CHAPTER 30
Urinary Incontinence
Renee McLeod-Sordjan, DNP, FNP-BC, Acute Care-BC
Urinary incontinence (UI) is defined by the International Continence Society (ICS) as the complaint of any involuntary leakage of urine that is a social or hygienic problem. UI is a symptom of an underlying process that affects more than 200 million people worldwide. The direct economic burden in the United States alone is of $16.3 billion, of which 75% is for the management of women with this condition (Tanagho, Bella, & Lue, 2008). UI is a storage symptom the prevalence of which increases with age. At least 50% of those affected do not report the problem to health care professionals. UI is not solely a physical problem: it may be debilitating psychosocially, significantly affecting quality of life. UI is associated with medical morbidity and hygienic issues. These include perineal Candida infection, cellulitis and pressure ulcers from constant skin moisture and irritation, urinary tract infections, and mechanical falls and fractures from slipping on urine. Psychosocial issues include depression, embarrassment, social isolation, impaired self-esteem, reduced activities outside the home, reduced sexual activity, and sleep disturbances (Kocaöz, Talas, & Atabekoğlu, 2010).
In older populations, UI may be a multifactorial syndrome representing the intersection of neurological pathology, age-related factors, comorbid conditions, medications, and functional and cognitive impairments (DuBeau, Johnson, Kuchel, Palmer, & Wagg, 2009). Patients and their caregivers perceive UI as restricting activities. UI contributes to embarrassment, increases caregiver burden, and affects social role functioning, thereby decreasing health-related quality of life (Coyne et al., 2009; DuBeau et al., 2009). The negative impact of UI on physical activity has significant implications for prevention of cardiovascular disease and other chronic illness. Given the increased morbidity, major impact on quality of life, and lack of patient disclosure, primary care providers (PCPs) are compelled to identify UI in their patients. The provider must be aware of UI and make an especially concerted effort to identify its existence and its classification to make appropriate treatment choices. In particular, patients older than 65 years should be routinely questioned about their voiding habits, as incontinence is not routine in “normal” aging.
UI can be described according to type, frequency, chronicity, severity, precipitating factors, social impact, effect on hygiene and quality of life, measures used to contain leakage, and the individual’s symptoms. Transient causes of UI include elements that form the mnemonic DIAPPERS: Delirium, Infection (usually urinary tract infections), Atrophic urethritis and vaginitis, Pharmaceuticals (e.g., α-adrenergic, cholinergic, or anticholinergic properties; diuretics; hypnotic sedatives; calcium channel blockers; and the prostaglandin inhibiter misoprostol), Psychiatric disorders (especially depression), Excessive urine output, Restricted mobility, and Stool impaction (Shenot, 2012).
Established causes of UI result from injury to bladder muscles or nerve innervation. Elements used to describe established UI are bladder outlet incompetence or obstruction, detrusor overactivity or underactivity, detrusor–sphincter dyssynergia, or a combination. Neurogenic UI is associated with detrusor muscle hyperreflexia, because of a loss of cerebral inhibition of bladder activity in patients with neurologic disease (e.g., spinal cord injury, stroke, multiple sclerosis, or Parkinson’s disease). Incomplete bladder emptying can result. Non-neurologic established causes of UI can result from voiding dysfunction in childhood, pelvic surgery (e.g., prostatectomy, hysterectomy), bladder carcinoma, chronic cystitis, and outlet obstructions.
In 2009, the ICS and the International Urogynecological Association established definitions of UI. The most prevalent types of chronic or established UI are characterized as stress, urge, overflow, functional, mixed, transient, or overactive bladder. Table 30.1 describes the various kinds of UI.
ANATOMY, PHYSIOLOGY, AND PATHOLOGY
Male and female urinary systems are similar in that both consist of the following elements: the bladder, surrounded by the detrusor muscle; an internal sphincter muscle; and an external sphincter muscle. The major differences include the prostate gland and a longer urethra in males. Figure 30.1 illustrates the basic structures. Knowledge of the anatomy, physiology, and functions of the male and female lower urinary tract provides a clear understanding of the potential areas where urinary continence can be affected.
