Monday, 9 January 2012


(Notes for Medical Students)

Consultant Urogynaecologist

·      In the US, over $10 billion is spent each year on urine incontinence
·      22-48% women leading independent lives have urine incontinence
·      Up to 50% of nursing home patients have urinary incontinence13% confide spouse, <50% seek treatment
·      GSI cause incontinence in 60%, DI increases with age

Anatomy & Physiology:
A) Female Continence Mechanism:
·      Continence is maintained by urethral closure and support of bladder & urethrovesical junction
·      3 systems produce urethral closure:
(i)  Internal urethral sphincter
n innervated by autonomic nervous system
n injury to pudendal nerve eg in childbirth, anti-incontinence surgery can affect this mechanism
(ii) External urethral sphincter
n under voluntary control
n resting tone contributes to intraurethral pressure
n intraurethral pressure higher than intravesical pressure maintains continence
n innervated by fibres from pudendal nerve, hence subject to injury in childbirth etc
(iii) Mucosal coaptation:
n filling of arteriovenous complex btw smooth ms coat of urethra & epithelium improves mucosal coaptation by causing urethral wall to seal, thus increasing resting urethral pressure
n HRT can improve blood flow to this area in postmenopausal women
·      Support to bladder & UV junction supplied by:
(iv) Pubocervical Fascia:
n attaches to cervix and travels beneath urethra and fuses with the perineal membrane of the urogenital triangle
n laterally connected to arcus tendineus (linear thickening of the parietal fascia of levator ani, which extends from ischial spine to the posterior aspect of the pubic bone and forms the lateral support of the vagina, bladder & rectum)
n forms a horizontal platform that supports the bladder
n anterior portion supports the urethra and maintains it in an almost  vertical  plane
n with increased increasing intraabdominal pressure, the lower urinary tract is pushed against pubocervical fascia and this urethrovesical trapping promotes continence
(v) Pelvic floor muscles:
n levator ani muscles assist in maintaining the proper position of the urethra and urethrovesical junction
n innervated by S2-S4 on their pelvic surface & branches from pudendal nerve on their perineal surface
n in constant state of contraction to allow the efficient positioning of the UV junction
·      Usually incontinence only occurs when multiple failures of these systems take place

B) Bladder Function:
·      Bladder function has 2 phases:
(i)  Filling phase:
n during filling phase, detrusor muscles remain in non-contractile  state (accommodation)
n when accommodation is impaired, spontaneous involuntary contractions of bladder occurs (detrusor instability)
n b-adrenergic sympathetic nerve stimulation causes detrusor ms relaxation and also inhibits parasympathetic activity
n a-adrenergic sympathetic stimulation causes internal sphincteric ms contraction
n external urethral ms and levator ani ms serve as backup voluntary continence control to forestall voiding for a short intended period
n once bladder reaches functional capacity (350-650ml), signals are sent to higher cortical centre to initiate emptying phase
(ii) Emptying phase:
n produced by relaxation of the urethra and levator ani, followed by detrusor ms contractions
n inhibition of pudendal & sacral efferent nerves produces relaxation of external urethral sphincter and levator ani, allowing posterior slackening of the fascial hammock
n cortical signals inhibit sympathetic relaxation of bladder
n activation of parasympathetic nervous system result in initiation of detrusor ms contraction and micturition begins
n voiding dysfunction can result from:
·      drug side effect and spinal cord disorder eg multiple sclerosis
·      impaired contractility with trauma, overdistension, fibrosis, inflammation
·      increased outlet resistance eg severe vaginal prolapse or tumours

Predisposing Factors:
A) Vaginal Childbirth:
·      vaginal childbirth can cause neuromuscular damage to the pelvic floor and/or detachment of pubocervical fascia
·      30% primigravidas new stress incontinence in pregnancy, <5% symptomatic 1 year later
·      postpartum GSI, 25% remained incontinent after 1 year
·      Risk factors for postpartum GSI:
·      prolonged stage 2
·      large fetus
·      episiotomy
·      obesity
·      parity >5
·      LSCS found to be protective of GSI, if one CS ( 5-11%), but risk increases if more than one CS(37%)
B) Aging and Genetic Factors:
·      aging causes microscopic and biochemical changes to endocervical fascia, esp collagen
·      symptoms of urine incontinence and other pelvic floor conditions often do not become evident until years after childbirth
C) Oestrogen Deficiency:
·      lower urinary tract rich in oestrogen receptors
·      when these receptors are stimulated, blood flow to the arteriovenous plexus is enhanced, thereby increasing coaptation of the urethral mucosa
D) Other Factors:
·      conditions which produce chronic raised intraabdominal pressure eg. constipation, chronic cough, obesity, heavy lifting
·      smoking aggravate incontinence by:
n causing chronic cough
n detrusor contractions induced by nicotine
n alteration of synthesis & quality of collagen
n anti-oestrogenic effect that diminish a-adrenergic receptor activity in internal urethral sphincteric ms

