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CHAPTER 37 Disorders of Urine Elimination CONTROL OF URINE ELIMINATION Bladder Structure Neural Control of Bladder Function Spinal Cord Centers Pontine Micturition Center Cortical and Subcortical Centers Micturition and Maintenance of Continence Pharmacology of Micturition Continence in Children Diagnostic Methods of Evaluating Bladder Function Physical Examination Laboratory and Radiologic Studies Ultrasound Bladder Scan Urodynamic Studies ALTERATIONS IN BLADDER FUNCTION Urinary Obstruction and Stasis Compensatory and Decompensatory Changes Treatment Neurogenic Bladder Disorders Spastic Bladder: Failure to Store Urine Flaccid Bladder: Failure to Empty Urine Nonrelaxing External Sphincter Treatment Urinary Incontinence Stress Incontinence Overactive Bladder/Urge Incontinence Overflow Incontinence Other Causes of Incontinence Diagnosis and Treatment Special Needs of Elderly Persons CANCER OF THE BLADDER Etiology and Pathophysiology Manifestations Diagnosis and Treatment A lthough the kidneys control the formation of urine and regulate the composition of body fluids, it is the bladder that stores urine and controls its elimination from the body. Alterations in the storage and expulsion functions of the bladder can result in incontinence, with its accompanying social and hygienic problems, or ob- struction of urinary flow, which has deleterious effects on ureteral and, ultimately, renal function. The discussion in this chapter focuses on normal control of urine elimination, urinary obstruction and stasis, neurogenic bladder, incontinence, and bladder cancer. Urinary tract infections are discussed in Chapter 35. Control of Urine Elimination After completing this section of the chapter, you should be able to meet the following objectives: ✦ Trace the innervation of the bladder and control of micturition from the detrusor muscle and external sphincter, the micturition centers in the sacral and thoracolumbar cord, the pontine micturition center, and the cerebral cortex ✦ Explain the mechanism of low-pressure urine storage in the bladder ✦ List at least three classes of autonomic drugs and explain their potential effect on bladder function ✦ Describe at least three urodynamic studies that can be used to assess bladder function The bladder, also known as the urinary vesicle, is a freely movable organ located behind the pelvic bone in the male and in front of the vagina in the female. It consists of two parts: the fundus, or body, and the neck, or posterior urethra. In the man, the urethra continues anteriorly through the penis. Urine passes from the kidneys to the bladder through the ureters, which are 4 to 5 mm in diameter and approximately 30 cm long. The ureters enter the bladder bilaterally at a location toward its base and close to the urethra (Fig. 37-1). The triangular area that is bounded by the ureters and the urethra is called the trigone. There are no valves at the ureteral openings, but as the pressure of the urine in the bladder rises, the ends of the ureters are compressed against the bladder wall to prevent the backflow of urine. BLADDER STRUCTURE The bladder is composed of four layers. The first is an outer serosal layer, which covers the upper surface and is contin851 852 UNIT VIII Epithelium when bladder is empty Renal Function Epithelium when bladder is full Detrusor muscle Ureters Trigone Internal sphincter External sphincter FIGURE 37-1 Diagram of the bladder, showing the detrusor muscle, ureters, trigone area, and urethral orifice. Note the flattening of epithelial cells when the bladder is full and the wall is stretched. uous with the peritoneum. The second is a network of smooth muscle fibers called the detrusor muscle. The third is a submucosal layer of loose connective tissue, and the fourth is an inner mucosal lining of transitional epithelium. The tonicity of the urine often is quite different from that of the blood, and the transitional epithelial lining of the bladder acts as an effective barrier to prevent the passage of water between the bladder contents and the blood. The inner layers of the bladder form smooth folds, or rugae. As the bladder expands during filling, these rugae spread out to form a single layer without disrupting the integrity of the epithelial lining. The detrusor muscle is the muscle of micturition (passage of urine). When it contracts, urine is expelled from the bladder. The abdominal muscles play a secondary role in micturition. Their contraction increases intra-abdominal pressure, which further increases intravesicular pressure. Muscles in the bladder neck, sometimes referred to as the internal sphincter, are a continuation of the detrusor muscle. They run down obliquely behind the proximal urethra, forming the posterior urethra in males and the entire urethra in females. When the bladder is relaxed, these circular muscle fibers are closed and act as a sphincter. When the detrusor muscle contracts, the sphincter is pulled open by the changes that occur in bladder shape. In the female, the urethra (2.5 to 3.5 cm) is shorter than in the male (16.5 to 18.5 cm), and usually affords less resistance to urine outflow. Another muscle important to bladder function is the external sphincter, a circular muscle composed of striated muscle fibers that surrounds the urethra distal to the base of the bladder. The external sphincter operates as a reserve mechanism to stop micturition when it is occurring and to maintain continence in the face of unusually high bladder pressure. The skeletal muscle of the pelvic floor also contributes to the support of the bladder and the maintenance of continence. NEURAL CONTROL OF BLADDER FUNCTION The control of bladder emptying is unique in that it involves both involuntary autonomic nervous system (ANS) reflexes and some voluntary control. The excitatory input to the bladder that causes bladder emptying is controlled by the parasympathetic nervous system. The sympathetic nervous system relaxes the bladder smooth muscle. There are three main levels of neurologic control for bladder function: the spinal cord reflex centers, the micturition center in the pons, and the cortical and subcortical centers. Spinal Cord Centers BLADDER FUNCTION ➤ The functions of the bladder are storage and emptying of urine. ➤ The control of the storage and emptying functions of the bladder involves both involuntary (autonomic nervous system) and voluntary (somatic nervous system) control. ➤ The parasympathetic nervous system promotes bladder emptying. It produces contraction of the smooth muscle of the bladder wall and relaxation of the internal sphincter. ➤ The sympathetic nervous system promotes bladder filling. It produces relaxation of the smooth muscle of the bladder wall and contraction of the internal sphincter. ➤ The striated muscles in the external sphincter and pelvic floor, which are innervated by the somatic nervous system, provide for the voluntary control of urination and maintenance of continence. The centers for reflex control of micturition are located in the sacral (S1 through S4) and thoracolumbar (T11 through L2) segments of the spinal cord1–3 (Fig. 37-2). The parasympathetic lower motor neurons (LMNs) for the detrusor muscle of the bladder are located in the sacral segments of the spinal cord; their axons travel to the bladder by way of the pelvic nerve. LMNs for the external sphincter also are located in the sacral segments of the spinal cord. These LMNs receive their control from the motor cortex by way of the corticospinal tract and send impulses to the external sphincter through the pudendal nerve. The bladder neck and trigone area of the bladder, because of their different embryonic origin, receive sympathetic outflow from the thoracolumbar (T11 to L2) segments of the spinal cord. The seminal vesicles, ampulla of the vas, and vas deferens also receive sympathetic innervation from the thoracolumbar segments of the cord. The afferent input from the bladder and urethra is carried to the central nervous system (CNS) by means of fibers that travel with the parasympathetic (pelvic), so- CHAPTER 37 Afferent fibers Efferent motor Efferent inhibitory Sympathetic neurons T12 L1 L2 Hypogastric nerve Parasympathetic pelvic nerves S1 S2 S3 S3 S4 Detrusor muscle Internal sphincter External sphincter 853 Micturition and Maintenance of Continence T11 S2 Disorders of Urine Elimination Somatic pudendal nerve FIGURE 37-2 Nerve supply to the bladder and the urethra. matic (pudendal), and sympathetic (hypogastric) nerves. The pelvic nerve carries sensory fibers from the stretch receptors in the bladder wall; the pudendal nerve carries sensory fibers from the external sphincter and pelvic muscles; and the hypogastric nerve carries sensory fibers from the trigone area.3 Pontine Micturition Center The immediate coordination of the normal micturition reflex occurs in the micturition center in the pons, facilitated by descending input from the forebrain and ascending input from the reflex centers in the spinal cord1,2 (Fig. 37-3). This center is thought to coordinate the activity of the detrusor muscle and the external sphincter. As bladder filling occurs, ascending spinal afferents relay this information to the micturition center, which also receives important descending information from the forebrain concerning behavioral cues for bladder emptying. Descending pathways from the pontine micturition center produce coordinated inhibition or relaxation of the external sphincter. Disruption of pontine control of micturition, as in spinal cord injury, results in uninhibited spinal reflex-controlled contraction of the bladder without relaxation of the external sphincter, a condition known as detrusor-sphincter dyssynergia. Cortical and Subcortical Centers Cortical brain centers enable inhibition of the micturition center in the pons and conscious control of urination. Neural influences from the subcortical centers in the basal ganglia, which are conveyed by extrapyramidal pathways, modulate the contractile response. They modify and delay the detrusor contractile response during filling and then modulate the expulsive activity of the bladder to facilitate complete emptying. To maintain continence, or retention of urine, the bladder must function as a low-pressure storage system; the pressure in the bladder must remain lower than urethral pressure. To ensure that this condition is met, the increase in