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Urinary Incontinence (2H)

1) Urinary incontinence is a major health issue affecting millions of people and costing billions annually. 2) It has various causes including dementia, bladder overactivity, weakness of the pelvic floor muscles, and neurological issues. 3) The pathophysiology involves an imbalance between bladder pressure and urethral closure mechanisms during activities that increase abdominal pressure like coughing, resulting in involuntary loss of urine.
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0% found this document useful (0 votes)
67 views94 pages

Urinary Incontinence (2H)

1) Urinary incontinence is a major health issue affecting millions of people and costing billions annually. 2) It has various causes including dementia, bladder overactivity, weakness of the pelvic floor muscles, and neurological issues. 3) The pathophysiology involves an imbalance between bladder pressure and urethral closure mechanisms during activities that increase abdominal pressure like coughing, resulting in involuntary loss of urine.
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPT, PDF, TXT or read online on Scribd
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URINARY INCONTINENCE

Sopheap Bou, MD
Urologist

1
Urinary Incontinence
• Major health issue that affect 10 million pt
• 50% of all nursing home residents
• Between15 and 30% of women over age 65
in retirement communities suffer from UI
• $15-20 billion is spent on this problem
annually.

2
3
Aetiology
A. Dementia and inappropriate voiding:
-many pt with dementia will have bladder
overactivity, but some have incontinence withouth
any demonstrable abnormality.
-the problem for these pt and for their carers is
the loss of normal social control over voiding,
which leads to pt passing urine at inappropriate
times or in inappropriate places.
-the resulting impact on pt and carer is exactly the
same as if the incontinence was due to a
demonstrable lower tract abnormality.
4
B. Overflow incontinence
• OI occurs when the UB becomes
overdistended, often within a short period of
time.
• It typically occurs in women following
childbirth and in pt who have had hip
fractures or hip surgery.
• The exact mechanism is not understood, but
it’s probably differs from the overflow
incontinence seen with high-pressure chronic
retention of urine.
5
B. Overflow incontinence

• It has been suggested that the


precipitating episode (labour, hip fracture
or surgery) and its associated
management may somehow alter
sensation from the lower urinary tract, so
that the bladder simply fills until it
overcomes the pressure at the bladder
outlet and urine then leaks continually.

6
C. Post-micturition dribble
• Common problem in men, thought to be due to
pooling of urine in the posterior urethra after
voiding.
• Typically, leakage occurs within a minute or two
of voiding, probably as a result of compression
of the urethra caused by walking, moving or
sitting after standing to void.
• The problem is managed by teaching the pt to
apply firm finger pressure from back to front
along the line of the urethra, thereby “milking”
out the retained in the urethra.
7
D. Bladder overactivity
• A normal bladder fills gradually to
accommodate urine with little or no rise in
pressure.
• When the degree of bladder wall stretch is
sufficient to activate enough sensory
receptors, the sensation of a full bladder is
perceived.
• This can usually be tolorated for up to 30min,
which allows time for socially convenient
voiding.
8
D. Bladder overactivity
• Bladder overactivity is characterised by the
presence of phasic or sustained detrusor
contractions during bladder filling.
• These result in a feeling of fullness at low
capacity, a sense of urgency or urge
incontinence. If such contraction can be
resisted, the desire to void may pass.
• Bladder overactivity may be idiopathic or
secondary to bladder outlet obstruction (BOO)
and neurological disease; those with BOO are
usually men with prostatic obstruction.
9
D. Bladder overactivity
• These men experience a poor stream
because they get a sensation of bladder
fullness at low capacity, so that they then void
with a stream that is spuriously poor.
• In general, overactive bladder has a greater
impact on quality of life than SUI.
• It’s likely that a combination of occult and
overt structural or functional changes in the
innervations of the lower urinary tract,
together with changes in the detrusor smooth
muscle itself, combine to cause bladder
overactivity. 10
Pathophysiology
• Elderly pt frequently accept UI as a sign of
aging and fail to seek help.
• In fact, it is a manifestation of an underlying
disease; occasionally it’s transient and
resolves spontaneously, but most often it is
chronic and progressive.
• Transient incontinence may occur after
childbirth or may be associated with an acute
bladder infection.

