URINARY INCONTINENCE

Prof. A.K.Sil

Definitions
What is continence? Ability to control urine in between two voluntary acts of micturition. What is incontinence? Involuntary leakage of urine which is objectively demonstrable and a social and hygienic problem.

Types of Incontinence
Congenital Epispadias

Transurethral

USI Neuropathic OAB Acquired Retention with overflow Misc.& functional Fistulae Ureteric, Vesical Urethral

Nonneuropathic

Congenital Extraurethral

Acquired

Mechanism of normal continence

Anatomy BladderDetrusor, Innervation. UrethraMuscles, Sphincters. Pelvic floor & supports. Physiology CNS, Spinal centres, Detrusor and urethral pressure.

Anatomy- Bladder
Multilayered- Mucosa, Submucosa, Muscle, Adventitia. Mucosa3 layers of transitional epithelium Superficial impermeable umbrella cell layer primary urine plasma barrier Secrete glycosaminoglycans protective barrier preventing bacterial adherence.

Bladder musculature
Outer longitudinal
Detrusor 3 layers smooth m act as syncytium

Middle circular

All rich in Ach esterase

Inner longitudinal
Sparse parasymp.n supply, continuous with that of prox urethra & ureter

Outer layer Trigone

At bladder neck, smooth m are separate from Detrusor no sphincteric effect

Inner layer

Same as rest of detrusor

Anatomy - Urethra
Length 3-5 cm Smooth muscleContinuous with Detrusor but minimal parasympathetic innervation. Striated muscle- Act as a single unit, circumferentially constricting upper 2/3rd and laterally compressing lower 1/3rd.

Slow twitch Wraps circumferentially External urethral sphincter/ Sphinter urethrae/ Rhabdosphincter at mid urethra

Striated m

Remains tonically contracted & maintains continence at rest

Act as single unit circumfere ntially constrictin g upper 2/3rd & laterally compressin g lower 1/3rd

Urethrovaginal sphincter &Compressor urethrae

Fast twitch
Arch ventrally over urethra and insert into fibromuscular tissue of anterior vagina Maintains continence during stress

Pelvic floor & supports

Levator ani muscles
Pubococcygeus Iliococcygeus Coccygeus

Endopelvic fascia
Levator ani muscles, ligaments, endopelvic fascia work in synergy. Defect of any of them cause support defect and incontinence.

Innervation - Bladder
S2,3,4 Muscarinic receptors in bladder wall M2, M3 predominant T10-L2, carried via hypogastric n.plexus Main Parasympathetic

Efferent

Contraction predominantly at bladder base & urethra

Aids continence Dome of bladder

Little Sympathetic

receptors

Afferent

Pass along sacral & thoracolum bar visceral afferents

receptors

Assists in urine storage.

Innervation - Urethra
Smooth muscle are supplied by
Parasympathetic which causes contraction, shortening & widening of urethra, no sphincteric function. Sympathetic predominantly adrenoceptors.

Striated muscle
Rhabdosphincter by pelvic splanchnic travelling with parasympathetic fibres. External periurethral m. by perineal br.of Pudendal nerve.

CNS Control
Discrete areas in cerebral cortex are responsible for
Perception of sensation of bladder fullness Inhibition of micturition Initiation of voiding.

Superior frontal gyrus & Anterior cingulate gyri Voluntary postponement of voiding Lesion causes abolition of conscious & unconscious inhibition of micturition.
Paracentral lobule Controls relaxation of sphincter Lesion causes spasticity of sphincter & retention.

CNS Control contd.

In cerebellum
Anterior vermis Fastigial nuclei.

Subcortical areas
Thalamus principal relay centre to cerebral cortex Reciprocal connection with lower spinal centres Basal ganglia Limbic system Hypothalamus Mesencephalic pontine medullary reticular formation 2 areas having inhibitory and excitatory effects on micturition centre.