intravesicular pressure that accompanies bladder filling is almost imperceptible. An increase in bladder volume from 10 to 400 mL may be accompanied by only a 5 cm H2O increase in pressure.1 Sustained elevations in intravesicular pressures (>40 to 50 cm H2O) often are associated with vesicoureteral reflux (i.e., backflow of urine from the bladder into the ureter) and the development of ureteral dilatation (see Chapter 35). Although the pressure in the bladder is maintained at low levels, sphincter pressure remains high (45 to 65 cm H2O) as a means of preventing loss of urine as the bladder fills. Micturition, or the act of bladder emptying, involves both sensory and motor functions associated with bladder emptying. When the bladder is distended to 150 to 250 mL in the adult, the sensation of fullness is transmitted to the spinal cord and then to the cerebral cortex, allowing for conscious inhibition of the micturition reflex.4 During the act of micturition, the detrusor muscle of the bladder fundus and bladder neck contract down on the urine; the ureteral orifices are forced shut; the bladder neck is widened and shortened as it is pulled up by the globular muscles in the bladder fundus; the resistance of the internal sphincter in the bladder neck is decreased; and the external sphincter relaxes as urine moves out of the bladder. Pharmacology of Micturition The ANS and its neuromediators play a central role in micturition. Parasympathetic innervation of the bladder is mediated by the neurotransmitter acetylcholine. Two types of cholinergic receptors affect various aspects of micturition: nicotinic and muscarinic. Nicotinic (N) receptors are found in the synapses between the preganglionic and postganglionic neurons of the sympathetic and the parasympathetic system, as well as in the neuromuscular end plates of the striated muscle fibers of the external sphincter and pelvic muscles. Muscarinic (M) receptors are found in the postganglionic parasympathetic endings of the detrusor muscle. Several subtypes of M receptors have been identified. The M2 and M3 receptors appear predominantly to mediate detrusor contraction and internal sphincter contraction. The M3 receptor also mediates salivary secretion and bowel activity.5 The identification of receptor subtypes has facilitated the development of medications that selectively target bladder structures while minimizing other, undesired effects. Although sympathetic innervation is not essential to the act of micturition, it allows the bladder to store a large volume without the involuntary escape of urine—a mechanism that is consistent with the fight-or-flight function subserved by the sympathetic nervous system. The bladder is supplied with α1- and β2-adrenergic receptors. The β2adrenergic receptors are found in the detrusor muscle; they produce relaxation of the detrusor muscle, increasing the bladder volume at which the micturition reflex is triggered. 854 UNIT VIII Renal Function Urine storage Bladder emptying Cortical facilitation Cerebral cortex Coordination of micturition motor function Pontine micturition center Thoracolumbar cord (T11-L2) Inhibition somatic neurons Stimulation parasympathetic neurons Coordination of bladder storage functions Stimulation sympathetic neurons Stimulation somatic neurons Sacral cord (S1-S3) Pelvic nerve Pudendal nerve Relaxation of external sphincter Cortical inhibition Detrusor muscle Bladder Contraction of detrusor muscle External sphincter and pelvic muscles Relaxation of detrusor muscle Contraction of external sphincter FIGURE 37-3 Pathways and central nervous system centers involved in the control of bladder (left) emptying and (right) storage functions. Efferent pathways for micturition (left) and urine storage (right). The α1-adrenergic receptors are found in the trigone area, including the intramural ureteral musculature, bladder neck, and internal sphincter. The activation of α1 receptors produces contraction of these muscles. Sympathetic activity ceases when the micturition reflex is activated. During male ejaculation, which is mediated by the sympathetic nervous system, the musculature of the trigone area and that of the bladder neck and prostatic urethra contract and prevent the backflow of seminal fluid into the bladder. Because of their effects on bladder function, drugs that selectively activate or block ANS outflow or receptor activity can alter urine elimination. Table 37-1 describes the action of drug groups that can impair bladder function or can be used in the treatment of micturition disorders. Many of the nonprescription cold preparations contain α-adrenergic agonists and antihistamine agents that have anticholinergic properties. These drugs can cause urinary retention. Many of the antidepressant and antipsychotic drugs also have anticholinergic actions that influence urination. Continence in Children In infants and young children, micturition is an involuntary act that is triggered by a spinal cord reflex; when the bladder fills to a given capacity, the detrusor muscle contracts, and the external sphincter relaxes. As the child grows, the bladder gradually enlarges, with an increase in capacity, in ounces, that approximates the age of the child plus 2.6 This formula applies up to ages 12 to 14 years. As the bladder grows and increases in capacity, the tone of the external sphincter muscle increases. Toilet training begins at about 2 to 3 years of age when the child becomes conscious of the need to urinate. Conscious control of bladder function depends on (1) normal bladder growth, (2) myelination of the ascending afferents that signal awareness of bladder filling, (3) development of cortical control and descending communication with the sacral micturition center, (4) ability to consciously tighten the external sphincter to prevent incontinence, (5) and motivation of the child to stay dry. Girls typically achieve continence before boys, CHAPTER 37 TABLE 37-1 Disorders of Urine Elimination 855 Action of Drug Groups on Bladder Function Function Drug Groups Mechanism of Action Detrusor Muscle Increased tone and contraction Cholinergic drugs Stimulate parasympathetic receptors that cause detrusor contraction Block β2 receptors that produce detrusor muscle relaxation Block the muscarinic receptors that cause detrusor muscle contraction May interfere with influx of calcium to support contraction of detrusor smooth muscle Inhibition of detrusor muscle relaxation during filling Decreased tone β2-Adrenergic–blocking drugs Anticholinergic drugs and drugs with an anticholinergic action Calcium channel–blocking drugs Internal Bladder Sphincter Increased tone α1-Adrenergic agonists Decreased tone α1-Adrenergic–blocking drugs External Sphincter Decreased tone Skeletal muscle relaxants and bowel control is typically achieved before bladder control. By 5 years of age, 90% to 95% of children are continent during the day and 80% to 85% are continent at night.6 DIAGNOSTIC METHODS OF EVALUATING BLADDER FUNCTION Bladder structure and function can be assessed by a number of methods.7 Reports or observations of frequency, hesitancy, straining to urinate or void, and a weak or interrupted stream are suggestive of outflow obstruction. Palpation and percussion provide information about bladder distention. Physical Examination Postvoid residual (PVR) urine volume provides information about bladder emptying. It can be estimated by abdominal palpation and percussion. Catheterization and ultrasonography can be used to obtain specific measurements of PVR. A PVR value of less than 50 mL is considered adequate bladder emptying, and more than 200 mL indicates inadequate bladder emptying.8 Pelvic examination is used in women to assess perineal skin condition, perivaginal muscle tone, genital atrophy, pelvic prolapse (e.g., cystocele, rectocele, uterine prolapse), pelvic mass, or other conditions that may impair bladder function. Bimanual examination (i.e., pelvic and abdominal palpation) can be used to assess PVR volume. Rectal examination is used to test for perineal sensation, sphincter tone, fecal impaction, and rectal mass. It is used to assess the contour of the prostate in men. Laboratory and Radiologic Studies Urine tests provide information about kidney function and urinary tract infections. The presence of bacteriuria or Activate α1 receptors that produce contraction of the smooth muscle of the internal sphincter Block contraction of the smooth muscle of the internal sphincter Decrease the tone of the external sphincter by acting at the level of the spinal cord or by interfering with release of calcium in muscle fiber pyuria suggests urinary tract infection and the possibility of urinary tract obstruction. Blood tests (i.e., blood urea nitrogen and creatinine) provide information about renal function. Bladder structures can be visualized indirectly by taking x-ray films of the abdomen and by using excretory urography (which involves the use of a radiopaque dye [see Fig. 37-1]), computed tomographic (CT) scanning, magnetic resonance imaging (MRI), or ultrasonography. Cystoscopy enables direct visualization of the urethra, bladder, and ureteral orifices. Ultrasound Bladder Scan The ultrasound bladder scan provides a noninvasive method for estimating bladder volume.9 The device measures ultrasonic reflections to differentiate the urinary bladder from the surrounding tissue. A computer system calculates and displays bladder volume. The device can be used to determine the need for catheterization, for evaluation and diagnosis of urinary retention, to measure PVR volumes, and for facilitating volume-dependent or timedependent catheterization or toileting programs. Urodynamic Studies Urodynamic studies are used to study bladder function and voiding problems. Three aspects of bladder function can be assessed by urodynamic studies: bladder, urethral, and intra-abdominal pressure changes; characteristics of urine flow; and the activity of the striated muscles of the external sphincter and pelvic floor. Specific urodynamic tests include uroflowmetry, cystometry, urethral pressure profile, and sphincter electromyography (EMG). It often is advantageous to evaluate several components of bladder function simultaneously. 