Incontinence and Sexual Dysfunction in the Elderly

Edmund Y. Ko

Sneha S. Vaish

Donald E. Novicki

Dean M. Wingerchuk

Elliot M. Frohman

Urinary incontinence (UI) is a very common complaint among the elderly and adversely affects the lives of millions of people. The prevalence of UI is 5% to 30% of people living in the community, 40% to 70% of elderly patients in an acute hospital setting, and up to 50% of people living in nursing homes (41). Currently, the health care cost of UI exceeds $20 billion annually in the United States (33). The total lifetime costs for treatment of UI in one older adult have been estimated at $60,000 (10).

Age-related changes of bladder function play a significant role in increasing UI. The aging bladder demonstrates increases in uninhibited detrusor contractions, impaired contractility, abnormal detrusor relaxation patterns, and reduced capacity. In addition, the aging population experiences a shift in nocturnal diuresis, and the frequency of nocturia increases (69). The aging male population can suffer from benign prostatic hyperplasia (BPH) with secondary bladder changes. BPH is evident in 50% of the male population by age 50 and 80% by age 80 (13). Beyond primary changes to the genitourinary tract, elderly adults can suffer from other risk factors that contribute to UI. These include decreased mobility and manual dexterity, difficulties accessing toilets, impaired mentation, and a variety of comorbid medical conditions and multiple medications outlined in Table 16-1.

Initial evaluation of elderly patients with UI should include a comprehensive history and physical exam including a thorough “brown bag review” of all medications used by the patient. The workup should include a comprehensive physical examination, a rapid screening for cognition using the Mini-Mental State Examination, neurologic exam, and evaluation of the patient’s mobility and manual dexterity. Useful diagnostic tests include urinalysis, urine culture, urine cytology, free flow and postvoid residual by catheter or ultrasound, 72-hour voiding diary, cough stress test, and urodynamics if empirical treatment has failed. Combining information gleaned from these tests can allow identification of the cause and contributing factors leading to the UI and can help the health care team to formulate and initiate an appropriate treatment plan.

Table 16-1. UI in the Older Adult: Risk and Predisposing Factors

Comorbid Disease

Diabetes

Congestive heart failure

Degenerative joint disease

Sleep apnea

Severe constipation

Neurologic/Psychiatric

Stroke

Parkinson’s disease

Dementia-all types

Depression

Normal pressure hydrocephalus

Medication

α-Adrenergic (blockers and agonists)

Cholinergics (blockers and agonist)

Angiotensin-converting enzyme inhibitors

Calcium blockers

Diuretics

Opiates

Anticholinergics

Antidepressants/antipsychotics

Functional

Impaired cognition

Impaired mobility

Inaccessibility of toilets

Lack of caregivers

Adapted from Dubeau CE. The aging lower urinary tract.

J Urol. 2006;175:S11-S15.

BLADDER INNERVATION

An understanding of bladder innervation and physiology is required to diagnose and treat UI. The lower urinary tract is innervated by three sets of peripheral nerves involving the parasympathetic, sympathetic, and somatic nervous systems. Pelvic parasympathetic nerves arise from S2-4 of the spinal cord in a region termed the sacral parasympathetic nucleus (SPN); they
send axons through the ventral roots to peripheral ganglia in the detrusor wall where they release acetylcholine. This action facilitates voiding by excitation of the detrusor muscle and relaxation of the urethra. Lumbar sympathetic fibers arising from the lumbar spinal cord follow a path through the sympathetic chain ganglion to the inferior mesenteric ganglia and then through the hypogastric nerve to pelvic ganglia. These fibers provide noradrenergic excitatory and inhibitory input, which relaxes the detrusor and contracts the sphincteric mechanism to facilitate urine storage. Finally, somatic influences are exerted via the pudendal nerve; motoneurons to the external urethral sphincter (EUS) arise from the lateral border of the ventral horn, known as the Onuf nucleus, and contract the EUS (16).

Afferent pathways through the pelvic, hypogastric, and pudendal nerves transmit information from the lower urinary tract to the lumbosacral spinal cord. Pelvic nerve afferents monitor the volume of the bladder and amplitude of bladder contractions via myelinated A-δ and unmyelinated C axons. A-δ fibers located in the bladder smooth muscle sense bladder fullness (i.e., wall tension) and serve as low-threshold mechanoreceptors. C fibers located in the mucosa respond to both stretch (i.e., bladder volume sensors) or nociception and overdistention. C fibers are largely insensitive to normal distention. They become mechanosensitive after activation by a chemical mediator during inflammation (16).

