OVERACTIVEBLADDER

DR.PREKSHA JAINDR. PRACHI DIXIT

CONTENTS• Introduction • Nerve supply• Physiology of Micturition• Urinary continence• Definition Overactive bladder • Etiology• Pathophysiology• Symptoms• Diagnosis• Treatment• Differential diagnosis

Introduction• Bladder- Detrusor, Trigone, Bladder neck

• Urethra- Proximal, Mid, Distal, Submucous & Mucous layers

• Supports to Bladder neck & urethra - 1. INTRINSIC: Rhabdosphincter, Cavernous plexus, Urethral

smooth muscles, Sympathetic activity, Estrogen 2. EXTRINSIC: Pubococcygeus, Pubourethral ligaments &

condensed endopelvic fascia, Urogenital diaphragm, uterus & cervix, Exercise

Nerve supply of Vesicourethral unit

Micturition Reflex Filling of bladder

Stimulation of stretch receptors

Afferent impulses via Pelvic nerve

Sacral segments of spinal cord

Efferent impulses via pelvic nerve

Contraction of detrusor Relaxation of sphincter

Flow of urine into urethra & stimulation of stretch receptors

Efferent impulses via pelvic nerve

Inhibition of pudendal nerve & relaxation external sphincter

• Once it begins it is self regenerative • Initial contraction increases sensory impulses from bladder &

urethra. These further increase in reflex bladder contraction• Cycle is repeated until force of bladder contraction reaches

maximum.• HIGHER CENTRES FOR MICTURITION-1. Inhibitory Areas: mid brain, Frontal cerebral cortex2. Facilitatory Areas: Pons & posterior hypothalamus

Physiology of MicturitionSTORAGE PHASE: • Fills at rate of 0.5- 5 ml/min. • Intravesical pressure 10 cm of water even with 500ml volume.

• Intravesical pressure kept lower by- 1. Proximal urethral musculature2. Detrusor stretching reflex contraction of neck3. Spinal centres inhibit cholinergic system4. Stimulation of β (relax detrusor) & α (contracts) adrenergic5. External sphincter

• VOIDING PHASE:

• Stimulation of stretch receptors

Untrained bladder Trained

At spinal level Hypothalamus & Frontal lobes

Controls spinal reflex arcInvoluntary voiding

Voluntary inhibited Voiding

Process of micturitionAbdominal ms contracts & pelvic floor relax

Drop in intraurethral pressure, sympathetic blockade, obliteration of post urethro vesicle angle

Detrusor contracts

Funneling of proximal urethra

Urine leaks into upper urethra

EUS opens & Voiding occurs

Distal end of urethra closes, milking back last drop into bladder

Post UrV angle restored & EUS closes

Urinary Continence • Intraurethral pressure > Intravesical at rest & stress

20-50 cm of water 10 cm of water

Pathophysiology of Continence • Maintained by: (at rest)1. Apposition of longitudinal mucosal folds2. Submucous vascular plexus (washer effect)3. Rhabdosphincter & levator ani4. Abundance of collagen & elastic tissue5. Tonic contraction of prox. urethra & bladder neck

• In stress-1. Intra abdominal pressure at bladder neck 2. Reflex contraction of external sphincter3. Kinking of urethra

1/3rd each

Urinary incontinence• Objectively demonstrable involuntary loss of urine so

as to cause hygienic &/ or social inconvenience for day to day activity.

• Pathophysiology- Intravesical > intraurethral pressure Due to- childbirth, surgery, ageing Injury to supports of bladder neck

Classification

URETHRAL

• Genuine Stress Incontinence• Overactive Bladder• Mixed• Overflow incontinence• Functional (DIAPPERS) • Congenital • Others (UTI)

EXTRAURETHRAL

• Congenital- Ectopic ureter• Acquired- Fistulae

Definitions (Abnormal storage)• INCONTINENCE- Involuntary leakage of urine.

• STRESS URINARY INCONTINENCE- Involuntary leakage due to sudden rise in intra-abdominal pressure.

• GENUINE STRESS INCONTINENCE- Involuntary loss of urine when intravesical pressure exceeds intraurethral pressure in absence of detrusor overactivity. (Following urodynamic assessment only)

• URGENCY- Sudden compelling desire to pass urine which is difficult to defer

• URGE INCONTINENCE- Involuntary loss of urine associated with urgency

• FREQUENCY- no. of voids per day from waking up until falling asleep at night. (pollakisuria)

• NOCTURIA- interruption of sleep one or more time because of need to micturate. (It excludes last void before going to bed & includes first void after waking up in morning)

• NOCTURNAL ENURESIS- Involuntary loss of urine that occurs during sleep.

