Approach to Urinary Incontinence
John D. Goodson
Urinary incontinence, defined as the involuntary loss of urine, is predominantly a condition of middle-aged and older women, affecting an estimated 30% to 60%. It ranks as a major source of physical and social impairment, having the potential to severely impact quality of life. In the setting of cognitive impairment, it is the culminating event that leads to nursing home placement. In men, urinary incontinence is a less frequent, typically less disruptive problem, mostly a consequence of chronic outflow obstruction from prostatic hyperplasia (see Chapter 138); however, when occurring as a complication or consequence of treatment for prostatic cancer (see Chapter 143), spinal cord injury, or dementia (see Chapter 173), it can be much more disruptive.
Substantial progress has been made in the evaluation and management of urinary incontinence; there are many useful strategies and interventions that do not require often-problematic pharmacotherapy or invasive measures. A very effective evaluation can usually be done in the office simply by means of a detailed history and directed physical examination, reserving urodynamic studies for those with complicated presentations. Behavioral measures, which can be implemented in the primary care setting and substantially improve quality of life, constitute the foundation of treatment programs. Because even successful solutions require readjustment, an ongoing dialogue around continence, complemented by continuous support, is an essential element of the management program.
The frequency and importance of urinary incontinence and the opportunity to significantly improve quality of life with relatively simple, readily implementable measures make it important that the primary care clinician and medical home team be able to conduct an effective and efficient evaluation, implement a basic treatment program, and identify those who need referral for consideration of more invasive measures. This chapter focuses largely on urinary incontinence in women (see Chapters 138, 143, and 173 for more additional discussions of the problem in men).
Normal Bladder Function and Continence
The detrusor muscle of the bladder is normally under simultaneous sympathetic and parasympathetic control. During the filling phase, sympathetic tone predominates, whereas parasympathetic tone is inhibited. The internal bladder sphincter tightens under a-adrenergic influence, and the detrusor relaxes under β-adrenergic influence. During voluntary emptying, parasympathetic stimulation via M3 muscarinic receptors in the bladder muscle produces detrusor contraction; at the same time, sympathetic tone decreases, the external sphincter of the pelvic floor relaxes, and abdominal muscles tighten. Normally, the urethra is oriented to the bladder so as to facilitate continence. With the initiation of voluntary voiding, the urethrovesical angle changes so as to permit full drainage. Complete bladder emptying depends on unimpeded flow.
The process of voiding usually begins with a sensation of bladder fullness mediated by proprioceptive fibers in the detrusor. A reflex arc between the detrusor and the brainstem initiates and amplifies bladder contraction by parasympathetic stimulation. This arc is under cortical inhibition. Voiding occurs with the release of inhibition and voluntary relaxation of the pelvic external sphincter.
Urinary Incontinence
The pathophysiology and clinical presentations of urinary incontinence can be divided on clinical and mechanistic grounds into categories of detrusor instability or overactivity (urge incontinence), sphincter or pelvic incompetence (stress incontinence), reflex incontinence, detrusor hypotonia or insufficiency (overflow incontinence), and functional incontinence. Clinically, two or more processes frequently coexist to varying degrees in the same patient.
Detrusor Instability or Overactivity (Urge Urinary Incontinence)
Detrusor instability or overactivity (urge urinary incontinence) is characterized by reduced bladder capacity resulting from excessive and inappropriate detrusor contraction. For many, the condition appears to arise as a concomitant of aging, although the mechanism is unclear and often referred to idiopathic urgency urinary incontinence. In some cases, it seems to be the result of decreased cortical inhibition of detrusor contraction. Loss of cortical input can ensue from such conditions as cerebral infarction, Alzheimer disease, brain tumor, and Parkinson disease. For
others, the detrusor instability or overactivity is linked to bladder irritation from such causes as trigonitis (a common accompaniment of cystitis), chronic interstitial cystitis, postradiation fibrosis, and detrusor hypertrophy from long-standing outflow tract obstruction from urethral stricture or benign prostatic hyperplasia (BPH). Patients note a few moments of warning, frequent episodes of urgency, moderate to large volumes, and nocturnal wetting. In roughly half of patients, detrusor instability is associated with poor detrusor function. For these patients, voiding is frequent and incomplete.
others, the detrusor instability or overactivity is linked to bladder irritation from such causes as trigonitis (a common accompaniment of cystitis), chronic interstitial cystitis, postradiation fibrosis, and detrusor hypertrophy from long-standing outflow tract obstruction from urethral stricture or benign prostatic hyperplasia (BPH). Patients note a few moments of warning, frequent episodes of urgency, moderate to large volumes, and nocturnal wetting. In roughly half of patients, detrusor instability is associated with poor detrusor function. For these patients, voiding is frequent and incomplete.