CLASSIFICATION | DESCRIPTION |
Stress incontinence | Involuntary loss of urine during coughing, sneezing, laughing, lifting, or other physical activities. Caused by sphincter insufficiency. Occurs when urethra pressure falls below bladder pressure. |
Urge incontinence | Leakage of large amounts of urine at unexpected times due to the patient’s inability to suppress the sensation of bladder fullness. The detrusor muscle is unstable. Patient experiences an abrupt and strong desire to void. |
Overflow incontinence | Also known as high post-void residual. Occurs when there is inadequate detrusor function due to hypotonia or insufficiency, inadequate sensory perception within the bladder wall, or significant outlet obstruction. Overflow incontinence is the second most common cause of UI in men due to prostatic stricture. |
Functional incontinence | Untimely urination secondary to impaired mobility, external obstacles, or impaired cognition that impedes a person’s toileting. |
Mixed incontinence | Symptoms of stress and urge incontinence. Characterized as an involuntary loss of urine associated with urgency and also with effort, physical exertion, sneezing, or coughing. |
Transient incontinence | Situational loss of urine from a temporary condition (i.e., infection, medication, or symptomatic cough). |
Overactive bladder | Urinary frequency or urgency, with or without UI. |
UI, urinary incontinence.
FIGURE 30.1
Bladder, urinary system, and sphincter muscle anatomy.
Source: Adapted from Rosse and Gaddum-Rosse (1997) and NKUDIC (2013).
Lower urinary tract structures function efficiently with low-pressure bladder filling, urine storage with perfect continence, and periodic complete voluntary urination. Micturition requires voluntary neural control with appropriate sensation of bladder fullness without urinary frequency, dysuria, or urgency. Lower urinary tract neuronal control differs from that of other visceral organs innervated by the autonomic nervous system, the regulation of which is solely involuntary. Urinary continence requires two discrete processes of the micturition cycle: (1) bladder filling and urine storage and (2) bladder emptying or voiding (Wein, 2011).
Bladder filling and urinary storage require the bladder outlet (urethra) to remain closed during increases in intra-abdominal pressure. Failure of bladder filling and urinary storage may be related to pathology of the bladder, the outlet (bladder neck, urethra, and external urethral sphincter), or both. Anatomic stress incontinence occurs due to a hypermobility of the bladder neck that transmits Intra-abdominal pressures below the pelvic floor muscles. This releases pressure from the bladder neck and urethra. The external urethral sphincter, overcome by the pressure, then releases urine. This form of anatomic-stress UI occurs during coughing and sneezing.
The intrinsic urethral sphincter may also be deficient, secondary to surgical procedures, such that mechanical incontinence ensues (Fauci et al., 2008). Typically, this type of stress incontinence is rare in males, but may occur after transurethral resection of the prostate (TURP) in which damage to the external and internal sphincter has occurred (McDougal et al., 2011). Loss of urethral sphinter control can also result from radiation treatments, fibrosis from an indwelling catheter, and ischemia.
Bladder emptying or voiding failures may result from detrusor muscle pathology, neural pathology, excessive bladder outlet resistance, or a combination of these. The detrusor muscle, responsible for the propulsive force in bladder emptying, is under parasympathetic autonomic control through the pelvic spinal somatic nerves (Fauci et al., 2008). Bladder contraction results from cholinergic stimulation. The internal and external sphincter muscles, located in the bladder outlet area, are responsible for maintaining urethral pressure. Comparably, the internal sphincter is innervated by the alpha-adrenergic pathway. Alpha stimulation results in muscle contraction, preventing urine flow (Wein, 2011). The external sphincter is composed of striated muscles that are under voluntary control.
The involuntary pathway of bladder emptying and voiding is located in the brainstem. Involuntary contractions of the bladder can be seen with neurologic disease or injury, related to neural degeneration in aging or due to increased afferent (sensory) pathways related to urethral or bladder wall irritation. As defined by the ICS, overactive bladder can lead to UI caused by reduced brainstem inhibition, spinal cord injury, or excitatory neurotransmitters along reflex pathways that control urination. Urinary tract infections and painful bladder syndromes (formerly known as interstitial cystitis) may also cause bladder emptying because of the increased afferent pathways.
In the female, estrogen receptors are located in both the internal and external sphincters. Estrogen receptor stimulation contributes to sphincter competence. In the absence of estrogen, as in postmenopausal women, the internal and external sphincters may not resist urine passage in situations of increased stress (e.g., coughing, sneezing, climbing stairs, and other physical activities), resulting in small amounts of urine leakage. This is secondary to the loss of estrogen-stimulated competence of these sphincters. In postmenopausal women, decreased estrogen levels may result in urogenital atrophy, atrophic urethritis, and vaginitis, thereby decreasing urethral resistance and promoting UI.
Overflow incontinence may result from obstruction of the bladder neck or urethra or from neurologic damage such as spinal cord injury. Bladder outlet obstruction often occurs in men with benign prostatic hypertrophy. When enlarged, the prostate gland, which surrounds the urethra, impedes urinary outflow from the bladder and increases strain on the detrusor muscle. This results in symptoms such as nocturia, reduced size and force of the urinary stream, straining to void, and terminal dribbling. Detrusor instability leads to uncontrollable bladder contractions and may arise from central nervous system diseases such as cerebrovascular accidents, dementia, neoplasia, and perhaps normal-pressure hydrocephalus (Fauci et al., 2008).