·      2 broad categories:
(a) Stress Incontinence
n leakage of urine with elevation of intraabdominal pressure
n eg. laughing, coughing, sneezing, walking, jumping
(b) Urge Incontinence
n involuntary loss of urine assoc with strong desire to void, whether or not the bladder is full
n eg. can’t get to bathroom in time
n other assoc symptoms include:
·      frequency (>7 times/day)
·      urgency ( strong desire to pass urine)
·      nocturia (>1 time/night)
·      enuresis ( bed wetting) and insensible urine loss may suggest a neurologic component
·      note that stress incontinence & urge incontinence are not diagnoses but rather symptom complexes reported by patient
·      Genuine stress incontinence is a diagnosis made by clinician based on objective evidence eg witnessing urine spurting out with coughing or through urodynamic study

Differential Diagnoses:
·      surgery should never be contemplated until a clear diagnosis can be objectively made
·      A) Genuine Stress Incontinence:
n = involuntary urine loss with increased intraabdominal pressure
n usually accompanied by loss of support for the UV junction
n O/E this loss of support can be seen as a posterior rotational descent of the anterior vaginal wall into vagina on straining
n In intrinsic sphincter deficiency (rare), urethral sphincter paradoxically opens during times of increased intraabdominal pressure, and the UV junction is relatively immobile on straining. This is often seen in patients who have had multiple anti-incontinence surgeries. Patients with this condition often experience continuous leakage or leakage with minimal exertion.
·      B) Detrusor Instability:
n = incontinence with strong urge to void which stems from involuntary detrusor contraction during the bladder filling phase
n symptoms suggestive frequency, urgency, nocturia
n differential diagnoses include (refer to plate 8) UTI, bladder cancer, bladder stones. (NB: 20% patients with bladder cancer present with irritative symptoms like this rather than haematuria)
n suburethral diverticulum can also result in UI (can contain chronically infected urine, stones or tumours)
n prior anti-incontinence surgery, eg retropubic suspension, can also result in UI
n Some neurologic conditions can also result in UI eg. Stroke, MS, Alzheimer, Parkinson’s.
·      C) Overflow Incontinence:
n can be due to outlet obstruction or secondary to acontractile or hypocontractile detrusor muscle
n  presentations include frequent or constant dribbling with SI & UI symptoms
n in women, can follow:
·      surgical procedures, eg retropubic suspension (partial urethral obstruction), urethral procedures (urethral stenosis), radical pelvic surgery
·      severe prolapse
·      drugs eg. anti-cholinergic
·      faecal impaction
·      neurological conditions eg. DM, MS, spinal cord tumour

·      D) Urinary Tract Abnormality:
n genitourinary fistulae
·      can result from obstetric trauma, pelvic radiation or surgery, tumour
·      presents with continuous urine leakage from vagina
·      if occurs postop, usually presents D5-14
n ectopic ureter
·      most common site of opening is along the urethra, below the level of bladder neck
·      causes continuous leakage and recurrent UTI
·      50% reports continuous dribbling despite a normal appearing voiding pattern
·      ectopic ureter can become dilated, creating a reservoir, mimicking the symptoms of stress incontinence
n suburethral diverticula
·      can be congenital or acquired (birth trauma, infection, instrumentation of urogenital tract)
·      classic triad of dysuria, dyspareunia and dribbling
·      other symptoms include localised pain, vaginal mass, chronic UTI, SI & UI
·      E) Pelvic Floor Defects:
n urethrocele, cystocele, uterine prolapse, enterocele, rectocele often accompany female urine incontinence

Clinical Evaluation:
·      history as described above
·      drug history important:
n (a) Cough & cold preparations (eg. pseudoephedrine, ephedrine, phenylpropanolamine)
·      increases urethral closure pressure and can result in urine retention
n (b) Antihypertensive agents (eg. prazosin, reserpine, guanethidine)
·      a-adrenergic antagonists which decrease urethral pressure and worsen GSI
n (c) Diuretics (eg. thiazides, loop diuretics, alcohol, caffeine)
·      increases urine output and worsens frequency and urge
n (d) Anticholinergic agents (eg. antihistamines, tricyclic anti-depressants, Haloperidol,  
·      causes detrusor relaxation and urine retention
n (e) Calcium channel blockers (eg.verapamil)
·      causes detrusor relaxation and urine retention

·      the value of urinary diary cannot be over-emphasised
·      examination should include abdominal, neurological and gynaecological
·      urine evaluation:
·      full ward test
·      measurement of post-void residual
·      mid stream urine

Diagnostic Testing:
·      simple cystometry:
n instil water slowly into bladder of standing patient
n note volume of water instilled when patient first noticed urge to void and the maximum volume that patient could tolerate
n fluid level that rises or overflows the syringe indicates unstable detrusor contraction
n other abnormalities seen include pain with bladder filling, first desire to void at bladder volume <100ml, and a bladder capacity of <350ml or >650ml
·      complex cystometry:
n specialised equipment to measure bladder, abdominal, and/or urethral pressure
·      videourodynamics:
n uses fluoroscope and radio-opaque media instead of water
n produces actual image of bladder as pressures are measured
n restricted to tertiary referral centres