11
Pathophysiology
• Chronic UI can result from a multitude of
causes and can be classified :
-Anatomic or genuine urinary stress
incontinence
-Urge incontinence (bladder overactivity)
-Neuropathic incontinence
-Congenital incontinence
-False (overflow) incontinence
-Post-traumatic or iatrogenic incontinence
-Fistulous incontinence. 12
A. Anatomic (Genuine Stress
Incontinence)
• Anatomic incontinence is primarily the result
of hypermobility of the vesicourethral
segment owing to pelvic floor weakness..
• It basic features are an essentially intact
sphinteric mechanism, a weak pelvic floor
support, and anatomic abnormality.
• It is easily demonstrable radiologically, and
restoration of the anatomy restores function.
13
A. Anatomic (Genuine Stress
Incontinence)
• This occurs when abd pressure rises abruptly
(coughing, sneezing, lifting or movement),
and the bladder outlet is unable to resist the
pressure rise.
• In normal individuals, there is a pelvic floor
contraction about 250ms before a cough,
which prevents leakage.
• The cause of stress urinary incontinence
(SUI) in any individual pt can be obscure, but
conditions associated with SUI are shown in
Table 2.
14
15
A. Anatomic (Genuine Stress
Incontinence)
• The mechanisms whereby lack of effective
urethral closure leads to SUI are shown in
Fig 3.

16
Stress urinary incontinence

17
Bonney maneuver
18
19
B. True Urge Incontinence:
• Detrusor instability with a normal sphinteric
component, normal anatomy, and no
neuropathy.
• Sphincteric instability is less common.
• Leakage occurs with either detrusor instability
and spontaneous contraction or, less
commonly, with sphinteric instability and
relaxation.

20
C. Neuropathic Incontinence
• Neuropathic incontinence varies, depending
on the nerve lesion.
• The neuropathy is usually identifiable.
• The incontinence can be active ( detrusor
hyperreflexia) or passive (sphinteric atony)
or, occasionally, a combination of the two.

21
D. Congenital Incontinence
• The cause of congenital incontinence are
ectopic ureters, duplicate or single system,
with epispadias, exstrophy, or cloacal
malformation.

22
E. False (Overflow) Incontinence

• False incontinence is usually the result of an


obstructive or neuropathic lesion. It is not
true incontinence.

23
F. Traumatic Incontinence
• TI is associated with a fractured pelvis or
with surgical damage to the sphincter
during bladder neck resection or extensive
internal urethrotomy; it also may result
from failure of urethral diverticulectomy or
repair of erosion of an artificial sphincter.

24
G. Fistulous Communication
• The fistula can be ureteral, vesical, or
urethral.
• Most of the time, the cause is iatrogenic,
from either pelvic or vaginal surgery.

25
Pathophysiology
This chapter discusses the most common and
significant disorders: Urinary stress
incontinence and neuropathic incontinence.
• UI is the involuntary loss of urine when the
intravesical pressure exceeds maximal urethral
pressure.
• Under resting conditions continence is effected
by an adequate urethral tone, which is the
result of smooth and striated muscle activity,
tension of the fibroelastic elements in the
urethral wall, and the cushioning effect of the
soft, compressible, submucosal vascular bed. 26
Pathophysiology
• The major contribution to urethral resistance
comes from the smooth and striated muscle
components.
• In experimental animals, as well as in
humans, the striated external sphincter
provides about 50% of static urethral
resistance, while smooth muscle is primarily
responsible for proximal urethral closure
pressure.

27
Pathophysiology
• The rise in pressure in the mid urethra
results from the combined function of the
smooth musculature and the striated musle
fibers around it .
• To maintain continence under stress
conditions, the striated urethral sphincter has
to resist a raised bladder pressure owing to
intra-abd pressure increase.

