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25
CHAPTER
Alterations in
Urine Elimination
CONTROL OF URINE ELIMINATION
Control of Urine Elimination
Bladder Structure
Micturition
Neural Control of Bladder Function
Spinal Cord Centers
Pontine Micturition Center
Cortical and Subcortical Centers
Development of Bladder Control in Children
Evaluation of Bladder Function
Alterations in Bladder Function
Urinary Obstruction and Stasis
Neurogenic Bladder Disorders
Spastic Bladder: Failure to Store Urine
Flaccid Bladder: Failure to Empty Urine
Urinary Incontinence
Stress Incontinence
Urge Incontinence/Overactive Bladder
Overflow Incontinence
Other Causes of Incontinence
Diagnosis and Treatment
Special Needs of Elderly Persons
Cancer of the Bladder
Diagnosis and Treatment
The urinary 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 ure-
ters. The ureters enter the bladder obliquely through the
trigone
,
a triangular area located above the bladder neck on the poste-
rior wall of the bladder (Fig. 25-1). There are no valves at the
ureteral openings, but because of their oblique position in
the bladder wall, the pressure of the urine keeps the ends of the
ureters compressed to prevent the backflow of urine from the
bladder into the ureters.
Bladder Structure
The bladder is composed of four layers. The first is an outer
serosal layer, which covers the upper surface and is continuous
with the peritoneum. The second is a network of smooth mus-
cle 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 blad-
der acts as an effective barrier to prevent the passage of water
between the bladder contents and the blood. The inner ele-
ments 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, form-
ing the posterior urethra in males and the entire urethra in fe-
males. When the bladder is relaxed, these circular muscle fibers
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 so-
cial and hygienic problems, or obstruction of urine flow, which
has deleterious effects on ureteral and, ultimately, renal func-
tion. The discussion in this chapter focuses on normal control
of urine elimination, urinary obstruction and stasis, neuro-
genic bladder, incontinence, and bladder cancer. Urinary tract
infections are discussed in Chapter 23.
446
447
Chapter 25: Alterations in Urine Elimination
scious inhibition of the micturition reflex. 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 de-
creased; and the external sphincter relaxes as urine moves out
of the bladder.
Epithelium when
bladder is empty
Epithelium when
bladder is full
Detrusor
muscle
Ureters
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 ANS and its neuromediators
play a central role in micturition. The somatic nervous system
controls the external sphincter and contributes to the voluntary
control of bladder emptying.
The parasympathetic nervous system produces contraction
of the detrusor muscle and bladder emptying. Parasympathetic
innervation of the bladder is mediated by cholinergic (mus-
carinic) receptors and the neurotransmitter acetylcholine.
2
Sympathetic innervation, although not essential to the act
of micturition, allows the bladder to store a large volume with-
out the involuntary escape of urine—a mechanism that is con-
sistent with the fight-or-flight function subserved by the sym-
pathetic nervous system. The bladder is supplied with
Trigone
Internal sphincter
External sphincter
■
FIGURE 25-1
■
Diagram of the bladder, showing the detrusor
muscle, ureters, trigone area, and urethral orifice. Note the flat-
tening of epithelial cells when the bladder is full and the wall is
stretched.
α
1
- and
β
2
-adrenergic 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. The
β
2
-adrenergic receptors. The
are closed and act as a sphincter. When the detrusor muscle
contracts, the sphincter is pulled open by the changes that oc-
cur in bladder shape. In the female, the urethra (2.5 to 3.5 cm)
is shorter than that 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
exter-
nal sphincter
, a circular muscle composed of striated muscle
fibers that surrounds the urethra distal to the base of the blad-
der. The external sphincter operates as a reserve mechanism to
stop micturition when it is occurring and to maintain conti-
nence in the face of unusually high bladder pressure. The skele-
tal muscles of the pelvic floor also contribute to the support of
the bladder and the maintenance of continence.
α
1
-adrenergic receptors are found in the
trigone area, including the intramural ureteral musculature,
bladder neck, and internal sphincter. The activation of
α
1
re-
ceptors produces contraction of these muscles. Sympathetic
activity ceases when the micturition reflex is activated. During
male ejaculation, which is mediated by the sympathetic ner-
vous system, the musculature of the trigone area and that of the
KEY CONCEPTS
BLADDER FUNCTION
Micturition
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 pres-
sure that accompanies bladder filling is almost imperceptible.
An increase in bladder volume from 10 to 400 mL may be ac-
companied by only a 5 cm H
2
O increase in pressure.
