Urinary Incontinence

Definition and Overview

Incontinence can be a significant problem for young, middle-aged, and older women. Life with incontinence, even mild incontinence, can become very stressful as it threatens self-image, body image, and self-esteem.

  • Urinary incontinence is defined as the involuntary loss of urine severe enough to cause unpleasant social and/or hygienic consequences.

This definition encompasses “involuntary urine loss” regardless of the environment. Voluntary or willful voiding into clothing or on furniture, walls, floors, and receptacle not designed for urinary eliminative needs is not included under this definition.

Rather than being a disease in itself, incontinence is a symptom of underlying disease processes. At least 10 million adult Americans are suffering from incontinence. Despite being more frequent among the elderly, it is not just a consequence of increasing age. The vast majority of older adult do not have incontinence.

Most people are not aware that young women can also have incontinence. Since incontinence is so frequently associated with aging, younger women are even less likely to talk about it or seek treatment. The good news is that there are now many ways to treat people of all ages who are incontinent.

Classification of Incontinence

Incontinence is often divided into five primary categories based on clinical presentation. These are urge, stress, overflow, functional, and mixed. Each category does not imply a specific etiology, and multiple etiologies may be involved in a patient. Each of the five types is briefly described in the table below.

Table X | Types of Urinary Incontinence

Urge incontinence Opens in new window

Involuntary loss of urine preceded by a sense of needing to urinate before reaching the bathroom.

Stress incontinence Opens in new window

Involuntary loss of urine as a result of some type of physical stress to the body such as with a cough, sneeze, physical activity, or laughing.

Overflow incontinence

Involuntary loss of urine occurring when the bladder is full but the bladder does not contract properly to push the urine out. The urine then trickles out of the overfull bladder.

Functional incontinence

Involuntary loss of urine that results from an inability to reach the toilet due to cognitive, functional or mobility impairments in the presence of an intact lower urinary tract system.

Mixed incontinence

Involuntary loss of urine with features of both stress and urge.

Proper classification will help identify the most likely cause of the incontinence. Determing the time of onset may be difficult, particularly in patients with mixed incontinence (Statements of the WHO Committees; Petros 1998; Norgaard et al 1998).

Normal Voiding

The sequence of events which occur during a normal void are as follows—bladder filling usually occurs at the rate of 2 ml per minute and the first sensation of fullness are felt when about 400 ml of urine has collected in the bladder. These sensations are transmitted to the spinal cord via the sympathetic nerves. The impulses are further conveyed to the area of the brainstem responsible for central control of micturition. Inhibiting impulses are then conveyed back to the bladder from this center.

As the urge to void increases, impulses from cortical areas are received at the micturition center in the pons and voluntary delay of voiding is maintained till an appropriate time. When the circumstances are favorable for normal voiding, facilitating impulses from the micturition center are transmitted to the detrusor muscle via the pelvic nerves, and bladder contraction occurs (Brading 1999; Chamorro et al 1998; Michielson and Wyndacle 1998).

Anatomicophysiologic Control of Continence

Neuroanatomy of Continence

Branches of the sympathetic, parasympathetic, and somatic nerves supply the bladder and urethra. Parasympathetic nerves convey the sensation of fullness and stretch in the bladder while the sympathetic nerves carry pain, touch and temperature.

The sympathetic endings are both beta- and alpha-adrenergic. Alpha-adrenergic endings predominate at the bladder base and proximal urethra, including prostatic urethra. The somatic nerve supply comes via the prudendal nerves, which supply the striated muscles of the sphincter in both sexes. There may be additional somatic contributions to the sphincter via fibres carried by the pelvic nerves (Chai and Steers 1997; Narayan et al 1995; Hollabaugh et al 1997).

Central Nervous System Control

Micturition integrates impulses arising from the higher centers in the cortex, brainstem, thoracolumbar sympathetic outflow and sacral parasympathetic neurons. The cortex, thalamus, limbic system, basal ganglia and hypothalamus receive impulses from the bladder and transmit inhibitory impulses to the detrusor nucleus in the pons.