28
Pathophysiology
• The activity of the external sphincter helped
by the pelvic floor provides for this increased
urethral resistance.
• Involuntary loss of urine with increased intra-
abd pressure, in the absence of detrusor
contraction, is usually labeled stress
incontinence.
• When loss of urine is associated with
increased intravesical pressure owing to
detrusor contraction, it is commonly referred
to as urge in continence.
29
Pathophysiology
• Genuine stress incontinence is invariably
associated with weakness of the pelvic floor
support, permitting hypermobility of the
vesicourethral segments, which in turn impairs
the efficiency of the sphincteric musculature.
• The increase in intraurethral pressure observed
during coughing results mainly from contraction
of the voluntary muscles with sphinteric action.
Part of the rise is passive (ie, by direct
transmission), but a significant component is
active (ie, caused by reflex musculature
contraction).
30
ASSESSMENT AND URODYNAMIC
STUDIES
• Most pt with UI can be assessed simply
without the need for urodynamics.
• A multidisciplinary approach to assessment
and management is strongly preferred and ,
in this respect, pt often relate better to non-
medical staff than doctors.

31
History and Examination
• The key features of the history are shown in
Table 1.
• Numerous st scoring system are available,
which may facilitate assessment and the
response to treatment.
• Hx taking may require a rather broader
assessment than is traditionally done by
general practitioners (GPs), including details
such as prolapse, sexual function and faecal
incontinence.
32
33
History and Examination
• Examination of the abd, prostate, urethra,
introitus, vagina and neurology are essential,
with particular attention to the presence of a
palpable bladder, estrogenisation status,
urethral abnormalities and any pelvic
masses.

34
Investigations
• Most important is simple urine testing to
exclude other diagnoses such as infection or
bladder cancer; many pt referred with
incontinence are found on simple testing to
have a previously undetected intravesical
abnormality.
• A frequency-volume chart is helpful for both
pt and clinician.
• It may show fewer st than the Hx might
suggest or clear evidence of, for example,
bladder overactivity with frequent, small-
volume voids. 35
Investigations
• The total daily urine output may also show
that most urine passage occurs at night
(nocturnal polyuria)← poor water handling by
the kidneys.
• A urine flow rate may be normal (Fig.1),
supranormal (bladder overactivity) or reduced
(← bladder hypocontractility).
• Significant residual urine (>100ml) on a post-
micturition US may also suggest detrusor
hypocontractility.
36
Investigations
• A pad test, with weighing of incontinence
pads over 24-72h, is helpful in estimating the
degree of urine loss.
• Pad tests have been shown to be an
objective and reproducible means of
assessing the degree of incontinence and
monitoring the response to treatment.

37
38
Urodynamics
• Reserved for those pt who fail conservative
management and who wish to consider
surgical treatment.
• The questions that need to be answered by
urodynamics are shown in Table 2.
• A urodynamic tracing from a pt with bladder
outlet obstruction is shown in Fig 2; there is a
high detrusor pressure and a low voiding flow
rate.

39
40
41
Urodynamics
• Urodynamics in SUI are used to confirm the
leakage and to exclude associated detrusor
overactivity or hypocontractility.
• Videourodynamics allow leakage into a pad
to be seen directly without the need to
inspect the pt’s perineum repeatedly.
• Detrusor overactivity (Fig.3) is found with
conventional urodynamics in 70% of those
who have it.
42
Urodynamics
• Using a low filling rate (20ml/mn or less)
improves the chances of detecting detrusor
overactivity, and unstable contractions may
be provoked during the study by standing,
coughing or handwashing

43
44
Treatment of Incotinence
• Conservative management, based on a clinical
diagnosis alone, is usually the optimum fist-line
treatment.
• Failure to respond to one form of conservative
management simply requires an alternative option to
be used and, if drug side-effects are a problem, these
are usually reversible on withdrawing the drug.
• However if surgical treatment is indicated, urodynamic
proof of the diagnosis is mandatory because st are not
a reliable predictor of urodynamic diagnosis.