1
Sustained
elevations in intravesicular pressures (
The storage and emptying of urine involve both in-
voluntary (autonomic nervous system) and voluntary
(somatic nervous system) control.
■
The parasympathetic nervous system promotes blad-
der emptying. It produces contraction of the smooth
muscle of the bladder wall and relaxation of the
internal sphincter.
■
40 to 50 cm H
2
O) 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 23). Although the pressure in
the bladder is maintained at low levels, sphincter pressure re-
mains high (45 to 65 cm H
2
O) as a means of preventing loss of
urine as the bladder fills.
Micturition involves both sensory and motor functions as-
sociated with bladder emptying. When the bladder is distended
to 150 to 300 mL, the sensation of fullness is transmitted to the
spinal cord and then to the cerebral cortex, allowing for con-
>
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.
■
448
Unit Six: Alterations in the Urinary System
bladder neck and prostatic urethra contracts and prevents the
backflow of seminal fluid into the bladder.
There are three main levels of neurologic control for blad-
der function: (1) the spinal cord reflex centers, (2) the mic-
turition center in the pons, and (3) the cortical and subcorti-
cal centers.
sphincter. As bladder filling occurs, and the muscle stretch re-
ceptors are activated, ascending spinal afferents relay this in-
formation to the micturition center, which also receives im-
portant descending information from the forebrain concerning
behavioral cues for bladder emptying. Descending pathways
from the pontine micturition center produce coordinated inhi-
bition of neurons controlling the internal and external sphinc-
ters. The onset of urinary flow through the urethra causes reflex
contraction of the bladder.
Spinal Cord Centers
The centers for reflex control of bladder emptying or micturition
are located in the sacral (S1 through S4) and thoracolumbar
(T11 through L2) segments of the spinal cord (Fig. 25-2). The
parasympathetic motor neurons that innervate 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
. Motor neurons for the external sphincter also are located
in the sacral segments of the spinal cord. These motor neurons
receive their control from the motor cortex by way of the corti-
cospinal tract and send impulses to the external sphincter
through the
pudendal nerve
. The bladder neck and trigone area
of the bladder are innervated by the sympathetic fibers from the
thoracolumbar segments of the spinal cord.
The afferent or sensory input, which detects stretch of the
bladder wall, is carried to the central nervous system (CNS) by
way of fibers that travel with the parasympathetic (pelvic), so-
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.
Cortical and Subcortical Centers
Cortical brain centers enable inhibition of the micturition cen-
ter in the pons and conscious control of urination. Neural in-
fluences from the subcortical centers in the basal ganglia, which
are conveyed by extrapyramidal pathways, modulate the con-
tractile response. They modify and delay the detrusor contrac-
tile response during filling and then modulate the expulsive ac-
tivity of the bladder to facilitate complete emptying.
Development of Bladder Control 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 bladder grows and increases
in capacity, the tone of the external sphincter muscle increases.
At 2 to 3 years of age, the child becomes conscious of the need
to urinate and can learn to contract the pelvic muscles to main-
tain closure of the external sphincter and delay urination. As
the nervous system continues to mature, inhibition of invol-
untary detrusor muscle activity takes place. After the child
achieves continence, micturition becomes voluntary.
Pontine Micturition Center
The immediate coordination of the normal micturition reflex
occurs in the micturition center in the pons, facilitated by de-
scending input from the forebrain and ascending input from
the reflex centers in the spinal cord
3,4
(Fig. 25-3). This center co-
ordinates the activity of the detrusor muscle and the external
Evaluation of Bladder Function
Bladder structure and function can be assessed by a number of
methods.
5
Reports or observations of frequency, hesitancy,
straining to void, and a weak or interrupted stream are sugges-
tive of outflow obstruction. Palpation and percussion provide
information about bladder distention.
Postvoided residual (PVR) urine volume provides informa-
tion about bladder emptying. It can be estimated by abdomi-
nal palpation and percussion. Catheterization and ultrasonog-
raphy 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 blad-
der emptying.
6
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.
Urine tests provide information about kidney function and
urinary tract infections. The presence of bacteriuria or pyuria
suggests urinary tract infection and the possibility of urinary
tract obstruction. Blood tests (
i.e.
, blood urea nitrogen and cre-
atinine) provide information about renal function.
Sympathetic
neurons
T11
Afferent fibers
Efferent motor
Efferent inhibitory
T12
L1
L2
Hypogastric nerve
Parasympathetic
pelvic nerves
S1
S2
S2
S3
S3
S4
Detrusor muscle
Somatic
pudendal
nerve
Internal sphincter
External sphincter
■
FIGURE 25-2
■
Nerve supply to the bladder and the urethra.