The sensorimotor cortex receives afferent sensations from the striated urethral sphincter (SUS) and pelvic muscle, and transmits afferent inhibitory impulses to the ventral pudendal motor neurons in the sacral spinal cord. The detrusor nucleus also receives afferent impulses from the bladder and relays impulses to the spinal cord micturition center, resulting in bladder contraction (Fletcher 1996; de Groat 1998).

Spinal and Peripheral Reflex Control

Spinal reflexes involving the sympathetic, hypogastric nerves, parasympathetic pelvic nerves and pudendal nerves mediate fine control of micturition. The parasympathetic reflex involves afferent impulses of bladder distension conveyed to the micturition center in the sacral spinal cord. Efferent impulses from the micturition center are transmitted through the pelvic nerves to the detrusor muscle, causing the bladder to contract. Efferent impulses originating in the sympathetic neurons can relax or contract urethral smooth muscle, depending on the need to void.

Stimulation of sympathetic efferent impulses prevents inappropriate voiding by blocking transmission of motor impulses to the detrusor nucleus. Impulses from the SUS and pelvic floor travel through the pudendal nerve, the spinal pudendal nucleus with some impulses relayed from there to the cerebellum medulla and sensorimotor cortex; other impulses from the SUS and pelvic floor reach the spinal detrusor nucleus. Efferent impulses arising in the spinal pudendal motor neurons course through the pudendal nerves to the striated urethral muscle and pelvic floor muscles and result in contraction or relaxation of the SUS, as necessary (Fletcher 1996; de Groat 1998).

Lower Urinary Tract Anatomy and Continence

There are three main structures responsible for urinary continence:

  1. normal storage function of the urinary bladder,
  2. sphincters of the bladder,
  3. pelvic floor musculature and
  4. other supporting structures such as the mucosa, ligaments and accessory muscles.

In men continence is maintained by :

  1. the smooth muscle of the detrusor, which forms a sling around the prostatic base (that is, pre-internal sphincter);
  2. an extension of the deep trigonal muscle as a sleeve around the proximal portion of the prostatic urethra, forming an internal sphincter;
  3. the prostatic urethra which has two layers of muscle and is surrounded by the prostatic tissue containing smooth contractile muscle; and
  4. the external sphincter, composed of striated muscle situated below the prostatic urethra which in its upper third extends onto the prostatic urethra.

Compressive effects of the levator ani and perineal muscles of the urogenital triangle enhance the internal and external sphincters (Chen 1974; de Leval 1993; Gosling et al 1977; Kaufman 1978; Oelrich 1980; Thuroff et al 1980; Strasser et al 1996; Seth 1987; Rosen 1981).

In women, continence is maintained mainly by the bladder neck, which is the internal smooth muscle sphincter, by the external sphincter supplemented by the levator ani and perineal muscles, and by a physiological angle between the proximal urethra and the neck of the bladder (Asmussen and Ulsten 1983; Benson 1994; Cardozo 1989).

Role of the Urinary Bladder in Continence

The urinary bladder is a hollow muscular structure which is responsible for storing the urine for a few hours before it comes out of the urethra. The kidneys continuously produce urine, which needs to be stored temporarily in the bladder.

The bladder therefore serves the dual function of storing the urine as well as expelling it during micturition. This paradoxical and somewhat antagonistic functional requirement actually results in the development of some unique anatomicophysiological properties of the urinary bladder. On the one hand, the bladder simply unfolds on itself during the filling phase of voiding. At this time, the bladder pressure does not rise to any appreciable levels due to the viscoelastic properties of the bladder. During this phase the bladder outlet remains closed due to the sphincteric action of the bladder neck, intrinsic rhabdosphicter and pelvic floor musculature (Michielsen and Wyndaele 1998; Petros 1999; Andersson 199; Lord and Eastwood 1994).

During the voiding phase however, the detrusor contracts and all sphincters relax and open up to allow quick and complete emptying of the bladder. It is therefore easy to visualize that any disease entity, which interferes with the storage capacity of the bladder or the sphincteric function of the lower urinary tract, can result in urinary incontinenece.