45
Stress urinary incontinence (SUI)
• Containment and management of fluids and
voiding may be the only practical options for
many frail or elderly pt unable to cooperate
with more complex treatments.
• As a general principle, however, treatment
should be directed at reducing the
incontinence rather than containing it.

46
Pelvic floor physiotherapy
• Very effective in controlled clinical trials, with
60% of women responding to pelvic floor
exercises.
• Standard pelvic floor exercises are more
effective than either kelgel exercises
( retaining graduated weights within the
vagina by pelvic floor contraction) or
electrostimulation via the rectum.

47
Medication
• Duloxetine, 60% respond; contrary to
expectation, there is some evidence that it is
effective regardless of the degree of SUI.
• It probably works by stimulating Onuf’s
nucleus in the sacral cord, resulting in an
increase in urethral sphincter activity.
• The principle side-effect is nausea, which
often resolves after the first month of
treatment.
48
Surgical treatment
• Reserved for those who failed conservative
treatment, but pt must be adequately
counselled in advance about the possible
side-effects of surgery ( Table 1)
• Following a suburethral sling procedure
(Fig.1) or colposuspension (Fig. 2), 90% of
women will be dry (or almost so), but the
success rate at 10 years decreases to 60%.
• There are, however, no long-term follow-up
data for autologous and prosthetic slings.
49
Surgical treatment
• Periurethral injections of inert, bulking
agents produce less durable effects and are
usually reserved for pt who are unfit for other
procedures, for the elderly and for those with
low-volume leakage.
• Too little attention has been paid to the
possible side-effects of surgery for SUI. A
women who exchanges SUI for an overactive
bladder post-op, without being aware that
this could happen, may feel badly treated.
50
Surgical treatment
• SUI in men is most often seen after
transurethral or open radical prostatectomy.
• If pelvic floor physiotherapy is ineffective,
periurethral injections may be used but, in
more severe cases, consideration should be
given to insertion of an artificial urinary
sphincter (AUS; Fig.3). This carries a 90%
satisfaction rate, but the revision rate is 30%,
usually for complications such as mechanical
failure and erosion into the urethra.
51
52
53
TVT

54
55
56
Overactive bladder (OAB)

• Consevative options for SUI are also


appropriate for OAB with the addition of
bladder training (Table.2).
• Bladder training introduced, prolonged
admission to the hospital for close
supervision.
• Bladder training at home may still be
effective in up to 85% of pt.
57
Medication
• An anticholinergic effect, probably on M3
receptors in the detrusor : oxybutynin,
tolterodine, propiverine, stropium and
solfenacin.
• 60% of pt obtain a useful response, and there is
a good evidence that this is sustained over a
period of time.
• The commonest side-effects of these drugs
include dry mouth and eyes, blurred vision,
dyspepsia, bowel disturbance and confuse (esp
in elderly). 58
Surgical treatment
Failed to conservative treatment:
-Major surgery to augment the bladder with a
bowel patch, which acted as a bladder
diverticulum to “mop up” sudden pressure
rises associated with inappropriate detrusor
contractions.
-In recent years, other techniques such as
neuromodulation and intravesical injections
of botulinum toxin have become popular
because they are less invasive.
59
60
Assessment and pathophysiology of
neuropathic bladder disorders
• Many neurological condition affect the LUT →
attention of urologists.
• In general, the role of urologist is to access the
urological conditions and then discuss with the pt
what potential management options are suitable for
that individual.
ex: 2 pts with the same problem (spinal cord injuries
-one choose simplest option (a long-term SPC)
-other may choose bladder augmentation, a
catheterisable stoma or an artificial sphincter as part
of a requirement to be free of an indwelling catheter.
61
Urological problems in neurological
conditions
• The fundamental concern for any pt with a
neurological condition is whether renal
function is at risk because of the effects of
neurological abnormality on their urinary tract.
• Before, the premature death from renal failure
was common, this was the commonest cause
of death in pt with spinal cord injury.

