Anatomy of Female LUT and its Continence Mechanisms

ANATOMY OF FEMALE LUT AND CONTINENCE MECHANISMS

Introduction
Upto 28% of women < 60 years of age and upto 35% > 60 years suffer from urinary incontinence.
Of all incontinence types, women are predominantly afflicted by SUI (estimated proportion - 60%).
Women with SUI report about a varying amount of urinary leakage during physical activity,
coughing, sneezing, laughing, or straining.
Basically, urinary incontinence occurs when the intravesical pressure rises above the urethral
pressure. In SUI, intra-abdominal pressure is transmitted to bladder and exceeds urethral pressure,
which leads to passive urinary leakage through urethra. Therefore, urethral closure insufficiency is
responsible for SUI. Understanding the continence mechanisms and the underlying causes of
urethral closure insufficiency helps to restore continence.
Relevant Anatomy
Urinary bladder is located in pelvis and surrounded by fatty tissue.
Urethra has a total length of about 4 5 cm; reaches from bladder neck to external meatus.
Bladder neck is located above the level of inferior margin of symphysis and lies on the endopelvic
fascia.
Endopelvic fascia is attached to levator ani muscle at both sides of urethra. Contraction of levator
ani muscle leads to simultaneous elevation of bladder neck.
Urethral wall consists of a mucosal lining, underneath a submucosal cushion of blood vessels
embedded in connective tissue and elastic fibers, and a longitudinal and circular layer of smooth
muscle cells
The urethra runs nearly parallel to the axis of the anterior vaginal wall and is closely attached to the
surrounding vaginal tissue
Posterior wall of the urethra is supported by the fibromuscular vaginal tissue, which is connected to
the pelvic bones via the pubovaginal portion of the levator ani muscle and the longitudinal muscle of
the anus.
Urethra is attached to posterior site of symphysis by pubourethral ligaments.
Accumulations of muscle cells exist around the urethra. The bladder neck is densely surrounded by
smooth muscle cells (internal urethral sphincter, 0 15th percentile of urethra) that are innervated by
sympathetic nerve fibers coming from the level Th11 L2 of the spinal cord.
The distal part of the proximal and midurethra is surrounded by striated muscle cells (20 60th
percentile of urethra); this rhabdomyosphincter (external urethral sphincter) is innervated by the
pudendal nerves, which leave the spinal cord at the level S2 S4.

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URINARY INCONTINENCE AND PELVIC PROLAPSE: PATHOPHYSIOLOGY

Definition and Classification of Pelvic Organ Prolapse
Pelvic organ prolapse is defined as the descent of one or more of the following: anterior vaginal
wall, posterior vaginal wall, and apex of the vagina (cervix/uterus) or vault (cuff) after hysterectomy.
Absence of prolapse is defined as stage 0 support.
Prolapse can be staged from stage I to stage IV.
Pelvic organ prolapse can occur in association with UI and other lower urinary tract dysfunction and
may occ. mask incontinence.
Anterior vaginal wall prolapse is defined as descent of the anterior vagina so that VUJ (a point 3 cm
proximal to the external urinary meatus) or any anterior point proximal to this is less than 3 cm
above the plane of the hymen.
Prolapse of the apical segment of the vagina is defined as any descent of the vaginal cuff scar (after
hysterectomy) or cervix, below a point that is 2 cm less than the total vaginal length above the plane
of the hymen.
Posterior vaginal wall prolapse is defined as any descent of the posterior vaginal wall so that a
midline point on the posterior vaginal wall 3 cm above the level of the hymen or any posterior point
proximal to this is less than 3 cm above the plane of the hymen.
Pelvic floor muscle function can be qualitatively defined by the tone at rest and the strength of a
voluntary or reflex contraction as strong, weak, or absent or by a validated grading system (e.g.,
Oxford 1 to 5).
A pelvic muscle contraction may be assessed by visual inspection, palpation, electromyography, or
perineometry.
Factors that must be assessed are strength, duration, displacement, and repeatability.
DRE allows description of observed and palpable anatomic abnormalities and is the easiest method
of assessing pelvic floor muscle function in children and men.
DRE is essential in children with UI to rule out faecal impaction.

