CHAPTER 2

VOIDING PHYSIOLOGY
JoAnn M. Ermer-Seltun

OBJECTIVES
1. Explain the physiology of normal voiding, to include the role of each of the following:
cerebralcortex, pontine micturition center, spinal cord and nerve pathways, bladder, urethral
sphincter mechanism, and pelvic floor.
2. Explain how kidney, bladder, and sphincter function change with aging and how these
changesaffect voiding patterns and continence.

TOPIC OUTLINE
Structures and Functions Critical to Normal Voiding and Continence
Structure and Function of the Lower Urinary Tract
Urinary Bladder Urothelium
Lamina Propria
Muscularis or Detrusor15Serosal Coat
Blood Supply to Bladder
Urethra and Urethral Sphincter Mechanism
Anatomic Features
Smooth Muscle (also known as internal sphincter) Striated
Muscle
Pelvis
Pelvic Floor
Pelvic Floor Part I & II Levator
Ani
Endopelvic Fascia
Perineal Membrane and Perineal Body
Role in Continence
Fast-Twitch versus Slow-Twitch Muscle Fibers
Guarding Reflex
Support for Voiding
Neural Control of Micturition
Central Nervous System
Cerebral Cortex and Midbrain Pons
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AN: 3322893 ; JoAnn Ermer-Seltun, Sandy Engberg.; Wound, Ostomy and Continence Nurses Society Core Curriculum: Continence Management
Account: s8507403.main.eds

Spinal Cord and Nerve Pathways

Autonomic Nervous System: Sympathetic and Parasympathetic Pathways
Sympathetic Pathways
Parasympathetic Pathways
Somatic Nervous System
Pudendal Nerve (Onuf Nucleus)

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 Signaling Neurons in the Detrusor and Urothelium Intact
Cognition
Summary of Normal Lower Urinary Tract Function
Storage Phase
Emptying Phase (Micturition)
Changes Across the Lifespan
Infants and Toddlers
Middle-Aged Adults
Elderly
Changes in Bladder Function
Changes in Sphincter Function
Changes in Pelvic Floor Function
Comorbid Conditions and Impact of Pharmacologic Agents
Conclusion

The lower urinary tract (bladder, urethra, and sphincter) is responsible for low pressure storage and
coordinated elimination of urine, with normal function characterized by cyclical filling and emptying. The
ability to delay voiding until a time and place that is socially acceptable and the ability to empty the bladder
effectively are important to quality of life for children past the age of toilet training, adolescents, and adults.
Normal voiding and urinary continence are dependent on normal bladder and sphincter function, neural
control, and intact cognition (Girard et al., 2017).

KEY POINT
Normal voiding and urinary continence are dependent on normal bladder and sphincter function, neural
control, and intact cognition. In order to understand the pathology of voiding dysfunction and the various
types of urinary incontinence, it is critical to understand normal function.

Voiding dysfunction and urinary incontinence are common disorders that have a major impact on quality
of life; voiding dysfunction and neurogenic bladder dysfunction can also potentially affect upper tract
function and overall health. In order to understand the pathology of voiding dysfunction and the various types
of urinary incontinence, it is critical to understand normal function. That is the focus of this chapter.

STRUCTURES AND FUNCTIONS CRITICAL TO

NORMAL VOIDING AND CONTINENCE
The individual with normal lower urinary tract function never really thinks about the components of bladder
control and effective voiding. The average adult with normal function voids approximately six to eight times
daily (every 3 to 4 hours) (Lukacz et al., 2009, 2011; Zderic & Chacko, 2012). He/she is able to sense bladder
filling, delay voiding if necessary (even if the bladder is quite full), and initiate voiding when a socially
acceptable time and place are found. The individual with normal lower urinary tract function can also initiate
urination even when there is very little urine in the bladder and no “need to void” should this be necessary
(e.g., when a urine sample is requested) (Griffiths, 2015). These abilities are supported by an anatomically
intact lower urinary tract (bladder, urethra, and sphincter) and pelvic floor, an intact and functional neural
control system (brain, spinal cord, and nerve pathways), and intact cognition (Birder et al., 2017; Girard et
al., 2017). The structure and function of each of these structures will be discussed, followed by a brief
discussion of changes in function across the life span.

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 KEY POINT
The child/adult with normal bladder function is able to sense bladder filling, delay voiding until a socially
acceptable time and place are found (even if the bladder is quite full), and initiate voiding when desired
(even if there is very little urine in the bladder and no sensation of “need to void”).

STRUCTURE AND FUNCTION OF THE LOWER

URINARY TRACT
The lower urinary tract consists of the bladder, urethra, and pelvic floor muscles. These structures work
together as a unit to maintain continence through storage and elimination of urine at a desirable time ( Fig.
2-1 ).

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 FIGURE 2-1 A, B. Female and male bladders. (From Tank, P. W., & Gest, T. R. (2009). Lippincott
Williams & Wilkins Atlas of anatomy . Baltimore, MD: Wolters Kluwer Health.)

URINARY BLADDER
The urinary bladder is a hollow, muscular organ that has a fixed base and quite a dispensable body designed
to fill with urine at low pressures, store approximately 300 to 600 mL in the healthy adult and eliminates
urine. The bladder lies within the pelvic cavity and is located posterior to the symphysis pubis and inferior
to the parietal peritoneum. In females, the anterior uterine wall and vagina come in contact with the bladder,
while in males, the posterior bladder neighbors the rectum (Shier et al., 2019). The pressure of surrounding
organs modifies the spherical shape of the bladder, but the size and shape of the bladder are dependent upon
the amount of urine being stored. Often, anatomic drawings inaccurately depict an air bubble in the bladder;
however, as the bladder empties, the walls collapse down upon the fixed base creating a tetrahedron
(triangular pyramid)-like shape.
As the bladder fills, the superior surface expands upward into a dome; it pushes above the pubic crest if
distended and near the umbilicus if greatly distended (Shier et al., 2019). The trigone is a triangular-shaped
smooth muscle at the base of the bladder with the apex extending into the bladder neck in women and the
verumontanum (an elevation in the floor of the prostrate where seminal ducts enter) in men. The trigone has
an inlet at each of the angles that resemble a flap-like fold of the mucous membrane. This fold acts like a
valve at the ureteral vesical junction (UVJ) that allows urine to enter the bladder but prevents backing up of
urine from the bladder to the ureter even during coughing, sneezing, and physical exertion (Shier et al., 2019).

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 KEY POINT
The UVJ plays a pivotal role in promoting antegrade urine flow from the kidney into the bladder and
preventing reflux (retrograde movement) from the bladder to the upper tracts.

The bladder has two critical and repetitive functions: to stretch and store moderate volumes of urine at
low pressures and to contract effectively to empty. The ability to distend with urine while maintaining low
intravesical pressures is a property known as compliance and is important both to preservation of upper tract
(renal) health and to normal voiding intervals and quality of life (Chai & Birder, 2015). Maintenance of low
filling pressures is essential to renal health because it permits continued delivery of urine from the kidneys
to the bladder; once the intravesical pressure rises to a level greater than that exerted by the low-pressure
ureters, delivery of urine ceases and there is resulting back pressure on the kidneys, which can eventually
result in hydronephrosis (distention of the kidney). In addition, a rapid rise in intravesical (within bladder)
pressure with low volumes of urine is associated with intense urgency in the patient who has normal sensation
(because the bladder feels and acts “full” when there is a marked increase in intravesical pressure).

KEY POINT
The bladder’s ability to distend with urine while maintaining low intravesical pressures is a property known
as compliance and is important both to preservation of upper tract (renal) health and to normal voiding
intervals and quality of life.

