Joanne Sandberg-Cook Urinary incontinence is the involuntary transient or persistent loss of urine (Box 145-1). It is experienced by 30% to 50% of women and 17% of men older than 60 years as well as up to 50% of elderly nursing home residents.1 Incontinence is considered to be one of the major causes of institutionalization in the geriatric population, but incontinence is not limited to the elderly. Twenty percent to 30% of young community dwellers are also affected by this disorder.1 Urinary incontinence should not be considered normal at any age and is not an expected outcome of aging. Impaired mobility, pelvic floor weakness, race and ethnicity, weight, other comorbidities (asthma, depression, heart disease, or a history of frequent urinary tract infection [UTI]), benign prostatic hyperplasia (BPH), medications, and bowel status may all contribute to incontinence.2 The annual cost of managing incontinence for all age groups in the United States was nearly $66 billion in 2007 with much of the cost associated with nursing home placement.3 However, despite its financial impact on society, incontinence is rarely addressed by patients with their health care providers. Thus, it behooves health care providers to identify patients who could benefit from therapeutic regimens to minimize the overall impact of incontinence. Urinary incontinence is usually the symptom of an underlying bladder or sphincter condition, but it may also be related to an extrinsic problem that can be easily treated. There are five main types of urinary incontinence: stress incontinence, urge incontinence, mixed incontinence, overflow incontinence, and functional or transient incontinence. Stress urinary incontinence (SUI) is leakage of urine with any maneuvers that increase intra-abdominal pressure (coughing, sneezing). The increase in intra-abdominal pressure is transmitted to the bladder, which then overcomes the sphincteric and urethral pressure, resulting in an open urethra and urinary leakage. Stress incontinence is seen in those who have either or both of the following issues. Previously termed genuine stress incontinence, anatomic incontinence refers to hypermobility of the bladder neck (vesicourethral junction). In general, the sphincter is competent at rest, and an increase in abdominal pressure leads to increased closure pressure. When the bladder neck is mobile, a rise in intra-abdominal pressure results in rotation of the bladder neck and urethra below the pelvic floor muscles so that intra-abdominal pressure is no longer transmitted to the bladder neck and urethra. The sphincter is overcome by the increase in abdominal pressure, which is transmitted to the bladder, and leakage occurs.4 Intrinsic sphincter deficiency (ISD) indicates an open bladder neck at rest. Even a mild increase in intra-abdominal pressure in individuals with ISD can result in leakage.4 Although ISD can occur naturally, patients who have had radical pelvic surgery may also experience a compromise of their intrinsic sphincter, predisposing them to incontinence. Contemporary theories suggest that all patients with sphincteric incontinence have some degree of ISD.4 Urge is the most common cause of incontinence in older adults and manifests as the sudden, often uncontrollable sensation to void.5 This urge can then lead to urinary urge incontinence (UUI). However, in patients with severe urge, incontinence may not be realized until actual leakage occurs. Overactive bladder is a newer term used to describe the phenomenon of urgency and frequency with or without UUI.5 Urge and urge incontinence occur because of a rise in detrusor pressure that may be a phasic contraction, detrusor overactivity (DO), or poor bladder compliance. DO is instability of the detrusor muscle during bladder filling as a result of idiopathic or neurogenic causes. In both idiopathic and neurogenic DO, bladder pressures surpass sphincter and urethral pressures, causing the bladder neck to open and incontinence to occur. When no defined neurologic contributor can be identified, DO is idiopathic. Prominent theories for DO include increased stimulation of alpha1 receptors in the bladder, disruption of somatic and autonomic nervous systems that help regulate voiding, disruption of afferent and efferent pathways, and increased activation of muscarinic (M2/M3) receptors in the bladder.4 Patients who have spinal cord injuries below T11-L1,2 or neurologic conditions, such as multiple sclerosis, diabetes mellitus, and spina bifida, can have a disruption in voluntary micturition control. Reflex micturition often results, leading to detrusor hyperactivity and urge incontinence.4 Normal bladder compliance allows large amounts of urine to be stored with minimum changes in bladder pressure.6 With poor compliance, large bladder pressures are seen with small increases in volumes.6 This can be a result of the loss of viscoelasticity in detrusor muscle or changes in neuroregulatory activity. A combination of SUI and UUI is referred to as mixed incontinence. Incomplete emptying of urine often results in passive loss of small amounts of urine when bladder pressures elevate, either episodically or continuously, as the bladder fills beyond capacity. The rise in bladder pressure may occur because of either transmitted abdominal pressure or an increase in detrusor pressure. Overflow incontinence is seen in patients with either bladder outlet obstruction or poor detrusor contractility. Bladder pressure surpasses sphincter and urethral pressure, which allows “overflow” of urine to occur. This is more commonly seen in men than in women, and