856 UNIT VIII Renal Function Uroflowmetry. Uroflowmetry measures the flow rate (milliliters per minute) during urination.7 It commonly is done using a weight-recording device located at the bottom of a commode receptacle unit. As the person being tested voids, the weight of the commode receptacle unit increases. This weight change is electronically recorded and then analyzed using weight (converted to milliliters) and time. Cystometry. Cystometry is used to measure bladder pressure during filling and voiding. It provides valuable information about total bladder capacity, intravesicular pressures during bladder filling, the ability to perceive bladder fullness and the desire to urinate, the ability of the bladder to contract and sustain a contraction, uninhibited bladder contractions, and the ability to inhibit urination. The test can be done by allowing physiologic filling of the bladder with urine and recording intravesicular pressure throughout a voiding cycle, or by filling the bladder with water and measuring intravesicular pressure against the volume of water instilled into the bladder.7 In a normally functioning bladder, the sensation of bladder fullness is first perceived when the bladder contains 100 to 200 mL of urine while bladder pressure remains constant at approximately 8 to 15 cm H2O. The desire to void occurs when the bladder is full (normal capacity is approximately 400 to 500 mL). At this point, a definite sensation of fullness occurs, the pressure rises sharply to 40 to 100 cm H2O, and voiding occurs around the catheter.7 Urinary continence requires that urethral pressure exceed bladder pressure. Bladder pressure usually rises 30 to 40 cm H2O during voiding. If the urethral resistance is high because of obstruction, greater pressure is required, a condition that can be detected by cystometry. Urethral Pressure Profile. The urethral pressure profile is used to evaluate the intraluminal pressure changes along the length of the urethra with the bladder at rest.7 It provides information about smooth muscle activity along the length of the urethra. This test can be done using the infusion method (most commonly used), the membrane catheter method, or the microtip transducer. The infusion method involves the insertion of a small double-lumen urethral catheter, followed by the infusion of water into the bladder and measurement of the changes in urethral pressure as the catheter is slowly withdrawn. Sphincter Electromyography. Sphincter EMG allows the activity of the striated (voluntary) muscles of the perineal area to be studied. Activity is recorded using an anal plug electrode, a catheter electrode, adhesive skin electrodes, or needle electrodes.7 Electrode placement is based on the muscle groups that need to be tested. The test usually is done along with urodynamic tests such as the cystometrogram and uroflow studies. In summary, although the kidneys function in the formation of urine and the regulation of body fluids, it is the bladder that stores and controls the elimination of urine. Micturition is a function of the peripheral ANS, subject to facilitation or inhibition from higher neurologic centers. The parasympathetic nervous system controls the motor function of the bladder detrusor muscle and the tone of the internal sphincter; its cell bodies are located in the sacral spinal cord and communicate with the bladder through the pelvic nerve. Efferent sympathetic control originates at the level of segments T11 through L2 of the spinal cord and produces relaxation of the detrusor muscle and contraction of the internal sphincter. Skeletal muscle found in the external sphincter and the pelvic muscles that support the bladder are supplied by the pudendal nerve, which exits the spinal cord at the level of segments S2 through S4. The micturition center in the brain stem coordinates the action of the detrusor muscle and the external sphincter, whereas cortical centers permit conscious control of micturition. Bladder function can be evaluated using urodynamic studies that measure bladder, urethral, and abdominal pressures; urine flow characteristics; and skeletal muscle activity of the external sphincter. Alterations in Bladder Function After completing this section of the chapter, you should be able to meet the following objectives: ✦ Describe the causes of and compensatory changes that occur with urinary tract obstruction ✦ Differentiate lesions that produce storage dysfunction ✦ ✦ ✦ ✦ ✦ associated with spastic bladder from those that produce emptying dysfunction associated with flaccid bladder in terms of the level of the lesions and their effects on bladder function Cite the pathology and causes of nonrelaxing external sphincter Describe methods used in treatment of neurogenic bladder Define incontinence and list the categories of this condition List the treatable causes of incontinence in the elderly Describe behavioral, pharmacologic, and surgical methods used in treatment of incontinence Alterations in bladder function include urinary obstruction with retention or stasis of urine and urinary incontinence with involuntary loss of urine. Although the two conditions have almost opposite effects on urination, they can have similar causes. Both can result from structural changes in the bladder, urethra, or surrounding organs or from impairment of neurologic control of bladder function. URINARY OBSTRUCTION AND STASIS In lower urinary tract obstruction and stasis, urine is produced normally by the kidneys but is retained in the bladder. Obstructions are classified according to cause (congenital or acquired), degree (partial or complete), duration (acute or chronic), and level (upper or lower urinary tract).10 Because it has the potential to produce vesicoureteral reflux and cause kidney damage, urinary obstruction and stasis is a serious disorder. CHAPTER 37 Congenital narrowing of the external meatus (i.e., meatal stenosis) is more common in boys, and obstructive disorders of the posterior urethra are more common in girls. Another common cause of congenital obstruction is the damage to sacral nerves that occurs in spina bifida and meningomyelocele. The acquired causes of lower urinary tract obstruction and stasis are numerous. In males, the most important cause of urinary obstruction is external compression of the urethra caused by the enlargement of the prostate gland. Gonorrhea and other sexually transmitted diseases contribute to the incidence of infection-produced urethral strictures. Bladder tumors and secondary invasion of the bladder by tumors arising in structures that surround the bladder and urethra can compress the bladder neck or urethra and cause obstruction. Constipation and fecal impaction can compress the urethra and produce urethral obstruction. This can be a particular problem in elderly persons. Compensatory and Decompensatory Changes The body compensates for the obstruction of urine outflow with mechanisms designed to prevent urine retention. These mechanisms can be divided into two stages: a compensatory stage and a decompensatory stage.10 The degree to which these changes occur and their effect on bladder structure and urinary function depend on the extent of the obstruction, the rapidity with which it occurs, and the presence of other contributing factors, such as neurologic impairment and infection. During the early stage of obstruction, the bladder begins to hypertrophy and becomes hypersensitive to afferent stimuli arising from bladder filling. The ability to suppress urination is diminished, and bladder contraction can become so strong that it virtually produces bladder spasm. There is urgency, sometimes to the point of incontinence, and frequency during the day and at night. With continuation and progression of the obstruction, compensatory changes begin to occur. There is further hypertrophy of the bladder muscle, the thickness of the bladder wall may double, and the pressure generated by de- Disorders of Urine Elimination 857 trusor contraction can increase from a normal 20 to 40 cm H2O to 50 to 100 cm H2O to overcome the resistance from the obstruction. As the force needed to expel urine from the bladder increases, compensatory mechanisms may become ineffective, causing muscle fatigue before complete emptying can be accomplished. After a few minutes, voiding can again be initiated and completed, accounting for the frequency of urination. The inner bladder surface forms smooth folds. With continued outflow obstruction, this smooth surface is replaced with coarsely woven structures (i.e., hypertrophied smooth muscle fibers) called trabeculae. Small pockets of mucosal tissue, called cellules, commonly develop between the trabecular ridges. These pockets form diverticula when they extend between the actual fibers of the bladder muscle (Fig. 37-4). Because the diverticula have no muscle, they are unable to contract and expel their urine into the bladder, and secondary infections caused by stasis are common. Along with hypertrophy of the bladder wall, there is hypertrophy of the trigone area and the interureteric ridge, which is located between the two ureters. This causes backpressure on the ureters, the development of hydroureters (i.e., dilated, urine-filled ureters), and eventually, kidney damage. Stasis of urine predisposes to urinary tract infections. When compensatory mechanisms no longer are effective, signs of decompensation begin to occur. The period of detrusor muscle contraction becomes too short to completely expel the urine, and residual urine remains in the bladder. At this point, the symptoms of obstruction— frequency of urination, hesitancy, need to strain to initiate NEUROGENIC BLADDER DISORDERS ➤ Neurogenic disorders of the bladder commonly are manifested by a spastic bladder dysfunction, in which there is failure to store urine, or as flaccid bladder dysfunction, in which bladder emptying is impaired. ➤ Spastic bladder dysfunction results from neurologic lesions above the level of the sacral cord that allow neurons in the micturition center to function reflexively without control from higher central nervous system centers. ➤ Flaccid bladder dysfunction results from neurologic disorders affecting the motor neurons in the sacral cord or peripheral nerves that control detrusor muscle contraction and bladder emptying. FIGURE 37-4 Destructive changes of the bladder wall with development of diverticula caused by benign prostatic hypertrophy. 