Dysfunction of the outlet causing obstruction has been well studied. Chronic outlet obstruction has been associated with many changes to the morphology of the bladder, including changes to the extracellular matrix, electrical gap junctions, and smooth muscle enzymes and mitochondria. Obstruction has been shown to lead to a rapid hypertrophy of the bladder smooth muscle and an increase in collagenous connective tissue deposits, but with decreased myosin concentration, which ultimately results in a decreased force of contraction. It is theorized that obstruction results in acute ischemia, thereby affecting all components of the bladder that embody its viscoelastic properties (epithelium, connective tissue, vasculature, and smooth muscle), resulting in acute muscle dysfunction. The degree of dysfunction is thought to be related to the degree of tissue hypertrophy and not necessarily the duration of the obstruction. However, the bladder has amazing ability to regenerate and has shown evidence of recovery as early as fourteen days after obstruction.

Primary dysfunction of the bladder without obstruction, on the other hand, is not as well understood. A number of changes have been found to impact the bladder secondary to aging, ischemia, and comorbidities. Diabetic neuropathy has been shown to affect the innervation to the bladder, dull the sensory input, and induce changes to the physiology of detrusor smooth muscle. In cases of chronic overdistention, there can also be subsequent reversible or irreversible changes to the detrusor muscle cells. Studies focusing on the effect of aging on the bladder have demonstrated decreased ratios of detrusor muscle to collagen and changes in the quantity of muscle and collagen with aging.

A number of theories exist to try to explain the development of bothersome symptoms from incomplete bladder emptying. It has been postulated that the detrusor is organized into circumscribed modules controlled by a peripheral myovesical plexus, interstitial cells, and intramural ganglia. Bladder outlet obstruction may cause reduced blood flow, causing a transient or permanent ischemia that then affects sensitive nerve terminals and leads to denervation to certain modules. Supersensitivity then develops in the affected muscle modules, causing a reflexive excitation. Eventually the denervation progresses to an extent that the detrusor no longer functions and decompensates. These secondary changes that occur may explain why treatment will not always cause a resolution of symptoms. Other studies looking at smooth muscle proteins Connexin 43 and 26, the most predominant subtypes in the bladder, have found that increased fluid pressure from urine retention caused four- to fivefold increase in their levels, noticed as early at 7–9 h after obstruction. There have also been found to be increases in alpha-1 adrenergic receptor subtypes, particularly subtype alpha-1 d, now being identified as having a marked role in the development of irritative symptoms that are associated with bladder outlet obstruction.

It is important to emphasize the value of having a common understanding of the terminology for purposes of reporting results and developing guidelines for treatment. The International Continence Society produced a report in 1988 to standardize definitions for a variety of lower urinary tract symptoms and conditions, which has subsequently been updated a number of times. Most recently in 2002 they published an updated report including urodynamic study findings. Appendix 1 reviews definitions from the report as they pertain to retention and bladder-emptying disorders.

“Lower urinary tract symptoms (LUTS)” now serves as a global term that applies to the variety of symptoms that may be representative of any bladder, urinary outlet, pelvic floor, endocrine, or neurologic abnormalities related to storage of urine and voiding. We are discovering that LUTS have a similar prevalence between men and women, and this prevalence increases in both groups with age. The EPIC study, a large multicenter survey study of 19,165 individuals 18 years or older in five countries using the 2002 ICS definitions for LUTS, found 64.3 % reported of at least one lower urinary tract symptom, with higher prevalence of storage symptoms in women compared to men (59.2 % vs. 51.3 %) and the opposite was true for voiding symptoms (men vs. women 25.7 % vs. 19.5 %). The overall presence of overactive bladder symptoms was 11.8 %, and the rate increased with age in both men and women.

Multiple potential sources contribute to incomplete bladder emptying (Fig. 13.2) and can be differentiated into dysfunction of the bladder or dysfunction of the bladder outlet.

The ICS 2002 defines detrusor underactivity (DU) as “a contraction of reduced strength and/or duration, resulting in prolonged bladder emptying and/or a failure to achieve complete bladder emptying within a normal time span.” A movement toward the use of the term “detrusor underactivity (DU)” has been advocated to encompass this spectrum of diseases and to replace prior terminology used such as “impaired detrusor contractility,” “underactive bladder,” “detrusor areflexia,” “hypotonic bladder,” and “detrusor/bladder failure.” Detrusor underactivity is impressed upon because it places the focus of the condition more on the symptoms rather than the etiology, which, as we will discuss, are broad and quite variable, resulting from neuropathic, myogenic, or pharmacologic sources. Currently there is not an accepted definition for the clinical syndrome associated with DU. It has been suggested that the term underactive bladder (UAB) syndrome could be applied to the “clinical syndrome that accompanies detrusor underactivity.” The problem with this definition, as opposed to the overactive bladder syndrome (OAB), is that the symptoms associated with DU are variable and nonspecific. Osman et al. suggested that UAB could be defined as “reduced sensation of the need to void (the opposite of urgency) that may be associated with frequency and nocturia or reduced voiding frequency often with a feeling of incomplete bladder emptying and incontinence that may predominate at nighttime.” This definition has its obvious limitations.

Bladder outlet dysfunction, also coined as “bladder outlet obstruction (BOO),” may be a result of a fixed anatomic obstruction. Less obviously, it may be due to a functional abnormality in which no distinct structural abnormality is present, but rather the patient “functionally” has obstruction due to a neurological, myogenic, or psychological condition.

The proper workup and evaluation of the patient is important to identify patients at risk, offer appropriate therapies in a timely fashion, and avoid unnecessary tests and treatments. Regardless of the etiology of incomplete emptying, the subsequent symptoms that develop may be debilitating despite very minimal objective findings, or the opposite may occur in which upper tract dysfunction is identified in a patient who has minimal to no symptoms. The goals of evaluation should be to establish a diagnosis, to define the characteristics of the patient’s storage and emptying, and to identify patients at risk for long-term sequelae.