Organ Prolapse Grading Systems

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RELATIONSHIP B/W INCONTINENCE AND PROLAPSE

Patients with severe prolapse may develop voiding symptoms as a result of urethral kinking, leading
to obstruction that is worsened during straining effort
Risk factors contributing to the symptoms of urgency and frequency include age and urogenital
atrophy
More than 40% of women with urethral sphincter incompetence will have a significant cystocele
However, complaints of stress incontinence a/w appearance of mild/moderate cystocele is not
specific for GSI
Occult or latent incontinence is urethral sphincteric incompetence masked by the presence of pelvic
prolapse
Incontinent women may note decrease or disappearance of stress incontinence episodes as degree
of prolapse worsens.
A large rectocele may cause incomplete bowel evacuation and tenesmus, leading some to splint or
manually reduce the posterior vaginal segment or perineum to assist in defecation. Patients may
describe stool becoming trapped in the rectocele pocket itself. Constipation and straining may
worsen the symptoms and lead to left lower quadrant abdominal pain if impaction occurs.
Prevalence of faecal incontinence
o 17% in pelvic organ prolapse and UI patients
o 2% to 3% in the general population.
o MC mechanisms are
Incompetent sphincter (20 to structural defect or pudendal nerve damage)
Overflow incontinence
Sexual problems have also been seen in patients with pelvic organ prolapse and UI

PATHOPHYSIOLOGY OF INCONTINENCE AND PROLAPSE

Summary of Normal Continence:
coordinated activity of smooth and striated muscles in the bladder, urethra, and pelvic floor is
required for continence.
bladder and urethra constitute a functional unit, which is controlled by central and peripheral
nervous systems and local regulatory factors
During bladder filling at physiologic rates, detrusor pressure remains nearly constant because of
property of accommodation ton s recepti e rela ation
Accommodation accounts for the nearly flat cystometric curve seen during normal bladder filling
The viscoelastic properties of the bladder normally produce a highly compliant structure. When
accommodation is impaired, low bladder compliance ensues. This is manifest as a steep rise in
detrusor pressure during bladder filling.
Important factors in the maintenance of urinary continence:
o Viscoelastic properties of bladder
o Anatomy and support of sphincteric unit
o Neural control of LUT
The micturition reflex is normally under voluntary control and is organized in the rostral brainstem
(the pontine micturition center [PMC]). Micturition is normally inhibited by Cortical areas
Release from inhibitor effect of higher centers stimulation of PMC Micturition.
It requires integration and modulation by
o Parasympathetic + somatic components of sacral spinal cord (sacral micturition center) and
o Thoracolumbar sympathetic component

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During micturition, the first recorded event is sudden and complete relaxation of the striated
sphincteric muscles, characterized by complete electrical silence of sphincter EMG
This is followed almost immediately by a rise in detrusor pressure and concomitant fall in urethral
pressure as the bladder and proximal urethra become isobaric
The bladder neck and urethra open, and voiding ensues.
Voluntary interruption of the stream is accomplished by a sudden contraction of the striated
periurethral musculature (which, through a reflex mechanism, shuts off the detrusor contraction,
aborting micturition).
The sphincteric system is also designed to resist physiologic increases in abdominal pressure and
thereby prevent development of incontinence.
Bladder abnormalities that cause UI include
o Detrusor Overactivity
o Low Bladder Compliance
Disordered LUT function can result from:
o Disruption of normal PNS/CNS control mechanisms
o Disordered bladder muscle function (10 or 20)