causes include BPH, radical pelvic surgery, detrusor inactivity, neurologic issues, and certain medications. Pathologic conditions external to the urinary tract can also cause incontinence. Such factors are indicated in Resnick’s DIAPPERS mnemonic (Box 145-2). Reversal of these conditions may improve the urinary incontinence. The presentation of incontinence can vary depending on the cause. A careful history and physical examination should exclude causes of transient incontinence that can be easily treated. SUI, UUI, mixed incontinence, and overflow incontinence can manifest similarly, so careful history taking may help delineate the type of incontinence experienced. A history should include a detailed review of symptoms related to incontinence; bowel habits; medications; medical, surgical, and genitourinary histories; history of pelvic trauma; and neurologic issues.5 Onset, precipitants, duration, characteristics (frequency, timing, and amount), alleviating factors, and treatments tried should all be documented. Alterations in bowel or bladder habits, number of pads used, and response to previous treatments should be noted as well. The physical examination for incontinence includes abdominal, genitourinary, pelvic, and rectal components. A neurologic and functional assessment as well as an assessment of the extremities for edema should also be made. Medication history (especially that of diuretic use), mental status, mobility, and social evaluations should be performed, especially in older adults, because impairment in any of these realms may contribute to functional incontinence. Examination findings in men including phimosis, balanitis or infection, rectal masses, prostate nodules or asymmetry, and fecal impaction suggest underlying causes of the incontinence. In women, an assessment of urethral mobility is performed by examining the bladder neck and urethra with the patient supine while she strains. A stress test is also performed by observing for urine loss when the patient performs a Valsalva maneuver or by having the patient cough. If incontinence is not seen when the patient is examined supine, the examination should be repeated with the patient standing. Bladder neck hypermobility can also be determined with the Q-tip test. If the Q-tip moves more than 30 degrees from a horizontal plane when it is inserted superficially into the urethra, lack of urethral support is delineated.7 Furthermore, pelvic organ prolapse and effectiveness of the patient’s ability to perform Kegel exercises (contraction of the pelvic floor) should be noted. General observation of pelvic anatomy should be made, and any abnormalities, including atrophy, should be documented. The relationship between estrogen and incontinence in perimenopausal and menopausal women has not been well defined. However, lack of estrogen and subsequent vaginal atrophy may contribute to symptoms of stress incontinence.8 UUI may not be detectable on physical examination. Subjective complaints may be most beneficial in detecting urge incontinence and UUI. However, examination of pelvic anatomy and pelvic floor strength may reveal contributors to bladder symptoms, such as constipation and vaginal atrophy. Mixed incontinence requires a physical examination to assess for SUI and UUI. This should be performed as previously discussed. Finally, overflow incontinence can often be determined through abdominal and vaginal examinations. Bladder distention may be easily palpated abdominally or vaginally. Evaluation of general pelvic anatomy should also occur. A urinalysis is performed to exclude hematuria, pyuria, glucosuria, or proteinuria. Hematuria, defined as more than three red blood cells per high-power field on urinalysis with a negative urine culture,9 warrants further workup with cytology, upper tract imaging, and bladder cystoscopy. Urine cytologic studies should also be performed in patients with gross or persistent microhematuria, risk factors for bladder cancer, or irritative symptoms.9 A urine culture is necessary to exclude a UTI in patients with pyuria or irritative symptoms, including urge and urge incontinence.5 Blood urea nitrogen (BUN) and creatinine levels should be obtained if compromised renal function is suspected, especially with overflow incontinence. If polyuria is suspected, serum glucose and calcium tests are also recommended. A postvoid residual (PVR) is helpful to exclude incomplete emptying and can be obtained through either pelvic ultrasound or catheterization.5 In general, a PVR of less than 50 mL is considered normal, whereas residuals of more than 100 mL are considered abnormal and require further evaluation.10 Additional testing is usually not needed for the basic evaluation of urinary incontinence unless onset is sudden, symptoms are severe, or suprapubic pain or hematuria is present. The patient should be referred to a urologist if further diagnostic testing (e.g., cystoscopy, urodynamics) is necessary or if the diagnosis is uncertain.5 The health care provider should refer the patient if an effective care plan cannot be devised, if hematuria is present without infection, if surgical intervention is being considered, or if therapy has failed.
Incontinence
Definition and Epidemiology
Pathophysiology
Stress Incontinence
Anatomic Stress Urinary Incontinence.
Intrinsic Sphincter Deficiency.
Urinary Urge Incontinence
Detrusor Overactivity.
Idiopathic Causes.
Neurogenic Causes.
Poor Bladder Compliance.
Mixed Incontinence
Overflow Incontinence
Functional or Transient Incontinence
Clinical Presentation
Physical Examination
Diagnostics
Incontinence
Chapter 145