858 UNIT VIII Renal Function urination, a weak and small stream, and termination of the stream before the bladder is completely emptied— become pronounced. With progressive decompensation, the bladder may become severely overstretched with residual urine volume of 1000 to 3000 ml.10 At this point, it loses its power of contraction and overflow incontinence occurs. The signs of urine retention are summarized in Chart 37-1. interrupted at any level. It can be interrupted at the level of the peripheral nerves that connect the bladder to the reflex micturition center in the sacral cord, the ascending and descending tracts in the spinal cord, the pontine micturition center, or the cortical centers that are involved in voluntary control of micturition.11,12 Neurogenic disorders of bladder function commonly are manifested in one of two ways: failure to store urine (spastic bladder dysfunction) or failure to empty (flaccid bladder dysfunction).11 Spastic bladder dysfunction usually results from neurologic lesions located above the level of the sacral micturition reflexes, whereas flaccid bladder dysfunction results from lesions at the level of sacral reflexes or the peripheral nerves that innervate the bladder. In addition to disorders of detrusor muscle function, disruption of micturition occurs when the neurologic control of external sphincter function is disrupted. Some disorders, such as stroke and Parkinson’s disease, may affect both the storage and emptying functions of the bladder. Table 37-2 describes the characteristics of neurogenic bladder according to the level of the lesion. Treatment Spastic Bladder: Failure to Store Urine CHART 37-1 Signs of Outflow Obstruction and Urine Retention Bladder distention Hesitancy Straining when initiating urination Small and weak stream Frequency Feeling of incomplete bladder emptying Overflow incontinence The immediate treatment of lower urinary obstruction and stasis is directed toward relief of bladder distention. This usually is accomplished through urinary catheterization (discussed later in this chapter). Constipation or fecal impaction should be corrected. Long-term treatment is directed toward correcting the problem causing the obstruction. NEUROGENIC BLADDER DISORDERS The urinary bladder is unique in that it is probably the only autonomically innervated visceral organ that is under CNS control. The neural control of bladder function can be TABLE 37-2 Failure to store urine results from conditions that cause reflex bladder spasm and a decrease in bladder volume. It commonly is caused by conditions that produce partial or extensive neural damage above the micturition reflex center in the sacral cord (see Fig. 37-3). As a result, bladder function is regulated by segmental reflexes, without control from higher brain centers. The degree of bladder spasticity and dysfunction depends on the level and extent of neurologic dysfunction. Usually, both the ANS neurons controlling bladder function and the somatic neurons controlling the function of the striated muscles in the external sphincter are affected. In some cases, there is a detrusor- Types and Characteristics of Neurogenic Bladder Level of Lesion Change in Bladder Function Common Causes Sensory cortex, motor cortex, or corticospinal tract Loss of ability to perceive bladder filling; low-volume, physiologically normal micturition that occurs suddenly and is difficult to inhibit Detrusor contractions are elicited suddenly without warning and are difficult to control; bladder contraction is shorter than normal and does not produce full bladder emptying Storage reflexes are provoked during filling, and external sphincter responses are heightened; uninhibited bladder contractions occur at a lower volume than normal and do not continue until the bladder is emptied; antagonistic activity occurs between the detrusor muscle and the external sphincter Areflexic bladder fills but does not contract; loss of external sphincter tone occurs when the lesion affects the α-adrenergic motor neurons or pudendal nerve Increased filling and impaired sphincter control cause increased intravesicular pressure Bladder overfilling occurs owing to a loss of ability to perceive bladder filling Stroke and advanced age Basal ganglia or extrapyramidal tract Pontine micturition center or communicating tracts in the spinal cord Sacral cord or nerve roots Pelvic nerve Autonomic peripheral sensory pathways Parkinson’s disease Spinal cord injury Injury to sacral cord or spinal roots Radical pelvic surgery Diabetic neuropathies, multiple sclerosis CHAPTER 37 sphincter dyssynergia with uncoordinated contraction and relaxation of the detrusor and external sphincter muscles. The most common causes of spastic bladder dysfunction are spinal cord lesions such as spinal cord injury, herniated intervertebral disk, vascular lesions, tumors, and myelitis. Other neurologic conditions that affect voiding are stroke, multiple sclerosis, and brain tumors. Bladder Dysfunction Caused by Spinal Cord Injury. One of the most common types of spinal cord lesions is spinal cord injury (see Chapter 51). The immediate and early effects of spinal cord injury on bladder function are quite different from those that follow recovery from the initial injury. During the period immediately after spinal cord injury, a state of spinal shock develops, during which all the reflexes, including the micturition reflex, are depressed. During this stage, the bladder becomes atonic and cannot contract. Catheterization is necessary to prevent injury to urinary structures associated with overdistention of the bladder. Aseptic intermittent catheterization is the preferred method of catheterization. Depression of reflexes lasts from a few weeks to 6 months (usually 2 to 3 months), after which the spinal reflexes return and become hyperactive. After the acute stage of spinal cord injury, the micturition response changes from a long-tract reflex to a segmental reflex. Because the sacral reflex arc remains intact, stimuli generated by bladder stretch receptors during filling produce frequent spontaneous contractions of the detrusor muscle. This creates a small, hyperactive bladder subject to high-pressure and short-duration uninhibited bladder contractions. Voiding is interrupted, involuntary, or incomplete. Dilation of the internal sphincter and spasticity of the external sphincter and perineal muscles innervated by upper motoneurons occur, producing resistance to bladder emptying. Hypertrophy of the trigone develops, often leading to vesicoureteral reflux and risk for renal damage. Spastic bladder due to spinal cord injuries at the cervical level is often accompanied by a condition known as autonomic hyperreflexia (see Chapter 51). Because the injury occurs above the CNS control of sympathetic reflexes in the spinal cord, severe hypertension, bradycardia, and sweating can be triggered by insertion of a catheter or mild overdistention of the bladder. Uninhibited Neurogenic Bladder. A mild form of reflex neurogenic bladder, sometimes called uninhibited bladder, can develop after a stroke, during the early stages of multiple sclerosis, or as a result of lesions located in the inhibitory centers of the cortex or the pyramidal tract. With this type of disorder, the sacral reflex arc and sensation are retained, the urine stream is normal, and there is no residual urine. Bladder capacity is diminished, however, because of increased detrusor muscle tone and spasticity. Detrusor-Sphincter Dyssynergia. Depending on the level of the lesion, the coordinated activity of the detrusor muscle and the external sphincter may be affected. Lesions that affect the micturition center in the pons or impair communication between this center and spinal cord centers interrupt the coordinated activity of the detrusor muscle and the external sphincter. This is called detrusor-sphincter Disorders of Urine Elimination 859 dyssynergia. Instead of relaxing during micturition, the external sphincter becomes more constricted. This condition can lead to elevated intravesicular pressures, vesicoureteral reflux, and kidney damage. Treatment. Among the methods used to treat spastic bladder and detrusor-sphincter dyssynergia are the use of anticholinergic medications to decrease bladder hyperactivity and urinary catheterization to produce bladder emptying (discussed later). A sphincterotomy (surgical resection of the external sphincter) or implantable urethral stent may be used to decrease outflow resistance in a person who cannot be managed with medications and catheterization procedures. An alternative to surgical resection of the external sphincter is the injection of botulinum-A toxin to produce paralysis of the striated muscles in the external sphincter. The effects of the injection last from 3 to 9 months, after which the injection must be repeated.11 Flaccid Bladder: Failure to Empty Urine Failure to empty the bladder can be due to flaccid bladder dysfunction, peripheral neuropathies that interrupt afferent or efferent communication between the bladder and the spinal cord, or conditions that prevent relaxation of the external sphincter (see Fig. 37-3). Flaccid Bladder Dysfunction. Detrusor muscle areflexia, or flaccid neurogenic bladder, occurs when there is injury to the micturition center of the sacral cord, the cauda equina, or the sacral roots that supply the bladder.12 Atony of the detrusor muscle and loss of the perception of bladder fullness permit the overstretching of the detrusor muscle that contributes to weak and ineffective bladder contractions. External sphincter tone and perineal muscle tone are diminished. Voluntary urination does not occur, but fairly efficient emptying usually can be achieved by increased intra-abdominal pressure or manual suprapubic pressure. Among the causes of flaccid neurogenic bladder are trauma, tumors, and congenital anomalies (e.g., spina bifida, meningomyelocele). Bladder Dysfunction Caused by Peripheral Neuropathies. In addition to CNS lesions and conditions that disrupt bladder function, disorders of the peripheral (pelvic, pudendal, and hypogastric) neurons that supply the bladder can occur. These neuropathies can selectively interrupt sensory or motor pathways for the bladder or involve both pathways. Bladder atony with dysfunction is a frequent complication of diabetes mellitus.13,14 The disorder initially affects the sensory axons of the urinary bladder without involvement of the pudendal nerve. This leads to large residual volumes after micturition, sometimes complicated by infection. There frequently is a need for straining, accompanied by hesitation, weakness of the