Mechanism of Continence
Complex dynamic process involving fascia, ligaments, muscles, with accompanying nerve & vascular supply and control of higher centres.
Maximum urethral pr. > Intravesical pressure

Mechanism of Continence contd. Intravesical pressure

1. Hydrostatic pressure of fluid in the bladder exerted at bladder neck. Vertical gravitation pr. with respect to atmospheric pr. at upper border of symphysis pubis. Rarely exceeds 10cm of water. 2. Transmission of intra-abdominal pr. 3. Tension in the bladder wall.

Mechanism of Continence contd.

Urethral closure
1. Hermetic seal or mucosal coaptation from submucous vascularity & secretion from mucosa. 1/3rd of urethral closure pr. 2. Intrinsic smooth muscle1/3rd of urethral closure pr. 3. Intrinsic & extrinsic striated muscle1/3rd of resting urethral pr. Highest pressure found in midurethra, 40-54th percentile.

Mechanism of Continence contd.

During stress Intra-abdominal pressure rises
Intra-vesical pressure rises.

Counteracted by simultaneous rise in intra-urethral pressure by Pressure transmission to proximal urethra and vesical neck Contraction of external sphincter Contraction of peri-urethral fibres of levator ani (fasttwitch fibres) Also shortening of levator ani lifting anterior vaginal wall pushing vesical neck against precervical arc Compression of urethra against anterior vaginal wall.

Pressure transmission to proximal urethra & vesical neck

Urethra is supported by a hammock anterior vaginal wall (VW) with its attachment to ATFP. Shortening of Levator ani (LAM) lifts vagina & pushes vesical neck (VN) against pre-cervical arc (PCA)

Mechanism of Continence concl.

In the young, continence is maintained at bladder neck. In advanced age, urethral sphincter mechanism is more important. During stress, 3 mechanisms for intraurethral pr.1. Reflex striated m.contraction occurs before voluntary striated m.contraction & pressure transmission come into action 2. Voluntary striated muscle contraction 3. Pressure transmission.

Normal Micturition
Filling and storage:
Bladder is filled at a rate of 0.5ml/min. Gradually distends but wall pressure is not increased due to relaxation Proprioceptive afferent from stretch receptor Pelvic nerves Sacral Dorsal roots of S 2,3,4 Ascend via Lateral Spinothalamic tract To reticular formation Detrusor contraction is inhibited by descending inhibitory impulses.

Normal micturition Filling & storage contd.

As bladder filling continues, afferent impulses ascend to cerebral cortex First sensation/desire to void occurs at of functional bladder capacity Conscious cortical inhibition to spinal centres Till suitable time, place & posture is found Also voluntary pelvic floor contraction occurs to increase urethral closure pressure.

Normal Micturition - Initiation

With suitable site, time & posture Voluntary relaxation of pelvic floor muscles

Relaxation of intrinsic striated muscle of urethra

Marked in intraurethral pressure. A few seconds later Descending inhibitory impulses are suppressed Rapid discharge of efferent parasympathetic impulses Detrusor contraction. Sympathetic discharge reduced causing further urethral relaxation Intravesical pr > Intraurethral pr

Urine flow starts.

Normal Micturition -Voiding

During voiding Intravesical pressure remains constant due to low P det radius of bladder decreases. At the end of micturition intravesical pressure falls

Urine flow diminishes. Pelvic floor and intrinsic striated muscles contracted
Urine flow is stopped at mid-urethra Urine in upper urethra is milked back into bladder Urethra closed cephalad

Mechanisms of Incontinence
During stress, increases in intra-abdominal pr leads to greater increase in intravesical pr than intraurethral pr due to lack of urethral support or abnormally positioned bladder neck & proximal urethra Leads to - GSI. Loss of intraurethral pr due to loss of urethral integrity i.e. lead pipeurethra Leads to GSI due to ISD Causes Menopause, Post RT, Post surgery.

Mechanisms of Incontinence contd.

Abnormal steep rise in Detrusor pr during bladder filling due to impaired bladder compliance Leads to DO Causes Post RT Chronic inflammation like TB, Interstitial cystitis. Increases in intravesical & intraurethral pr occurs but latter increase is insufficient Leads to DO Example Detrusor sphincter dyssynergia.