Figure 16-1. Diagram illustrating the anatomy of the lower urinary tract and the “switchlike” function of the micturition reflex pathway. During urine storage, a low level of afferent activity activates efferent input to the urethral sphincter. A high level of afferent activity induced by bladder distention activates the switching circuit in the CNS, producing firing in the efferent pathways to the bladder, inhibition of the efferent outflow to the sphincter, and urine elimination. CNS, central nervous system. (From Walsh PC, Retik AB, Vaughan ED, et al., eds. Campbell’s Urology. 8th ed. Philadelphia: Saunders; 2002. Copyright (c) 2002 Saunders, An Imprint of Elsevier.)

REFLEX CIRCUIT

The lower urinary tract has two major functions: (a) low-pressure bladder filling and storage of urine with continence and (b) low-pressure periodic voluntary emptying. The micturition cycle is organized via a simple on-off switching circuit (Fig. 16-1) that maintains a reciprocal relationship between the urinary bladder and the urethral outlet (16). During bladder filling and urine storage, three functions must occur: (a) the bladder must continue to maintain low pressure and accommodate an increasing volume of urine, (b) the bladder outlet must remain closed, and (c) there should be an absence of abnormal bladder contractions. In contrast, during bladder emptying/voiding three things must happen: (a) the bladder must contract for an adequate magnitude and duration, (b) a concomitant lowering of resistance at the level of the smooth and striated sphincter must occur, and (c) there must be an absence of anatomic obstruction (67).

Voiding dysfunction may occur from damage to the micturition reflex at the storage level or at the elimination level. Thus, voiding dysfunction may be categorized as the failure to store urine or the failure to empty urine secondary to the bladder or the outlet (Table 16-2). In addition, a mixture of both of these classifications can exist. By extrapolating from a basic switchlike framework, many different etiologic possibilities that affect storage, emptying, or both can be defined as illustrated in Table 16-3.

Table 16-2. Functional Classification of Voiding Dysfunction

Failure to Store
	Bladder dysfunction
	Outlet dysfunction
Failure to Empty
	Bladder dysfunction
	Outlet dysfunction
Mixed Failure to Store and Empty

Table 16-3. Types of Incontinence Based on Function

Female
	Failure to Store
		Bladder dysfunction
			OAB-wet or dry
			Decreased bladder compliance
			Fistula
		Outlet dysfunction
			SI-anatomic urethral hypermobility
			Intrinsic sphincteric deficiency
	Failure to Empty
		Bladder dysfunction
			Detrusor decompensation
			Bladder denervation with hypocontractile bladder
		Outlet dysfunction
			Neurogenic sphincter dysfunction
			Iatrogenic urethral obstruction
	Combined
		Detrusor instability with hypocontractile bladder
Male
	Failure to Store
		Bladder dysfunction
			OAB-wet or dry
			OAB secondary to bladder outlet obstruction
			Decreased compliance
			Bladder decompensation with overflow incontinence
		Outlet dysfunction
			SI: iatrogenic after prostatectomy
			Neurogenic denervation
	Failure to Empty
		Bladder dysfunction
			Bladder decompensation
			Bladder denervation
		Outlet dysfunction
			Benign prostatic hyperplasia with obstruction
			Neurogenic sphincter dysfunction
	Combined
		OAB with hypocontractile bladder
		Parkinson’s disease
		Cerebrovascular accident
OAB, overactive bladder; SI, stress incontinence.
Modified from Wein AJ. Pathophysiology and classification of voiding dysfunction. In: Walsh PC, Retik AB, Vaughan ED, et al., eds. Campbell’s urology. 8th ed. Philadelphia: Saunders; 2002:887-899; and Kobashi KC, Leach GE. Bladder dysfunction and urinary incontinence. In: Noble J, Greene HL, Levinson W, et al., eds. Noble: textbook of primary care medicine. 3rd ed. St. Louis: Mosby; 2001:1409-1417.

STORAGE AND ELIMINATION PHASES OF THE BLADDER

By viewing micturition as a simple on-off circuit, adding the complexity of the afferent and efferent neural control of the urinary tract yields a complex but understandable circuit, as described below (16). Intravesical pressure measurements during bladder
filling should show constant low pressure and low levels of afferent pelvic nerve activity. The responding efferent pathways produce pudendal nerve outflow and contraction of the EUS, sympathetic nerve stimulation causing detrusor inhibition with activation of the continence mechanism, and finally, inactivation of the sacral parasympathetic outflow (Fig. 16-2A).