stream, dribbling, and a sensation of incomplete bladder emptying.14 The chief complications are vesicoureteral reflux and ascending urinary tract infection. Because persons with diabetes are already at risk for development of glomerular disease (see Chapter 35), reflux can have serious effects on kidney function. Treatment consists of client education, including the need for frequent voiding (e.g., every 3 to 4 hours while 860 UNIT VIII Renal Function awake), use of abdominal compression to effect more complete bladder emptying, and intermittent catheterization when necessary.12 Nonrelaxing External Sphincter Another condition that affects micturition and bladder function is the nonrelaxing external sphincter. This condition usually is related to a delay in maturation, developmental regression, psychomotor disorders, or locally irritative lesions. Inadequate relaxation of the external sphincter can be the result of anxiety or depression. Any local irritation can produce spasms of the sphincter by means of afferent sensory input from the pudendal nerve; included are vaginitis, perineal inflammation, and inflammation or irritation of the urethra. In men, chronic prostatitis contributes to the impaired relaxation of the external sphincter. Treatment The goals of treatment for neurogenic bladder disorders focus on preventing bladder overdistention, urinary tract infections, and potentially life-threatening renal damage and reducing the undesirable social and psychological effects of the disorder. The methods used in treatment of neurogenic bladder disorders are individualized based on the type of neurologic lesion that is involved; information obtained through the health history, including fluid intake; report or observation of voiding patterns; presence of other health problems; urodynamic studies when indicated; and the ability of the person to participate in the treatment. Treatment methods include catheterization, bladder training, pharmacologic manipulation of bladder function, and surgery. Catheterization. Catheterization involves the insertion of a small-diameter latex or silicone tube into the bladder through the urethra.15 The catheter may be inserted on a one-time basis to relieve temporary bladder distention, left indwelling (i.e., retention catheter), or inserted intermittently. With acute overdistention of the bladder, usually no more than 1000 mL of urine is removed from the bladder at one time. The theory behind this limitation is that removing more than this amount at one time releases pressure on the pelvic blood vessels and predisposes to alterations in circulatory function. Permanent indwelling catheters sometimes are used when there is urine retention or incontinence in persons who are ill or debilitated or when conservative or surgical methods for the correction of incontinence are not feasible. The use of permanent indwelling bladder catheters in patients with spinal cord injury has been shown to produce a number of complications, including urinary tract infections, urethral irritation and injury, pyelonephritis, and kidney stones. Intermittent catheterization is used to treat urine retention or incomplete emptying secondary to various neurologic or obstructive disorders.15 Properly used, it prevents bladder overdistention and urethral irritation, allows more freedom of activity, and provides periodic distention of the bladder to prevent muscle atony. It often is used with phar- macologic manipulation to achieve continence; when possible, it is learned and managed as a self-care procedure (i.e., intermittent self-catheterization).16 It may be carried out as an aseptic (sterile) or a clean procedure. Aseptic intermittent catheterization is used in persons with spinal shock and in those who need short-term catheterization. The clean procedure typically is used for selfcatheterization. It is performed at 3- to 4-hour intervals to prevent overdistention of the bladder. The best results are obtained if only 300 to 400 mL is allowed to collect in the bladder between catheterizations. The use of the clean instead of the sterile procedure has been defended on the basis that most urinary tract infections are caused by some underlying abnormality of the urinary tract that leads to impaired mucosal resistance to bacterial infection, the most common cause of which is decreased blood flow because of bladder overdistention.15 Bladder Retraining. Bladder retraining differs with the type of disorder.17 Methods used to supplement bladder retraining include monitoring fluid intake to prevent urinary tract infections and control urine volume and osmolality, developing scheduled times for urination, and using body positions that facilitate micturition. Among the considerations when monitoring fluid intake is the need to ensure adequate fluid intake to prevent unduly concentrated urine, which may serve to stimulate afferent neurons of the micturition reflex. In hyperreflexive bladder or detrusor-sphincter dyssynergia, the stimulation of afferent nerve endings by irritating urinary constituents results in increased vesicular pressures, vesicoureteral reflux, and overflow incontinence. Fluid intake must be balanced to prevent bladder overdistention from occurring during the night. Adequate fluid intake also is needed to prevent urinary tract infections, the irritating effects of which increase bladder irritability and the risk for urinary incontinence and renal damage. Developing scheduled times for urinating prevents overdistention of the bladder. The methods used for bladder retraining depend on the type of lesion causing the disorder. In spastic neurogenic bladder, methods designed to trigger the sacral micturition reflex are used; in flaccid neurogenic bladder, manual methods that increase intravesicular pressure are used. Trigger voiding methods include manual stimulation of the afferent loop of the micturition reflex through such maneuvers as tapping the suprapubic area, pulling on the pubic hairs, stroking the glans penis, or rubbing the thighs. Credé’s method, which is done with the person in a sitting position, consists of applying pressure with four fingers of one hand or both hands to the suprapubic area as a means of increasing intravesicular pressure. The use of Valsalva’s maneuver (i.e., bearing down by exhaling against a closed glottis) increases intra-abdominal pressure and aids in bladder emptying. This maneuver is repeated until the bladder is empty. For the best results, the patient must cooperate fully with the procedures and, if possible, learn to perform them independently. Biofeedback methods have been useful for teaching some aspects of bladder control. They involve the use of EMG or cystometry as a feedback signal for training a per- CHAPTER 37 son to control the function of the external sphincter or raise intravesicular pressure enough to overcome outflow resistance. Pharmacologic Manipulation. Pharmacologic manipulation includes the use of drugs to alter the contractile properties of the bladder, decrease the outflow resistance of the internal sphincter, and relax the external sphincter. The usefulness of drug therapy often is evaluated during cystometric studies. Anticholinergic drugs, such as tolterodine (Detrol), oxybutynin (Ditropan), and propantheline (generic; Pro-Banthine), decrease detrusor muscle tone and increase bladder capacity in persons with spastic bladder dysfunction.12,18 Cholinergic drugs that stimulate parasympathetic receptors, such as bethanechol chloride (generic; Urecholine), provide increased bladder tonus and may prove helpful in the symptomatic treatment of milder forms of flaccid neurogenic bladder. Muscle relaxants, such as diazepam (Valium) and baclofen (Lioresal), may be used to decrease the tone of the external sphincter. A nasal spray preparation of desmopressin (DDAVP), a synthetic antidiuretic hormone, can be used to treat persons with nighttime frequency due to spastic bladder symptoms. Surgical Procedures. Among the surgical procedures used in the management of neurogenic bladder are sphincterectomy, reconstruction of the sphincter, nerve resection of the sacral reflex nerves that cause spasticity or the pudendal nerve that controls the external sphincter, and urinary diversion. Urinary diversion can be done by creating an ileal or a colon loop into which the ureters are anastomosed; the distal end of the loop is brought out and attached to the abdominal wall. Other procedures include the attachment of the ureters to the skin of the abdominal wall or the attachment of the ureters to the sigmoid colon, with the rectum serving as a receptacle for the urine. Extensive research is being conducted on methods of restoring voluntary control of the storage and evacuation functions of the bladder through the use of implanted electrodes. Single and multiple electrodes can be placed on selected nerves and then coupled to a subcutaneous receiver.12 URINARY INCONTINENCE The Urinary Incontinence Guideline Panel defines urinary incontinence as an involuntary loss of urine that is sufficient to be a problem.19 This panel was convened by the Agency for Health Care Policy and Research in 1992 and again in 1996 for the purpose of developing specific guidelines to improve the care of persons with urinary incontinence.19 Urinary incontinence affects approximately 13 million Americans. Many body functions decline with age, and incontinence, although not a normal accompaniment of the aging process, is seen with increased frequency in elderly persons.19 For elderly persons living in the community, the prevalence of incontinence ranges from 15% to 35%,20,21 with women being affected twice as often as men.20 The increase in health problems often seen in elderly persons Disorders of Urine Elimination 861 INCONTINENCE ➤ Incontinence represents the involuntary loss of urine due to increased bladder pressures (overactive bladder with urge incontinence or overflow incontinence) or decreased ability of the vesicourethral sphincter to prevent the escape of urine (stress incontinence). ➤ Stress incontinence is caused by the decreased ability of the vesicourethral sphincter to prevent the escape of urine during activities, such as lifting and coughing, that raise bladder pressure above the sphincter closing pressure. ➤ Overactive bladder/urge incontinence is caused by neurogenic or myogenic disorders that result in hyperactive bladder contractions. ➤ Overflow incontinence