Evaluation of Incontinence
1. Urinary symptoms Number of voids Pads used/day Type of pad Frequency of pad changing Degree of pad saturation Circumstances & manouevres inciting leakage

Evaluation of Incontinence contd.

2. Quality of life assessment IIQ-7, UDI-6 3. Midstream urine for R/E & culture 4. Urinary diary Completed in 5 days How much & how frequently she drinks and voids Leakage episodes with precipitating events Acts as baseline for monitoring of bladder retraining. 5. Pad Test significant or +ve if 1 hr > 1 gm or 24hr > 4 gm.

6.

Q Tip test Excursion > 20-30o Hypermobile urethra

Evaluation of Incontinence contd.

7. Uroflowmetry Maxm flow rate 15ml/sec with voided volume > 150ml. 8. Cystometry Static & Ambulatory Simple & Twin-channel Studies pressure/volume relationship of bladder during filling & voiding Indications:
i. ii. iii. iv. v. Urinary incontinence, OAB symptoms Voiding disorder Prior to bladder neck surgery Previous unsuccessful continence surgery Neuropathic bladder disorder.

Cystometry contd.
All measurements in cm of water, upper edge of symphysis pubis as zero reference 12 F catheter Filling rate 10100ml/min Slow fill <10ml/min indicated in neuropathic bladder Assessment of Pves Pabd Pdet = Pves - Pabd

Cystometry contd.

Normal values
Residual volume < 50ml First desire to void at 150-200ml Capacity (strong desire to void) >400ml No Detrusor pressure during filling Absence of systolic Detrusor contraction No leakage on coughing Detrusor pr rises on voiding maximum voiding pr < 50cm of water with peak flow rate >15ml/sec for a voided volume > 150ml.

Cystometry contd.

Abnormality
Leakage on coughing in absence of rise in Pdet GSI Spontaneous or provoked Detrusor contraction during filling phase DO Phasic Detrusor contraction Systolic overactive bladder Pressure rise > 15cm of water on filling the bladder with 500ml of fluid which does not settle after filling is stopped Low compliance bladder

Evaluation of Incontinence contd.

9. Radiology : i. Plain abdominal Xray
Bladder calculi Osteitis pubis Spina bifida, meningomyelocele Spinal cord problem, disc prolapse

ii. IVP
Only for neuropathic bladder, suspected ureterovaginal fistula

iii. VCU
Not routinely used. Helpful in vesico-ureteric reflux, post-micturition dribble.

Radiology contd.
iv. Micturating Cystogram
Not useful in assessment of incontinence Useful in demonstrating vesico-ureteric reflux, diverticula, bladder/urethral fistula

v. Lateral Chain Xray

Downward and backward displacement of bladder neck during coughing & straining can be demonstrated, PUV angle can be assessed but it is neither reliable nor consistent in clinical practice.

Evaluation of Incontinence contd.

10. Ultrasound :
Post void residual urine (l w d) 0.625 Bladder neck position by TAS, TVS, TPS. Uses lower border of symphysis pubis as a fixed reference. Descent of bladder base & bladder neck opening seen both in DO & GSI. Difficult to differentiate without cystometry Vaginal probe may compress bladder neck preventing leakage. Bladder wall thickened in OAB rather than GSI Urethral USG detects opening of urethral diverticulum Urethral sphincter cross-sectional area - decreased in GSI; can also be assessed by 3D USG.

Evaluation of Incontinence contd.

11. Urethral Pressure Profilometry Done by catheter(7F) tip dual sensor microtransducer 2 transducers 6cm apart, each 1.2cm long, 1.6-2.3cm in diameter. Withdrawl at 1mm/s Resting ur. Pr. and Ur. Closure Pr.Normal > 20cm of water < 20cm of water Low pressure urethra i.e. ISD 50% chance of failure rate after conventional continence surgery. VCU and Urethral Pr Profile - good evaluation

12. VLPP
Abdominal Leak point pressure measure of urethral resistance to intraabdominal pr by valsalva. Leakage at Intravesical pr < 60cm of water sphinter incompetence or ISD

Evaluation of Incontinence contd. 13. Urethral electrical conductance

BNEC & DUEC Investigation & treatment of OAB and sensory urgency Demonstrates bladder neck opening Deflection > 8mA with quick return to baseline GSI Deflection > 8mA lasting > 3sec Overactive bladder.