449
Chapter 25: Alterations in Urine Elimination
Bladder emptying
Urine storage
Cortical facilitation
Cerebral
cortex
Cortical inhibition
Coordination of bladder
storage functions
Coordination of micturition
motor function
Pontine
micturition
center
Thoracolumbar
cord (T11-L2)
Stimulation
sympathetic
neurons
Stimulation
somatic
neurons
Inhibition
somatic
neurons
Stimulation
parasympathetic
neurons
Sacral cord
(S1-S3)
Pelvic
nerve
Detrusor
muscle
Pudendal
nerve
Bladder
Relaxation of
detrusor
muscle
Contraction of
external
sphincter
Relaxation of
external
sphincter
Contraction of
detrusor muscle
External
sphincter
and pelvic
muscles
■
FIGURE 25-3
■
Pathways and central nervous system centers involved in control of bladder function.
Efferent pathways for micturition (
left
) and urine storage (
right
).
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, computed tomo-
graphic (CT) scanning, magnetic resonance imaging (MRI), or
ultrasonography. Cystoscopy enables direct visualization of
the urethra, bladder, and ureteral orifices. The ultrasound blad-
der scan provides a noninvasive method for estimating bladder
volume. Urodynamic studies may be used to study bladder
function and voiding problems.
Skeletal muscle found in the external sphincter and the pelvic
muscles that support the bladder are supplied by the puden-
dal nerve, which exits the spinal cord at the level of segments
S2 through S4. The micturition center in the brain stem coor-
dinates 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 stud-
ies that measure bladder, urethral, and abdominal pressures;
urine flow characteristics; and skeletal muscle activity of the
external sphincter.
In summary,
although the kidneys function in the forma-
tion of urine and the regulation of body fluids, it is the blad-
der that stores and controls the elimination of urine. Micturi-
tion is a function of the peripheral ANS, subject to facilitation
or inhibition from higher neurologic centers. The parasympa-
thetic nervous system controls the motor function of the blad-
der detrusor muscle and the tone of the internal sphincter; its
cell bodies are located in the sacral spinal cord and communi-
cate with the bladder through the pelvic nerve. Efferent sym-
pathetic 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.
ALTERATIONS IN BLADDER FUNCTION
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 al-
most 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 neuro-
logic control of bladder function.
450
Unit Six: Alterations in the Urinary System
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).
7
Because it
has the potential to produce vesicoureteral reflux and cause kid-
ney damage, urinary obstruction and stasis is a serious disorder.
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 com-
mon 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 uri-
nary 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 sec-
ondary invasion of the bladder by tumors arising in structures
that surround the bladder and urethra can compress the blad-
der 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.
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.
7
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, some-
times to the point of incontinence, and frequency during the
day and at night.
With continuation and progression of the obstruction, com-
pensatory 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 detrusor contraction can
increase from a normal 20 to 40 cm H
2
O to 50 to 100 cm H
2
O
to overcome the resistance from the obstruction. As the force
needed to expel urine from the bladder increases, compen-
satory mechanisms may become ineffective, causing muscle fa-
tigue 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 con-
tinued outflow obstruction, this smooth surface is replaced
with coarsely woven structures (
i.e.
, hypertrophied smooth
muscle fibers) called
trabeculae
. Small pockets of mucosal tis-
sue, called
cellules
, commonly develop between the trabecular
ridges. These pockets form diverticula when they extend be-
tween the actual fibers of the bladder muscle (Fig. 25-4).
Because the diverticula have no muscle, they are unable to con-
tract and expel their urine into the bladder, and secondary in-
fections caused by stasis are common.
■
FIGURE 25-4
■
Destructive changes of the bladder wall with de-
velopment of diverticula caused by benign prostatic hypertrophy.
Along with hypertrophy of the bladder wall, there is hyper-
trophy 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, vesicourethral re-
flux, and eventually, kidney damage (see Chapter 23). Stasis of
urine predisposes to urinary tract infections.
When compensatory mechanisms no longer are effective,
signs of decompensation begin to appear. The period of detru-
sor 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, a need to strain to initiate urination, a weak and
small stream, and termination of the stream before the bladder
is completely emptied—become pronounced. The amount of
residual urine may increase to 1000 to 3000 mL, and overflow
incontinence occurs. There also may be acute retention of urine.
The signs of urine retention are summarized in Chart 25-1.
CHART 25-1
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
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