Mixed urinary incontinence (MUI) is the complaint of involuntary leakage associated with urgency and also with exertion, effort, sneezing, or coughing (1). Thus, it is a complex clinical condition of the leakage of urine with acute rises in abdominal pressure (stress urinary incontinence) and leakage that occurs as a result of spontaneous or triggered rises in bladder pressure (urge urinary incontinence). The rises in abdominal pressure that typically occur with exertion, cough, laugh, or sneeze result in transient spikes in bladder pressure. More persistent rises in bladder pressure are commonly associated with urgency. Urgency can be spontaneous, as a result of a detrusor contraction, or can occur as a result of socialized and environmental cues, such as being startled, passing a restroom, acute drops in outside temperature, and hearing or feeling water run. On occasion, detrusor contractility and urinary leakage may be insensible.

A distinction should be made between the symptom, sign, urodynamic observation, and condition of urinary incontinence. For the purposes of this chapter, the definitions as specified by the International Continence Society (1,2) will be used unless otherwise specified. Overactive bladder (OAB) is a symptomatic diagnosis whereby a patient has urgency and frequency with or without urge incontinence. Detrusor overactivity is a urodynamic diagnosis of OAB associated with urodynamic evidence of detrusor contractions. Urge incontinence is the actual leakage of urine with urge, either reported by the patient (symptom) or observed during bladder filling (sign). Since stress incontinence also has its own nuances, even welldone research studies are sometimes difficult to interpret due to confusion over the definition of MUI. For instance, a woman with urodynamic stress incontinence and urodynamically recorded urge incontinence has mixed incontinence. This situation happens only 27% of the time (3). The sensitivity (specificity) of urodynamics in women with a history of mixed incontinence is only 0.51 (0.66) (4). Those patients with MUI symptoms show only urodynamic stress incontinence on urodynamics 55% of the time and detrusor overactivity incontinence in 38% (5). Since detrusor overactivity can be missing on as many as 46% of urodynamics in those with OAB (6), it seems prudent to use a combination of symptomatic and objective evidence in the definition of MUI. The woman who has observed stress leakage in the office but also reports symptoms of OAB would also qualify as having MUI. This dichotomy affects the diagnosis, decision to treat, and eventual treatment outcomes of MUI.

MUI is one of the most common types of urinary incontinence in patients presenting to their physicians with complaints of urinary loss. It has been estimated that 29% to 62% of women with urinary incontinence have MUI (7, 8, 9, 10, 11, 12, 13). MUI is associated with an increasing number of vaginal deliveries, a history of operative vaginal delivery, and a history of chronic obstructive pulmonary disease and neurologic disease (12). Women with MUI tend to have a more severe degree of incontinence symptoms
than do women with pure stress or urge incontinence (10,13) and have greater degrees of bother (13). Patients who undergo surgical procedures for the stress component of their condition and have urgency or urge incontinence have a reduced patient satisfaction, and in many series the urge component reduces the overall continence rates (14). Although the weekly MUI rate is as low as 3% in young, pregnant patients primiparas who had vaginal deliveries were found to have a higher risk of stress or MUI than their nulliparous counterparts (odds ratio 5.7) (15). The incidence of MUI is known to rise in women after the sixth decade.

Incontinence has been shown to have a detrimental effect on health-related quality of life (HRQL), and those with urge incontinence or MUI may be more greatly affected (16). Women with MUI have more reported incontinent episodes when compared with stress incontinence. Indeed, the stress and urge components have a synergistically negative effect on patient symptomatology, distress (17), and quality of life (18). Nocturia can lead to sleep deprivation and either worsen or trigger depression, resulting in even further functional and quality-of-life deficits. Women with MUI are 13.5 times more likely to have major depression than women with stress incontinence (11).

There are several theories of the etiology of mixed incontinence, one of which is iatrogenic. The first, and most commonly held, is that MUI is merely a combination of stress incontinence and urge incontinence, with their individual respective etiologies. In this scenario, correcting the stress component would be expected not to change the urge component. However, in a significant number of cases of surgical correction of the stress component of MUI, the urge component is cured or improved.

Another theory is that MUI is due to a urethral event. By forcing urine (or passive urine leakage) into the bladder neck, the patient is set up for the normal neurologic response of voiding: triggering a conscious urgency and/or bladder contractions that are initially suppressed. Eventually, however, neuropathic or myopathic changes may occur that make the spread of contractile signals more effective, resulting in the unconscious let-down of urethral and sometimes pelvic floor tone. McLennan et al describe a shorter functional urethral length in women with urethral instability (19). This shortening is a physiologic event coordinated with detrusor contraction and posterior slackening of the endopelvic fascial hammock that occurs during normal voiding. Bump et al have supported this theory: they found that the main determining factor as to whether urge incontinence symptoms were present in their MUI subjects seemed to be incontinence severity (8). Others have not found this to be the case (20).

It also has been suggested that there is a myogenic (21, 22, 23, 24) and/or neurologic (9,25) basis for the development of urge incontinence. Myocytes have stretch-sensitive cation channels that can depolarize and trigger action potentials, and this can result from stretching part of the bladder wall (22). Unlike skeletal muscle, denervated smooth muscle becomes hypersensitive to acetylcholine and small rises can trigger a large reaction. If the stimulus for the action potential is persistent, electrically coupling can happen, leading to a spreading of the muscular action potential (23). Vaginal electromyographic changes are seen in urge, stress, and mixed incontinence and successively decrease with age (9). Others have proposed that the pelvic nerves stretch as a result of increased abdominal pressure and that this stimulates a bladder contraction (26).

However, there is an important subgroup of mixed incontinence that deserves particular attention: those who present with MUI after a stress incontinence surgical procedure (27). Worsening or de novo urge symptoms after surgery may indicate bladder outlet obstruction, a vesical or urethral foreign body (such as a stitch or sling material), or a urinary tract fistula or diverticulum (28). Cystourethroscopy and interval urodynamics with pressure-flow studies should be entertained for this subset of patients.

The evaluation of urinary incontinence is covered in Chapters 5, 6 and 7.

Although the true etiology may be in question, most experts agree that MUI is a difficult problem to treat. The expectations of the patient are that whatever treatment the physician recommends will stop the leakage, when in fact a total cure may not be attainable. Treating the urge component of MUI alone may not change the stress component. Treating the stress component may not only result in an unchanged urge component (18) but in 10% to 15% can exacerbate urge symptoms (29).

The most common recommendation is to treat the predominant symptom first. If the patient suffers from stress-predominant MUI, surgical repair of the stress component can cure or improve the urge component in 25% to 75% of cases. Since surgery for SUI can cause bladder outlet obstruction, the worsening of urge incontinence symptoms after surgery should trigger investigation (28). Lower urinary tract symptoms such as urge incontinence have been shown to be more bothersome and more distressing than the occasional leakage of urine with a cough or sneeze (27). If the predominant symptom is urge incontinence, the prudent choice would be to aggressively treat the urge component until stable, then address any residual stress incontinence. This achieves two things: it identifies a therapy already proven to control the patient’s urge, and it establishes a baseline (on treatment) that can be used to determine if the patient’s urge symptoms change or worsen after surgical correction of stress incontinence.

Since most MUI treatment approaches hinge on addressing the individual symptom components, various therapies have been employed to treat MUI over the years. Many of these are addressed, at length, in previous chapters (Chapters 11, 12, 13, 14, and 15). A summary of treatment options is listed in Table 16.1. The evidence-based literature available about MUI-specific treatments and outcomes will be discussed.