It is also important for the bladder to mount a strong and sustained contraction to effectively empty the
urine. A weakly contractile bladder is associated with significant volumes of retained urine, which causes
increased urinary frequency and urgency, nocturia, and increased risk of urinary tract infection (UTI).
The bladder is very well designed for alternate storage and expulsion of urine (see Fig. 2-2 ).
Depending upon anatomy texts, multiple equivalent terms are used for the four layers of the bladder
(mucosal, submucosal, muscular, and serous coat). It has three main microscopic layers (urothelium or
mucosa; lamina propria, suburothelium or submucosal; muscularis or detrusor), each of which plays an
important role in bladder filling, sensory inputs to the central nervous system (CNS) regarding state of filling,
and effective emptying. In addition, it has an outer serosal coat or adventitia (Bolla & Jetti, 2019; Chai &
Birder, 2015; Kurz & Guzzo, 2017; Shier et al., 2019).

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 FIGURE 2-2 Layers of the Bladder.

Urothelium
The mucosa coat is composed of several thicknesses of the transitional epithelial cells or uroepithelium that
are similar to the lining of the renal pelvis and ureters as well as the upper portion of the urethra. The thickness
of this layer becomes reduced (only one to two cells deep) as the bladder fills and distends and returns to five
to seven cells deep with urine elimination, thereby earning its “transitional” name. The apical or umbrella
cell is the inner most urothelium layer that comes in contact with urine and microorganisms (Chai & Birder,
2015).
The uroepithelium is impermeable to the contents of the urine and coated with a thick, mucoid-like
substance called glycosaminoglycans (GAG layer) that is thought to limit adherence of bacteria and
penetration of urine irritants. Damage to this layer might permit penetration by noxious substances, bacterial
adherence and infection, and/or abnormal release of inflammatory molecules by the urothelium, resulting in
symptoms such as pain, urgency, and frequency. Recently, it is believed that proteins within the umbrella cell
membranes (uroplakins) and tight junction proteins play a greater role in the impermeability and barrier
function of the bladder urothelium (Chai & Birder, 2015).
The urothelium was previously conceptualized as a passive layer that primarily provided separation
between the bladder wall and the constituents of the urine. However, it is now recognized that there are a
number of ion channels and receptors located in the urothelial layer that detect mechanical, thermal, and
chemical stimuli; in response to these stimuli, the urothelium secretes signaling molecules (such as ATP,
ACh, and NO) that provide input to the brain regarding bladder filling and messaging to the bladder muscle
that help to modulate relaxation and contractility (Gonzalez et al., 2014a,b). For example, nitric oxide (NO)
released by the urothelium may contribute to normal bladder filling via two mechanisms: (1) There is
evidence that NO modulates and down-regulates activation of sensory pathways signaling bladder filling and
(2) NO is known to contribute to detrusor muscle relaxation. There is also evidence that activation of stretch
receptors in the bladder wall causes release of ATP by the urothelium, which stimulates the sensory pathways
signaling bladder filling. Finally, emerging evidence suggests that, in the “normal” bladder, there is a balance
between release of NO and ATP and that the ATP/NO ratio is one factor determining the frequency of bladder

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 contractions (Chai & Birder, 2015; Fry & Vahabi, 2016). Disease, injury, stress, or inflammation may alter
the urothelium’s ability to release signaling molecules potentially contributing to bladder dysfunction (Girard
et al., 2017).

KEY POINT
The bladder is lined with urothelium, which was previously thought to be a passive layer separating the
bladder wall from the constituents of the urine; it is now recognized that the urothelium secretes signaling
molecules that provide input to the brain regarding bladder filling and input to the bladder that modulates
bladder relaxation and contractility.

Lamina Propria
The lamina propria is also known as the suburothelium and is the layer lying between the urothelium and
the detrusor. It is often referred as the “functional center” of the bladder by coordinating detrusor muscle and
uroepithelium activities (Chai & Birder, 2015). It includes interstitial cells called myofibroblasts that may
have a pacemaker role, fibroblasts, blood vessels, and both afferent (sensory) and efferent (motor) nerves.
This layer is thought to contribute to normal bladder distensibility (compliance) by maintaining a balance
between type III and type I collagen (25% and 75%, respectively) and by production of the elastic fibers that
allow the bladder to return to its normal shape following emptying (Andersson & McCloskey, 2014). Recent
studies suggest that the lamina propria may also contribute to modulation and signaling related to bladder
filling and contractility (Andersson & McCloskey, 2014; Gonzalez et al., 2014b).

Muscularis or Detrusor
The third layer consists of a complex meshwork of smooth muscle bundles (unlike the organized circular and
longitudinal layers of the intestine) surrounded by an extracellular matrix known as the detrusor muscle. The
muscle layer contains 50% collagen and 2% elastin to provide structural integrity to the bladder (Chai &
Birder, 2015). The long slender smooth muscle cells of the bladder are known as single unit smooth muscle,
meaning that the ratio between muscle cells and nerve endings is almost 1:1; this rich innervation provides
high-level neural control of bladder contractility (Chai & Birder, 2015). The smooth muscle cells of the
bladder have length and tension properties that permit them to stretch slowly without inducing a contraction
until emptying is initiated voluntarily or until capacity has been reached. In the event of rapid stretch (e.g.,
rapid bladder filling due to diuresis or rapid filling during cystometrogram), the muscle cells respond initially
with a marked increase in tension that dissipates before a detrusor contraction is produced; this phenomenon
is known as the stress relaxation response and is dependent in part on normal viscoelastic properties of the
detrusor muscle and extracellular matrix (collagen). Excessive stretch on the detrusor muscle cells, as occurs
with marked overdistention of the bladder, results in irreversible changes in the muscle; this explains why
inadequate management of acute urinary retention can result in chronic urinary retention (Wyndaele et al.,
2011; Zderic & Chacko, 2012).
Detrusor contraction occurs in response to parasympathetic stimulation and is normally characterized by
a contraction of sufficient force and duration to expel all or most of the urine; normal contractility is
dependent both on normal innervation and normal contractility (Chai & Birder, 2015).

KEY POINT
The inner layer of the bladder (detrusor muscle) is comprised of smooth muscle cells with length and
tension properties that permit them to stretch slowly without inducing a contraction until emptying is
initiated voluntarily or until capacity has been reached.
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 In addition to the myocytes (muscle cells), the detrusor contains stretch receptors that signal bladder
filling. Further, there is some evidence for a motor–sensory system within the bladder that may increase
sensory awareness of the need to void. Specifically, there are data suggesting that, as the bladder becomes
progressively more distended with urine, there is increasing low-level muscle activity (localized low
amplitude contractions, or “twitches,” in the muscle); these low amplitude contractions in response to stretch
do not produce voiding but are thought to contribute to the afferent “noise” produced by the distending
bladder that signals the CNS regarding the need to void (Eastham & Gillespie, 2013).
Serosal CoatThe fourth and most outer layer of the bladder is the serosal coat or adventitia. It covers
most of the bladder with fibroelastic connective tissue except the upper portion of the bladder where simple
squamous epithelium covers the area along with a small amount of connective tissue. The primary role of the
serosal/adventitia is to connect to surrounding tissues and protect the bladder from friction from adjacent
organs. Perivesical fat covers beyond the serosa/adventitia (Bolla & Jetti, 2019; Girard et al., 2017).

Blood Supply to Bladder

The bladder receives its arterial blood supply via the superior, inferior, and medial vesical arteries, in addition
to branches of the obturator, inferior gluteal, or internal iliac arteries. Females also receive arterial blood to
the bladder from uterine and vaginal arteries. This profuse blood supply to the bladder accounts for blood in
the urine (hematuria) that easily arises with UTIs, trauma, or surgery (Huether, 2019).