Detrusor Overactivity
Detrusor overactivity is a urodynamic observation characterized by involuntary detrusor
contractions during the filling phase, which may be spontaneous or provoked
Detrusor overactivity may be phasic, terminal, or both
Patterns of DO
o Phasic Detrusor Overactivity
o Terminal Detrusor Overactivity
o Detrusor Overactivity incontinence
o Other Patterns
DO can also be qualified according to cause:
o Neurogenic detrusor overactivity (due to a relevant neurologic cause). This term replaces
the term detrusor hyperreflexia.
o Idiopathic detrusor overactivity (when there is no defined cause). This term replaces
detrusor instability.
A. Phasic detrusor overactivity
Is defined by a characteristic wave form
May or may not lead to urinary incontinence
Not always accompanied by any sensation
May be interpreted as a first sensation of bladder filling or as a normal desire to void.
B. Terminal detrusor overactivity: It is a new ICS term
Is defined as a single, involuntary detrusor contraction, occurring at cystometric capacity, which
cannot be suppressed and results in incontinence usually resulting in bladder emptying (voiding).
A/w reduced bladder sensation
However, in complete spinal cord injury patients there may be no sensations whatsoever.
C. Detrusor overactivity incontinence
Incontinence due to an involuntary detrusor contraction.
In a patient with normal sensation, urgency is likely to be experienced just before the leakage
episode.

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D. Other patterns
Combination of phasic and terminal detrusor overactivity
Sustained high pressure detrusor contractions seen in spinal cord injury patients when attempted
voiding occurs against a dyssynergic sphincter
Provocative manoeuvres during UDS to provoke DO:
Rapid filling
Use of cooled or acid medium
Postural changes
Hand washing
Causes of DO:
Neurogenic Detrusor Overactivity Idiopathic Detrusor Overactivity
1. Supraspinal neurologic lesions No neurologic abnormality is evident, but associated
a. Stroke abnormalities include:
b. Parkinson disease 1. Bladder infection
c. Hydrocephalus 2. BOO (Men) prostatic and bladder neck, strictures
d. Brain tumour 3. BOO (Women) pelvic organ prolapse, postsurgical,
e. Traumatic brain injury urethral diverticulum, primary bladder neck, strictures
f. Multiple sclerosis 4. Bladder tumour
2. Suprasacral spinal lesions 5. Bladder stones
a. Spinal cord injury 6. Foreign body
b. Spinal cord tumour 7. Aging
c. Multiple sclerosis
d. Myelodysplasia
e. Transverse myelitis
3. Diabetes mellitus
Interpretation of Vesicourethral Dysfunction
The most important points to clarify in clinical practice are
o Presence/absence of Neurogenic DO
o Behaviour of distal urethral sphincter mechanism during voiding.
High-pressure bladders with DESD prone to develop VUR may lead to renal impairment.
Preservation of renal function is of utmost importance in chronic neurologic conditions.
As a rule of thumb, patients with a competent bladder outflow and DLPP cm H O, are at
particular risk of developing upper urinary tract back pressure changes.
Neurologic conditions can alter vesicourethral function by impairing:
o Detrusor activity
o Striated sphincter activity
o Bladder and urethral sensation
o Urethral smooth muscle activity
Classification of Neuropathic Bladder Dysfunction
Supraspinal lesions Suprasacral lesions: Infrasacral lesions:
All cerebral diseases such as: All spinal cord lesions above Conus or Sacral roots
Cerebral haemorrhage and conus May be further subdivided into
thrombosis Cauda equina lesions
Dementia (within spinal canal)
Tumours Peripheral lesions
Arteriosclerosis (outside spinal canal)
Parkinson disease

