Presented at the NIH State-of-the-Science Conference: Prevention of Fecal and Urinary Incontinence in Adults - Bethesda, MD - December 10-12, 2007

The lower urinary tract (LUT) functions as a group of interrelated structures with a joint function in the adult to bring about efficient and low-pressure bladder filling, low-pressure urine storage with perfect continence, and periodic complete voluntary urinary expulsion, again at low pressure.

Urinary incontinence (UI) is defined as the involuntary loss of urine. The term is used in various ways. It may denote a symptom, a sign, or a condition. The pathophysiology of failure of the LUT to fill with or store urine adequately or to empty adequately must logically be secondary to reasons related to the bladder, the outlet, or both. A simple classification of the various subtypes of UI is seen in Table 1.

There are situations in which urethral incontinence cannot be considered merely as an isolated abnormality of either bladder contractility or sphincter resistance. These situations, listed in Table 2 are more complicated to deal with, first, because they are more difficult to diagnose, and second, because one entity may adversely affect or compromise treatment of the other.

Absolute or relative failure to fill with and store urine adequately results from bladder overactivity (involuntary contraction or decreased compliance), decreased outlet resistance, heightened or altered sensation, or a combination.

Bladder Overactivity

Overactivity of the bladder during filling or storage can be expressed as phasic involuntary contractions (detrusor overactivity), as low compliance, or as a combination. Detrusor overactivity is most commonly seen in association with neurologic disease or injury; however, it may be associated with increased afferent input due to inflammation or irritation of the bladder or urethral wall, bladder outlet obstruction, stress urinary incontinence (perhaps due to sudden entry of urine into the proximal urethra), aging (probably related to neural degeneration), or may be idiopathic. Some hypothesize that decreased stimulation from the pelvic floor can contribute to phasic overactivity. Decreased compliance during filling or storage may be secondary to neurologic injury or disease, usually at a sacral or infrasacral level, but may result from any process that destroys the viscoelastic or elastic properties of the bladder wall.

Outlet Underactivity

Decreased outlet resistance may result from any process that damages the innervation or structural elements of the smooth and/or striated sphincter or support of the bladder outlet in the female. This may occur with neurologic disease or injury, surgical or other mechanical trauma, or aging. Classically, sphincteric incontinence in the female was categorized into relatively discrete entities: (1) so-called genuine stress incontinence (GSI) and (2) intrinsic sphincter deficiency (ISD), originally described as “type III stress incontinence.” GSI in the female was described as associated with hypermobility of the bladder outlet because of poor pelvic support and with an outlet that was competent at test but lost its competence only during increases in intra-abdominal pressure. ISD described a nonfunctional or very poorly functional bladder neck and proximal urethra at rest. The original implication of classical ISD was that a surgical procedure designed to correct only urethral hypermobility would have a relatively high failure rate, as opposed to one designed to improve urethral coaptation and compression. The contemporary view is that the majority of cases of effort-related incontinence in the female involve varying proportions of support-related factors and ISD. It is possible to have outlet-related incontinence due only to ISD but not due solely to hypermobility or poor support—some ISD must exist.

Stress- or effort-related UI is a symptom that arises primarily from damage to muscles and/or nerves and/or connective tissue within the pelvic floor. The urethra is normally supported by the action of the levator ani muscles through their connection to the endopelvic fascia of the anterior vaginal wall. Damage to this connection, or to the nerve supply, or direct muscle damage can, therefore, influence continence. Bladder neck function is likewise important, and loss of normal bladder neck closure can result in UI despite normal urethral support. In older writings, the urethra was sometimes ignored as a factor contributing to continence in the female, and the site of continence was thought to be exclusively the bladder neck. However, in approximately 50% of continent women, urine enters the urethra during increases in abdominal pressure. The continence point in these women (highest point of pressure transmission) is at the mid urethra.

Urethral hypermobility implies weakness of the pelvic floor-supporting structures. During increases in intra-abdominal pressure, there is descent of the bladder neck and proximal urethra. If the outlet opens concomitantly, stress UI ensues. In the classic form of urethral hypermobility, there is rotational descent of the bladder neck and urethra. However, the urethra may also descend without rotation (it shortens and widens), or the posterior wall of the urethra may be pulled (sheared) open while the anterior wall remains fixed. However, urethral hypermobility is often present in women who are not incontinent; thus, the mere presence of urethral hypermobility is not sufficient to make a diagnosis of a sphincter abnormality unless UI is also demonstrated. The “hammock hypothesis” of John DeLancey proposes that for stress incontinence to occur with hypermobility, there must be a lack of stability of the suburethral supportive layer: the effect of abdominal pressure increases on the normal bladder outlet, if the suburethral supportive layer is firm, is to compress the urethra rapidly and effectively. If the supportive suburethral layer is lax and/or movable, compression is not as effective. Intrinsic sphincter dysfunction denotes an intrinsic malfunction of the urethral sphincter mechanism itself. In its most overt form, it is characterized by a bladder neck and proximal urethra which are open at rest and is usually the result of prior surgery, trauma with scarring, or a neurologic lesion.

Urethral instability refers to the rare phenomenon of episodic decreases in outlet pressure unrelated to increases in bladder or abdominal pressure. The term urethral instability is probably a misnomer, because many believe that the drop in urethral pressure represents simply the urethral component of a normal voiding reflex in an individual whose bladder does not measurably contract, because of either myogenic or neurogenic reasons. In theory at least, categories of outlet-related incontinence in the male are similar to those in the female. Sphincteric incontinence in the male is not, however, associated with intrinsic hypermobility of the bladder neck and proximal urethra but is similar to what is termed sphincter dysfunction in the female. It is generally due to prostatectomy, pelvic trauma, or neurologic disease or injury.

Overflow Incontinence

This descriptive term denotes leakage of urine associated with urinary retention. This is more common in the male than female. The primary pathophysiology is actually a failure of emptying, leading to urinary retention with “overflow” UI, resulting from either continuous or episodic elevation of intravesical pressure over urethral pressure. This generally results from outlet obstruction or detrusor inactivity, either neurologic or pharmacologic in origin, or may be secondary to inadvertent overdistention of the bladder.

Written by: Wein A., M.D., Ph.D. (Hon.)

General References

1. Wein AJ. Pathophysiology and classification of voiding dysfunction; In: Wein AJ, Kavoussi LR, Novick AC, Partin AW, Peters CA, eds. Campbell-Walsh Urology. 9th ed. Philadelphia, PA: Saunders/Elsevier; 2007:1973–1985.
2. Wein AJ, Moy ML. Voiding function and dysfunction: urinary incontinence. In: Hanno PM, Malkowicz SB, Wein AJ, eds. Penn Clinical Manual of Urology. Philadelphia, PA: Saunders/Elsevier; 2007:341–478.

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