results from overfilling of the bladder with escape of urine. probably contributes to the greater frequency of incontinence. Despite the prevalence of incontinence, most affected persons do not seek help for it, primarily because of embarrassment or because they are not aware that help is available. Incontinence can be caused by a number of conditions. It can occur without the person’s knowledge; at other times, the person may be aware of the condition but be unable to prevent it. The Urinary Incontinence Guideline Panel has identified four main types of incontinence: stress incontinence, urge incontinence, overflow incontinence, and mixed incontinence, which is a combination of stress and urge incontinence.19 Recently, the term overactive bladder has been designated as a term to replace urge incontinence.20 Table 37-3 summarizes the characteristics of stress incontinence, urge incontinence/overactive bladder, and overflow incontinence. Incontinence may occur as a transient and correctable phenomenon, or it may not be totally correctable and TABLE 37-3 Types and Characteristics of Urinary Incontinence Type Characteristics Stress Involuntary loss of urine associated with activities, such as coughing, that increase intra-abdominal pressure Urgency and frequency associated with hyperactivity of the detrusor muscle; may or may not involve involuntary loss of urine Involuntary loss of urine when intravesicular pressure exceeds maximal urethral pressure in the absence of detrusor activity Overactive bladder/ urge incontinence Overflow 862 UNIT VIII Renal Function occur with various degrees of frequency. Among the transient causes of urinary incontinence are confusional states; medications that alter bladder function or perception of bladder filling and the need to urinate; diuretics and conditions that increase bladder filling; restricted mobility; and stool impaction.22 Stress Incontinence Stress incontinence is the involuntary loss of urine during coughing, laughing, sneezing, or lifting that increases intraabdominal pressure. With severe urinary stress incontinence, any strain or increase in bladder pressure leads to urinary leakage. In women, the angle between the bladder and the posterior proximal urethra (i.e., urethrovesical junction) is important to continence.23 This angle normally is 90 to 100 degrees, with at least one third of the bladder base contributing to the angle when not voiding24 (Fig. 37-5). During the first stage of voiding, this angle is lost as the bladder descends. In women, diminution of muscle tone associated with normal aging, childbirth, or surgical procedures can cause weakness of the pelvic floor muscles and result in stress incontinence by obliterating the critical posterior urethrovesical angle. In these women, loss of the A B X FIGURE 37-5 Importance of the posterior urethrovesical (PU-V) angle to the continence mechanism. (A) In the presence of the normal PU-V angle, sudden changes in intra-abdominal pressure are transmitted optimally (indicated by the arrows with dotted lines) to all sides of the proximal urethra. In this way, intraurethral pressure is maintained higher than the simultaneously elevated intravesicular pressure. This prevents loss of urine with sudden stress. (B) Loss of the PU-V angle results in displacement of the vesicle neck to the most dependent portion of the bladder, preventing the equal transmission of sudden increases in intra-abdominal pressure to the lumen of the proximal urethra. Thus, the pressure in the region of the vesicle neck rises considerably more than the intraurethral pressure just beyond it, and stress incontinence occurs. (Green J.T., Jr. [1968]. Obstetrical and Gynecological Survey 23, 603. Reprinted with permission) posterior urethrovesical angle, descent and funneling of the bladder neck, and backward and downward rotation of the bladder occur, so that the bladder and urethra are already in an anatomic position for the first stage of voiding. Any activity that causes downward pressure on the bladder is sufficient to allow the urine to escape involuntarily. Another cause of stress incontinence is intrinsic urethral deficiency, which may result from congenital sphincter weakness, as occurs with meningomyelocele. It also may be acquired as a result of trauma, irradiation, or sacral cord lesion. Stress incontinence in men may result from a congenital defect or from trauma or surgery to the bladder outlet, as occurs with prostatectomy. Neurologic dysfunction, as occurs with impaired sympathetic innervation of the bladder neck, impaired pelvic nerve innervation to the intrinsic sphincter, or impaired pudendal nerve innervation to the external sphincter, may also be a contributing factor. Overactive Bladder/Urge Incontinence The Urinary Incontinence Guideline Panel has defined urge incontinence as the involuntary loss of urine associated with a strong desire to void (urgency).19 To expand the number and types of patients eligible for clinical trials, the U.S. Food and Drug Administration adopted the term overactive bladder to describe the clinical syndrome that describes not only urge incontinence but also urgency, frequency, dysuria, and nocturia.20 Although overactive bladder often is associated with urge incontinence, it can occur without incontinence.18 Although some cases of overactive bladder result from specific conditions such as acute or chronic urinary tract infections, in many cases, the cause is unknown. Regardless of the primary cause of overactive bladder, two types of mechanisms are thought to contribute to its symptomatology: those involving CNS control of bladder sensation and emptying (neurogenic), and those involving the smooth muscle of the bladder itself (myogenic).18 The CNS functions as an on-off switching circuit for voluntary control of bladder function. Therefore, neurologic damage to central inhibitory pathways or sensitization of peripheral afferent terminals in the bladder may trigger bladder overactivity owing to uncontrolled voiding reflexes. Neurogenic causes of overactive bladder include stroke, Parkinson’s disease, and multiple sclerosis. Other neurogenic causes of overactive bladder include increased peripheral afferent activity or increased peripheral sensitivity to efferent impulses. Myogenic causes of overactive bladder are thought to result from spontaneous elevations in bladder pressure arising from changes in the properties of the smooth muscle of the bladder itself. One example is overactive bladder associated with bladder outlet obstruction. It is hypothesized that the sustained increase in intravesicular pressure that occurs with the outlet obstruction causes a partial destruction of the efferent nerve endings that control bladder excitability.18 The result is urgency and frequency of urination due to spontaneous bladder contractions resulting from detrusor muscle hyperexcitability. Disorders of detrusor muscle structure and excitability also can occur as the result of the aging process or disease conditions such CHAPTER 37 as diabetes mellitus. Overactive bladder symptoms usually are exaggerated by incomplete bladder emptying. In persons with overactive bladder, urge incontinence may occur because the interval between knowing the bladder needs to be emptied and being able to stop it from emptying may be less than the time needed to reach the lavatory. Musculoskeletal disorders, such as arthritis and joint instability, also may prevent an otherwise continent person from reaching the toilet in time. Drugs such as hypnotics, tranquilizers, and sedatives can interfere with the conscious inhibition of voiding, leading to urge incontinence. Diuretics, particularly in elderly persons, increase the flow of urine and may contribute to incontinence, particularly in persons with diminished bladder capacity and in those who have difficulty reaching the toilet. Treatment methods for overactive bladder include the use of behavioral methods and pharmacologic agents. Behavioral methods include fluid management, modification of voiding frequency, and bladder retraining.25 Bladder retraining and biofeedback techniques seek to reestablish cortical control over bladder function by having the person ignore urgency and respond only to cortical signals during waking hours. Two newer anticholinergic medications, tolterodine (Detrol) and extended-release oxybutynin (Ditropan XL), may be used to inhibit detrusor muscle hyperactivity and thereby increase overall bladder capacity.18,25,26 Overflow Incontinence Overflow incontinence is an involuntary loss of urine that occurs when intravesicular pressure exceeds the maximal urethral pressure because of bladder distention in the absence of detrusor activity. It can occur with retention of urine owing to nervous system lesions or obstruction of the bladder neck. With this type of incontinence, the bladder is distended, and small amounts of urine are passed, particularly at night. In males, one of the most common causes of obstructive incontinence is enlargement of the prostate gland. Another cause that commonly is overlooked is fecal impaction (i.e., dry, hard feces in the rectum). When a large bolus of stool forms in the rectum, it can push against the urethra and block the flow of urine. The Standardization Sub-Committee of the International Continence Committee recommends that the term overflow incontinence should no longer be used, indicating that the term is confusing and lacking definition.27 Instead, it suggests that more specific terms such as reduced urethral function or overactivity/low bladder compliance be used. Other Causes of Incontinence Another cause of incontinence is decreased bladder compliance or distensibility. This abnormal bladder condition may result from radiation therapy, radical pelvic surgery, or interstitial cystitis. Many persons with this disorder have severe urgency related to bladder hypersensitivity that results in loss of bladder elasticity, such that any small increase in bladder volume or detrusor function causes a sharp rise in bladder pressure and severe urgency. Incontinence also may be caused by factors outside the lower urinary tract, such as the inability to locate, reach, or receive assistance in reaching an appropriate place to Disorders of Urine Elimination 863 void.14 This may be a particular problem for elderly persons, who may have problems with mobility and manual dexterity or find themselves in unfamiliar