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Supraspinal Lesions
Patients who have supraspinal lesion generally empty their bladders efficiently unless they have
associated BOO.
Pre-existing bladder dysfunction is common
Urodynamics plays a major role in defining the abnormality and formulating treatment strategies.
Suprasacral Lesions
Patients who have cord lesions above the sacral micturition center initially go through a period of
spinal shock in which there is loss of neurologic activity below the level of the injury.
Detrusor areflexia and maintenance of some residual sphincteric competence usually results in
urinary retention requiring either indwelling or intermittent catheterization.
Recovery is characterized by the gradual return of reflex bladder activity or neurogenic detrusor
overactivity mediated through the sacral micturition center, which is intact but separated from
higher centers.
It usually occurs within 2 to 3 months, but in a small number of patients it may take up to 2 years for
reflex activity to return.
As reflex bladder activity increases during the recovery phase, the bladder may empty well at the
expense of incontinence or high detrusor voiding pressures may develop, resulting in
hydronephrosis.
Infrasacral Lesions
Detrusor activity may be absent or diminished if there are lesions of the cell bodies or
parasympathetic efferents to the bladder from the sacral roots (S2 to S4).
This may be due to trauma to the spinal cord or pelvic nerves or destruction of the cord segment by
lesions such as a plaque of multiple sclerosis
Injury to the conus or sacral roots results in:
o Detrusor areflexia
o Denervated open bladder neck
o Paralyzed closed external sphincter
o In most patients, urinary retention
Weakened urethral sphincter mechanism and paralyzed pelvic floor make patients prone to stress
incontinence, especially women.
Some patients empty their bladders by abdominal straining or suprapubic compression (Credé s
manoeuvre), but the majority need CISC to empty efficiently.
A minority of patients are at risk of developing poorly compliant high-pressure bladders that can
lead to renal damage.
Partial infrasacral lesions may result in a mixed pattern of
o Weak or absent detrusor activity
o Poor compliance,
o Considerable reflex activity in the pelvic floor muscles

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Idiopathic Detrusor Overactivity

Associated with a variety of non-neurogenic clinical conditions such as bladder outlet obstruction,
dysfunctional voiding, and inflammatory reactions
Elbadawi and colleagues
o Have proposed a possible explanation for age-related DO based on ultrastructural studies of
bladder.
o Electron microscopic changes (abundant, distinctive protrusion junctions and abutments)
Diminished electrical resistance between detrusor muscle cells Hyperexcitable state
IDCs.
BOO Increased voiding pressures and a prolonged duration of voiding Ischemic damage to
intramural ganglia Partial denervation of detrusor (Hypothesis). Experiments have shown that
denervation of smooth muscle cells Supersensitivity to agonists + Excitability + Increased
electrical coupling Detrusor more susceptible to IDCs.
Detrusor muscle hypertrophy on obstruction does not necessarily play a causative role.
Bladder Compliance
Bladder compliance describes the relationship between change in bladder volume and change in
detrusor pressure.
Compliance is calculated by dividing the volume change ΔV by the change in detrusor pressure
ΔPdet during that change in bladder volume C V ΔPdet). It is expressed in mL/cm H2O.
Calculating bladder compliance
o 2 standard points are commonly used
o Both points are measured excluding any detrusor contraction
o PDet at start of bladder filling and corresponding bladder volume (usually zero)
o PDet (and corresponding bladder volume) at cystometric capacity or immediately before start
of any detrusor contraction that causes significant leakage
With normal compliance there is little or no pressure change as the bladder fills.
At present, there are no standardized or international agreed values to define normal, high, and low
compliance.
Calculated value of compliance is less important than actual bladder pressure during filling.
This is because compliance value can change depending on the volume over which it is calculated.
For this reason, numeric values of compliance are usually not reported.
Low bladder compliance
Denotes an abnormal volume pressure relationship in which there is a high incremental rise in
detrusor pressure during bladder filling.
Clinically, low bladder compliance is MC seen in neurologic conditions, especially LMN lesions (spina
bifida and cauda equina syndrome).
Obstructive uropathy effect on bladder ultrastructure low bladder compliance. It has been
identified as a urodynamic risk factor.
Leng and McGuire (2003) showed that relief of obstruction by TUIP/TURP can improve compliance.
Causes of Low Bladder Compliance
Neurogenic Non-Neurogenic (Increased Collagen)
Myelodysplasia Tuberculous cystitis
Shy-Drager syndrome Radiation cystitis
Suprasacral spinal cord injury/lesion Chronic indwelling catheter
Radical hysterectomy Bladder outlet obstruction
Abdominoperineal resection