Evaluation of Incontinence contd. 13. Cystourethroscopy

Indications:
Reduced bladder capacity at cystometry Recent (<2yr) h/o frequency/ urgency Suspected urethrovaginal or vesicovaginal fistula Suspicion of interstitial cystitis presence of split which bleeds on decompression Haematuria unrelated to UTI To exclude neoplasm Part of operative technique TVT, Inj of GAX Collagen.

Evaluation of Incontinence contd. 14. Electrophysiology

EMG of pelvic floor muscles Assessment of sacral reflexes PTML Partial denervation of pelvic floor following childbirth contributes to vaginal prolapse and incontinence.

USI or GSI
Urethral sphincter incompetence/ Urodynamic stress incontinence

USI or GSI
Prevalence 25-55% exact figure not known 1 in 4 seek med. adv. due to embarrassment, limited access to med care & poor screening USI comprises 29-75% of incontinent pts Stress incontinence is a
Symptom Sign Underlying disease GSI/USI

Defined as involuntary loss of urine when intravesical pr exceeds maximal urethral pressure in the absence of detrusor activity.

USI or GSI contd.

Difficult to differentiate clinically between USI and DI. 30% of USI have co-existent DI. Anatomic Stress incontinence loss of bladder neck support Intrinsic Sphincter deficiency (ISD) MUCP < 20cm of water, low VLPP. Green Classification: Type I Loss of PUV angle, no urethral hypermobility Type II Loss of PUV angle + urethral hypermobility Type III Low urethral closure pr < 20cm of water, urethra fixed (ISD Lead pipe urethra)

Aetiology of USI
Parturition Direct injury to muscles of pelvic floor & supports of lower urinary tract Indirectly by damage to supplying nerves. Aging Urethral closure pr & functional urethral length decrease Associated medical problems & medications. Menopause Oestrogen deficiency causing atrophy of vagina & supporting structures. Obesity Causes greater fluctuation of intraabdominal pr

Aetiology of USI contd.

Pelvic support defects Ant vaginal wall supports urethra like hammock POP results in bladder neck mobility (Q Tip mobility 20-30%) Due to this there is lack of pressure transmission to bladder neck & proximal urethra leading to leak.
Urologists opine that it is primarily an intrinsic sphincter defect.

Pressure transmission to proximal urethra & vesical neck

Assessment of patient
Thorough history
Urinary/defaecatory/sexual dysfunction Complaints related to prolapse Exacerbating/relieving factors Effect of medical problems/medications Exploration of her daily activities QoL assessment by IIQ-7, UDI-6.

Assessment of patient contd.

Physical Examination
Thorough assessment of pelvic support & function Anterior compartment, Middle compartment, Posterior compartment. Should be examined in full bladder. Should be examined after reducing prolapse to detect occult incontinence. Examined in both supine & upright position with straining. Re-examined after bladder evacuation Assessment of S 2-4 nerve roots - Anal wink reflex, Bulbocavernosus reflex. Assessment of pelvic floor muscle strength.

Investigations
Urine R/E & C/S Q Tip test Pad test Pessary test Post void residual urine USG for PVR, Assessment of bladder neck mobility, bladder wall thickness, Urethral diverticula. 3D for cross-section of urethral sphincter. Radiology Fluoroscopy voiding cystometrogram. Urodynamic studies Cystometry, Uroflowmetry Urethral pressure profilometry VLPP BNEC, DUEC

MANAGEMENT
USI to be differentiated from DO All patients should be offered conservative therapy Even partial improvement may help in improving QoL and thereby may be more acceptable

Behavioral therapies
PFE- subjective cure rate upto 36%; improvement 17-75% patient education for proper ms recognition Biofeedback- auditory, visual, tactile weighted vaginal cones Electrical stimulation of pudendal nv vaginal or rectal probe IFT Extracorporeal Magnetic Innervation

