There are two broad categories of problems that can present with voiding dysfunction (see Table 10.2). These are detrusor muscle weakness and bladder outlet obstruction. Iatrogenic voiding dysfunction may occur following pelvic surgery such as stress urinary incontinence surgery. Finally, storage abnormalities such as detrusor overactivity may occasionally present with symptoms suggestive of voiding dysfunction.

Detrusor muscle strength can range from normal to acontractility in a continuum. Gross detrusor dysfunction can easily be identified by a constellation of clinical and urodynamic findings including poor flow, large residuals, and obvious detrusor muscle weakness on urodynamics. Unfortunately, many women present with less obvious features.

Detrusor muscle weakness is an important cause of voiding dysfunction which may exist in isolation or in combination with bladder outlet obstruction. Poor detrusor muscle strength varies in a continuum from mild weakness (detrusor underactivity) to a total loss of contractility (acontractility) (see Fig. 10.2). There are several causes for detrusor underactivity (see Table 10.2). Detrusor underactivity is widely prevalent in older women with an estimated prevalence of 12–45 % [4]. It has long been observed that older individuals are more likely to present with underactivity. Research indicates up to two-thirds of elderly nursing home residents show detrusor underactivity. Bladder biopsy reveals changes in the detrusor muscle including axonal degeneration, loss of muscle fibers, and fibrosis [8].

Detrusor underactivity can also occur due to untreated bladder outlet obstruction or retention due to any other cause. Chronic or severe acute stretch injury can lead to detrusor dysfunction. Postpartum urinary retention is a classic example of such injury.

Diabetes is an important medical cause of underactive detrusor. The classical clinical picture of patients with florid diabetic cystopathy is one of acontractility. Such patients usually have long-standing diabetes of more than 10 years’ duration and often have other evidence of diabetic peripheral neuropathy. However, studies have shown a higher prevalence of other patterns such as overactive bladder in patients with diabetic cystopathy [9]. Diabetes impacts all levels of neuromuscular control of the lower urinary tract. There is altered afferent sensation possibly linked to changes in the urothelium and detrusor. Afferent and efferent nerves demonstrate degenerative changes in function. Depending on the relative impact on different aspects of lower tract dysfunction, one can expect a wide variety of bladder manifestations [10].

Several drugs can impact lower urinary tract function either by exacerbation of a preexisting voiding dysfunction or by inducing acute-onset symptoms in otherwise normal individuals [11]. Drugs with anticholinergic side effects such as antidepressants and antipsychotic drugs as well as calcium channel blockers are some of the examples. Older women are more likely to be impacted by these side effects due to alterations in neurotransmission, receptor sensitivity, and blood-brain barrier defects. Also, elderly women are more likely to have preexistent lower tract dysfunction such as underactive detrusors that might make them especially susceptible to the adverse effects.

Neurogenic lower urinary tract dysfunction can produce a variety of effects on the lower urinary tract. Classically, lesions above the brainstem do not have an impact on detrusor contractility. Some studies have shown up to 6 % of patients with CVA have acontractile detrusors [12]. It is difficult to judge what proportion of this might be due to preexisting detrusor dysfunction in this elderly age group. Detrusor underactivity may conceivably occur following CVA.

Unrecognized postpartum retention can be a disaster for the bladder with short- or long-term damage. This is now a rare event in the developed world. Pifarotti et al. noted postpartum retention in 105 out of 11,108 (1 %) women undergoing a vaginal delivery. They defined postpartum retention as inability to void within 6 h of delivery. On multivariate analysis, only vacuum-assisted delivery and uterine fundal pressure during the second stage of labor were noted to be independent risk factors [13].

Protracted second stage of labor and vacuum delivery were noted to be risk factors in another large study [14]. In this study, 55 women (0.18 %) developed postpartum retention. Of these, two-thirds recovered by 2 weeks and the remaining by 4 weeks. However, the author has seen anecdotal instances of long-term voiding dysfunction. This is unusual in the Western world where strict labor room protocols are enforced and women are identified before they develop florid bladder damage.

Pelvic organ prolapse (POP) is an important cause for lower urinary tract dysfunction in women. However, one must remember that the only symptom of feeling a vaginal bulge shows consistent correlation with POP. No urine symptoms have been shown to be consistently associated with POP. The situation might be different in women who primarily present with voiding dysfunction and have severe prolapse. Uncorrected prolapse may alter the dynamics of the lower urinary tract and elevated residuals are common in such women. In women with significant POP, which usually implies that the prolapsing organ is beyond the introitus, an important clinical question is whether correcting the prolapse will improve voiding. Such women may habitually reduce the prolapse before voiding [15]. One method of resolving this issue is to use a pessary and perform urodynamic evaluation or flow tests with and without the pessary. Women with obvious improvement in lower urinary tract function are likely to improve with surgery (see Fig. 10.3).

Genuine urethral stricture in women is an uncommon entity. Conversely, a large number of women continue to be subjected to urethral dilatation for various forms of lower urinary tract dysfunction.

Functional bladder neck obstruction is less common in women since the bladder neck smooth muscle is not as well organized into a sphincter in women as compared to men (see Fig. 10.4). As such, in most series only a small number of women have urodynamically confirmed functional bladder neck obstruction [16]. However, in a recent prospective multicenter study from China, the commonest form of voiding dysfunction was noted to be functional bladder neck obstruction. It is unclear whether this result represents methodological differences, variations in diagnostic criteria, or a genuine difference in prevalence [17].

Large uterine fibroids can have an impact on urinary tract function. This is more likely in women, when the uterine size is over 12 weeks of gestation size. These women often complain of voiding difficulty and the symptoms usually improve following surgery [18]. Isolated case reports have found leiomyoma of the urethra as a cause of voiding difficulty [19].

The ICS-IUGA terminology defines dysfunctional voiding as “an intermittent and/or fluctuating flow rate due to involuntary intermittent contractions of the peri-urethral striated or levator muscles during voiding in neurologically normal women” [2]. As discussed in a previous review, this author has made a case for modifying this definition to reflect the two key components of dysfunctional voiding, namely, dyssynergia of the striated urethral sphincter-pelvic floor complex and lack of a clear neurological etiology [6]. In a small but significant proportion of these patients, neurological abnormalities may manifest subsequently [20]. Hence, it is important to evaluate these patients carefully for subtle clues to an underlying neurological abnormality and to perform additional assessment judiciously, including MRI of the spine or other forms of nerve-muscle evaluation. In some women, dysfunctional voiding may represent faulty toilet training in childhood. A related condition in which women with polycystic ovarian disease have urinary retention due to an increased sphincteric tone that has hormonal associations has been termed “Fowler’s syndrome” [21].

Most women will have a “staccato flow” with fluctuations in excess of the square root of the maximum flow (see Fig. 10.5). Some women may have slow but non-staccato flow or even normal flow rates [6]. Hence, in suspected dysfunctional voiding, urodynamic evaluation is important for diagnosis and management.