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SPHINCTERIC MECHANISMS:
Innermost mucosal layer in both sexes
o is organized in longitudinal folds
o during storage phase, when urethra is closed, this appears in a stellate configuration on
cross section
o Such a configuration allows significant distensibility during urethral opening
The submucosal layer contains a vascular plexus, which may be involved in improving the seal of a
closed urethra by transmitting the tension of the urethral muscle to the mucosal folds
Male vs. Females:
o 2 powerful sphincter mechanisms in males
o Single weaker intrinsic sphincter mechanism + weaker bladder neck + shorter urethra in
female
Traditionally, the urethral sphincter is composed of:
o Internal sphincter (direct continuation of detrusor smooth muscle)
o External Striated sphincter
Clinically, bladder neck proximal urethra normally functions as a sphincter in both sexes.
Anatomically there is a unique mixture of smooth and striated muscle, intracellular matrix, and
mucosal components contributing to the functional sphincter.

Male Sphincteric Mechanism:

2 important sphincteric mechanisms:
o Proximal bladder neck mechanism
o Distal urethral mechanism at apex of prostate.
Proximal mechanism:
Bladder neck + prostate + prostatic urethra till verumontanum
Receives a dual innervation from ANS(PSNS + SNS)
Main motor control sympathetic, although there is some evidence for a contribution from
detrusor muscle (PSNS)
It provides a powerful mechanism in both maintaining urinary continence and preventing
retrograde ejaculation

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In patients with damaged distal urethral sphincter (e.g., PFUDD), continence can be maintained
solely by proximal mechanism.
Ultrastructurally, it consists of a powerful inner layer of muscle bundles arranged in a circular
orientation.
This portion of continence mechanism is removed during prostatectomy, leaving only distal
mechanism to prevent urinary leakage
Distal urethral mechanism
At apex of prostate, from verumontanum to proximal bulb
It has ability to also maintain continence even when proximal mechanism has been rendered
incompetent
It is confined to the 3- to 5-mm thickness of wall of membranous urethra from level of
verumontanum down to distal aspect of membranous urethra.
Composed of
o Prostatomembranous urethra
o Cylindrical rhabdosphincter (external sphincter muscle) surrounding prostatomembranous
urethra
o Extrinsic paraurethral musculature and connective tissue structures of pelvis.
Rhabdosphincter
o is a concentric muscular structure
o consists of longitudinal smooth muscle and slow-twitch (type I) skeletal muscle fibers that
maintain resting tone
o Skeletal muscle fibers of rhabdosphincter intermingle with smooth muscle fibers of proximal
urethra
o It is invested in a fascial framework and supported below by a musculofascial plate that
fuses with the midline raphe (which is also a point of origin for the rectourethralis)
o Superiorly, the fascial investments of rhabdosphincter fuse with puboprostatic ligaments.
This dorsal and ventral support probably contributes to competence of sphincter.
Extrinsic paraurethral muscle (Levator ani complex)
o Striated fibers of fast-twitch (type II) variety
o During sudden increases in abdominal pressure, these fibers can contract rapidly and
forcefully to provide continence.
Female urethral support compromised due to childbirth & aging
In males, compromise to rhabdosphincter usually occurs after trauma or surgery (e.g.,
prostatectomy).
Sphincter Abnormalities in Men
Caused by trauma or neurologic injury
In Prostatectomy, distal urethral sphincter (particularly the rhabdosphincter) can be damaged by
direct injury or injury to the nerve supply or supporting structures
Radiation and neurologic lesions can cause sphincteric dysfunction.
Pelvic trauma or instrumentation that results in trauma to the distal urethral sphincter can result in
incontinence, particularly when the PUS is absent or deficient.