Physiological age-related changes occur in continent persons as well as those who develop incontinence. Thus, the predisposition to incontinence is multifactorial and incompletely described by only physiological changes.
EPIDEMIOLOGY
Prior to 2001, when the ICS developed a standardized epidemiologic definition of UI, the true prevalence of this disorder was difficult to establish (Luber, 2004). Risk factors are multifactorial and include aging, gender, obesity, cognitive impairment, physical inactivity, diabetes, perimenopausal oral estrogen use, pregnancy, and childbirth (Wein, 2011). Although UI is not exclusive to the elderly population, it does occur most frequently in this group of patients, with women more affected than men. The prevalence of female incontinence is reported at 38%, increasing with age from 20% to 30% during young-adult life to almost 50% in the elderly (Anger et al., 2006). This number rises to 35% of patients in the acute care hospital setting and up to 70% of residents in long-term facilities (Burkhardt & Resin, 2013). As much as 70% of cases of UI in the elderly may be attributed to detrusor instability (Fauci et al., 2008). United States Census population projections predict that the number of American women with UI will increase 55% from 18.3 million to 28.4 million between 2010 and 2050 (Wu et al., 2009). UI should not be considered normal at any age. Up to 30% of younger community residents are affected by this disorder (Hamill-Lemay, 2012).
Current evidence indicates that UI affects 4% to 14% of younger women, 30% to 50% of those older than 60 years, and 17% of men older than 60 years (Coyne et al., 2014; Luber, 2004). There is a substantial variation in reported incidence of UI (Stewart et al., 2014). Involuntary loss of urine secondary to activity has been reported by 50% of nulliparous women 18 to 25 years of age (Fink et al., 2008). The prevalence of UI is underestimated as a result of the social stigma and assumption that UI is part of normal aging (DeMaagd et al., 2008; Lukacz et al., 2011; Markland, Richter, Fwu, Eggers, & Kusek, 2011). Of the reported cases, the incidence of UI is highest in Caucasians (7.3/100 person-years), followed by Asians (5.7/10 person-years) and African Americans (4.8/100 person-years; Townsend et al., 2010).
As previously noted, UI has both medical and psychosocial consequences. The overall cost of health care is increased for patients with UI, and the morbidity and perhaps mortality rates of these patients may also be affected. UI is not a disease, but rather a symptom of an underlying problem. Once that process has been identified, successful treatment may be chosen to improve or cure UI.
DIAGNOSTIC CRITERIA
Though definitive criteria may be elusive, the ICS urges clinicians to base diagnosis on symptomatology gathered from the history and physical examination. Depending on the type and severity of UI, patients may present with a variety of symptoms. The importance of a correct diagnosis cannot be overemphasized. A complete review of the patient’s history, including comorbidities, and investigation of reversible causes are necessary for the development of a thorough treatment plan. Urodynamic studies may assist clinicians in determining the precise cause of UI and are an important part of the diagnostic process. However, the use of urodynamic testing is not routinely found in the primary care setting (Abrams et al., 2010; Ghoniem et al., 2008).
Evaluation of UI with urodynamics provides objective data and may indicate changes in bladder function, but the clinical significance is irrelevant unless symptoms are also evaluated. Moreover, the use of urodynamic testing does not necessarily carry over into improvements in clinical outcomes (Hartmann et al., 2009). Post-void residuals >100 mL may be indicative of overflow incontinence, and >200 mL is considered inadequate and suggestive of either detrusor weakness or bladder outlet obstruction.
HISTORY AND PHYSICAL EXAMINATION
The evaluation of UI begins with the identification of its presence. If a reversible cause such as drug therapy or urinary tract infection cannot be identified, further workup for chronic UI begins. As seen in Table 30.2, the first step is gathering a complete patient history.
After the history, a physical examination helps classify the type of UI. Key aspects include urinalysis, palpation of the bladder, a neurologic examination, examination of the rectum and pelvic areas (appropriate to gender), and catheterization of the bladder (Kenton, 2014). Urinalysis may be performed to identify the presence of leukocytes, blood, or nitrites, which may be indicative of infection, a cause of reversible UI if appropriately treated. A palpable bladder is suggestive of overflow incontinence. The neurologic examination of the perineal area provides information regarding a potential neurologic cause for the UI. While doing this examination, the provider assesses sensation in the perineal area using fine touch and also observes the presence of voluntary anal sphincter tone (DuBeau et al., 2009). The rectal examination can identify fecal impaction and, in men, prostatism.
