This document discusses urinary incontinence and provides information on various related topics. It defines urinary incontinence and discusses its epidemiology and various causes. The causes of urinary stress incontinence are explained. Diagnosis and investigations for stress incontinence are outlined, including pelvic exams, postvoid residual measurement, and urodynamic studies. Conservative and surgical management options for stress incontinence are summarized. Overactive bladder is also defined.

1. Urinary Incontinence
Dr Bahgat Yassin

2. Definition
• Urinary incontinence is defined by the International Continence Society as
‘the complaintof any involuntary leakage of urine’.

3. EPIDEMIOLOGY
1) Age
Theincidenceofurinary incontinenceincreaseswithincreasingage.
2) Race
there is evidence that there is a lower incidence of both urinary incontinence and
urogenitalprolapse inblackwomen

4. EPIDEMIOLOGY
3) Pregnancy
Urgency and urge incontinence have been shown to increase in pregnancy. Stress
incontinencehas also been reported tobe more common in pregnancy.
4) Childbirth
Childbirth may result in damage to the pelvic floor musculature as well as injury to
the pudendal and pelvic nerves. The association between increasing parity and
urinary incontinencehas beenreported in several studies.

5. 5) Menopause
The urogenital tract and lower urinary tract are sensitive to the effects of
oestrogen and progesterone throughout adult life. Urge incontinence in
particular is more prevalent following the menopause and the prevalence
would appear torise withincreasingyears of oestrogen deficiency.
EPIDEMIOLOGY

6. THE CAUSES OF URINARY INCONTINENCE
1. Urodynamic stressincontinence(USI);
2. Detrusor overactivity;
3. Overflow incontinence;
4. Fistulae(vesicovaginal, ureterovaginal,urethrovaginal);
5. Congenital(e.g.ectopicureter);
6. Urethraldiverticulum;
7. Other (e.g.UTI,faecalimpaction,medication);
8. Functional(e.g.immobility).

7. Urinary symptomscan bebroadly divided.
Detrusor overactivity is classically associated with frequency, urgency, urge
incontinence,nocturiaandnocturnal enuresis.
Urodynamic stress incontinence is classically associated with involuntary leakage
on effortor on exertionor oncoughing or sneezing
Continuous incontinence and/or post-micturition dribbling are more likely to be
associatedwith neurologicaldisorders, overflow,urethral diverticulaeor a fistula.
Manywomencomplainofamixtureofsymptoms.

8. URODYNAMIC STRESS INCONTINENCE
• Definition
Urodynamic Stress Incontinence (USI) is noted during filling cystometry and is defined as ‘the
involuntary leakage of urine during increased abdominal pressure, in the absence of a detrusor
contraction’.
Incidence
Urodynamic stress incontinence is the commonest cause of incontinence in women. 1 in 10 women
willsuffer from USI atsome point intheir lives.
Aetiology
There are various factors that are thought to predispose to the development of USI.

9. 1. Increasedintra-abdominalpressure:
o – pregnancy
o – chronic cough
o – abdominal, pelvic mass
o – constipation
o – ascites.
2. Damagetothepelvicfloor:
– childbirth
– radical pelvic surgery.
3. Fixed,scarredurethra:
– previous surgery
– radiotherapy.

10. Pathophysiology
• Theexactpathophysiologyisunclear, butseveralhypotheses havebeenputforward.
1. Failure of the supporting structures such as the pubourethral and pubovesical
ligaments.
2. Failure of the intrinsic sphincter mechanism as a result of damage to the
rhabdosphincter, poor collagen or reduced urethral vascularity (intrinsic sphincter
deficiency–ISD).
3. Failure of the extrinsic sphincter mechanism as a result of weakness or damage to the
pelvic floor musculature. This allows displacement of the bladder neck from within the
intra-abdominalpressure zone.

11. ‘integral theory’
This hypothesises that the distal and mid urethra have an important role in the continence
mechanism and that maximal urethral closure pressure is controlled at the mid-urethral point.
The theory also proposes that damage to the pubo-urethral ligaments, which support the
urethra, impaired support of the anterior vaginal wall to the mid urethra, and weakened
function of part of the pubo- coccygeal muscles, which insert adjacent to the urethra, are
responsible for causingstress incontinence.

12. Diagnosis of genuine SUI
1) History : ........usually MP.....
Complaint: escape of urineduringstress e.gcoughsneezing, laughing.
Identifypredisposing and precipitating factors.
ExcludeUTI, DM-neurologicaldisorders –interstetialcystitis.