Female Sphincteric Mechanisms:

Females are more likely to suffer from UI due to sphincter deficiency
Female bladder neck is weaker than male bladder neck and is often incompetent
Bladder neck is poorly defined (muscle fibers have mainly longitudinal orientation)
Continence usually relies on integrity of urethral sphincteric mech.

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Like the male distal mechanism, female sphincter is composed of

o Longitudinal intrinsic urethral smooth muscle
o Larger extrinsic striated muscle
This sphincter extends through proximal 2/3rd of urethra
It is most developed in middle 1/3rd of urethra
Therefore in women the majority of urethra should be considered to be sphincter active.
Damage to NS of urethral sphincter (esp. pudendal nerve) by obstetric trauma reduces effectiveness
of this mechanism and predisposes to SUI
Sphincter Abnormalities in Women
In females with SUI a degree of sphincter weakness in all cases.
The sphincter abnormality = spectrum ranges from Mild to Severe
Mild degree where predominant pathophysiologic abnormality is urethral hypermobility (urethral
support defect)
Severe, where irrespective of urethral support defect there is severe ISD.
Urethral hypermobility is MC a/w
o Pregnancy and vaginal delivery
o Pelvic surgery
o Chronic abdominal straining (e.g., Chronic constipation).
In some cases, loss of support many be 20 to neurologic injury.
4 major mechs. by which vaginal delivery sphincter damage:
o Injury to connective tissue support (process of vaginal delivery)
o Vascular damage to pelvic structures (compression by foetus)
o Damage to pelvic nerves/muscles/both (trauma during parturition)
o Direct injury to urinary tract (labour and delivery)
Important factors leading to pudendal nerve injury
o Vaginal delivery can cause partial denervation with consequent re-innervation in most 1st
deliveries
o Multiparity
o Forceps delivery
o Increased duration of 2nd stage of labour partially related to epidural anaesthesia
o 3rd degree perineal tear
o High birth weight (>4000 g)
Conditions a/w increased risk for ISD in women:
o Previous urethral or periurethral surgery: periurethral fibrosis, scarring, or denervation
o Neurologic insult: In complete sacral parasympathetic lesions, the bladder is Areflexic and is
in urinary retention. When, in addition to a parasympathetic lesion, there is a sympathetic
lesion, the proximal urethra loses its sphincteric function. Clinically, this results in
incomplete bladder emptying, caused by the acontractile detrusor, and sphincteric
incontinence, caused by the non-functioning proximal urethra
o Somatic neurologic lesions affect pudendal afferent and efferent nerves. In addition to loss
of perineal and perianal sensation, these lesions abolish the bulbocavernosus reflex and
impair the ability to contract the urethral and anal sphincters voluntarily.
o Sacral neurologic lesions are caused by herniated disks, diabetic neuropathy, multiple
sclerosis, and spinal cord tumors.
o They are also commonly encountered after extensive pelvic surgery such as
abdominoperineal resection and radical hysterectomy
Pelvic radiation therapy

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Mechanisms believed to contribute to female urinary continence - “Stress Continence Control System”
1. Active Sphincteric System: Smooth and striated muscle cells in and around the urethra close the
urethral lumen
2. Passive Sphincteric System/Urethral Wall Factor: The length of the urethra and urethral wall
tension (collagen and elastic fibers, mucosa and submucosal cushion of blood vessels in the urethral
wall) guarantee additional positive pressure in the urethra in the resting position
3. Passive Pressure Transmission: Pressure transmission from the abdominal cavity to the proximal
urethra
4. Active Pressure Transmission: Activation of the coughing reflex via the pudendal nerve leads to a
fast contraction of the urethral rhabdomyosphincter and pelvic floor before and during vesical
pressure increase
5. Hammock system: Posterior urethral wall support by fibromuscular tissue of the anterior vaginal
wall and the tendinous arch of the pelvic fascia
6. Integral Theory: Ventral kinking of the urethra during contraction of the levator ani muscle,
longitudinal muscle of the anus, and the hammock muscle pulls the vagina and bladder base back-
and downward and presses the urethra against the pubic bone