The initiation of micturition can be activated either voluntarily or involuntarily. The activation of micturition incites high levels of afferent pelvic nerve activity, which stimulates the brainstem micturition center. The pontine micturition center (PMC) then inhibits somatic nerve output (pudendal nerve) to cause relaxation of the EUS and inhibits sympathetic outflow (hypogastric nerve) to cause a release of inhibition on the relaxation of bladder and contraction of the urethra. The PMC stimulates parasympathetic outflow, which excites the bladder and relaxes the internal sphincter smooth muscle of the urethra. Voiding occurs by initial relaxation of the urethral sphincter, and then a few seconds later, contraction of the bladder, increase in bladder pressure, and flow of urine.

Maintenance of the voiding reflex is through ascending afferent input from the spinal cord, which may pass through the periaqueductal gray matter (PAG) before reaching the PMC (Fig. 16-2B).

Figure 16-2. Mechanism of storage and voiding reflexes. A: Storage reflexes. During the storage of urine, distention of the bladder produces low-level bladder afferent firing. Afferent firing in turn stimulates (i) the sympathetic outflow to the bladder outlet (base and urethra) and (ii) pudendal outflow to the EUS. These responses occur by spinal reflex pathways and represent “guarding reflexes,” which promote continence. Sympathetic firing also inhibits detrusor muscle and transmission in bladder ganglia. B: Voiding reflexes. At the initiation of micturition, intense vesical afferent activity activates the brainstem micturition center, which inhibits the spinal guarding reflexes (sympathetic and pudendal outflow to the urethra). The PMC also stimulates the parasympathetic outflow to the bladder and internal sphincter smooth muscle. Maintaining the voiding reflex is through ascending afferent input from the spinal cord, which may pass through the PAG before reaching the PMC. EUS, external urethral sphincter; PMC, pontine micturition center; PAG, periaqueductal gray matter. (From Walsh PC, Retik AB, Vaughan ED, et al., eds. Campbell’s Urology. 8th ed. Philadelphia: Saunders; 2002. Copyright (c) 2002 Saunders, An Imprint of Elsevier.)

PATHOPHYSIOLOGY OF VOIDING DYSFUNCTION

Dysfunction at any level of the urinary mechanism outlined in the previous section can cause loss in the regulation of voiding and result in UI. Loss of detrusor inhibition and relaxation of the internal sphincter occur, which results in uninhibited bladder contractile activity, causing urgency and UI. Injuries to the PMC or to the descending spinal pathways cause a loss of coordination between the bladder and the urinary sphincter, which results in an uninhibited contraction and a nonrelaxing urinary sphincter (detrusor sphincteric dyssynergia). This causes a high-pressure, poor emptying bladder, which eventually can decompensate and cause upper urinary tract damage. This type of dysfunction is seen with dementia, stroke, multiple sclerosis (MS), tumors, or other brain injuries. Exceptions to this framework are lesions of the internal capsule (typically strokes), which result in uninhibited and poorly sustained detrusor contractions and inadequate voiding pressure with sphincteric dysfunction.

Injuries at the level of the spinal cord can be from trauma, disk herniation, vascular lesions, MS, tumors, syringomyelia, myelitis, or iatrogenic causes. In the acute phase, they lead to a hypocontractile bladder with low pressure and large bladder capacity. Over time, these injuries lead to a loss of innervation and sphincteric spasticity and voiding dyssynergia. Bladder wall fibrosis occurs and can result in detrusor hypertrophy, high voiding pressure, ureteral reflux or obstruction leading to renal damage, and UI. Cervical spinal cord injuries may cause autonomic dysreflexia. Injuries above the level of the sympathetic outflow from the cord result in hypertensive blood pressure fluctuations, bradycardia, and sweating with stimulation of the lower urinary tract.

Pathologic lesions that occur at or below the sacral micturition center (S2-4) may be caused by spinal cord injury, damage to the anterior horn cells from poliovirus or herpes zoster, or iatrogenic causes such as radiation or surgery. These lesions are often incomplete and cause a mixture of overactive bladder (OAB) activity with weakened muscle contractility. Sphincter tone is diminished, and bladder pressure is low, but capacity is high and can lead to UI. Voiding is accomplished through straining.

Hypocontractile bladders can result from other neurologic conditions including diabetes mellitus, tabes dorsalis, pernicious anemia, and posterior spinal cord lesions. The pathology is not damage to the detrusor muscle nucleus, but rather a loss of sensory input through the afferent feedback pathway. Eventually, this may lead to a loss of neurotransmission in the dorsal horn of the cord and loss of perception in bladder filling, resulting in overstretching of the detrusor. An atonic detrusor with a large volume capacity and high residual urine may eventually occur.