13. Diagnosis of genuine SUI
 Past Medical History:
• Obstetric trauma → damage to pelvic floor support : history of prolonged
labour , macrosomia , instrumental delivery.
medical conditions : “DIAPPERS”: dementia/delirium, infection, atrophic
vaginitis, psychological, pharmacologic, endocrine, restricted mobility, and
stool impaction.

14. Pelvic examination :
1.Cough stresstest:
Patient lies in lithotomy position while the UB is semi-full ask the patient to strain
to see escape of urine. repeat the test while the patient is standing on towel or
sheet
2.Q tiptest :
A lubricatedcotton swabis insertedintotheurethra tothe levelofUrethro-Vesical
junction. The patient is asked to strain as if urinating . If the angle ranges between
30 -60o abovethehorizontalplane= hypermobility.(controversial)

15. • 3. Bonney’s’Marshal’ test :
Done in case of prolapse with + ve cough stress test to differentiate if incontinence is dt prolapse or
sphincteric weakness . Elevate UBbase by 2 fingers . If SUI stopped
SUI is dt descent of UB base ??.

16. Investigations for genuine SUI :
1) Basictests :
• Mid stream urine analysis & culture: no infection .blood, glucose, protein,
leucocytes and nitrites in theurine.
• Urinary diary & pad test (simple pad test 1 h & extended pad test 24 h) .not
recommendedin the routineassessment of UI by NICE

17. Investigations for genuine SUI :
2) Postvoid Residual (PVR):
• - measured with: a handheld sonographic bladder scanner , transurethral
catheterizationand 3D ultrasound devices.
• - A large PVR reflect : recurrent infection, urethral obstruction or
neurologic deficits.

18. Investigations for genuine SUI :
• - A normally small PVR is often found in those with SUI.
• - Postoperative PVR after anti-incontinence surgery, helpful
indicator of a
• patient’s ability to completely empty her bladder. This evaluation
may be
• completed with a “passive” or an “active” voiding trial.
• - A voided volume of at least 300 mL and PVR less than 100 mL is
desirable.
• or if the PVR is less than one third of the voided volume.

19. 3) Urodynamic study
itis basic investigationnow.
• - Bladder functions is measured by set of tests called Cystometrics which
may be simple or multichannel.
• - Multi-channel cystometry, ambulatory urodynamics or video
urodynamics is not recommended before starting conservative treatment.
(NICE 2006)

20. • - Multi-channelfillingand voidingcystometryis recommendedin before
surgery for UIif thereare: (NICE 2006)
• Symptomssuggestiveofvoiding dysfunctionor detrusoroveractivity .
• previous surgery forstress UIor anteriorprolapse,
4) Video cysto-uretherography:
not routinely recommended...
Loss of posteriorangle– Bladderbasedescent .Micturatingcystourethrography:
toassessthe angle,fillingdefects& fistula.

21. MANAGEMENTOF USI
Conservative management
• USI interferes with a woman’s quality of life but it is not a life-threatening condition
and therefore conservative measures should be tried in every woman prior to
resorting to surgical treatment.
• Conservative treatment is effective, has few complications and does not compromise
further surgical procedures. It is particularly useful in those women who are medically
unfit for surgery and those who have not completed their family, are breastfeeding or
are less thansix monthspostpartum.
• Conservative measures include:

22. 1. Pelvic floor exercises.
2. Biofeedback.
3. Electrical stimulation.
4. Vaginalcones.
5. Urethral devices.

23. Pelvic floormuscletraining
• women learn to consciously pre-contract the pelvic floor muscles before and
duringincreases in abdominal pressure toprevent leakage(‘the knack’);
• ● strength training builds up long-lasting muscle volume and thus provides
structural support;
• ● abdominal muscletrainingindirectly strengthensthepelvic floor muscles.

24. Electrical Stimulation
Electrical stimulation uses an electrical pulse to augment the ability to produce a
voluntary contraction. A probe is put into the vagina near the muscles of the pelvic
floor and a pulse of electricity is passed. The pulse frequency is debated, but it is
usually in the 35–40 Hz range. This method cannot be used in pregnancy or in
those with an IUCD in situ. It is not suitable for most women as it is excessively time
consuming.

25. Vaginal cones and urethral devices
These devices elevate the bladder neck and in some cases partially obstruct the flow
of urine. They are particularly suitable for women who find they are incontinent only
at specific times, for instanceduringaerobics or playing tennis.