Devices
Vaginal pessaries Urethral occlusion devices- intraurethral or at ext. urethral meatus

Pharmacotherapy
Principal- to increase urethral resistance by adrenoceptors, bladder relaxation by adrenoceptors/ anticholinergic ephredrine, pseudoephedrine, norephedrine,phenylpropanolamine Imipramine- agonist + anticholinergic 1025mg po qd Oestrogen 2-4 gm vaginally 3-7 times/wk

USI Surgical management

Main principles

1) High rate of relief of incontinence, subjective & objective , and improved QOL 2) Low rate of complication 3) Primary surgical procedure should have maxm cure rate

Determinants of choice of surgery

Descent of bladder neck outside intraabdominal pr. Zone Intrinsic sphincter deficiency

Loss of urethral support

Route of surgery depend upon concomitant presence of genital prolapse

Cases with bladder neck descent

Retropubic urethropexy - Open or Laparoscopic

MMK
Burch colposuspension Gynaecologist prefer retropubic urethropexy as 1st choice Urologist prefer sling procedure as primary procedure

Cases with ISD Sling operation: Autologous fascia Cadaveric donor fascia Synthetic mesh

Cases with loss of urethral support

Mid-urethral tape procedure:
TVT- Tension Free Vaginal Tape TVT-O / TOT- Trans obturator tape

Recurrent incontinence
Sling procedure: After failed urethropexy Periurethral injection of Bulking Agent : specifically for fixed scarred low pressure urethra Artificial urinary sphincter At the same time ,one should look for undected UTI, Fistula, associated Detrusor Instability or de novo DI

Other surgeries
Anterior Colporraphy with Kellys buttressing suture Needle suspension procedure- Pereyra ,Raz , Stamey

Paravaginal repair of associated DISPLACEMENT CYSTOCELE

Burch colposuspension
Initial procedure same as MMK Two sutures 1st 2 cm. lat. to UV junc. 2nd 2cm. Lat to proximal urethra Fixed with ipsilateral ileopectineal lig Suture no. 0 PDS or Ethibond There should not be any suture bridge After tying , 2 finger should pass between urethra and pubis Cure rate: subj 90% ,obj 84% ( Jervis et al) overall 90% at 1yr. 70% at 10yr.(Alcay et al )

Burch colposusp. Contd.

Complications : Voiding dysfunctions (5-27%) Infection ,hg. , injury to bladder, urethra, ureter( post op. cystoscopy suggested ) Pelvic organ prolapse through post. compt ( also with MMK) - obliteration of POD by MOSCOWITCH or HALBAN should be done.

Mid urethral tape procedure

TVT- First reported by Nilsson in 1998 Suburethral sling prolene tape supporting mid urethra Minimal dissection Tape not sutured to any structure & not under any tension Placing a mayo scissors between tape & urethra Higher obj. cure rate 97% at 1 yr., at 7 yr. 81% Voiding dysfunction, de novo DI much less Can be done in both hypermobile and low pr. Urethra Can be done in recurrent cases

Other Mid urethral tape

TVT-O / TOT Tape introduced through obturator foramen by specially designed helical needle Avoidance of retropubic space Less chance of bladder injury No need of cystoscopy Much less operative time Efficacy same as TVT Two procedures outside-in & inside-out

Peri-urethral injection of bulking agent

GAX collagen, Macroplastique, Durasphere Submucosal injection transurethral or periurethral Several wheals are formed mucosa of one side touches mucosa of other side Subj. cure rate 82%, obj. cure 60% - in long term,failure is more with collagen inj. Often retention needing self catherisation

Anterior colporrhaphy and bladder neck buttress

Easy operation Initial subj. cure rate 81% , obj. cure rate 72% but medium-to-long-term outcome poor (30-35%) Cochrane review comparing Ant. Colporrhaphy with open colposuspension, failure rate at 1 yr.29% & 14% and beyond 1 yr. 41% & 17% respectively For cases with distension cystocele Ant. Colporrhaphy with either sling or mid-urethral tape procedure should be done