surroundings. It occurs when a person cannot find or reach the bathroom or manipulate clothing quickly enough. Failing vision may contribute to the problem. Embarrassment in front of other persons at having to use the bathroom, particularly if the timing seems inappropriate, may cause a person to delay emptying the bladder and may lead to incontinence. Treatment with drugs such as diuretics may cause the bladder to fill more rapidly than usual, making it difficult to reach the bathroom in time if there are problems with mobility or if a bathroom is not readily available. Night sedation may cause a person to sleep through the signal that normally would waken a person so that he or she could get up and empty the bladder and avoid wetting the bed. Diagnosis and Treatment Urinary incontinence is a frequent and major health problem. It increases social isolation, frequently leads to institutionalization of elderly persons, and predisposes to infections and skin breakdown. Urinary incontinence is not a single disease but a symptom with many possible causes. As a symptom, it requires full investigation to establish its cause. This usually is accomplished through a careful history, physical examination, blood tests, and urinalysis.20,22 A voiding record (i.e., diary) may be used to determine the frequency, timing, amount of voiding, and other factors associated with the incontinence.20 Because many drugs affect bladder function, a full drug history is essential. Estimation of PVR volume is recommended for all persons with incontinence. Provocative stress testing is done when stress incontinence is suspected. This test is done by having the person relax and then cough vigorously while the examiner observes for urine loss. The test usually is done in the lithotomy position; if no leakage is observed, it is repeated in the standing position.20 Urodynamic studies may be needed to provide information about urinary pressures and urine flow rates. Treatment or management depends on the type of incontinence, accompanying health problems, and the person’s age. Exercises to strengthen the pelvic muscles and surgical correction of pelvic relaxation disorders often are used for women with stress incontinence. Noncatheter devices to obstruct urine flow or collect urine as it is passed may be used when urine flow cannot be controlled. Indwelling catheters (discussed earlier), although a solution to the problem of urinary incontinence, usually are considered only after all other treatment methods have failed. In some types of incontinence, such as that associated with spinal cord injury or meningomyelocele, self-catheterization provides the means for controlling urine elimination. Treatment of Stress Incontinence. Stress incontinence can be treated by physiotherapeutic measures, surgery, or a combination of the two. Surgical correction of cystocele and pelvic relaxation disorders may be needed for women. Active muscle-tensing exercises of the pelvic muscles may prove effective.20,28,29 These exercises were first advocated by Kegel, and they commonly are called Kegel’s 864 UNIT VIII Renal Function exercises.30 Two groups of muscles are strengthened: those of the back part of the pelvic floor (i.e., muscles used to contract the anus and control the passing of stool) and the front muscles of the pelvic floor (i.e., muscles used to stop the flow of urine during voiding). In learning the exercises, a woman concentrates on identifying the muscle groups and learning how to control contraction. After this has been accomplished, she can start an exercise program that consists of slowly contracting the muscles, beginning at the front and working to the back while counting to four and then releasing. The exercises can be done while sitting or standing and usually are performed in repetitions of 10, three times each day. A vaginal cone, a tampon-like device, may be used to enhance the benefits of the exercise. The cone is placed in the vagina, and the woman instructed to hold it in place by contracting the proper inner muscles.31 The α-adrenergic agonist drugs, such as pseudoephedrine, increase sympathetic relaxation of the detrusor muscle and internal sphincter tone and may be used in treating stress incontinence.20 Imipramine, a tricyclic antidepressant agent that has α-adrenergic and anticholinergic properties, has proved useful in some women. Surgical intervention may be considered when other treatment methods have proved ineffective. Three types of surgical procedures are used: procedures that increase outlet resistance, surgeries that decrease detrusor muscle instability, and operations that remove outflow obstruction to reduce overflow incontinence and detrusor muscle instability. A new development for the treatment of stress incontinence is the tension-free vaginal tape procedure.32 The procedure, which is minimally invasive and performed under local anesthesia, involves recreating suburethral support with a polypropylene mesh, without repositioning the bladder or urethra. Initial results from the procedure appear to be promising, with one study reporting a 90% cure rate.32 Another minimally invasive procedure for the treatment of stress incontinence is periurethral injection of a bulking agent (glutaraldehyde cross-linked bovine collagen or carbon-coated beads). Both of these agents typically require multiple treatment sessions to achieve cure.20,23 Noncatheter Devices. Two types of noncatheter devices commonly are used in the management of urinary incontinence: one obstructs flow, and the other collects urine as it is passed. Obstruction of urine flow is achieved by compressing the urethra or stimulating contraction of the pelvic floor muscles. Penile clamps are available that occlude the urethra without obstructing blood circulation to the penis. Clamps must be removed at 3-hour intervals to empty the bladder. Complications such as penile and urethral erosion can occur if clamps are used incorrectly. In females, compression of the urethra usually is accomplished by intravaginal devices. Surgically implanted artificial sphincters are available for use in males and females. These devices consist of an inflatable cuff that surrounds the proximal urethra. The cuff is connected by tubing to an implanted fluid reservoir and an inflation bulb. Pressing the bulb, which is placed in the scrotum in males, inflates the cuff. It is emptied in a similar manner. When urinary incontinence cannot be prevented, various types of urine collection devices or protective pads are used. Men can be fitted with collection devices (i.e., condom or sheath urinals) that are worn over the penis and attached to a container at the bedside or fastened to the body. There are no effective external collection devices for women. Pants and pads usually are used. Dribbling bags (males) and pads (females) in which the urine changes to a nonpourable gel are available for occasional dribbling but are unsuitable for considerable wetting. Special Needs of Elderly Persons Urinary incontinence is a common problem in elderly persons. An estimated 15% to 30% of community-dwelling elders and 50% of institutionalized elders have severe urinary incontinence.21,33 The economic and social costs of incontinence are staggering. Annually, more than $3 billion is spent managing incontinence in nursing homes alone.34 Many factors contribute to incontinence in elderly persons, a number of which can be altered. More than half of normal elderly persons experience nocturia. The overall capacity of the bladder is reduced, as is the urethral closing pressure.21 Detrusor muscle function also tends to decline with aging; thus, there is a trend toward a reduction in the strength of bladder contraction and impairment in emptying that leads to larger PVR volumes.2,21,35 It has been proposed that many of these changes are due to degenerative detrusor muscle changes rather than neurologic changes, as was once thought. The combination of involuntary detrusor contraction (detrusor hyperactivity) leading to urge incontinence, along with impaired contractile function, leads to incomplete bladder emptying. Pelvic relaxation disorders are also more frequent in older than in younger women, and prostatic hypertrophy is more common in older than in younger men. Furthermore, advancing age often results in restricted mobility, an increasing number of medications being taken, comorbid illness, infection, and stool impaction, all of which can precipitate urinary incontinence.21,35 Many elderly persons have difficulty getting to the toilet in time. This can be caused by arthritis that makes walking or removing clothing difficult or by failing vision that makes trips to the bathroom precarious, especially in new and unfamiliar surroundings. Medication prescribed for other health problems may prevent a healthy bladder from functioning normally.21,23,35 Potent, fast-acting diuretics are known for their ability to cause urge incontinence. Psychoactive drugs, such as tranquilizers and sedatives, may diminish normal attention to bladder clues. Impaired thirst or limited access to fluids predisposes to constipation with urethral obstruction and overflow incontinence and to concentrated and infected urine, which increases bladder excitability. Diagnosis and Treatment. According to Stanton, “there are two guiding principles in management of incontinence in the elderly. First, growing old does not imply becoming incontinent, and second, incontinence should not be left untreated just because the patient is old.”36 CHAPTER 37 The treatment of urinary incontinence in elderly persons requires a thorough history and physical examination to determine the cause of the problem. A voiding history is important. A voiding diary provides a means for the person to provide objective information about the number of bathroom visits, the number of protective pads used, and even the volume of urine voided. A medication history is also important because medications can affect bladder function.21 There are many nonurologic conditions that predispose to urinary incontinence. The transient and often treatable causes of urinary incontinence in elderly persons may best be remembered with the acronym DIAPPERS, in which the D stands for dementia/dementias, I for infection (urinary or vaginal), A for atrophic vaginitis, P for pharmaceutical agents, P for psychological causes, E for endocrine conditions (diabetes), R for restricted