A) Conservative Management:
·      Behavioural therapy
·      monitor progress with urine diary
·      important 1st line therapy for DI & some mild GSI
·      patients must be motivated & cognitively intact
·      most can achieve 50-90% symptomatic improvement
·      can be combined with pharmacologic treatment
·      Pelvic floor exercise & Biofeedback
·      1st described by Kegel >50 years ago
·      however, studies have shown that only 30% women who receive verbal instructions can perform PFE correctly (therefore, give instruction while doing bimanual exam)
·      if done properly, patients can expect 70-80% symptomatic improvement over 12 weeks
·      PFE can be enhanced with biofeedback devices eg intravaginal pressure probe, graduated vaginal cones
·      Absence of a levator contraction during bimanual examination precludes the use of these
·      Electrical stimulation & physical therapy
·      ES of pelvic floor results in reflex contraction of peri & paraurethral muscles while inhibiting detrusor activity
·      requires intact pelvic floor innervation
·      symptomatic improvement in 50%
·      portable, home usage available
·      with physical therapy, patients can strengthen the levator muscles by exercising hip girdle muscles (these muscles work together in groups)
·      Pharmacologic therapy
·      cholinergic agonists eg bethanechol, have been used to induce bladder contractions, but studies have shown little benefit in urine retention
·      anti-cholinergics eg. imipramine, oxybutynin; produce detrusor relaxation and are used in DI
·      a-adrenergic agonists which can cause urethral sphincter contractions may be helpful in for GSI, particularly when combined with PFE
·      a-adrenergic antagonists eg, prazosin, have a role in treatment of urine retention caused by a lack of coordination btw the UV junction & the bladder during micturition (but may worsen GSI)
·      imipramine also useful in stress incontinence by increasing urethral contractility
·      oestrogen replacement therapy helps to restore collagen and improve urethral mucosal coaptation in postmenopausal women
·      Devices for control of incontinence
·      tampons or pessaries can improve mild stress incontinence
B) Surgical Management:
·      with the exception of paravaginal repair and artificial sphincters, all anti-incontinence procedures aims to restore the UV junction and hence the hammock effect to prevent urinary loss
·      all except artificial sphincters place sutures in the pubocervical fascia
·      GSI is the most commonly treated condition
·      Surgical treatment of GSI:
·      Anterior colporrhaphy:
n one of the oldest technique
n often performed together with suburethral plication
n objective success rate 70% at 1 year, 37% at 5 years
·      Retropubic suspension:
n eg. Burch, Marshall-Marchetti-Krantz
n sutures are placed into pubocervical fascia around the urethra & UV junction and secured to structures in the bony pelvis
n Burch -> objective success rate 87% at 1 yr, 82% at 5 yrs and 82% at 10 yrs
n Burch complication:
n detrusor instability, de novo 10%
n enterocele/rectocele, 5-17%; 13% at 5 years
n voiding dysfunction 2-12%
n sexual dysfunction poorly reported
n failure of colposuspension:
n incorrect preop diagnosis
n faulty technique, inadequate vaginal elevation
n previous bladder neck surgery, 65% 5 years
n preop DI
n increasing age & weight
n MUCP<20cm H20
n poor bladder neck mobility

·      Needle suspension:
n eg. Stamey, Peyrera, Gittes, Raz procedures
n sutures placed on either sides of UV junction transvaginally , then brought thru ant abd wall and anchored over rectus abdominus fascia
·      Sling procedures:
n  tension free vaginal tape (TVT) where tape applied midurethrally transvaginally & then brought through anterior abdominal walll
n Transobturator tape (TOT) where tape applied midurethrally transvaginally and brought through obturator foramen
n Mini-sling where tape applied midurethrally transvaginally and the tape is pushed towards the obturator foramen
n autologous tissue (eg. fascia lata, rectus fascia, round ligament etc) can also be used
n synthetic material eg. Polypropylene, Teflon, Goretex
n sling versus Burch:
·      success, 4 prospective studies showed no difference (all had power <50%)
·      RCT success rates 90%, bladder irritability & voiding dysfunction 29% in sling and 10% in colpo
·      retrospective study; sling 79%, colpo 95%
·      Now sling procedure is the gold standard for treatment of USI
n complication: voiding dysfunction 13% and DI 17%
·      Paravaginal repair:
n can be transabdominal or transvaginal
n reapproximates pubocervical fascia to white line
n used in lateral wall defect
n 1 study quoted 95% satisfaction
n RCT objective success:
n 100% colposuspension
n 61% paravaginal
n paravaginal assoc with less voiding difficulties
·      Transurethral injections:
n agents eg. autologous fat, teflon, collagen, macroplastique
n day case, minimal morbidity, easily repeated
n transurethral or periurethral injections
n indications:
n elderly, frail, poor health
n well supported bladder neck
n macroplastique:
n GSI 73% cured or improvement at 3 months, 58% at 3 years
n expensive
·      artificial sphincters:
n mechanical cuffs placed around UV junction
n  deflate cuff when voiding desired
n can break down


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