Paravaginal repair
Indicated in Displacement cystocele Endopelvic fascia reattached to ATFP eventually elevating bladder neck Results are not lasting So along with paravaginal repair Burch colposuspension should be done

Artficial Urinary Sphincter (AUS)

Indicated in low pr. scarred urethra due to multiple operation failure or Implantable device occluding urethra having pressure regulating reservoir, cuff and control pump (AMS 800) following radiation Alternative to suburethral sling or periurethral bulking agent where there is pre-op. voiding problem unable to self-catheterisation post op. Success rate 80 100% Disadvantage : cost , device malfunction (25%), infection ,erosion

Conclusion
USI not life threatening , but affects QOL considerably Conservative measures should be tried first Proper councelling before operation Results assessed not only by obj. cure rate but also by improved QOL

Overactive bladder or Detrusor instability

OVERACTIVE BLADDER SYNDROME

Refers to spectrum of lower urinary tract symptoms, namely frequency (>8 voids/day), urgency( sudden compelling desire to pass urine which is difficult to defer) nocturia (waking >1time during night to void) and often incontinence as a result of urgency

Detrusor Instability
Detrusor Instability is one that is shown objectively to contract spontaneously or on provocation , during the filling phase whilst the patient is attempting to inhibit micturtion Quite common 10% of population who not learnt bladder control at proper age 10% of postmenopausal woman 30-50% of adult woman investigating for ur. incontinence. commonest cause( upto 80%) in elderly undergoing urodynamic assessment Worldwide 50-100 million people suffering from OAB syndrome

Aetiology
Not known ; probabilities are Idiopathic: common in subjects who had h/o poor potty or bladder training in childhood Psychosomatic: OAB pt. has higher psychoneurotic score poor responder to oxybutinin has higher psychoneurotic score Neuropathic: Multiple sclerosis, spinal injuries, CNS lesi ons of frontal lobe, paracentral lobule, ponti ne reticular formation etc. Following incontinence surgery & outflow obstruction

Pathophysiology .
Remains a mystery Partial denervation of detrusor, postjuctional supersensitivity, hypertrophy of cells production of elastin & collagen within ms. fascicles, excitability and spreading between cells resulting in coordinated myogenic contraction of whole detrusor In Detrusor hyperreflexia ,altered spontaneous motor activity consistent with electrical coupling of cells, patchy denervation, supersensitivity to potassium P2X receptors (purinergic)in DO No. of VIP immunoreactive Nvs Reduced blood flow (ischaemia) to detrusor

Clinical presentation
Multiplicity of Symptoms Frequency Urgency 80% of pt.s Nocturia Urge incontinence > preceded by urgency > unaware of any sensation Nocturnal enuresis Coital incontinence > during penetration USI > orgasm - DI Increased risk of OAB with 1)Obesity, 2) Smoking, 3)Carbonated drinks Decreased ,, ,, ,, 1)Vegetables, 2)Bread, 3)Chicken

Infinite variability of symptomatology

Some severely incapacitated when at work, but asymptomatic on holiday Some severe urgency & frequency in morning but normal in rest of the day Some incontinent when washing up Some incontinent when putting doorkey in lock ( latch-key incontinence) QoL worse with OAB than USI

Signs
No specific cl. Sign Look for Vulval excoriation Urogenital atrophy Residual urine Stress incontinence Neurologic lesions - cranial, spinal Integrity of sacral reflex arc

Investigations
Urine c/s Frequency/vol. Chart : for 5 days - to some acting as bladder drill Uroflowmetry : to exclude voiding difficulty Cystometry : subtracted provocative cystometry >Uninhibited systolic contraction during filling same sympyom >Steep rise in PDET during filling low compliance diff to differen >Abnormal rise PDET on change of posture >Detrusor contraction provoked by coughing Symptoms with cystometric finding Common features are early first sensation, small bladder capacity, inability/difficulty in interrupting urine flow, slow or absent milk-back (in VCU)