mobility, and S for stool impaction.37 These eight transient causes of incontinence should be identified and treated before other treatment options are considered. Treatment may involve changes in the physical environment so that the older person can reach the bathroom more easily or remove clothing more quickly. Habit training with regularly scheduled toileting—usually every 2 to 4 hours—often is effective. Many elderly persons who void on a regular schedule can gradually increase the interval between toileting while improving their ability to suppress bladder instability. The treatment plan may require dietary changes to prevent constipation or a plan to promote adequate fluid intake to ensure adequate bladder filling and prevent urinary stasis and symptomatic urinary tract infections. In summary, alterations in bladder function include urinary obstruction with retention of urine, neurogenic bladder, and urinary incontinence with involuntary loss of urine. Urine retention occurs when the outflow of urine from the bladder is obstructed because of urethral obstruction or impaired bladder innervation. Urethral obstruction causes bladder irritability, detrusor muscle hypertrophy, trabeculation and the formation of diverticula, development of hydroureters, and eventually, renal failure. Neurogenic bladder is caused by interruption in the innervation of the bladder. It can result in spastic bladder dysfunction caused by failure of the bladder to fill or flaccid bladder dysfunction caused by failure of the bladder to empty. Spastic bladder dysfunction usually results from neurologic lesions that are above the level of the sacral micturition reflex center; flaccid bladder dysfunction results from lesions at the level of the sacral micturition reflexes or peripheral innervation of the bladder. A third type of neurogenic disorder involves a nonrelaxing external sphincter. Urinary incontinence is the involuntary loss of urine in amounts sufficient to be a problem. It may manifest as stress incontinence, in which the loss of urine occurs as a result of coughing, sneezing, laughing, or lifting; overactive bladder, characterized by frequency and urgency associated with hyperactive bladder contractions; or overflow incontinence, which results when intravesicular pressure exceeds the maximal urethral pressure because of bladder distention. Other Disorders of Urine Elimination 865 causes of incontinence include a small, contracted bladder or external environmental conditions that make it difficult to access proper toileting facilities. The acronym DIAPPERS—D (dementia) I (infection) A (atrophic vaginitis) P (pharmaceutical) P (psychological) E (endocrine) R (restricted mobility) S (stool impaction) emphasizes the transient and often treatable causes of incontinence in the elderly. The treatment of urinary obstruction, neurogenic bladder, and incontinence requires careful diagnosis to determine the cause and contributing factors. Treatment methods include correction of the underlying cause, such as obstruction due to prostatic hyperplasia; pharmacologic methods to improve bladder and external sphincter tone; behavior methods that focus on bladder and habit training; exercises to improve pelvic floor function; and the use of catheters and urine collection devices. Cancer of the Bladder After completing this section of the chapter, you should be able to meet the following objectives: ✦ Discuss the difference between superficial and invasive bladder cancer in terms of bladder involvement, extension of the disease, and prognosis ✦ State the most common sign of bladder cancer Bladder cancer is the most frequent form of urinary tract cancer in the United States, accounting for more than 57,700 new cases and 12,500 deaths each year.38 It is three times more common in men than women and has an average age of onset of 65 years. Its incidence is higher in whites than African Americans.39 Approximately 90% of bladder cancers are derived from the transitional (urothelial) cells that line the bladder.40–42 These tumors can range from low-grade noninvasive tumors to high-grade tumors that invade the bladder wall and metastasize frequently. The low-grade tumors, which may recur after resection, have an excellent prognosis, with only a small number (2% to 10%) progressing to higher-grade tumors.41,42 The high-grade tumors tend to have greater invasive and metastatic potential and are potentially fatal in approximately 60% of cases within 10 years of diagnosis.40 ETIOLOGY AND PATHOPHYSIOLOGY Although the cause of bladder cancer is unknown, evidence suggests that its origin is related to local influences, such as carcinogens that are excreted in the urine and stored in the bladder. These include the breakdown products of aromatic amines used in the dye industry, products used in the manufacture of rubber, textiles, paint, chemicals, and petroleum.42 Smoking also deserves attention.41,42 Fifty percent to 80% of bladder cancers in men are associated with cigarette smoking.40 Chronic bladder infections and bladder stones also increase the risk for bladder cancer. Bladder cancer is more frequent among persons harboring the parasite Schistosoma haematobium in their bladder.40 866 UNIT VIII Renal Function The parasite is endemic in Egypt and Sudan. It is not known whether the parasite excretes a carcinogen or produces its effects through irritation of the bladder. MANIFESTATIONS The most common sign of bladder cancer is painless hematuria.38,39,42 Gross hematuria is a presenting sign in 75% of persons with the disease, and microscopic hematuria is present in most others. Frequency, urgency, and dysuria occasionally accompany the hematuria. Because hematuria often is intermittent, the diagnosis may be delayed. Periodic urine cytology is recommended for all persons who are at high risk for the development of bladder cancer because of exposure to urinary tract carcinogens. Ureteral invasion leading to bacterial and obstructive renal disease and dissemination of the cancer are potential complications and ultimate causes of death. The prognosis depends on the histologic grade of the cancer and the stage of the disease at the time of diagnosis. DIAGNOSIS AND TREATMENT Diagnostic methods include cytologic studies, excretory urography, cystoscopy, and biopsy. Ultrasonography, CT scans, and MRI are used as aids for staging the tumor. Cytologic studies performed on biopsy tissues or cells obtained from bladder washings may be used to detect the presence of malignant cells.39,42 A technique called flow cytometry is helpful in screening persons at high risk for the disease and for monitoring the results of therapy. In flow cytometry, the interaction between fluorochromes or dyes with DNA causes the emission of high-intensity light similar to that produced by a laser.39 Flow cytometry can be carried out on biopsy specimens, bladder washings, or cytologic preparations. The treatment of bladder cancer depends on the extent of the lesion and the health of the patient. Endoscopic resection usually is done for diagnostic purposes and may be used as a treatment for superficial lesions. Diathermy (i.e., electrocautery) may be used to remove the tumors. Segmental surgical resection may be used for removing a large single lesion. When the tumor is invasive, cystectomy with resection of the pelvic lymph nodes frequently is the treatment of choice. In males, the prostate and seminal vesicles often are removed as well. Until the 1980s, most men who underwent radical cystectomy became impotent. Newer surgical approaches designed to preserve erectile function now are being used. Cystectomy requires urinary diversion, an alternative reservoir, usually created from the ileum (e.g., an ileal loop), that is designed to collect the urine. Traditionally, the ileostomy reservoir drains urine continuously into an external collecting device. External beam radiation therapy is an alternative to radical cystectomy in some patients with deeply infiltrating bladder cancer.39 Although a number of chemotherapeutic drugs have been used in the treatment of bladder cancer, no chemotherapeutic regimens for the disease have been established. Perhaps of more importance is the increasing use of intravesicular chemotherapy, in which the cytotoxic drug is instilled directly into the bladder, thereby avoiding the side effects of systemic therapy. These drugs can be instilled prophylactically after surgical resection of all demonstrable tumor or therapeutically in the presence of residual disease. Among the chemotherapeutic drugs that have been used for this purpose are thiotepa, mitomycin C, and doxorubicin (Adriamycin).39 The intervesicular administration of bacillus Calmette-Guérin (BCG) vaccine, made from a strain of Mycobacterium bovis that formerly was used to protect against tuberculosis, causes a significant reduction in the rate of relapse and prolongs relapse-free interval in persons with cancer in situ. The vaccine is thought to act as a nonspecific stimulator of cell-mediated immunity. It is not known whether the effects of BCG are immunologic or include a component of direct toxicity. Several strains of this agent exist, and it is not known which is the most active and least toxic. In summary, cancer of the bladder is the most common cause of urinary tract cancer in the United States. Bladder cancers fall into two major groups: low-grade noninvasive tumors, and high-grade invasive tumors that are associated with metastasis and a worse prognosis. Although the cause of cancer of the bladder is unknown, evidence suggests that carcinogens excreted in the urine may play a role. Microscopic and gross, painless hematuria are the most frequent presenting signs of bladder cancer. The methods used in treatment of bladder cancer depend on the cytologic grade of the tumor and the lesion’s degree of invasiveness. The methods include surgical removal of the tumor, radiation therapy, and chemotherapy. In many cases, chemotherapeutic or immunotherapeutic agents can be instilled directly into the bladder, thereby avoiding the side effects of systemic therapy. REVIEW EXERCISES A 23-year-old man is recovering after the acute phase of a cervical (C6) spinal cord injury with complete loss of motor and sensory function below the level of injury. He is now experiencing spastic bladder contractions with involuntary and incomplete urination. 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