62
Urological problems in neurological
conditions
• More recently, It has been recognized that
other issues such as bladder emptying,
continence, UTI, erectile dysfunction and
fertility are also important in these pt.
• Other non-urological concerns may also be
relevant in pt neuropathic bladder disorders
(Table 1).

63
64
Static and progressive neurological
conditions
• Whether the neurological condition is static
or progressive (Table 2) is of crucial
importance to urological management.
• It also important to appreciate that some
treatment options may require good eyesight
as well as a degree of mental or manual
dexterity (Table 3).

65
Static and progressive neurological
conditions
• condition If these faculties are
subsequently affected by progression of
the neurological, as is often case in
multiple sclerosis, not only may
management need to change, but the pt
may already have undergone a procedure
associated with significant morbidity with
little or no benefit.

66
67
Classification of lower urinary tract
function in neurological disorders
• A number of classifications have been used
over the years.
• However, the simplest methode is to consider
seperately the effects on the bladder and the
bladder outlet and to determine whether each
is overactive, normal or underactive.
• The consequences of this classification are
shown in Table 4.
68
69
Classification of lower urinary tract
function in neurological disorders
• An overactive sphincter may produce a
condition called detrusor-sphincter
dyssynergia, whereby the normal process of
coordination between bladder contraction and
bladder outlet relaxation is lost; there is
intermittent contraction of the outlet during
voiding, leading to dramatic rises intravesical
pressure.

70
Classification of lower urinary tract
function in neurological disorders
• Figure 1 shows a urodynamic study in detrusor-
sphincter dyssynergia, together with
electromyographic (EMG) recordings from the
sphincter (sphincter EMG); there is evidence of
intermittent sphincter activity during a voiding
contraction.
• If there are sufficient overactive bladder
contractions to raise the bladder pressure to a
level higher than the renal filtration pressure,
upper tract dilatation develops and may
progress to renal impairment. 71
Classification of lower urinary tract
function in neurological disorders
• Fortunately, conditions that cause an overactive
sphincter are rare, so renal impairment in
neurological conditions is uncommon; it
generally occurs only in spinal cord injury, spina
bifida and, to a lesser extent, in Parkinson’s
disease. The first two conditions carry the
greatest risk of upper tract deterioration.

72
73
Assessment
• Assessment requires consideration of the
issues in Tables 1-4.
• Pt with spinal cord injury pr spina bifida are
usually referred to urologists from a spinal
injuries centre or from a paediatric urologist
respectively; their management should
already be in place when they are first
assessd.
• Most other pt come from a neurologist or
general pratitioner.
74
Assessment
• Assessment should also take into account
how bladder emptying occurs ( spontaneously
or drained by a catheter), whether
incontinence is a problem and whether urinary
tract infections are occurring.
• The need for urodynamics is determined by
whether the pt is at risk of upper tract damage
and whether the current management plan is
satisfactory.

75
Treatment of neuropathic bladder
disorders
• Need to be tailored to the urological
problems of each individual pt.
• Options for management are shown in
Table 1 according to the underlying
urological problem; some options may
need to be considered in combination.

76
77
A. Urinary Tract Infection

• Repeated, symptomatic lower tract infections


are best managed by low-dose prophylactic
antibiotics.
• The choice of antibiotic should be
determined by the risk of side-effects and the
capacity for an undesirable elimination of the
normal bowel flora in the long term.
• The optimum antibiotics in this respect are
trimethoprim, cephalexin, nitrofurantoin or
norfloxacin, given as a single daily dose.
78
B. Chronic retention
• An indwelling catheter will relieve chronic retention
and prevent upper tract damage if there is
urodynamic evidence of a high-pressure bladder.
• Suprapubic catheterisation (SPC) is usually
preferred because changing the catheter is easy
and retains dignity for the pt.
• Urethral catheters should be avoided in women
because, in the long term, they cause erosion of
the bladder neck, which causes the catheter to
drop out with its balloon inflated.