Sphincter or Pelvic Incompetence (Stress Urinary Incontinence)
Sphincter or pelvic incompetence (stress urinary incontinence) is usually a consequence of pelvic floor laxity and is the most common form of urinary incontinence in women. Less frequently, it develops from partial denervation that reduces sphincter tone. Pelvic laxity is seen as a concomitant of normal aging or as a consequence of difficult or multiple vaginal deliveries or direct perineal injury. In some cases, a cystocele forms and further impedes control. Estrogen deficiency in women may reduce the competency of the internal sphincter and can also cause urethral symptoms (dysuria and frequency). In men, stress incontinence may result from prostatic surgery, most commonly prostatectomy, although in most cases, the abnormality resolves within 6 to 12 months if innervation remains largely intact. Patients complain of incontinence, which occurs predominantly at times of straining (coughing, laughing, sneezing, lifting). There is loss of small to moderate volumes of urine, very infrequent nighttime leakage, and little postvoid residual.
Reflex Urinary Incontinence
Reflex incontinence derives mostly from spinal cord damage above the sacral level. Interference with sensation and coordination of detrusor and sphincter activity secondary to inhibited or absent central control leads to detrusor spasticity and overactivity and functional outlet obstruction. The patient is unable to sense the need to void. Diabetes and spinal cord injury are the most common causes. Multiple sclerosis, tabes dorsalis, and intrinsic or extrinsic cord compression from tumor, disk herniation, or spinal stenosis account for many other cases. Reflex incontinence takes place day and night with equal frequency and without warning or precipitating stress. Volumes are moderate, and voiding is frequent. Voluntary sphincter control and perineal sensation are reduced; sacral reflexes remain intact.
Detrusor Hypotonia or Insufficiency (Overflow Urinary Incontinence)
Detrusor hypotonia or insufficiency (overflow urinary incontinence) results from long-standing outlet obstruction, detrusor insufficiency, or impaired sensation. The bladder becomes hypotonic, flaccid, and distended. Voiding consists primarily of overflow spillage. In outflow tract obstruction (seen most often in men, largely from long-standing BPH—see Chapter 138), the detrusor is constantly overstretched and gradually becomes incapable of generating sufficient pressure to ensure bladder emptying. Often, detrusor hypotonia or insufficiency is a consequence of lower motor neuron damage, as occurs with injury to the sacral cord or the development of peripheral neuropathy (as in diabetes or vitamin B12 deficiency). Perineal sensation and sacral reflexes may be lost. Of importance, anticholinergic agents and drugs with anticholinergic activity (e.g., tricyclic antidepressants) can reduce detrusor tone and exacerbate detrusor weakness.
Distinguishing clinical characteristics include a palpably distended bladder and a large postvoid residual. Patients report urinary frequency, especially at night and after fluid loads and diuretics. Incomplete emptying, slow or interrupted flow, hesitancy, and the need to strain are common complaints. There may be reports of concurrent stress incontinence. Retrograde flow of urine and increased ureteral pressures can compromise renal function if the condition is left uncorrected, and an occasional patient will present with renal failure.
Functional Urinary Incontinence
Functional incontinence refers to situations in which physical or mental disability makes it impossible to void independently, even though the urinary tract may be intact. Patients with disabling illness or simply an acute change to a bedridden state may be unable to maintain sufficient control over lower urinary function to avoid incontinence. Sedating drugs in such situations may only exacerbate the problem. Patients who are aware of their condition will describe their unsuccessful attempts to maintain continence. Patients with frontal lobe dysfunction secondary to cortical degenerative disease or normopressure hydrocephalus may be unaware of their voiding and therefore be functionally incontinent. Rarely, deliberate incontinence is part of a mental health condition.
Mixed Presentations
Mixed forms of incontinence are the most common presentation in older women, with about half reporting a combination of urge and stress incontinence symptoms. Functional impairment also commonly contributes to the clinical picture.
Other Symptoms of Urinary Tract Dysfunction
Persons with urinary incontinence may also experience other urinary tract symptoms, which can provide important clues as to the underlying pathology. Moreover, other urinary tract symptoms may dominate the clinical presentation and represent the principal problem.