The urinary bladder consists of an outer covering of connective tissue, a smooth muscle layer, and an inner mucosal membrane lining. The smooth muscle layer is composed of sheets of muscle fibers, which lack a particular orientation, unlike striated or cardiac muscle. The bundles of smooth muscle extend down into the trigone in such a way that they can cause occlusion of the bladder neck when contracted (Michielsen and Wyndaele 1998; Evans and Castleden 1998; Elbadawi et al 1998; Moore and Richardson 1998; Zinner 1998; Griffiths 1998; Wiskind et al 1994; de Groat 1994; Lord and Eastwood 1994; Scaldazza 1993).

Changes with Ageing

In older persons, there are changes involving the neurological control of micturition and in the anatomic structure of the bladder and bladder outlet. In addition, age-related changes in other functions (for example, cognition, musculoskeletal) may affect continence. Although bladder function alters with age, age-related changes as such are never the cause of urinary incontinence (Bishop et al 1992; Burton 1984; Campbell et al 1985; Ouslander and Schnelle 1995; Pinkowski 1996; Resnick and Yalla 1987; Romanowski et al 1988; Rudd 1968; Snape et al 1989).

Neurological Changes

Central nervous system inhibition of the brainstem micturition center may diminish in old age, and may be markedly reduced in the presence of central nervous system disorders (as in Parkinson’s disease, stroke). Detrusor instability, expressed as poorly coordinated contraction of the bladder and bladder outlet, may reflect age-related neurological changes and is found in up to 50 percent of healthy older persons (Bishop et al 1992; Burton 1984; Hooyman and Cohen 1986; Lentz and Homesley 1998; Ouslander 1989, 1992, 1997; Ouslander and Schnelle 1995).

Bladder Changes

Loss of muscle fibers and decreased elastic content of the bladder wall contribute to diminished bladder capacity and decreased bladder emptying in older men and women. Moreover, there may be some degrees in tone of the internal urethral sphincter (Bishop et al 1992; Campbell et al 1985; Chutka et al 1996; Hooyman and Cohen 1986; Houston 1993; Koyama et al 1998).

Bladder Outlet Changes

In older males, increased collagen content of the neck of the bladder may contribute to bladder outlet obstruction. Benign prostatic hypertrophy, present in up to 50 percent of men over the age of 65, further obstructs normal urine flow.

In multiparous women, the normal angle between the proximal urethra and the bladder may be decreased, diminishing the valve function of this angle. Loss of the effects of estrogen in older women leads to atrophy of urethral smooth muscle and the urethral epithelium, diminishing the urethral-closing pressure. Dorschner et al has described the unique function and form of several different muscle systems of the urinary bladder neck (Dorschner and Hofner 1989).

If these systems have different functional responsibilities, then the muscles must undergo different ageing processes, as stated in the theory of function-dependent ageing. One characteristic of histologic ageing is the change over time in the proportion of muscle cells to connective tissue, a phenomenon that has been demonstrated in both the ciliary muscle and in the two muscle systems of the small intestine.

Using a SIS-Image Analysing System, we have now measured automatically the ratios of muscle cells to connective tissue in sections from several regions of the urinary bladder neck, taken from 50 male and 15 female cadavers. Our results confirm new functional explanations of the different muscle systems in the bladder neck.

The relative volume of muscle cells diminishes continuously with age. The volume of muscle cells first increases and then begins to decrease (the decrease starting in the late thirties and continuing till senescence). Contrary to earlier presumptions, the proportion of muscle cells in the detrusor does not decline during the later decades. The volume of muscle cells and fibers in both urethral sphincter muscles, however, decrease with age, beginning in early childhood (Rother et al 1996).

Non-urinary Tract Changes

Urinary continence may be challenged by changes that affect the older person’s ability to get to the bathroom (due to muscle weakness, arthritis) or by medication that places an undue burden on control of micturition (for instance polyuria due to vigorous diuresis) (Dorschner et al 1994).

Urinary continence is achieved through an interplay of complex neurological, vesical, muscular and sphincteric functions. The fine balance between voiding and continence may be disturbed by several pathological and physiological factors. Detailed understanding of these concepts is a prerequisite before undertaking any surgical methods for correcting incontinence.