KEY POINT
The detrusor also contains stretch receptors that signal bladder filling as well as a rich blood supply.

URETHRA AND URETHRAL SPHINCTER MECHANISM The

urethra serves as a conduit for elimination of urine from the bladder (and for semen in men) and plays an
important role in both effective bladder emptying and in maintenance of continence. Normally, the urethra
functions synergistically with the bladder; during the storage cycle, the urethra remains closed to maintain
continence (even during periods of increased abdominal pressure), and during voiding, the urethra funnels
and opens to permit unobstructed flow. Normal function is dependent on structural integrity of the bladder
neck, urethral sphincter mechanism, and pelvic floor as well as intact neural structures, pathways, and
activity. KEY POINT

Normally, the urethra functions synergistically with the bladder; during the storage phase, the urethra
maintains closure, and during the emptying phase, the urethral funnels and opens to permit unobstructed
flow.
Anatomic Features
Anatomically, the urethra is short and straight in women, averaging 4.0 cm (2.5 to 5.0 cm), and long and
curved in men, averaging 20 cm (15.0 to 25.0 cm) ( Figs. 2-3 and 2-4 ). The greater urethral length and
curvature in men provides increased urethral resistance, and this anatomic difference between men and
women is thought to be one factor contributing to the increased risk of incontinence among women ( Gill,
2019; Kurz & Guzzo, 2017). The male urethra can be subdivided into three sections: the prostatic urethra
(the section surrounded by the prostate gland), the membranous urethra (the section involving the voluntary
sphincter mechanism), and the penile urethra. Like the upper urinary tract and bladder, the urethra is
composed of the same four histological layers (urothelium, lamina propria, muscularis, and serosa or
adventitia) but differs in that it is composed of both smooth and specialized striated muscle that aids in
maintaining continence. The smooth muscle maintains a level of tonic contraction that helps to maintain
urethral closure during the filling cycle (Sadananda et al., 2011) while the specialized striated muscle that

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 contains both fast-twitch and short-twitch muscle fibers aid in tone of the urethra during periods of sudden
increase in abdominal pressure (i.e., cough) and prolong periods needed for continence between voids.

FIGURE 2-3 Female Urethra.

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 FIGURE 2-4 Male Urethra. Asset provided by Anatomical Chart Co.

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 Additional support for continence is provided by a rich vascular plexus that is located in the subepithelial
layer. This network of vessels acts as a fluid-filled sponge that provides compressive support to the urethra,
which seems to be particularly important to continence in women (Sadananda et al., 2011). In addition, to
promote female continence even further, the anterior vaginal wall is fused with the distal two thirds of the
urethra and shares vascular components, muscular and endopelvic fascial support (Pradidarcheep et al., 2011;
Sampselle & DeLancey, 1998; Siccardi & Valle, 2019). Finally, in women, anatomic support for continence
is provided by coaptation of the urethral walls, which helps to maintain urethral closure and to resist leakage;
coaptation is dependent on soft moist urethral tissue and may be adversely affected by estrogen deficiency
(Alperin et al., 2019). In males, passive support is provided by the prostate gland as another contributing
factor to continence although late in life, prostatic hypertrophy may result in outlet obstruction and urinary
retention (Wagg et al., 2017).
KEY POINT
Anatomic features of the male urethra contributing to continence include the greater length and curvatures,
which increases resistance, and support provided by the prostate gland. In women, the suburethral vascular
plexus, anterior vaginal wall fusion to the distal urethra, and coaptation of the urethral walls seem to play
an important role upholding continence.

Smooth Muscle (also known as internal sphincter)

The bladder neck is comprised of smooth muscle innervated by the autonomic nervous system (ANS) and
controlled by descending nerve pathways from the pontine micturition center (PMC); the internal sphincter
is tonically contracted throughout the filling phase and provides primary support for continence. As noted,
neural control of the bladder neck and detrusor muscle assures synergistic response of the bladder and its
outlet. Specifically, during the storage phase, sympathetic pathways are activated; sympathetic stimulation
of the alpha-adrenergic receptors in the smooth muscle of the bladder neck causes increased urethral tone,
while sympathetic stimulation of the beta-adrenergic receptors in the bladder wall causes detrusor relaxation.
Conversely, during voiding, sympathetic stimulation to the bladder neck and detrusor is turned “off,” causing
relaxation of the bladder outlet, and parasympathetic stimulation of cholinergic/muscarinic receptors in the
bladder wall causes detrusor contraction.
There is evidence that the smooth muscle of the bladder neck is more highly developed in the male than
in the female. There is also evidence that interstitial cells interspersed throughout the smooth muscle of the
bladder neck may function as “pacemakers” to promote contractility and maintain urethral closure during the
filling cycle and that there is direct input from the pontine storage center (PSC) to the bladder neck promoting
closure (Birder et al., 2017; Chai & Birder, 2015; Sadananda et al., 2011).

KEY POINT
The “internal sphincter” is comprised of smooth muscle fibers within the bladder neck, which are innervated
by the autonomic nervous system and controlled by the pons.

Striated Muscle
The voluntary sphincter (also known as the external urethral sphincter [EUS] or rhabdosphincter) consisting
of striated muscle is located just distal to the prostate gland in men (at the level of the membranous urethra)
and at approximately midurethra in women. In men, the rhabdosphincter is one omega-shaped muscle; in
women, it is more semicircular (horseshoe) in shape and consists of three separate but connected muscles
(sphincter urethrae, compressor urethrae, and sphincter urethrovaginalis) that work together to support,
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 compress, and elongate the urethra (Fig. 2-6B) (Hinata & Murakami, 2014 ; Jung et al., 2012). The EUS
contains both fast-twitch (quick and strong contraction) and slow-twitch (sustained contraction) fibers. Ratio
of fast-twitch to slow-twitch fibers in women is 13% to 87% and 35% to 65% in men, respectively (Chai &
Birder, 2015). Fast-twitch fibers provide a rapid burst of contractile force when sudden increases of
abdominal pressure, that is, cough, while the slow-twitch offers a sustained contraction that is slow to fatigue
to maintain continence. The voluntary sphincter is innervated by branches of the pudendal nerve; voluntary
contraction significantly increases urethral closure pressure and helps to prevent leakage during periods of
increased intra-abdominal pressure.
KEY POINT
The “external” urethral sphincter is comprised of striated muscles located just distal to the prostate gland
in men and at midurethra in women; it is under voluntary control and can be strengthened by pelvic muscle
exercises.

PELVIS
The pelvis is a ring of bones composed of the sacrum and fusion of paired bones of the iliac, ischial, and
pubic bones. The female pelvis accommodates both locomotion and childbirth by being larger and broader
than that of a male (tall, narrow, and compact) as well as having an ovoid-shaped inlet in contrast to the male
heart-shaped inlet.

PELVIC FLOOR
The pelvic floor consists of several muscle groups, fascia, and ligaments that help support the pelvic viscera
(urethra, bladder, vagina, uterus, prostate) and promote anal and urethral sphincter function ( Fig. 2-5 A and
B); there are many descriptors given to these muscles by authors, which creates confusion even for the
savviest continence specialist. Basically, the pelvic floor is made up of three primary layers beginning from
the inferior to the most superior view of the pelvis: (1) superficial perineum (houses erectile tissues, external
genitalia muscles, superficial perineal space, created by superficial facia interfacing with the perineal
membrane); (2) urogenital diaphragm (deep perineum) contains the deep perineal space (superior aspect or
roof of the perineal membrane), urethral and vaginal sphincter muscles; and (3) pelvic diaphragm that consist
of the levator ani, coccygeus, and pelvic wall muscles (Bordoni et al., 2019). See Figure 2-6 A–C.