Urinary Frequency in Conjunction with Difficulty Voiding
When associated with slow stream, hesitancy, and a sense of incomplete emptying, frequency is likely to be a manifestation of outflow tract obstruction (extrinsic or intrinsic). At first, the patient may notice only minor slowness of stream. If the obstruction persists, bladder instability may ensue and cause frequent voiding of small volumes, followed later by chronic distention and overflow incontinence (see prior discussion). Strictures, tumor (especially prostatic enlargement), and occasionally stones are responsible for most cases of obstruction. In the setting of severe constipation, the rectal vault can become sufficiently impacted that it actually blocks the urethra and prevents bladder emptying. a-Adrenergic agents and β-blockers can increase sphincter tone and impair voiding acutely, especially in patients with preexisting lower urinary tract dysfunction. Anticholinergic drugs may interfere with bladder contraction.
Urinary Frequency and Polydipsia
When frequency presents in association with increased thirst, it suggests a diabetic condition leading to increased urine volume and the resultant polyuria. Diabetes mellitus is distinguished by significant glycosuria (see Chapter 102). Neurogenic (idiopathic central) diabetes insipidus is manifested by sudden onset, craving for huge volumes of cold water, and prodigious urine outputs (5 to 10 L/d). Inability to concentrate the urine after overnight
fluid deprivation and response to parenteral antidiuretic hormone (ADH), with formation of a concentrated urine, characterize the condition. Patients with nephrogenic diabetes insipidus differ from those with the neurogenic variety, in that their kidneys do not respond to intrinsic or parenteral ADH. Hypercalcemia, lithium therapy, and pregnancy are precipitants of the acquired variety. Patients with psychogenic polydipsia may be hard to distinguish from those with nephrogenic diabetes insipidus because they have washed out their renal concentrating system and also do not adequately respond to parenteral ADH. They do respond normally to fluid deprivation, which is a diagnostically useful finding, although some patients with neurogenic disease respond in a similar fashion (see Chapter 101).
fluid deprivation and response to parenteral antidiuretic hormone (ADH), with formation of a concentrated urine, characterize the condition. Patients with nephrogenic diabetes insipidus differ from those with the neurogenic variety, in that their kidneys do not respond to intrinsic or parenteral ADH. Hypercalcemia, lithium therapy, and pregnancy are precipitants of the acquired variety. Patients with psychogenic polydipsia may be hard to distinguish from those with nephrogenic diabetes insipidus because they have washed out their renal concentrating system and also do not adequately respond to parenteral ADH. They do respond normally to fluid deprivation, which is a diagnostically useful finding, although some patients with neurogenic disease respond in a similar fashion (see Chapter 101).
Isolated Urinary Frequency
Isolated frequency may be a manifestation of reduced bladder capacity or a presentation of mild diabetes mellitus, mild diabetes insipidus, minor urinary tract infection, or bladder irritation. A large extrinsic or intrinsic mass impinging on the bladder can reduce its capacity and produce frequent urination, usually of small volumes, which distinguish it from other forms of polyuria. Pelvic surgery, chronic interstitial cystitis, or irradiation can have a similar effect by reducing bladder capacity. Patients who surreptitiously abuse diuretics rarely complain of frequency, but those who take them for therapeutic purposes are often bothered by the side effect. Nocturnal urinary frequency and occasional incontinence can represent the mobilization of fluid in patients with dependent edema associated with congestive heart failure or intake of certain medications, such as some of the calcium channel blockers. Similarly, excess volume may ensue from the stimulation of atrial natriuretic peptide production by obstructive sleep apnea, exacerbating nocturnal frequency.
TABLE 134-1 Important Causes of Urinary Incontinence | |||||||||||||||||||||
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The differential diagnosis of incontinence can be classified according to clinical presentation and mechanism (Table 134-1). The differential diagnosis of dysuria and frequency is that of urinary tract infection and its related syndromes (see Chapters 133 and 140). Most patients with difficulty voiding are men with BPH (see Chapter 138). Among other causes of difficult voiding are drugs (anticholinergics, β-blockers, sedatives), urethral stricture, congenital valves, stone, tumor, pelvic abscess, and fecal impaction. Causes of urinary frequency in the absence of other urinary tract symptoms include diabetes mellitus, diabetes insipidus, psychogenic polydipsia, diuretics, and bladder compression.
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