Investigation (contd.)
Ambulatory cystometry : more physiological, more accurate DI detected 50% more often than routine cystometry Cystourethroscopy: to exclude Bladder tumour, calculus Coarse trabeculation, interstitial cystitis Bladder/ urethral diverticulae, fistulae Suture material in bladder from previous surgery Urethral pressure profilometry BNEC DUEC : TYPE III - >8mA , lasting 3sec USG : bladder wall thickness increased

Management
Behavioral modification: less drinking- 1-1.5l/day avoiding tea, coffee, alcohol tampon in vag. dur. sport. act. Alteration in medication-diuretics Drug therapy Behavioral therapy Maximal electrictal stimulation, Neuromodulation Transvesical phenol Surgery

Drug therapy
A. Inhibit bladder contractility

B. Affect sensory nerves C. Increase outlet resistance D. Decrease urine production

Antimuscarinic &musculotropic
Oxybutinin: 5mg tds ; 70% cure rate Tolteradine : selective M2, M3 blocker; 2mg bd / 2-4 mg SR od; less side effect Derifenacin : 5 times more selective; 7.5/15 mg p.o. daily Solifenacin : 5-10 mg p.o. daily Trospium chloride: 20 mg bid

Other drugs
Imipramine: 50 mg bd Flavoxate : 200 mg tds Calcium channel blocker: nifedipine Potassium channel opener: cromokaline , pinacidil PG synthetase inhibitor: flubiprophen Desmopressin (DDAFP): 2mg po at night Oestrogen

Intravesical application
Capsaicin: Neurotoxin of C fibres thereby removing affarent limb of reflex arc Indication: Detrusor Hyperreflexia, Detrusor Sphincter Dyssynergia Resiniferatoxin: 1000 times more potent, fewer side effects

Behavioral therapy
Bladder drill: Biofeedback: Hypnotherapy: Acupuncture: Endorphins & Encephalins which inhibit detrusor contraction

Transvesical applications

Phenol Injecting 10 ml. Of 6% phenol submucosally midway between blad. neck & ureteric orifice Effective in Neurogenicbladder Idiopathic overactive bladder BOTOX injection

Surgery
For severe/ intractable cases 10% Clam enterocystoplasty:Bladder bisected in coronal plane patch of gut (ileum) 25cm. Sewn around circumference may need self-catheterisation , risk of adenocarcinoma Detrusor myomectomy Urinary diversion Ileal bladder

Others
Cystodistension

Conclusion
OAB is more common than USI , may co-exist Idiopathic DO more common in mid-reproductive age Cystometry is the key urodynamic test Behavioral therapy should be tried first, then medical therapy. Surgery is the last resort. It is a disease of spontaneous exacerbations & remissions, so short courses of med. Therapy when symptom worse When co-existent with USI , DO should be treated first

Genito-urinary Fistulae

Definition
Abnormal communication between urinary system ( ureter , bladder , urethra ) and genital system (uterus , cervix , vagina ) .
True incidence not known ; av. 0.3 5% Most common is Vesico-vaginal fistula

Pathophysiology
Disruption of normal wound healing following tissue injury/trauma (which involves inflammation , angiogenesis , collagen deposition , scar remodelling) , leads to fistula formation Healing adversely affected by hypoxia, ischaemia, malnutrition, radio/chemotherapy Most present 1-3 wks after tissue injury Edges epithelialise & chronic fistula tract formed

Etiology
Congenital : e.g. ectopic ureter Acquired : obstetric pelvic surgical malignancy radiation miscellaneous : infection- LGV,TB,Actinomycosis others : forgotten pessary, other foreign body, penetrating trauma, vesical calculi etc.