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 FIGURE 2-5 A. Pelvic floor, male and female. B. Medial view pelvic floor muscles. (From Oatis,
C. A. (2004). Kinesiology—The mechanics and pathomechanics of human movement .
Baltimore, MD: Lippincott Williams & Wilkins.)

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 FIGURE 2-6 Three Layers of the Pelvic Floor Muscles. A. Layer 1: Superficial Perineum. B.
Layer 2: Urogenital Diaphragm. C. Layer 3: Pelvic Diaphragm. (Used with permission from Moore,
K. L., DAlley, A. F., & Agur, A. M. R. Clinically oriented anatomy . Philadelphia, PA: Wolters
Kluwer.)

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 PELVIC FLOOR PART I & II
Key support structures within these three layers provide vital support to the pelvic soft organs (viscera) and
the urethral continence mechanism: (1) levator ani muscle; (2) endopelvic fascia; and (3) perineal membrane,
perineal body (PB) and external anal sphincter (Bordoni et al., 2019).

Levator Ani - Within the third layer (pelvic floor diaphragm) resides the principal source of support of
the pelvic floor, the levator ani, which consists of the (1) pubococcygeous (includes pubourethralis,
pubovaginalis), the central and major muscle, which extends from the symphysis pubis to the coccyx; (2)
puborectalis, which forms a sling behind the anorectal junction; and (3) ileococcygeous, a smaller muscle
that lies superior to the pubococcygeus (Fig. 2-6C). Although the levator ani is a group of muscles, they
function as a single unit (Pradidarcheep et al., 2011; Sampselle & DeLancey, 1998). The principle function
of the levator ani is to lift the anus, vagina, and urethra and to pull them forward; this anterior pull creates a
compressive force against the lumen of these organs that promotes closure through increased intraurethral,
intravaginal, and intra-anal pressures (Bordoni et al., 2019; Sampselle & DeLancey, 1998). The muscles are
covered by endopelvic fascia, which condenses into ligaments that attach the pelvic organs to the bony
pelvis (Siccardi & Valle, 2019).
Endopelvic Fascia
The pelvic floor layers and viscera must anchor to the bony structures of the pelvis in order to provide optimal
support. The endopelvic fascia is complex internal system made of dense connective tissue composed of
collagen, elastin, and smooth muscle. It provides suspensory support by encapsulating the pelvic viscera
(urethra, vagina, bladder, uterus) as well as the levator ani and connecting them to the boney pelvis as well
to each other. In general, endopelvic fascia serves to compartmentalize organs and muscles to maintain form
and function, assists in sliding yet limits friction during motion, responds to stretch and distention and serves
as a shock absorber (Siccardi & Valle, 2019).

Perineal Membrane and Perineal Body - The perineal membrane, PB, and anal sphincter
comprise an inferior supportive layer of the pelvic floor (Siccardi & Bordoni, 2018) (Fig. 2-6 A,B; and Fig.
2-7). The perineal membrane (urogenital diaphragm) is a triangular fibrous structure that spans the anterior
pelvis, the vagina, and urethra pass through a central hole in this supportive membrane. The primary function
of the perineal membrane is to limit descent of the pelvic organs by attaching the PB to the pubic bones. The
perineal membrane provides secondary support by limiting descent of the PB and vagina when the levator
ani is relaxed during the processes of defecation, urination, and birth (Sampselle & DeLancey, 1998).

The PB is a fibrous muscular structure that is centrally located between the urogenital and anal triangles.
In women, it’s between the anus and vagina and men, between the bulb of the penis and anus. It is often
referred as the “central tendon” of the perineum because of the multiple attachments to the superficial and
deep perineal muscles, urethral and anal sphincters, as well as a midline anchor for the perineal membrane
and rectovaginal or recto prostatic facia (Siccardi & Bordoni, 2018). See Figure 2-7. Due to these
attachments, the PB strengthens the pelvic floor. Some authors describe the PB as a knot made of many
strings to simplify its image and visualization of function. For example, if tension is applied to one of the
strings attached to the knot, the PB (knot) becomes imbalance or changes position (Nayak et al., 2008).
Recently, the PB has received greater attention in the literature due to its crucial role in maintaining pelvic
floor integrity especially in women (Larson et al., 2010; Siccardi & Bordoni, 2018). Injury often occurs
during childbirth causing it to rupture from spontaneous tears, episiotomy or overstretching leading to nerve,
muscle or fascial defects such as prolapse of the uterus, rectum, and occasionally the bladder leading to bowel
and bladder dysfunction (Siccardi & Bordoni, 2018). Assessment of the PB is encouraged during the
assessment of pelvic floor function (Chevalier et al., 2014). See Chapter 4 for further discussion. The role of
the anal sphincter mechanism is outlined in Chapter 20.
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 FIGURE 2-7 Perineal Body (A) and Anterior Posterior Triangle (B). (Used with permission from
Agur, A. M. R., & Dalley, A. F. Grant’s atlas of anatomy . Philadelphia, PA: Wolters Kluwer.)

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 Role in Continence
A healthy pelvic floor has sometimes been compared to a trampoline; when increased intra-abdominal
pressure pushes pelvic organs caudally, the pelvic floor normally provides counterpressure and sufficient
support to maintain the organs (vagina, bladder, and urethra) in their normal positions ( Ashton-Miller et al.,
2001). This is important because there is some evidence that loss of normal intrapelvic position compromises
function of the striated sphincter; urethral “hypermobility” (distal displacement of the urethra in response to
increased intra-abdominal pressure) is thought to be one factor contributing to stress incontinence in women
(Aleksic & De, 2016; Bauer & Huebner, 2013). Pelvic floor support is enabled by the fact that there are
connections between the pelvic floor and striated sphincter muscles, so contraction of the striated sphincter
also causes contraction of the pelvic floor muscles. This means that pelvic muscle exercise programs
strengthen both the striated sphincter and the pelvic floor muscles, thus providing improved support for
pelvic organs in addition to increasing sphincter muscle contractility and endurance (McLean et al., 2013;
Dumoulin et al., 2017; Qaseem et al., 2014).

KEY POINT
A healthy pelvic floor has sometimes been compared to a trampoline; it serves to support the pelvic organs
in normal anatomic position and to oppose downward displacement during activities that cause increased
intra-abdominal pressure.

Fast-Twitch versus Slow-Twitch Muscle Fibers

The pelvic floor muscles are comprised of approximately 2/3 slow-twitch fibers and 1/3 fast-twitch fibers.
Slow-twitch fibers provide sustained tonic contraction and improve baseline support for pelvic organs, while
fast-twitch fibers provide rapid strong contractions that prevent leakage during periods of increased
abdominal pressure (Marques et al., 2010). Pelvic muscle exercise programs are generally designed to
strengthen both slow-twitch and fast-twitch fibers and thus to improve both continence at rest and continence
during activities that increase stress on the continence mechanism (Dumoulin et al., 2017; Madill et al., 2013;
Marques et al., 2010; Qaseem et al., 2014).

KEY POINT
Pelvic floor muscles contain both slow-twitch and fast-twitch fibers, which means they provide both
baseline support for continence and increased contractility during periods of increased abdominal pressure.