• OVERACTIVE BLADDER- urgency, usually with frequency and nocturia, with or without incontinence, in the absence of UTI or other obvious pathology

Abnormal sensory symptoms• Increased bladder sensation• Reduced• Absent

• HESITANCY- delay in initiating micturition

• RETENTION- inability to pass urine despite persistent effort.

• INTERMITTENCY- urine flow that stops & starts on one or more occasions during voiding.

Abnormal emptying

Others• OVERFLOW INCONTINENCE: involuntary release of urine from

overtly full bladder, often in absence of urge to urinate

• PAINFUL BLADDER SYNDROME: Chronic inflammatory condition resulting in painful voiding

• Urge incontinence two types 1. Motor- overactive bladder2. Sensory- unable to control escape of urine once there is urge

to void. Can be controlled with adequate encouragement. Infection may be present. Cystometry is normal

Overactive Bladder• Definition – symptom complex of urgency, usually with

frequency and nocturia, with(wet) or without(dry) incontinence, in the absence of UTI or other obvious pathology.

• Prevalence – 16.9% in North America, increases with age • Overall 12-15%

• Detrusor overactivity - Ach induced stimulation of muscarinic receptors (urodynamic diagnosis)

• 64% of OAB have detrusor overactivity.• 83% of patients with detrusor overactivity have OAB.

Etiology • Idiopathic• Psychosomatic• Following surgery for incontinence• Neurogenic- Multiple sclerosis, diabetic neuropathy,

spinal injuries, parkinsonism, CVA

Pathophysiology • OUTFLOW OBSTRUCTION HYPOTHESIS-Lead to partial denervation & in AchEsterase.Supersensitivity to Ach.Instability of membrane potentialFacilitation of Spinal reflex mediated by C-fibres. NGF & tachykinins

• NEUROGENIC HYPOTHESIS-When cause is Idiopathic.Increased α adr activity causes increased detrusor contractility.

Incompetent bladder neck

Urine in proximal urethra

Detrusor overactivity

Incontinence

• URETHRAL REFLEX-

• MYOGENIC HYPOTHESIS-Common in all cases of detrusor overactivityAlteration of properties of smooth musclesLoss of nerves & hypertrophy of cells with collagen & elastin.Increased excitability & cell to cell propagationCoordinated myogenic contractions of whole detrusor

• UROTHELIAL AFFERENT HYPOTHESIS- C- fibres afferent activation in the urothelium & suburothelial myofibroblasts.Bladder distension releases NO (inhibitory)& prostanoids (stimulatory)in urotheliumSupported by use of Capsaicin & Resiniferatoxin intravesically

Symptoms• Urgency• Frequency• Nocturia• Nocturnal enuresis

• SIGNS- vulval excoriation, urogenital atrophy, residual urine & stress incontinence

Diagnosis• History & QOL Questionnaire & Urgency severity scales• Physical examination

• Pelvic examination with bladder full – Stress test, Q-tip, cystocele, levator ani & anal sphincter function

• Simple (primary care level) Tests-1. Voiding Diary2. Urinalysis 3. Post Void Residual volume4. Cough stress test5. Pad test

Advanced Testing

• Urodynamics-1. Uroflowmetry2. Filling Cystometry3. Urethral pressure profile4. Leak point pressure5. Voiding cystometrogram

• Imaging tests- USG, Fluoroscopy, Functional neuroimaging, MRI

• Neurophysiologic test-1. Pudendal nerve

terminal motor latency2. Sacral reflexes 3. Somatosensory evoked

potentials4. EMG5. Emerging techniques-

PET

Urodynamics• I/c- 1. Diagnosis is uncertain/mixed disorder2. Surgery is being considered3. Failure of multiple surgical corrections4. Elevated PVR 5. Neurological condition 6. Frequency/voiding difficulties/nocturia7. Marked pelvic organ prolapse

UROFLOWMETRY• Volume of urine voided plotted over time• Flow rate- 15-25ml/sec• Peak flow rate • Time to peak flow