26. Pharmacologicalmanagement
• ⍺1-adrenoceptor agonists
• oestrogens
• tricyclic antidepressants
• duloxetine

27. Duloxetine
• is a potent and balanced serotonin (5-
hydroxytryptamine) and noradrenaline re-uptake
inhibitor (SNRI) which enhances urethral striated
sphincter activity via a centrallymediated pathway.
• Duloxetine was associated with significant and dose-
dependent decrease in incontinence episode frequency
whilst the most frequently reported adverse event was
nausea.

28. Surgical procedures
• Colposuspension
The patient is placed in themodifiedlithotomy positionusingLloyd–Davies
stirrups. A Foley catheteris inserted into the bladder and allowed to drain
freely. A low transverse incision is made justabove thesymphysis pubis (i.e.
lowerthana pfannenstiel).

29. Surgical procedures
The retropubic space is dissected until the white paravaginal tissue lateral to
the bladder neck is exposed. Two to four polydioxanone (PDS), Ethibond or
polyglycolic acid sutures are inserted into the paravaginal fascia. Each suture
is tied and the needle is then re-inserted into the ipsilateral ilio- pectineal
ligament. The first suture is placed at the level of the bladder neck and the
subsequentsuturesare placed 1 cm laterally and 1 cm cranially

31. Pubovaginal sling
• tension-free vaginal tape

32. •

33. •

34. Trans-obturator sling procedures

37. OVERACTIVE BLADDER

38. Overactive bladder is the term used to describe the symptom
complex of urgency with or without urge incontinence,
usually with frequency and nocturia, in the absence of UTI or
any other obvious cause.
The symptoms of OAB are due to involuntary contractions of
the detrusor muscle during the filling phase of the
micturition cycle. These involuntary contractions are termed
detrusor overactivity and are mediated by acetylcholine-
induced stimulation of bladder muscarinic receptors

39. Detrusor overactivity
• Detrusor overactivity is defined as ‘a urodynamic observation
characterised by involuntary detrusor contractions during the filling phase
whichmay bespontaneousor provoked’
• Detrusor overactivity is a urodynamic diagnosis and usually presents with
symptoms of frequency, urgency, urge incontinence, nocturia, nocturnal
enuresis and sometimesincontinenceat orgasm.

40. Prevalence
• Epidemiological studies have reported the overall prevalence of OAB in
women tobe 16.9%
• the normal micturition contraction is through muscarinic acetylcholine
receptors (five receptor sub-typesM1–M5 )

41. Pathophysiology
A detrusor contraction is initiated in the rostral pons. Efferent pathways emerge
from the sacral spinal cord as the pelvic parasympathetic nerves (S2, S3, S4) and
run forwards to the bladder. Whilst preganglionic neurotransmission is
predominantly mediated by acetylcholine acting on nicotinic receptors
transmission may also be modulated by adrenergic, muscarinic, purinergic and
peptidergic presynaptic receptors.

42. • Acetylcholine is released by the post-ganglionic nerves at the
neuromuscular junction and results in a coordinated detrusor contraction
mediated through muscarinic receptors. However ATP also has a role,86
mediatedthrough non-adrenergic,non-cholinergic(NANC) receptors.
Pathophysiology

43. • Conversely sympathetic innervation is from the hypogastric and pelvic
nerves acting on ℬ-adrenoreceptors causing relaxation of the detrusor
muscle. Thus a balance between sympathetic and parasympathetic
stimulationis required for normal detrusor function.
Pathophysiology

44. Management of detrusor overactivity
• The treatment options for detrusor overactivity can be divided into
conservative, pharmacological, neuromodulationand surgical options.

45. Conservative management
• Conservative measures includeadvice regarding fluid intake. It may be that
simply cutting down on the volume of fluid consumed throughout the day
or altering the times at which drinks are taken will be enough to reduce the
symptoms and improve QoL. Women should be advised to consume
between 1 L and 1.5 L in any 24-hour period. It is not advisable to restrict
fluidintakeseverely,

46. Conservative management
• as a low urine outputtogetherwithfrequentvoiding can lead to a
reduction in the bladder’s functionalcapacity. Caffeineand alcohol are
known to irritate the bladder, and women shouldbe advised to try to avoid
caffeine-baseddrinks or substitutethem with decaffeinateddrinks.