GUARDING REFLEX
The guarding reflex helps to maintain continence by progressively increasing outlet resistance in response to
bladder filling or sudden increase in bladder pressure, that is, cough (Birder et al., 2017; Vo & Kielb, 2018).
There appears to be at least two pathways involved in the guarding reflex: (1) As the bladder distends with
urine, stretch receptors in the bladder wall are activated, and these receptors send signals regarding bladder
filling to the sacral cord; this activates the pudendal nerve (in addition to sending messages regarding bladder
filling to the brain). The pudendal nerve then activates efferent (motor) pathways to the external sphincter
that act on nicotinic receptors in the external sphincter muscle to increase outlet resistance. (2) In addition,
afferent (sensory) signals from the distending bladder activate a pathway from the sacral cord to the
thoracolumbar cord; this causes increased sympathetic stimulation of the bladder neck and bladder, which
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 results in increased bladder neck tone and detrusor relaxation; (Chai & Birder, 2015; Vo & Kielb, 2018).
Recently, there is a greater emphasis that sensory fibers within the urethra itself may in fact initiate the
guarding reflex when urine is presented in the proximal urethra activating both pudendal motor pathways
and sympathetic activation as described above (Birder et al., 2017).

KEY POINT
The guarding reflex helps to maintain continence by progressively increasing outlet resistance in
response to bladder filling or an abrupt increase in bladder pressure.

Support for Voiding

In addition to maintaining closure during the filling cycle and thereby preventing incontinence, the normal
urethra funnels and opens to provide unobstructed emptying during voiding. There is some evidence that
afferent nerves in the urethra may contribute to effective bladder emptying by sensing flow rates and
providing feedback that maintains the detrusor contraction as long as flow rates remain high (Deckmann et
al., 2014; Girard et al., 2017).

NEURAL CONTROL OF MICTURITION

As noted, the bladder and its outlet constantly cycle between filling and periodic emptying, with synergistic
activity during each phase (bladder relaxation and sphincter contraction during filling, followed by bladder
contraction and sphincter relaxation during emptying). This coordinated and cyclical activity requires
complex interaction among multiple signaling pathways and neurologic centers, in addition to an intact lower
urinary tract (Birder et al., 2017; de Groat et al., 2015; Gill & Kim, 2018). The primary nervous systems
involved include (1) CNS including the brain, brain stem, and spinal cord; (2) peripheral nervous system
including the ANS providing sympathetic outflow tracts located in the thoracolumbar cord (T10–L2) and
parasympathetic outflow tracts located in the sacral cord (S2–S4) and somatic nervous system controlling
striated muscles through outflow tracts at Onuf nucleus also located in the sacral cord (S2–S4); and lastly (3)
signaling neurons in the urothelium and detrusor (Birder et al., 2017; Chai & Birder, 2015; Gill & Kim, 2018;
Girard et al., 2017; Griffiths, 2015 ) (see Figs. 2-8 and 2-9 ).

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 FIGURE 2-8 Divisions of the Nervous System. (Image created by JoAnn Ermer-Seltun.)

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 FIGURE 2-9 Neural Control of Voiding. (Reprinted with permission from Newman, D. K., DNP,
Society of Urologic Nurses and Associates Core Curriculum.)

CENTRAL NERVOUS SYSTEM

Cerebral Cortex and Midbrain
The actual switch between bladder filling (storage) and bladder emptying (voiding) is controlled by midbrain
structures (particularly the periaqueductal gray, or PAG) and the PMC; however, decision -making regarding
voiding (social continence) is the responsibility of higher brain centers, specifically the prefrontal cortex
(Yao et al., 2018). The decision regarding voiding is based on sensory input from mechanoreceptors within
the bladder regarding bladder filling as well as environmental input and can involve delay of voiding despite
a very full bladder (until an appropriate time and place can be found) or can involve volitional initiation of
voiding in the absence of any urgency to void, such as the decision to void “prophylactically” before
beginning a long car trip (Griffiths, 2015). The primary centers involved in processing signals regarding
bladder filling include the periaqueductal gray, the insula, the locus coeruleus, the anterior cingulate gyrus,
and the prefrontal cortex (Birder et al., 2017; Griffiths, 2015). This information is then relayed to the
decision-making center (prefrontal cortex) to defer or initiate the micturition (voiding) reflex depending upon
social acceptability. This reflex is usually under voluntary control by the higher brain center by age 3 to 5

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 but if any injuries or disease occur where the CNS cannot inhibit the micturition reflex when the bladder
becomes full, involuntary voiding will result (reflex voiding) (Gill & Kim, 2018; Girard et al., 2017).
Functional neuroimaging suggests the following sequence of events: (1) The PAG processes sensory
input regarding bladder filling and relays the information to the hypothalamus, insula, anterior cingulate
gyrus, and lateral prefrontal cortex; (2) the information is then transmitted from these centers to the medial
prefrontal cortex, which maintains inhibitory control of the PAG; (3) the medial prefrontal cortex makes a
decision regarding whether or not to void; (4) if the decision is not to void, inhibition of the PAG is maintained
and voiding is delayed; and (5) when the decision is made to void, inhibitory control of the PAG is withdrawn
and the PAG then activates the PMC (Barrington nucleus) to initiate coordinated voiding (de Groat et al.,
2015; Girard et al., 2017; Griffiths, 2015; Yao et al., 2018). New insights regarding regulation of voiding
validate the presence of other urination-related cortical neurons that may signal the PMC to permit or
suppress voiding (Yao et al., 2018).

KEY POINT
The actual switch between bladder filling and bladder emptying is provided by the midbrain structures (e.g.,
periaqueductal gray and pons); however, decision-making regarding voluntary voiding is the responsibility
of the prefrontal cortex.

PONS
The pons is located within the brainstem, which serves as specialized relay center between the brain and the
bladder. The pons has two areas involved with continence and voiding: the pontine micturition center (PMC
or Barrington nucleus) and the pontine storage center (PSC) (Birder et al., 2017). The PMC is responsible
for assuring that both the bladder neck (internal sphincter) and rhabdosphincter (external sphincter) are
relaxed before the bladder contracts, in order to provide unobstructed voiding. When activated by the PAG
to initiate the micturition reflex, the PMC sends input to the cord that inhibits sympathetic stimulation of the
bladder neck and innervation of the external sphincter via Onuf nucleus (thus causing both internal and
external sphincter relaxation) and activates the parasympathetic pathways causing detrusor contraction
(Birder et al., 2017; Gill & Kim, 2018; Griffiths, 2015). When the PSC is activated, there is direct stimulation
of a somatic pathway to Onuf nucleus triggering continued contraction of the striated sphincter via pudendal
nerve (Birder et al., 2017). Bladder filling (storage) begins again with sympathetic activation once the PAG
inhibits the PMC (Birder et al., 2017; Gill & Kim, 2018; Vo & Kielb, 2018).

KEY POINT
The PMC is responsible for assuring that both the bladder neck (internal sphincter) and rhabdosphincter
(external sphincter) are relaxed before the bladder contracts, in order to provide unobstructed voiding.

SPINAL CORD AND NERVE PATHWAYS

The spinal cord and its peripheral nerve pathways are essential to continence and to normal voiding, because
these structures comprise the communication center of the controlled voiding system, transmitting messages
from the bladder and sphincter to the brain and brain stem, and from the brain and brain stem to the bladder

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 and sphincter. Thus, any disruption in the spinal cord causes loss of continence and disruption in effective
coordinated voiding, a condition known as neurogenic bladder (Gill & Kim, 2018) (see also Chapter 9).

KEY POINT
Any disruption in the spinal cord causes loss of continence and disruption in effective coordinated
voiding, a condition known as neurogenic bladder.

