflex center, due to either its underinhibition or overfacilitation. Pathologic relaxation and weakness of the striated muscles of the pelvic floor and perineum can result in underactivity of the perineodetrusor inhibitory reflex, causing underinhibition of the sacral micturition reflex center, and may predispose a patient to detrusor instability.

Other scientists, who support a correlation between urethral afferents and the micturition reflex, suggest that it is rather urine entering the proximal urethra that stimulates the urethral afferents and therefore the voiding reflex.²⁹ It is widely held that urethral relaxation occurs in the initial phase of micturition. In the healthy adult, urine enters the urethra only during micturition. However, urine is present in the urethra in patients with SUI because of poor pelvic support and/or sphincteric deficiency. It is proposed that the entry of urine into the proximal urethra could act as a stimulus to potentiate or even initiate a detrusor contraction.²⁹

Urethral instability, as seen as fluctuations in urethral pressure, is evidenced in women with detrusor instability. In one study, urethral instability was reported to have occurred in 42% of patients with detrusor instability and was associated with the sequence of urethral relaxation before an unprovoked contraction.³⁰ In a report by Low,³¹ bladder and urethral pressures were simultaneously measured during bladder filling in 77 women with idiopathic detrusor instability. Low found that 85% of patients developed urethral relaxation 5 seconds before detrusor contraction. He concluded that the involuntary detrusor contractions were preceded by a fall in urethral pressure, similar to that observed in normal voiding. Hindmarsh and coworkers³² also demonstrated urethral relaxation preceding detrusor contractions in a series of patients with detrusor instability, not only supporting the concept that urethral instability can be associated with unstable bladder contractions but also suggesting that detrusor instability may be initiated from the bladder outlet region or proximal urethra.

Mahony and colleagues³³ described two urethrodetrusor reflexes that could increase the excitability of the micturition reflex and trigger a detrusor contraction when activated by urine flow across urethral mucosa. The theory that urine or fluid in the posterior urethra could result in a detrusor contraction has been supported by several animal models. As early as 1931, Barrington³⁴ reported that running water through the urethra or distending the proximal urethra in the cat caused contraction of the detrusor. Also using the cat model, Kiruluta and colleagues³⁵ noted that urethral perfusion triggered spontaneous bladder contractions of such intensity that bladder filling was not possible. More recently, Jung and associates²⁹ sought experimental support for the hypothesis that stimulation of urethral afferent nerves can induce reflex detrusor contractions. By measuring urethral perfusion pressure and isovolumetric bladder pressure with catheters inserted through the bladder dome of female rats, they demonstrated that fluid passing though the urethra can result in activation of the mechanosensitive urethral afferents, which can in turn increase the excitability of the micturition reflex.

Therefore, in patients with SUI, leakage of urine into the proximal urethra may stimulate urethral afferents and facilitate the voiding reflex. This would imply that SUI can induce and/or increase detrusor instability. There is little direct support for this theory in humans,^4,36 and some believe that the effect may be species specific. However, the fact that this phenomenon has not been demonstrated convincingly in humans may be a result of study design. For example, although Sutherst and Brown³⁶ did not detect such facilitatory reflexes in the human, they believed that the transurethral catheter might have interfered with the activation of afferent receptors that respond to flow through the urethra. Furthermore, not all women with MUI symptoms have both urodynamically proven SUI and detrusor instability. Absence of urodynamic “proof” may be a result of an inhibitory effect of the patient during the study.

In short, it is likely that women with MUI symptoms have SUI as their primary problem and that detrusor overactivity results secondarily when urethrodetrusor facilitative reflexes are activated, either because an incompetent bladder neck allows urine to enter into the proximal urethra during physical activity or because of traction on the pelvic nerves due to a weakened pelvic floor.

IMPORTANCE OF URODYNAMICS

An accurate diagnosis is essential for effective treatment of the incontinent patient. Although a detailed history is important, symptoms alone are often a poor guide to a final diagnosis. The urologist is therefore encouraged to rely on a combination of symptoms, physical findings, and objective testing. In addition to a routine evaluation, secondary testing in patients with mixed symptomatology should include urine cytology and cystourethroscopy to rule out pathologic conditions of the bladder, especially carcinoma in situ.

Urodynamic evaluation is integral in determining the true underlying etiology of a patient’s incontinence, especially in the patient with mixed symptomatology. Videourodynamic evaluation, which combines the use of fluoroscopy with measurement of bladder and urethral pressures, allows simultaneous evaluation of structure and function and is the preferred method.³⁷

The most important reason to perform videourodynamic studies in a patient with MUI is to rule out poor bladder compliance. A high-pressure or poorly compliant bladder poses significant risk to ureteral and renal function. It can be caused by a number of conditions, including neurologic conditions, prolonged catheter drainage, radiation therapy, prior pelvic or urethral surgery, interstitial cystitis, and obstructive uropathy. If there is suspicion of altered bladder compliance in any incontinent patient, that patient should undergo urodynamic testing to determine the condition of the bladder’s storage function. Poor compliance adversely influences the outcome of any procedure done to increase bladder outlet resistance and could create a situation in which the upper tracts are at risk from high bladder pressures. Fortunately, urodynamic testing is accurate and sensitive in the diagnosis of poor compliance.

CONSERVATIVE THERAPY

Behavioral Therapy, Biofeedback, and Pelvic Floor Rehabilitation

Behavioral therapies such as timed voiding, avoidance of bladder irritants, and bladder retraining have been used with some success in patients with both SUI and UUI. Additionally, pelvic floor electrical stimulation or biofeedback has been used successfully in both UUI and SUI, with excellent success rates and high levels of patient satisfaction.⁴⁰ Several studies have investigated the response of pelvic floor stimulation in patients with MUI specifically. Sand⁴¹ found a greater than 50% improvement in approximately 38% of subjects, with 8% being completely dry after 8 weeks of treatment. In this study, symptoms of urgency, frequency, and stress incontinence improved significantly, whereas symptoms of UUI remained relatively stable. Bent and colleagues⁴² reported a 52% success rate in patients with MUI, whereas Caputo and associates⁴³ reported a 70% response rate in these patients. Siegel and coworkers⁴⁰ studied patients with both UUI and MUI undergoing 20 weeks of pelvic floor electrical stimulation, either daily or every other day. Treatment resulted in significantly lower urge and stress leakage, with decrease in urge episodes and total number of voids and improvement in quality-of-life measures. Overall, 72% of patients were satisfied with their therapy.

When compared directly to drug therapy, electrical stimulation has been shown to have better results and higher patient satisfaction. Goode⁴⁴ studied 197 women with UUI or MUI in a randomized controlled trial comparing biofeedback-assisted behavioral treatment with anticholinergics and placebo. The biofeedback group demonstrated the best results, with an 80% decrease in incontinence episodes, 78% of patients being “completely satisfied”, and 97% wanting to continue treatment. A modified crossover trial was conducted, which showed that combination treatment is more effective than monotherapy with either drug or biofeedback alone, a finding supported by other studies.^40,41,45

In short, treatment of patients with MUI can be challenging and should be tailored to the individual. In those patients with MUI, it is wise to direct treatment at the dominant symptom first. When in doubt, it is most reasonable to proceed with conservative treatment of the urge component before consideration of surgical therapy for SUI.²

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