Download Ch37_Urinary Disorde..

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. Urodynamic studies reveal spastic contraction of the external sphincter
with urine retention and high bladder pressures.
A. Explain the reason for the involuntary urination and
incomplete emptying of the bladder despite high
bladder pressures.
B. What are possible complications associated with
overdistention and high pressure within the bladder?
A 66-year-old woman complains of leakage of urine during coughing, sneezing, laughing, or squatting down.
A. Explain the source of this woman’s problem.
B. One of the recommended treatments for stress incontinence is use of Kegel’s exercises, which focus on
strengthening the muscles of the pelvic floor. Explain how these exercises contribute to the control
of urine leakage in women with stress incontinence.
CHAPTER 37
References
1. Kandel E.R., Schwartz J.H., Jessel T.M. (2000). Principles of
neural science (4th ed.). New York: McGraw-Hill.
2. Fowler C.J. (1999). Neurological disorders of micturition and
their treatment. Brain 122, 1213–1231.
3. Guyton A.C., Hall J.E. (2000). Textbook of medical physiology
(10th ed., pp. 364–367). Philadelphia: W.B. Saunders.
4. Rhoades R.A., Tanner G.A. (2003). Medical physiology (2nd ed.,
pp. 423–424). Philadelphia: Lippincott Williams & Wilkins.
5. Dmochowski R.R., Appell R.A. (2000). Advances in pharmacologic management of overactive bladder. Urology 56(Suppl. 6A),
41–49.
6. Elder J.S. (2004). Voiding dysfunction. In Behrman R.E.,
Kliegman R.M., Jenson H.B. (Eds.), Nelson textbook of pediatrics
(17th ed., pp. 1808–1809). Philadelphia: W.B. Saunders.
7. Tanagho E.A. (2004). Urodynamic studies. In Tanagho E.A.,
McAninch J.W. (Eds.), Smith’s general urology (16th ed.,
pp. 453–472). New York: Lange Medical Books/McGraw-Hill.
8. Fantl J.A., Newman D.K., Colling J., et al., for the Public Health
Service, Agency for Health Care Policy and Research. (1996).
Urinary incontinence in adults: Acute and chronic management.
Clinical Practice Guideline no. 2, 1996 update. AHCPR publication no. 96-0682. Rockville, MD: U.S. Department of Health
and Human Services.
9. Schott-Baer F.D., Reaume L. (2001). Accuracy of ultrasound
estimates of urine volume. Urological Nursing 21(3), 193–195.
10. Tanagho E.A. (2004). Urinary obstruction and stasis. In
Tanagho E.A., McAninch J.W. (Eds.), Smith’s general urology
(16th ed., pp. 175–187). New York: Lange Medical Books/
McGraw-Hill.
11. Elliott D.S., Boone T.B. (2000). Recent advances in management of neurogenic bladder. Urology 56(Suppl. 6A), 76–81.
12. Tanagho E.A., Lue T.F. (2000). Neuropathic bladder disorders.
In Tanagho E.A., McAninch J.W. (Eds.), Smith’s general urology
(16th ed., pp. 435–452). New York: Lange Medical Books/
McGraw-Hill.
13. Sasaki K., Yoshimura N., Chancellor M.B. (2003). Implication
of diabetes mellitus in urology. Urological Clinics of North
America 30(1), 1–12.
14. Vinik A.I., Maser R.E., Mitchell B.D., Freeman R. (2003). Diabetic autonomic neuropathy. Diabetes Care 26(5), 1553–1579.
15. Cravens D.D., Zwieg S. (2000). Urinary catheter management.
American Family Physician 61, 369–376.
16. Barton R. (2000). Intermittent self-catheterization. Nursing
Standard 15(9), 47–52.
17. Addison R., Lopez J. (2001). Bladder retraining. Nursing Times
97(5), 45–46.
18. Dmochowski R.R., Appell R.A. (2000). Advancements in
pharmacologic management of overactive bladder. Urology
56(Suppl. 6A), 41–49.
19. Agency for Health Care Policy and Research (AHCPR). Public
Health Service, U.S. Department of Heath and Human Services.
(1996). Urinary incontinence in adults: Acute and chronic management. Clinical Practice Guideline (AHCPR Pub. No 96-0682).