AUTONOMIC NERVOUS SYSTEM: SYMPATHETIC AND

PARASYMPATHETIC PATHWAYS
Sympathetic Pathways
As explained earlier, sympathetic stimulation activates alpha-adrenergic receptors in the bladder neck (via
neurotransmitters such as norepinephrine) to produce increased tone and resistance and also activates beta-
adrenergic receptors in the bladder wall to cause detrusor relaxation. Thus, sympathetic pathways are active
during the storage phase and quiescent during voiding. Sympathetic pathways exit the cord at the
thoracolumbar level (T10–L2) via the hypogastric nerve (de Groat et al., 2015).

Parasympathetic Pathways
In contrast, parasympathetic stimulation causes bladder contraction and reflex relaxation of the bladder neck;
the primary neurotransmitter is acetylcholine, which mediates contraction via muscarinic receptors (M2 and
M3) in the bladder wall. In addition to its direct effects on detrusor contractility, acetylcholine is thought to
affect sensory awareness of bladder filling (Sellers & Chess-Williams, 2012). Parasympathetic pathways are
active during voiding and quiescent during filling. Parasympathetic pathways exit the cord at S2–S4 via the
pelvic nerves (de Groat et al., 2015; Girard et al., 2017).

KEY POINT
Sympathetic pathways are active during the storage phase, causing bladder neck contraction and detrusor
relaxation; parasympathetic pathways are active during voiding, causing reflex relaxation of the bladder
neck and detrusor contraction.

SOMATIC NERVOUS SYSTEM

Pudendal Nerve (Onuf Nucleus)
The striated sphincter is under voluntary control, via a collection of cells in the sacral cord known as Onuf
nucleus and the pudendal nerve. The cells of Onuf nucleus appear to receive direct input from the
PSC; activation provides contraction of the striated sphincter via the pudendal nerve, which exits the cord at
S2–S4 (de Groat et al., 2015). (As noted, inhibition of Onuf nucleus via the PMC causes striated sphincter
relaxation.)

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 KEY POINT
The striated sphincter and pelvic floor are under voluntary control (pudendal nerve).

SIGNALING NEURONS IN THE DETRUSOR AND UROTHELIUM

As previously discussed, the urothelium and detrusor contain a number of receptors that respond to
progressive bladder distention. The gradual increase in intravesical pressures that accompanies bladder filling
activates thinly myelinated fibers that send increasingly strong signals of bladder filling along autonomic
sensory nerve pathways to the cord; from the cord, they are transmitted to the brain, where there is a gradual
increase in awareness that prompts decision-making regarding when and where to void (Birder et al., 2017;
Chai & Birder, 2015). Studies of normal subjects revealed that bladder filling is perceived as “tingling” or
“pressure” and that awareness proceeds along the following continuum: no sensation, weak awareness,
stronger awareness, weak need to void, stronger need to void, and absolute need to void (Heeringa et al.,
2011). Extreme distention may also activate C fibers, which transmit signals of severe discomfort and pain;
C fibers are also activated by noxious substances in the urine or inflammation of the bladder wall (Birder et
al., 2017; Girard et al., 2017; Gonzalez et al., 2014b).

INTACT COGNITION
Bladder control is dependent in part on normal cognitive function. The individual must be able to accurately
interpret messages related to bladder filling, determine or locate a socially appropriate place to void, move
to that location, and remove clothing in order to permit voiding (Griffiths, 2015; Yao et al., 2018). While the
controlled voiding process is “automatic” for most individuals, it is in fact a complex process governed at
each step by the CNS. This is reflected by the fact that incontinence is common among individuals with
cognitive impairment, such as those who are sedated and those with advanced dementia. These individuals
tend to void whenever the bladder reaches a certain point of filling, regardless of time and place (reflexive
voiding) (de Groat et al., 2015; Gill & Kim, 2018). Incontinence due to cognitive impairment is labeled
“functional incontinence” and is discussed in detail in Chapter 13.

KEY POINT
While the controlled voiding process is “automatic” for most individuals, it is in fact a complex
process governed at each step by the central nervous system.

SUMMARY OF NORMAL LOWER URINARY TRACT FUNCTION

KEY POINT
The lower urinary tract cycles between “storage” and “emptying” via a complex sequence of events
controlled by a myriad of signaling molecules and nerve pathways.

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 STORAGE PHASE
During storage, the sympathetic pathways are active, and the parasympathetic pathways are quiescent.
Sympathetic stimulation of the alpha-adrenergic receptors in the bladder neck and proximal urethra maintains
bladder neck closure, and sympathetic stimulation of the beta-adrenergic receptors in the bladder wall
maintains bladder relaxation. The slow-twitch fibers in the pelvic floor muscles maintain resting tone, and
direct input from the PSC to Onuf nucleus (in the sacral cord) maintains closure of the external sphincter via
pudendal nerve innervation (Birder et al., 2017; Griffiths, 2015).
Progressive filling of the bladder activates stretch receptors in the bladder wall and release of signaling
molecules by the urothelium that provide progressively stronger messages to the midbrain (via the cord)
regarding bladder filling. Microcontractions of the detrusor muscle may also contribute to signaling regarding
bladder filling. This progressive filling also activates the guarding reflex (i.e., activation of pathways that
increase tone within the bladder neck and the voluntary sphincter via sympathetic stimulation and pudendal
nerve stimulation, respectively). The guarding reflex assures that urethral resistance increases in proportion
to the demands placed by a progressively distending bladder and increasing intravesical pressures (Birder et
al., 2017; Griffiths, 2015).
Messages regarding bladder filling are integrated by the midbrain, primarily the PAG; these synthesized
messages are forwarded to the medial prefrontal cortex, which maintains inhibitory control of the PAG and
where decision-making regarding when and where to void takes place. If the decision is made to defer
voiding, inhibitory control of the PAG is maintained, as is sympathetic input to the bladder and bladder neck
and pudendal nerve input to the voluntary sphincter (Birder et al., 2017; Griffiths, 2015).

EMPTYING PHASE (MICTURITION)

If the decision is made to initiate voiding, inhibitory control of the PAG is released; the PAG then directs the
PMC to mediate coordinated voiding (sphincter relaxation prior to detrusor contraction). The PMC
inactivates sympathetic pathways and the pathways controlling Onuf nucleus, thus causing relaxation of the
internal and external sphincters; the PMC also activates the parasympathetic pathways, thus causing detrusor
contraction via acetylcholine stimulation of muscarinic receptors (Birder et al., 2017; Griffiths, 2015; Yao et
al., 2018).

CHANGES ACROSS THE LIFESPAN

There are a number of changes that occur in lower urinary tract structure and function across the lifespan that
impact on continence and the ability to empty the bladder effectively; these changes will be discussed briefly
in this chapter and in more depth in Chapters 13 and 14.

INFANTS AND TODDLERS

Lower urinary tract development and urine production begin early in fetal life, at about 4 to 6 weeks gestation;
by the 12th week of gestation, the three-layered structure of the bladder wall is evident, and by 16 weeks, the
bladder exhibits limited reservoir capacity. During infancy, bladder function is characterized by lack of
coordination between the bladder and sphincter and by interrupted voiding (two separate voids during a 5-
to 10-minute period). For many years, it was thought that voiding in infants was a simple spinal reflex;
however, recent studies suggest involvement of the CNS, based on evidence of varying degrees of arousal
preceding voiding. When the child has matured to the level where she/he recognizes bladder filling and can
control bladder emptying, toilet training is appropriate. Once the child has established voluntary control of
voiding, the loss of coordination between bladder and sphincter disappears (sacral reflex voiding) and the
filling emptying cycle characteristic of adult bladder function is established (de Groat et al., 2015). For most
children, daytime continence is established first (attained by age 4 to 5), followed by nighttime control; girls
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 typically achieve continence at an earlier age than boys (Bauer & Huebner, 2013; Milsom et al., 2017).
Prevalence of daytime urinary incontinence (diurnal) at age 7 is 3.2% to 11.2% and nocturnal enuresis
(bedwetting) at age 7 (11%), 11 to 12 (3.5%), and 16 (1.3%). In most cases, children who suffer diurnal
incontinence or combination of day and nighttime incontinence are caused by overactive bladder (Milsom et
al., 2017).