Obstetric trauma
Most common cause in developing country: >90% Obstructed labour Caesarean section Difficult forceps Destructive operation

Pelvic surgery
In developed countries 90% cause is pelvic surgery ; incidence of fistula following surg is 0.1 2% Laparoscopic hysterectomy , abdominal hyst, vaginal hyst. Radical hyst, endometriosis With routine intra op. Cystoscopy case detection rate is 6.2/1000 for ureteral inj and 10.4/1000 for bladder injury

Classification
Simple Complicated: tissue loss, scarring, impaired access, ureteric orifice involvement, coexistent RVF according to siteUrethral , bladder neck, subsymphysial, midvaginal, juxtacervical, vault fistula, massive fistulae, vesicouterine, vesicocervical fistulae

Classification

from Goh

Type 1: distal edge >3.5cm from ext ur meatus Type 2: " " >2.5 3.5 cm Type 3: " " 1.5 >2.5cm " Type 4: " " < 1.5cm " Size in the largest diameter : a)<1.5cm , b) 1.5-3cm ,c) >3cm i)no/mild fibrosis and/or vag >6cm, normal capacity ii)mod./severe fibrosis &/or reduced vaginal length/capacity iii)special: postradiation,ureteric involvement, circumferencial , previous repair

Clinical presentation
Continuous dribbling of urine per vagina In large fistula , no sensation of bladder filling Sometimes levator hypertrophy , in small fistula, helps in controlling incontinence In ureterovaginal fistula, cont dribbling plus normal voiding Cyclical menouria in vesicouterine fistula Amenorrhoea , vulval excoriation Socially ostracised due to uriniferous smell

Diagnosis
History Typical uriniferous smell Identifying fistulous tract in ant vag wall/vault Finding no. of fistulous tract and coexistent other fistula Differentiating fistula from stress incontinence Measurement of Cr. content of vag fl. value >17mg/dl consistent with urine

Diagnosis

contd.

Dye test 3 swab test Cystourethroscopy : no. of fistula, prximity to ureteral opening IVP: to see renal function , ureteral involvement ; use of oral phenazopyridine with dye test/3 swab test help to identify ureteral involvement Voiding cystourethrography

Diagnosis
Retrograde pyelography Fistulography Colpography and HSG EUA

contd.

Treatment
Conservative Continuous bladder drainage by folleys catheter for 19 54 days. Small 2-3mm fistula closes in 10%cases. At least size will become smaller Fibrin sealant

Surgical
High cure rate with first attempt Appropriate pre & intra operative preparation Timely repair Multilayer , tensionfree , watertight closure Proper haemostasis Assessment of surrounding tissue viability Adequate postoperative bladder drainage

Timing of surgery
Immediately when detected at the time of surgery /within 24 hrs After 3 months : detected late .can be done early if surrounding tissue infection/ inflammation is controlled After 8 wks of failed surgery

Route of surgery
Vaginal : proper exposure is necessary scuchardts incision may be helpful position lithotomy ;reverselithotomy with head up tilt in subsymphysial fistula Abdominal :in high fistula,fixed to vault, stenosed vagina, co existent ureteral or gut fistulae Transperitoneal Transvesical Both

Specific repair technique

Saucerisation Latzkos technique Classical flap-splitting method Laparoscopic repair

Flap splitting method

Round incision around fistula;extended longitudinally in midvaginal fistula, transversely in vault fistula Proper dissection & mobilisation Exicising bladder-wall debatable Bladder repaired in 2 layers; interrupted inverting suture; 2-0 vicryl Vagina closed; watertight closure checked

Interposition grafting
Martius graft: labial fat & bulbocavernosus graft. Useful in urethral or bladder neck repair Gracilis graft Omental pedicle graft Peritoneal flap graft

Ureteric fistula
Reimplantation direct reimplantation with psoas hitch Boari-Ockerblad technique Ureterouretorostomy end to side anastomosis or interposing a loop of small bowel

Post operative management

Post op continuous bladder drainage . Urethral or suprapubic or both; non balloon urethral catheter used in vesical neck fistula ; surgical fistula- 12 days; obst fistula 21 days radiation fistula 42 days Daily fluid intake at least 3L, urine output 100 ml/hr maintained till urine clear of blood After catheter removal hrly voiding encouraged Tampoon, pessary, douching, intercourse avoided for 3 months post op

Results
Cure rate of obst fistula is higher: 81.7% with 1st attempt, 65% with 2nd/3rd procedure Post operative stress incontinence occurs in 10%cases specially in obst fistula involving sphincter mechanism and involving urethra or bladder neck

Subsequent pregnancy

Managed by El. Caesarean delivery