Pelvic trauma may injure the nerves to the sphincter, and selective denervation can lead to an incompetent sphincter mechanism and UI. Peripheral nerve injuries can also occur with radical pelvic surgeries or radiation therapy. During pelvic surgeries, damage to the peripheral nerves may result in a bladder that cannot accommodate with filling; the smooth muscle is intact, but no central reflex organizes muscle activity, and a hypertonic bladder wall with high-pressure filling and poor storage of urine can occur. Radiation can result in denervation of the detrusor or sphincter. At the detrusor level, it can cause fibrosis and loss of compliance of the detrusor, with failure to both store and empty urine adequately.

Incomplete neural lesions can cause variable lower urinary tract dysfunction that is often not predictable based on the level of the injury. In disease processes such as MS, the neural lesions can be present at multiple levels and can confuse clinical presentations in patients (16,39,63,67).

PERIPHERAL PHARMACOLOGY

Normal human detrusor muscle has been studied pharmacologically, yielding evidence for both prejunctional and postjunctional receptors as locations of action for potential drugs. At least five different cholinergic muscarinic receptor subtypes (M1 to M5) have been cloned. M1, M4, and M5 receptor subtypes are found in the human nervous system. M2 and M3 receptors are predominate as the cholinergic receptors in the bladder smooth muscle. M2 receptors play a role in inhibition of bladder relaxation and modulation of bladder contraction in denervation injuries or spinal cord disease, whereas M3 receptors mediate direct detrusor muscle contractions. In turn, multiple muscarinic receptor antagonists have been developed and are widely prescribed for the treatment of UI (3). Antimuscarinics depress both voluntary and involuntary bladder contractions and increase total bladder capacity. However, antimuscarinics lack receptor specificity, and side effects include dry mouth, tachycardia, constipation, and blurred vision from accommodation paralysis. Such adverse events may be unpleasant or annoying for younger individuals but dangerous for the elderly.

MECHANISTIC CLASSIFICATION OF UI

Defining the overarching causes of UI can be difficult due to nonstandard terminology. However, each clinician should choose one of the classifications and
apply it to his or her practice. UI can be divided into five major categories: OAB, including both OAB wet and dry; stress incontinence (SI); overflow incontinence; functional incontinence; and mixed incontinence, which can have elements of all these categories (69). Figure 16-3 illustrates the extensive overlap between categories (2).

Figure 16-3. Urinary incontinence (UI) may be urge UI (UUI), stress UI (SUI), or mixed in any type. Overactive bladder (OAB) syndrome includes those who are wet and dry. (Adapted from Abrams P, Cardozo L, Fall M, et al. The standardisation of terminology in lower urinary tract function: report from the standardisation sub-committee of the International Continence Society. Urology. 2003;61:37-49.)

OVERACTIVE BLADDER

OAB is defined by the International Continence Society (ICS) as urgency with or without urge UI (UUI) usually associated with frequency and nocturia (2). The ICS defines urgency as “sudden compelling desire to void that is difficult to defer” (2). OAB overlaps with other subtypes of lower urinary tract symptoms (LUTS). Data from the National Overactive Bladder Evaluation study reveal that the prevalence of OAB is 16.5% of the general adult population, or approximately 33 million people in the United States. Of people meeting the criteria for OAB, only 37% of patients afflicted with OAB will experience UUI (OAB wet), whereas the remaining patients remain dry (OAB dry) (62). OAB has a significant impact on quality of life, affecting physical activity, psychological well-being, social activity, sexual activity, occupational productivity, and domestic logistics (38).

Many different causes of OAB have been described, including neurogenic and myogenic detrusor damage, bladder urothelium causes, and neurotransmitter abnormalities. In the neurogenic circumstance, the micturition reflex is disturbed; baseline bladder storage function occurs through relaxation of the bladder, activation of the sphincter, and deactivation of the parasympathetic neural stimulation. Suprapontine lesions can affect the reflex and cause increased lower urinary tract afferent nerve input, loss of peripheral inhibition, and enhancement of excitatory neurotransmission in the micturition reflex pathway (18). Common causes include stroke, Parkinson’s disease, spinal cord injury, MS, and transverse myelitis.

The myogenic situation is applicable to individuals with bladder outlet obstruction. Over time, the increase in intravesical pressure causes partial neurologic denervation of the bladder smooth muscle. The smooth muscle denervation causes an increase in the number of spontaneous actions potentials, which in turn propagate from cell to cell causing “micromotions” in the detrusor. These micromotions increase vesicular pressure and activate the afferent receptors, and the feedback to the central nervous system (CNS) will cause the sensations associated with OAB (68).