KEY POINT
Once the child has matured to the level where she/he recognizes bladder filling and can control emptying,
toilet training is appropriate. For most children, daytime continence is established first, followed by
nighttime continence; girls usually achieve continence at an earlier age than boys.

MIDDLE-AGED ADULTS
Urinary incontinence is especially prevalent in middle-age women (Burgio et al., 1991; Danforth et al., 2006;
Hunskaar et al., 2000; Khoudary et al., 2019; Milsom et al., 2017). A longitudinal cohort study with an
ethnically and racially diverse sample of women (age 42 to 52 years) from seven geographical sites across
the United States named SWAN (Study of Women’s Health at Midlife) reported 68% of the 3,302 participants
suffered from at least one urinary incontinent episode per month (Khoudary et al., 2019). Danforth et al.
(2006) reported in a cross-sectional analysis of 83,335 participants in the Nurses’ Health Study II, 43% of
women experienced at least one urinary incontinent episode per month. In addition, data identified primary
risk factors: age, race/ethnicity, body mass index, parity, smoking, diabetes, and hysterectomy (Danforth et
al., 2006). Prevalence data regarding UI in middle-age men are sparse (Milsom et al., 2017), but data indicate
that lower urinary tract symptoms (LUTS) begin to manifest during the fourth decade of life in both sexes;
among women, storage symptoms are more common, while voiding symptoms are more common among
men. For both men and women, LUTS are associated with negative impact on quality of life, resulting in
anxiety and depression. For women, symptoms associated with increased anxiety include nocturia, urgency,
stress incontinence, leakage during sexual activity, weak stream, and split stream; symptoms associated with
increased anxiety in men include nocturia, urgency, incomplete emptying, and bladder pain. Among women,
stress incontinence, urgency, and weak stream are associated with depression; symptoms associated with
depression in men include frequency and incomplete emptying (Bauer & Huebner, 2013).

KEY POINT
Urinary incontinence is especially prevalent in middle-age women compared to men. Women tend to suffer
storage problems (stress incontinence) at midlife while men experience voiding problems.
ELDERLY
The elderly population has the highest prevalence rate of urinary incontinence (UI) compared to any other
age group (Wagg et al., 2017). A novel study reported by Gorina et al. (2014) of national estimates for UI
prevalence in the United States among people 65 years and older living in different care settings employed
data from CDC (Centers for Disease Control), NCHS (Prevention’s National Center for Health Statistics),
and CMS (Centers for Medicare & Medicaid Services) based upon interviews with 2,625 noninstitutionalized
individuals, 6,856 assisted living residents, 3,226 home care patients, 3,918 hospice discharges, and
2,416,705 nursing home residents. Prevalence rates of UI in men and women by place of residence includes
(1) noninstitutionalized: women (54.8%), men (29.9%); (2) residential care facility: women (39.4%), men
(32.7%); (3) long-term facility: women (73.5%), men (64.9%); (4) home care services; women (49.%), men
(32.4%); and (5) hospice care: women (48.2%), men (39.9%). These data support previous reports of UI and
voiding dysfunction as prevalent conditions among the elderly that increase with age (Wagg et al., 2017).
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 The prevalence of UI and voiding dysfunction is due in part to changes in bladder and sphincter function and
in part to increasing comorbid conditions and use of pharmacologic agents that can adversely affect bladder
and sphincter function (Vahabi et al., 2017). Likewise, Inouye et al. (2007) classified multiple interacting
risk factors in this age group as a “geriatric syndrome” that could greatly impact the elder’s bladder health
involving multiple comorbidities, polypharmacy, age-related physical and cognitive function (Wagg et al.,
2017). Regrettably, studies have also confirmed a lack of knowledge by health care providers at all levels of
licensure regarding the “symptom of incontinence” may in fact limit meaningful assessment and treatment
and mistakenly promote the “normalization” of incontinence in the aged (Wagg et al., 2017). Conversely, it
is important to realize that urinary incontinence and voiding dysfunction are not inevitable consequences of
aging; it is also important to realize that most elderly men and women can be effectively treated.

KEY POINT
Elderly population have significant risk factors to develop urinary incontinence due to age-related changes
to the lower urinary tract, comorbidities, and polypharmacy. Nevertheless, incontinence is not a normal
part of the aging process but a symptom that deserves proper assessment and treatment.

Changes in Bladder Function

Aging is associated with increased collagen content in the bladder wall, which reduces elasticity and bladder
capacity and also adversely affects contractility. There is also a reduction in M3 receptors and a loss of
caveolae (specialized areas in the muscle cell that affect bladder smooth muscle contractility), which may
further reduce contractility. Reduced contractility results in less effective emptying and higher postvoid
residual volumes, and the combination of reduced bladder capacity and higher postvoid residuals can produce
urinary frequency, a common complaint among older adults (Chai & Birder, 2015 ; Ranson & Saffrey, 2015;
Wagg et al., 2017). In addition, older adults report less ability to inhibit bladder contractions, which may be
due in part to failure of CNS centers or to increased presence of white matter hyperdensities (Wagg et al.,
2017). Moreover, study findings posit that in older adults, detrusor hyperactivity and underactivity can occur
simultaneously due to an imbalance of purinergic and muscarinic signaling. Increased purinergic signaling
in aging bladders leads to bladder overactivity but also suppresses muscarinic signaling, thereby reducing
the ability to empty the bladder effectively as seen in detrusor hyperactivity with impaired contractility
(DHIC) (Chai & Birder, 2015; Wagg et al., 2017). When one considers the fact that many elderly individuals
have reduced mobility, changes in bladder function and CNS function that cause increased urinary frequency
and urgency place them at significant risk for leakage.

KEY POINT
Aging is associated with reduced bladder capacity and contractility, which results in higher postvoid
residuals and increased urinary frequency.

Changes in Sphincter Function

Changes in sphincter function and in bladder outlet resistance are due in part to hormonal changes resulting
in benign prostatic enlargement in men (and increased risk of voiding dysfunction) and estrogen loss in
women. Estrogen deficiency is known to adversely affect urethral coaptation and to increase the risk for
storage symptoms such as urgency and frequency; in addition, estrogen affects the synthesis of collagen and
muscle in the lower urinary tract and may influence neurologic control of voiding (Wagg et al., 2017).

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 Changes in Pelvic Floor Function
Currently, there are no studies that link ageing as a “direct” cause in the reduction of total collagen in pelvic
muscles and fascia as well enhanced cross-linking and reduced elasticity (Wagg et al., 2017). The difficulty
lies in the ability to differentiate the changes in pelvic floor structure from consequences of hormonal changes
and number of vaginal deliveries (Wagg et al., 2017).

