Authors: Macfarlane, Michael T.
Title: Urology, 4th Edition
Copyright 2006 Lippincott Williams & Wilkins
> Table of Contents > Part One - Chief Presentations > Chapter 5 - Incontinence
Involuntary loss of urine is a frequent presenting complaint to the urologist. What constitutes significant loss can be defined by the degree of psychosocial impairment or by more objective evidence, such as the number of pads used per day. A detailed history will usually lead toward the correct diagnosis and will require only a few confirmatory tests. As with any voiding disorder (see Chapter 21), incontinence can be approached using the Wein classification as either a failure to store or a failure to empty. The major categories of incontinence follow.
Types of Incontinence
Total incontinence is characterized by the constant or periodic loss of urine without normal voiding and no postvoid residual. It can be thought of as a true leak in the tank. Causes include major sphincteric abnormalities such as those that occur with exstrophy of the bladder or epispadias and abnormal anatomic connections such as those that occur with vesicovaginal fistulas or ectopic ureteral orifices.
Stress incontinence is characterized by the involuntary loss of urine not caused by bladder contraction and is associated with physical activities such as coughing, laughing, sneezing, lifting, or exercise. This usually occurs in females with weakened pelvic floor support, urethral hypermobility, and descensus of the bladder neck. It is often associated with multiple vaginal deliveries. The net result is a loss of the normal transmission of intraabdominal pressures to the proximal urethra. Increased intraabdominal pressures will therefore cause only elevated intravesical pressures
Urgency incontinence is the result of an involuntary rise in intravesical pressure secondary to bladder contraction, which overcomes outlet resistance. Bladder instability or hyperreflexia generally produces a sensation of urgency of urination in most patients; however, it can present with incontinence alone. Common causes of detrusor instability include loss of cortical inhibition of the voiding reflex (e.g., those that occur after strokes or dementia or with parkinsonism). However, the more common local causes of detrusor instability, such as infection, bladder stone, tumor (carcinoma in situ), interstitial cystitis, or foreign body, must always be ruled out first.
Overflow incontinence is said to be paradoxical because urine loss is the result of a failure of the bladder to empty, rather than an inability to properly store urine. Causes include bladder outlet obstruction, detrusor weakness, or a combination. Males with outlet obstruction secondary to benign prostatic hyperplasia or strictures typically present with symptoms of frequency; slow, weak stream; and voiding small volumes. The hallmark of overflow incontinence is a high postvoid urine volume. Females more typically have detrusor hypotonicity with poor emptying and high residuals secondary to diabetes mellitus, autonomic neuropathy, or anticholinergic medications (e.g., tranquilizers).
Enuresis refers to involuntary wetting in children. It is generally a problem at night and should be referred to as nocturnal enuresis as opposed to diurnal enuresis. However, these qualifiers are often omitted, and enuresis is usually taken to mean bedwetting. Enuresis is a common problem and should be viewed as a developmental lag in the inhibitory influence of the central nervous system on the urinary bladder. However, behavioral or stress factors are believed also to be involved in some children. Twelve percent of 6-year-olds, 3% of 12-year-olds, and 1% of 18-year-olds wet their beds.
Primary enuretics are children who have been wet since birth, whereas secondary enuretics have had a period of dryness before reverting to wetting. Most primary enuresis resolves by the second or third year of life; however, some children will continue to wet into later years. No objective organic lesion will be identified in the true enuretic other than a lower functional bladder capacity. The most characteristic trait of enuretics is their sound sleeping habits. The diagnosis is made by excluding urologic disease that could be responsible (e.g., urinary tract infections, reflux, meatal stenosis, bladder outlet obstruction, or neurologic disease). A careful history, urinalysis, and plain film of the abdomen are generally sufficient to work up the enuretic child. If the history or urinalysis suggests organic disease, then a more thorough investigation, including voiding cystourethrogram (VCUG), intravenous urography, and cystoscopy, is in order.
Spontaneous resolution can be expected with regularity, requiring only parental reassurance, toilet training, and fluid restriction before bedtime. More aggressive measures should be considered in the child reaching school age.
A good voiding history is essential and will often reveal the correct diagnosis without the need for an elaborate evaluation. Inquire about specific details of symptoms, including urgency, frequency, dysuria, stress leakage, and times of leakage. A detailed history of other medical problems, including all medications, surgical history, and parity, is important. Note caffeine intake. Ask if the patient uses protection and, if so, how many pads per day are needed. A voiding diary can be helpful.
Abdominal, pelvic, and rectal examinations should be routine, along with a neurologic assessment. Note any masses, cystoceles, rectoceles, rectal sphincter tone, fecal impaction, or evidence of estrogen deficiency in females. A Q-tip test can be performed to test for pelvic floor relaxation in women.
Urinalysis, urine culture, serum electrolytes, blood urea nitrogen (BUN), creatinine, and fasting blood sugar should be obtained. Atypical vaginal cultures may be productive in difficult cases of overactive bladder.
Postvoid Residual Urine
Measurement of postvoid residual urine (PVR) is probably the single most useful piece of information in understanding incontinence. It helps categorize the disorder as failure to store or failure to empty.
Urodynamic studies, including uroflow and cystometry, should be obtained when indicated. Abdominal leak point pressure measurement can identify intrinsic sphincter dysfunction.
A VCUG is often helpful, particularly in patients with suspected stress urinary incontinence. Bladder descensus with cystocele can be readily appreciated. An intravenous urogram is indicated in patients with hematuria, persistent infections, or suspected tumor.
Cystoscopy can be reserved for patients with hematuria, persistent infections, suspected tumor, or a history of prior surgical intervention.
Intraurethral and bladder neck injections with collagen can give short-term improvement. Retropubic slings and suspensions,
Urgency Incontinence (Detrusor Instability)
Pharmacotherapy (oxybutynin, tolterodine, solifenacin, trospium, darifenacin), bladder denervation, and augmentation cystoplasty are treatment options.
Intermittent self-catheterization is appropriate for patients with bladder atony. Males with outlet resistance should benefit from surgical relief of the obstruction if detrusor function can be salvaged. Indwelling urethral catheters should be avoided if possible. Intermittent self-catheterization would be preferable.
Patients with documented anatomic problems such as exstrophy, epispadias, ectopic ureters, or fistulas will require appropriate surgical intervention. Artificial urinary sphincters may be necessary in some instances.
True enuresis will generally resolve spontaneously between age 2 and 6 years. Objective urologic disease must be ruled out if suspected. Alarm conditioning and pharmacotherapy may be necessary. Pharmacologic therapy includes imipramine [Tofranil 25 mg orally (PO) at bedtime] or oxybutynin (Ditropan 5 mg PO at bedtime). Intranasal or oral arginine vasopressin [DDAVP 20 g at bedtime (qhs)] can be tried in children age 6 years or older.