Washington D.C.: U.S. Government Printing Office.
20. Culligan P.J., Heit M. (2000). Urinary incontinence in women:
Evaluation and management. American Family Physician 62,
2433–2452.
21. Klausner A.P., Vapnek J.M. (2003). Urinary incontinence in
the geriatric population. Mount Sinai Journal of Medicine 70(1),
54–61.
Disorders of Urine Elimination
867
22. Gray M., Burns S.M. (1996). Continence management. Critical Care Clinics of North America 8, 29–38.
23. Tanagho E.A. (2004). Urinary incontinence. In Tanagho E.A.,
McAninch J.W. (Eds.), Smith’s general urology (17th ed.,
pp. 473–491). New York: Lange Medical Books/McGraw-Hill.
24. Green T.H. (1975). Urinary stress incontinence: Differential
diagnosis, pathophysiology, and management. American Journal of Obstetrics and Gynecology 122, 368–382.
25. Wein A.J. (2001). Putting overactive bladder into clinical perspective. Patient Care for the Nurse Practitioner (Spring Suppl.),
1–5.
26. Roberts R.R. (2001). Current management strategies for overactive bladder. Patient Care for the Nurse Practitioner (Spring
Suppl.), 22–30.
27. Abrams P., Cardozo L., Fall M., et al. (2003). The standardization of terminology in lower urinary tract function: Report of the standardization sub-committee of the International
Continence Society. Urology 61, 37–49.
28. Wells T.J., Brink C.A., Kiokno A.C., et al. (1991). Pelvic muscle exercise for stress urinary incontinence in elderly women.
Journal of the American Geriatrics Society 39, 785–791.
29. Thakar R., Stanton S. (2000). Management of urinary incontinence in women. British Medical Journal 321, 1326–1330.
30. Kegel A.H. (1948). Progressive resistance exercises in the functional restoration of the perineal muscles. American Journal of
Obstetrics and Gynecology 56, 238–248.
31. Boourcier A.P., Jurat J.C. (1995). Nonsurgical therapy for
stress incontinence. Urologic Clinics of North America 22,
613–627.
32. Carlin B.I., Klutke J.J., Klutke C.G. (2000). The tension-free
vaginal tape procedure for treatment of stress incontinence in
the female patient. Urology 56(Suppl. 6A), 28–31.
33. Lee S.Y., Phanumus D., Fields S.D. (2000). Urinary incontinence: A primary guide to managing acute and chronic
symptoms in older adults. Geriatrics 55(11), 65–71.
34. Weiss B.D. (1998). Diagnostic evaluation of urinary incontinence in geriatric patients. American Family Physician 57,
2675–2684, 2688–2690.
35. Dubeau C.E. (2002). The continuum of urinary incontinence
in an aging population. Geriatrics 57(Suppl 1), 12–17.
36. Stanton S.L. (1984). Surgical management of female incontinence. In Brocklehurst J.C. (Ed.), Urology in the elderly (p. 93).
New York: Churchill Livingstone.
37. Resnick N.M., Yalla S.V. (1998). Geriatric incontinence and
voiding dysfunction. In Walsh P.C., Retik A.B., Vaughan E.D.,
Wein A.J. (Eds.), Campbell’s urology (7th ed., p. 1045). Philadelphia: W.B. Saunders.
38. American Cancer Society (2003). Bladder cancer: Overview.
[On-line]. Available: http://www.cancer.org/cancerinfo.
39. Grossfeld G.D., Carroll P. (2004). Urothelial carcinoma: Cancers of the bladder, ureter, and renal pelvis. In Tanagho E.A.,
McAninch J.W. (Eds.), Smith’s general urology (16th ed.,
pp. 324–345). New York: Lange Medical Books/McGraw-Hill.
40. Cotran R.S., Kumar V., Collins T. (1999). Robbins pathologic
basis of disease (6th ed., pp. 1003–1008). Philadelphia: W.B.
Saunders.
41. Lee R., Droller M.J. (2000). The natural history of bladder cancer. Urologic Clinics of North America 27(1), 1–13.
42. Murphy G.P. (2001). Urologic and male genital cancer. In
Lenhard R.E., Osteen R.T., Gansler T. (Eds.), Clinical oncology
(pp. 408–415). Atlanta: American Cancer Society.