Comorbid Conditions and Impact of Pharmacologic Agents

Perhaps, the greatest impact of aging on bladder and sphincter function relates to the increasing number of
comorbid conditions and the pharmacologic agents used for control of those conditions. Many commonly
used pharmaceuticals can adversely affect bladder function, including diuretics, antihypertensives, alpha-
adrenergic agonists and antagonists, angiotensin-converting enzyme (ACE) inhibitors, and drugs with
anticholinergic effects (e.g., antipsychotics and antidepressants). Multiple comorbid conditions are linked in
causing or promoting urinary incontinence in the frail elderly such as diabetes, congestive heart failure, sleep
apnea, neurological disorders such as stroke, Parkinson disease, dementia, depression, functional
impairments, as well as environmental factors such as inaccessible or unsafe toilet facilities or lack of
toileting assistance or caregivers (Wagg et al., 2017). Thus, effective management of the older individual
with urinary incontinence or voiding dysfunction must involve a holistic approach that includes a careful
review of all medications being taken and management of comorbid conditions (Vahabi et al., 2017; Wagg
et al., 2017).

KEY POINT
Factors contributing to bladder dysfunction in the elderly include hormonal changes and the increasing
number of comorbid conditions and pharmacologic agents used to control those conditions.

CONCLUSION
Urinary continence and effective emptying require an intact lower urinary tract (bladder, sphincter, and pelvic
floor), normal neural innervation and control, and normal cognitive function. Neural control involves the
cortex, midbrain, pons, and spinal cord pathways; the storage phase of the voiding cycle is primarily mediated
by sympathetic inputs, while the voiding phase is primarily mediated by parasympathetic stimulation. Any
neurologic lesion at any level can adversely affect bladder control and the ability to empty effectively. There
are a number of changes in bladder and sphincter function associated with aging that can increase the risk of
incontinence or impaired emptying; however, urinary incontinence and voiding dysfunction are never
“normal” findings.

REFERENCES

Aleksic, I., & De, J. B. (2016). Surgical management of female voiding dysfunction. Surgical Clinics of North America
, 96 (3), 469–490.
Alperin, M., Burnett, L., Lukacz, E., et al. (2019). The mysteries of menopause and urogynecological health: clinical
and scientific gaps. Menopause , 26 (1), 103–111.
Andersson, K. E., & McCloskey, K. (2014). Lamina propria: The functional center of the bladder? Neurourology and
Urodynamics , 33 , 9–16.

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QUESTIONS
1. The continence nurse is assessing bladder compliance in an older adult. Which of the
followingaccurately describes this property of the urinary tract system?
A. The ability to delay voiding until a socially acceptable time and place are found
B. The ability of the bladder to distend with urine while maintaining low intravesical
pressuresC. The ability of the bladder to contract with enough force and duration to expel all or
most of stored urine
D. Detrusor relaxation in response to beta-adrenergic stimulation

2. Which layer of the bladder secretes signaling molecules that provide input to the brain
regardingbladder filling and messaging to the bladder muscle that help to modulate relaxation and
contractility?
A. Urothelium
B. Trigone
C. Propria
D. Detrusor

3. The lamina propria contributes to normal bladder distensibility by maintaining the balancebetween
type III and type I collagen and
A. Secreting signaling molecules that provide input to the brain regarding bladder filling
B. Secreting signaling molecules that provide input to the brain regarding the need to voidC.
Allowing smooth muscle cells to stretch slowly without inducing a contraction until emptying is
initiated
D. Producing elastic fibers that allow the bladder to return to normal shape after voiding
4. Which of the following describes the main function of the urethra?
A. Serving as a conduit for elimination of urine from the bladder
B. Providing stretch receptors that signal bladder filling
C. Preventing leakage during periods of increased intra-abdominal pressure
D. Supporting the pelvic organs in normal anatomic position

5. Which anatomic feature of the male urethra predominately contributes to the maintenance
ofcontinence?
A. Rich suburethral vascular plexus
B. Coaptation of the urethral walls
C. Greater length and curvature
D. Prostatic hypertrophy

6. A continence nurse recommends pelvic muscle exercises for a female patient experiencing
stressincontinence. What anatomical structure is strengthened by these exercises?
A. Internal sphincter
B. External sphincter
C. Detrusor muscleD. Urethra

7. What mechanism is involved in the guarding reflex function that helps to maintain continence?

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 A. Increased detrusor contractility in response to increased abdominal pressure
B. Closing of the urethra during the storage phase
C. Support of the pelvic organs in normal anatomic position
D. Progressive increase in outlet resistance in response to bladder filling

8. Which structure controls the actual switch between bladder filling (storage) and bladderemptying
(voiding)?
A. Midbrain
B. Prefrontal cortex
C. Spinal cord
D. Neuronal pathways

9. Which structure is responsible for assuring that both the bladder neck (internal sphincter)
andrhabdosphincter (external sphincter) are relaxed before the bladder contracts, in order to provide
unobstructed voiding?
A. Periaqueductal gray (PAG)
B. Onuf nucleus
C. Pontine micturition center (PMC)
D. Sympathetic pathways

10. A continence nurse assessing elderly patients in a nursing home takes into considerationage-related
changes in the urinary system, such as
A. Lower postvoid residuals
B. Reduced bladder contractility
C. Increased bladder capacity
D. Decreased urinary frequency

ANSWERS AND RATIONALES

1. B. Rationale: The ability to distend with urine while maintaining low intravesical pressures is a
property known as compliance and is important both to preservation of upper tract (renal) health and
to normal voiding intervals and quality of life.

2. A. Rationale: Numerous receptors located in the urothelium detect mechanical, thermal, and
chemical stimuli; in response to these stimuli, the urothelium secretes signaling molecules (such as
ATP, ACh, and NO) that provide input to the brain regarding bladder filling and messaging to the
bladder muscle that help regulate bladder relaxation and contractility.

3. D. Rationale: The lamina propria is the layer lying between the urothelium and the detrusor and
often referred as the “functional center” of the bladder by coordinating detrusor muscle and
uroepithelium activities. It contributes to normal bladder distensibility (compliance) by maintaining a
balance between type III and type I collagen (25% and 75%, respectively) and by production of the
elastic fibers that allow the bladder to return to its normal shape following emptying.

4. A. Rationale: The urethra serves as a conduit for elimination of urine from the bladder (and for
semen in men) and plays an important role in both effective bladder emptying and in maintenance of
continence.

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 5. C. Rationale: The male urethra can be subdivided into three sections: the prostatic urethra (the
section surrounded by the prostate gland), the membranous urethra (the section involving the
voluntary sphincter mechanism), and the penile urethra. The greater urethral length and curvature in
men provides increased urethral resistance to promote continence.

6. B. Rationale: The “external” sphincter is comprised of striated muscles located just distal to the
prostate gland in men and at midurethra in women; it is under voluntary control and can be
strengthened by pelvic muscle exercises.

7. D. Rationale: The guarding reflex helps to maintain continence by progressively increasing outlet
resistance by sympathetic stimulation of the internal bladder sphincter resulting in enhance urethral
tone and pudendal nerve stimulation of striated external sphincter to boost outlet closure in response
to bladder filling or sudden increase in bladder pressure.

8. A. Rationale: The actual switch between bladder filling (storage) and bladder emptying (voiding) is
controlled by midbrain structures (particularly the periaqueductal gray, or PAG) and the pontine
micturition center (PMC); however, decision-making regarding voiding (social continence) is the
responsibility of higher brain centers, specifically the prefrontal cortex.

9. C. Rationale: When activated by the PAG to initiate the micturition reflex, the PMC sends input to
the cord that inhibits sympathetic stimulation of the bladder neck and innervation of the external
sphincter via Onuf nucleus (thus causing both internal and external sphincter relaxation) and
activates the parasympathetic pathways causing detrusor contraction.

10. B. Rationale: Aging is associated with increased collagen content in the bladder wall, which reduces
elasticity and bladder capacity and adversely affects contractility.

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