Bladder Neck: Intrinsic Sphincter Deficiency, Urethral Hypermobility, and the “Hammock Hypothesis”
The active and passive sphincteric systems, active and passive pressure transmissions, as well as the
hammock h po hesis poin s 5, above) support the concept that the bladder neck and proximal
urethra are responsible for urinary continence.
Sphincters guarantee that urethral lumen is water-tight closed in the filling phase of bladder
Together with the surrounding tissue, Sphincters give structural support to keep the proximal
urethra from moving during abdominal pressure increase.
Anatomical or functional damage of the sphincteric systems may cause an insufficient
approximation of the urethral lumen.
Two causes are identified for sphincteric insufficiency:
o ISD
o Urethral Hypermobility
In ISD
o the urethral sphincters are too weak to close the urethral lumen
o Urinary leakage may be associated with a minimal increase in intravesical pressure or even
may be gravitational.
o Patients with this type of incontinence have a low leak point pressure during coughing or
straining (<60 cm H2O) and a low urethral closure pressure at rest in urethral pressure
profilometry (<20 cm H2O)
o During video-urodynamic investigation, the bladder neck and proximal urethra, regardless of
the anatomic position, are open at rest.
In urethral hypermobility
o Sphincters remain strong in resting position but become insufficient during stress
o Patients have a pathological cotton swab (Q-tip) test (difference of urethrovesical angle
from the horizontal plane >30°)
o Leak point pressure (>60 cm H2O) and urethral closure pressure at rest remain high (>20 cm
H2O)
o Loss of anchoring system of bladder neck and proximal urethra believed to cause urethral
hypermobility insufficiency of pressure transmission to proximal urethra.

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o During VUDS, bladder neck and proximal urethra are closed at rest but open and descend
during stress.
o Ultrasound investigations demonstrated that the rhabdomyosphincter is significantly thicker
in continent than incontinent women and significantly thicker in women with urethral
hypermobility than ISD
o Based on these two distinct findings, a classification system of stress urinary incontinence
consisting of five subtypes has been established. Types 0 IIb refer to urethral
hypermobility and type III refers to ISD.
Types of SUI based on ISD and Urethral Hypermobility
Type O
The patient has a typical history of stress incontinence, which, however, cannot be reproduced
during clinical or urodynamic investigation.
The bladder neck and proximal urethra are closed at rest and situated at or above the inferior end of
the symphysis.
The bladder neck and proximal urethra descend and open during stress.
Failure to demonstrate urinary incontinence may be due to momentary voluntary contraction of the
external urethral sphincter during the examination
Type I
The bladder neck is closed at rest and located above the inferior margin of the symphysis.
Bladder neck and proximal urethra open and descend < 2 cm during stress.
Urinary incontinence is apparent during periods of increased abdominal pressure.
There is a small or no cystocele
Type II a
The bladder neck is closed at rest and located above the inferior margin of the symphysis.
The bladder neck and proximal urethra open during stress and a rotational descent is observed
(cystourethrocele)
Type II b
The bladder neck is closed at rest and situated at or below the inferior margin of the symphysis.
During stress, there may or may not be further descent but the proximal urethra opens and urinary
leakage occurs
Type III
The bladder neck and proximal urethra are open at rest.
The proximal urethra does not function as a sphincter anymore