Bladder urothelial-based causes occur when bladder distention increases the amount of acetylcholine released from the urothelium; this feedback to the CNS creates a sensation of urgency, which drives the OAB (19). A final hypothesis in patient with OAB is an abnormal leak of acetylcholine from efferent nerve fibers, which causes micromotions in the bladder smooth muscle that stimulate the CNS, recreating the sense of urgency in OAB (3).

The management of OAB includes a variety of treatments, ranging from noninvasive management with behavior modifications to pharmacologic therapy to treatment as invasive as surgery. Behavior modification is initially education for the patient about the micturition reflex and dysfunction and includes the use of a voiding diary to better elucidate the patient’s voiding habits. Simple solutions include adjustment of fluid intake (time, quantity, or type) and a timed voiding regimen at predetermined intervals. Pelvic floor exercise and biofeedback can be introduced to abort unwanted sensation of urgency. Pharmacologic treatments include five antimuscarinics agents: darifenacin (Enablex), oxybutynin (Ditropan), solifenacin (VesiCare), tolterodine (Detrol), and chlordiazepoxide (Tropium); these drugs are currently approved for treatment of OAB in the United States. Studies of these drugs have shown similar efficacy (70% to 75%) in decreasing episodes of UUI (68).

Novel trends for treatment of OAB include injections of botulinum toxin (BTX) into the bladder or the urethra or sacral nerve stimulation (SNS) for those
who are refractory to antimuscarinic therapy. BTX causes paralysis by inhibiting the release of acetylcholine from the motor nerve into the neuromuscular junction, leaving the bladder unable to contract. The temporary relaxation generally lasts between 3 and 6 months before full muscle strength returns (25). Neuromodulation through SNS involves percutaneous surgical placement of electrodes through the sacral foramen, typically S3, under local anesthesia. After a trial of 3 to 7 days, the temporary leads can be internalized with a permanent implant, currently produced under the name InterStim therapy. The electrical stimulation modulates neural reflexes to impact the bladder and pelvic floor to reduce the UUI. Brazzelli et al. (11) systematically reviewed the efficacy and safety of SNS for severe UUI, and results show that 67% of patients become dry or achieve a 50% improvement in symptoms after implantation.

STRESS INCONTINENCE

In women, stress UI is defined as anatomic incontinence secondary to the hypermobility of the vesicourethral segment due to pelvic floor weakness (63). Pregnancy and childbirth can affect the lower genitourinary tract through anatomic changes, denervation injury, or traumatic injury. Up to one third of premenopausal women and almost one half of postmenopausal women experience some type of pelvic floor disorder in their lifetime, including UI, anal incontinence, or pelvic organ prolapse. Pelvic organ prolapse is the herniation of the pelvic organs to or through the vaginal opening. One in nine women will have surgery for pelvic floor disorders by age 80, and 30% will require reoperation. Symptoms of pelvic organ prolapse include bulge sensation in the perineum, urinary or bowel symptoms, sexual symptoms, and pain (56). In neurologically healthy men, SI is very unusual and occurs only after lower urinary tract surgery, such as transurethral resection of the prostate (TURP) or radical prostatectomy (1). Symptoms generally present as involuntary loss of urine when a patient laughs, coughs, sneezes, changes position, or performs an activity that increases intra-abdominal pressure.

Standard nonsurgical treatments include medications, biofeedback, pelvic floor exercises, behavioral therapy, periurethral injections, and corrective surgery. Pharmacologic agents include alpha-agonists, vaginal or oral estrogen, and tricyclic antidepressants. Pharmacologic intervention usually does not lead to a cure and is often combined with the behavioral therapy described earlier (55,58). Periurethral injections have been done with a variety of different substances, including collagen, fat, Teflon, and silicone polymers, and provide reasonably good short-term symptomatic improvement. The results are not long lasting in most individuals.

Surgical techniques to correct SI in female patients include pubovaginal slings, retropubic suspension, needle suspension, and anterior colporrhaphy. The history of bladder suspensions began with the Marshall-Marchetti-Krantz and Burch procedures (63). However, in the last 20 years, pubovaginal and needle suspension have become popular because of the ease and approach of the procedure. Slings are placed beneath the proximal urethra and bladder to provide a “hammock” for support and direct urethral compression. Pubovaginal slings have been created from a variety of materials, including synthetic, autologous, allogeneic, and xenogenic tissues (39).

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