47. Bladder retraining
The principles of bladder retraining are based on the ability to suppress
urinary urge and to extend the intervals between voiding. The regimen is
generally initiated at set voiding intervals and the patient is not allowed to
void between these predetermined times, even if she is incontinent. When
she remains dry, the time interval is lengthened. This continues until a
suitabletime span is achieved, usuallyaround 3–4 hours.

48. Bladder retraining
Cure rates using bladder retraining alone and no pharmacological agents
have been reported between44 - 90 %.

49. Pharmacology
• Antimuscarinicdrugs
The detrusor is innervated by the parasympathetic nervous system (pelvic
nerve), the sympathetic nervous system (hypogastric nerve) and by NANC
neurones. The motor supply arises from S2, 3 and 4 and is conveyed by the
pelvic nerve. The neurotransmitter at the neuromuscular junction is
acetylcholine, which acts upon muscarinic receptors. Antimuscarinic drugs
shouldthereforebe of usein thetreatmentof detrusor overactivity.

50. Tolterodine
Tolterodine is a competitive muscarinic receptor antagonist with relative functional selectivity for
bladder muscarinic receptors. Tolterodine has also been developed as an extended-release once-daily
preparation
Solifenacin
Solifenacin is a potent M3 receptor antagonist that has selectivity for the M3 receptors over M2 receptors and has much higher potency against M3
receptors in smooth muscle than it does against M3 receptors in salivary glands. The most frequently reported adverse events leading to
discontinuation weredry mouthand constipation.

51. Drugs that have a mixed action
• Oxybutynin
Is a tertiary amine that undergoes extensive first- pass metabolism to an
active metabolite, N-desmethyl oxybutynin, which occurs in high
concentrations and is thought to be responsible for a significant part of the
action of the parent drug. It has a mixed action consisting of both an
antimuscarinic and a direct muscle relaxant effect in addition to local
anaestheticproperties.

52. Drugs that have a mixed action
• Oxybutynin has been shown to have a high affinity for muscarinic
receptors in the bladder and has a higher affinity for M1 and M3 receptors
over M2.The effectiveness of oxybutynin in the management of patients
withdetrusor overactivity is welldocumented.

53. Tricyclic antidepressants
These drugs have a complex pharmacological action. Imipramine has
antimuscarinic, antihistamine and local anaesthetic properties. It may
increase outlet resistance by peripheral blockage of noradrenaline uptake
and it also acts as a sedative. The side effects are antimuscarinic, together
with tremor and fatigue. Imipramine is particularly useful for the treatment
of nocturia and nocturnal enuresis.

54. Intravesical therapy
• Botulinumtoxin
The use of intravesical botulinumtoxin type A (onobotulinumtoxin)was first
described in the managementof patientswithneurogenic detrusor
overactivity, althoughthereis now considerable evidence to support its usage
in patients with idiopathic detrusor overactivity as well.

55. Botulinumtoxin
• Consequently onobotulinumtoxin may be effective in
managing women with refractory OAB symptoms and may
be administered either under general anaesthetic with a
rigid cystoscope or under local anaesthetic with a flexible
cysto- scope. Whilst botulinum toxin type A (Botox®) is
currently licensed in the UK for the treatment of
neurogenic detrusor overactivity it is not currently
licensed for the management of idiopathic OAB.

56. Neuromodulation
• Sacral neuromodulation
Stimulation of the dorsal sacral nerve root using a permanent implantable device in the S3
sacral foramen has been developed for use in patients with OAB and neurogenic detrusor
overactivity. The sacral nerves contain nerve fibres of the parasympathetic and sympathetic
systems providing innervation to the bladder as well as somatic fibres providing
innervation to the muscles of the pelvic floor. The latter are larger in diameter and hence
have a lower threshold of activation, meaning that the pelvic floor may be stimulated
selectively without causingbladder activity.

57. URINARY FISTULAE
The development of a genitourinary fistula has profound effects on both the
physical and psychological health of a woman. The most common simple
genitourinaryfistulaeare

58. Fistulae types
vesicovaginal,
42%
ureterovaginal34%
urethrovaginal,
11%,
vesicocervical,
3%,

59. • The development of a fistula following surgery has considerable legal
implications. Whilst most gynaecologists accept that the development
of a fistula is deeply regrettable, it was generally thought that this was,
on occasion, unavoidable. However, more recent legal cases involving
ureteric injury would seem to refute that. There is a body of opinion
that holds the view that ureteric damage can always be avoided and
thatnottodoso constitutesnegligence