79
B. Chronic retention
• Permanent catheterisation is inevitably
associated with chronic bacteriuria, but this
does not require antibiotic treatment unless it
causes systemic st.
• Regular bladder washouts with citrate
solution may prevent long-term problems
such as catheter blockage and bladder stone
formation.

80
B. Chronic retention
• Intermittent self-catheterisation (ISC) is
preferable if the pt has good eyesight and
manual dexterity.
• Hydrophilic catheters are easy for the pt to
insert, and the frequency of catheterisation
is determined by measuring residual urine
throughout the day.
• ISC does not run the risk of introducing
infection, but actually reduces infections
by removing any residual urine after
voiding.
81
C. Overactive bladder (OAB)
• The aim of treatment for ABO should be to
reduce the pressure within the bladder,
thereby protecting the upper tracts.
• Denervation of the bladder by subtrigonal
phenol injections or by endoscopic/open
transection of the bladder is no longer used
because the effect is short-lived.
• Catheterisation or ISC should be the first
measure in order to protect the kidneys.
82
C. Overactive bladder (OAB)
• More permanent effects can be achieved by
bladder augmentation with an isolated path of
bowel (Fig.1); ileum is most commonly used
(clam ileocystoplasty).
• This effectively creates a large diverticulum in
the vault of the bladder, which absorbs
pressure rises and prevents their transmission
to the upper tract.
• The long-term sequelae of this procedure can
be troublesome (Table 2).
83
84
85
C. Overactive bladder (OAB)
• Alternative Tx include dorsal rhizotomy,
where the dorsal sacral roots are divided
surgically to disrupt the micturation reflex arc,
and implantation of a sacral root stimulator,
which produces detrusor contractions and
stimulates voiding.
• Pt undergoing dorsal rhizotomy usually
require ISC after the procedure to allow
bladder emptying
86
C. Overactive bladder (OAB)
• Intravesical botulinum toxin is currently
the preferred option for OAB due to
neurological disease. The toxin is injected
into the bladder wall under local anesthetic
through a flexible cystoscope.
• St are relieved in 60-70% of pt, but this
improvement may last only a few months;
long-term follow-up data are not available.

87
C. Overactive bladder (OAB)
• Sacral root neuromodulation is used in
some centers for OAB (Fig.2).
• Following confirmation that the patient’s st
respond to stimulation of the S3 motor root
(using a temporary electrode inserted
under LA), a programmable stimulator is
implanted in a subcutaneous pocket above
the buttock, and the S3 root is stimulated
continuously.
88
C. Overactive bladder (OAB)
• 60% of pt with OAB refractory to other
treatments respond to neuromodulation.
• Urinary diversion, usually into an ileal
conduit, may be necessary for some pt
whose st are refractory to other Tx or who
want a “one-off” solution to their problem.

89
90
D. Sphincter weakness
• A simple condom drainage device or
indwelling catheter may be appropriate for
many pt, and insertion of an artificial
urinary sphincter (AUS), while a major
procedure, produces good functional
results provided the pt has adequate
manual dexterity to activate the device.

91
D. Sphincter weakness

• One surgical alternative is to close off the neck


of the bladder through a suprapubic incision and
construct a catheterisable stoma on the abd.
• This involves fashioning a conduit between the
bladder and the ant abd wall using a flap of
bladder, the appendix, a fallopian tube or an
isolated segment of bowel (Mitrofanoff
procedure).
• The stoma is catheterised regularly to empty the
bladder.

92
E. Detrusor-sphincter dyssynergia

• Division of the external sphincter (external


sphincterotomy) is occasionally used to
prevent high bladder pressures.
• This inevitably causes incontinence, but
the incontinence can be managed either
with a condom drainage device or, if the pt
prefers, by implantation of an artificial
urinary sphincter.

93
94

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