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THE HAMMOCK SYSTEM

is a supportive anatomical structure that can explain closure of the bladder neck and proximal
urethra during abdominal pressure increase. According to this hypothesis, BN and proximal urethra
lie in a position where they can be compressed against a backboard and sealed during abdominal
pressure increase. The hammock consists of the anterior vaginal wall and the surrounding
connective tissue that are connected with the pelvic bones via the pubovaginal portion of the
levator ani muscle and the tendinous arch of the pelvic fascia. If the hammock system is intact but in
a more caudal position, continence still may be maintained. The stability of the supporting layers
and muscles therefore are responsible for continence during stress situations. Laxity of the
hammock would give less resistance during abdominal pressure increase and lead to urinary
incontinence.
DeLancey described this system like a water hose: stepping on the hose would stop the water flow if
the hose would lie on a firm, noncompliant ground [4, 9] . The results after anterior colporrhaphy
support this hypothesis. In a prospective randomized trial comparing the outcome of three different
operation techniques 37% of women reported to be dry 5 years after colporraphy [19] .

MIDURETHRA: THE INTEGRAL THEORY

The integral theory supports the concept that the midurethra is responsible for urinary continence.
The integral theory is a complex musculoelastic concept whereby muscle forces pull on the vaginal
tissue to open and close the urethra
This theory adds a dynamic extrinsic mechanism contractions of specific pelvic floor muscles to
the concept of urethral closure.
Closure of urethra occurs when three muscle forces interact together, pulling the vagina
simultaneously to the dorsal, caudal, and ventral direction.
Levator ani muscle contracts and pulls vagina and attached bladder base and urethra to dorsal
direction
Longitudinal muscle of the anus contracts and pulls vagina to a caudal direction
So-called hammock m scle con rac s and p lls agina o en ral direc ion
Midurethra: The Integral Theory
As a result of the muscle contractions, the upper urethra moves to a horizontal and the lower
urethra to a vertical position, causing kinking of the midurethra and closure of the urethral lumen.
Mechanical obstruction of the urethral lumen occurs only during muscle contraction; this effect was
named “dynamic mid-urethral knee angulation” or “iris effect”
Possible mechanisms of damage of this system during childbirth with regard to urinary incontinence,
prolapse, and voiding disorders were described
Laxity of any of the involved muscles or ligaments prevents the urethra, vagina, and bladder base
from stretching, and therefore weakens the transmission of muscular forces, leading to urinary
incontinence.
Application of a forceps on one side of the vagina at the midurethral area can control supine urine
loss while coughing by preventing abnormal descent and funneling of the bladder base (midurethral
one-sided Bonney test)

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 Anatomy of Female LUT and its Continence Mechanisms

Conclusions
Concepts aim to explain the mechanisms of urinary continence. The bladder neck and midurethra have
become the center of interest. Clinical, urodynamic, and radiological signs seem to support the
individual theory. However, many women have risk factors for urinary incontinence (e.g., overweight,
childbirth, hysterectomy, advanced age), urethral hypermobility, a low urethral closure pressure, laxity
of the anterior vaginal wall, or cystourethrocele without being incontinent [14, 33] . Furthermore, no
strict relationship exists between the degree of urethral hypermobility and the severity of stress
incontinence [33, 34] .
Additionally, urethral hypermobility or ISD after midurethral operations and urethral closure pressure
after bladder neck operations remain unchanged; nevertheless, these women become continent [21,
35 37]. Obviously, insufficiency of one mechanism can be compensated for by others. Therefore,
continence seems to be produced by several mechanisms. However, damage of one part of the
continence system may be more severe than damage of other parts.
Conclusions
Randomized studies demonstrated that operation techniques (suspension operations vs. TVT) are
equally effective in restoring continence in 65 90% of patients.
Surgical restoration of one part of the continence mechanism at the level of the bladder neck or
midurethra compensates for the existing loss of urethral support and functions by creating new areas
for urethral compression.
However, some women remain incontinent after the operation, indicating that reconstruction of the
individual system was wrong or not sufficient enough to restore continence
Consequently, it is hypothesized to choose an operation based on the other continence concept after
failed primary surgery.
This strategy is clinical reality; however, it remains to be proved in randomized studies.

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