CYSTOMETRY• Assess bladder & urethral function during filling phase• Single channel & multi channel • Steps conducting multichannel urodynamic study-1. Insert pressure & filling bladder catheter. 2nd in vg/ rectum 2. Infuse saline @ 50-100ml/min. Record volume & pressure3. Note the point at which any leakage occurs.4. Record first desire to void & strongest desire to void &

maximum cystometric capacity5. If no detrusor overactivity, do provocative test.• Pdet = Pves - Pabd

Normal findings in cystometry

• Residual volume 0-50ml

• First sensation of urination 150-200ml

• Strong desire to void >250ml

• Cystometric Capacity 400-600ml

• Intravesical pressure on filling & standing 0-15 cm of water

• Bladder compliance after 60sec of reaching capacity 20- 100ml/cm of water

• Maximum detrusor pressure during voiding <50 cm of water

• Peak urinary flow rate >15ml/sec

• No uninhibited detrusor contraction despite provocation

• No stress or urge despite provocation

• Cystometrogram-• Graphical registration of pressure changes in bladder in relation

to rise in the volume of urine. • Segment 1, 2 & 3

URETHRAL FUNCTION TEST1. Urethral pressure profilometry-

catheter with microtip pressure transducer slowly pulled along urethra measuring intravesical & urethral pressure.

P ure – P ves = P clos <20cm of water poor prognosis after surgery

2. Fluoroscopic & cystoscopic assessment of bladder neck

3. Leak point pressure- urodynamic measure of the minimum intra abdom or intravesical pressure to cause incontinence .1. Valsalva LPP2. Cough LPPIntrinsic sphincter deficiency found in women cutoff 60 cm water

Bulking agents (collagen) are used <100cm water LPP when bladder is filled with 150ml

Voiding Cystometrogram• Valsalva voiding, low preoperative flow rate & high detrusor

pressure during voiding are risk factors for postoperative voiding dysfunction

Treatment• General measures- Psychotherapy for psychosomatic

problems, treating other medical conditions

• Behavioral therapy- o Limit fluid intake (1-1.5 litres/d)o Reduce tea, coffee, alcoholo Diuretics stoppedo Weight loss o Bladder retraining : bladder drill, biofeedback,

hypnotherapy. 83% asymp 6mth 40% relapse in 3 yrs

Drug Therapy• Inhibit bladder contractility, • Increase bladder neck & urethral resistance.• Antimuscarinic agents- Reduce incontinence episodes per day Reduce frequency, urgency• Immediate release- Oxybutinin, tolterodine • Extended release- Trospium, solifenacin • Conjugated Estrogen- should not be prescribed • Ephedrine, pseudoephedrine, phenylpropanolamine- risks

of complications , hemorrhagic cerebral vascular accident

NATURE DRUGS & DOSES RELIEVES SIDE EFFECT CONTRAINDICATION

ANTI CHOLINERGICM1 & M3 antagonist

Oxybutinin 5mg BD PO/ transdermal patch 3.9mg twice a wk

Frequency

Urgency

Dry mouth

Blurred vision

Constipation

Glaucoma

Myasthenia

Intestinal obstruction

Ulcerative colitis

Urinary retention

ANTI MUSCARINIC M3 antagonist

Tolterodin

1-2mg PO BD

ANTI MUSCARINICM3 anatgonist

Solifenacin

5-10 mg OD

Flatulence

Chest pain also

TCA Imipramine

50mg HS

Nocturia Sedation Hip fractureOrthostatic htn

Coronary Artery Dis

HTN

SYNTHETIC ANTIDIURETIC HORMONE ANALOGUE

DDAVP

Intranasal 20-40µg HS

Nocturnal enuresis

Fluid retentionRhinitisNauseaHyponatremia

Cardiac insufficiency

Other drugs • Darifenacin- same as solifenacin• Fesoterodine- Prodrug, active metabolite 5 hydroxy methyl

tolterodine • Flavoxate (similar to oxybutinin)- 200mg TDS urinary frequency,

urgency, dysuria• Propiverine- antichl & CCB, urgency frequency, urge incontinence,

M3 antagonist• Trospium- cautiously in renal & hepatic, parasympatholytic,

reduces tone of smooth ms in bladder, not distributed to CNS because of large molecular size & hydrophilicity• Bumetanide- loop diuretic, decrease nocturia• Furesemide- mid afternoon. Decrease night time urine

production

Refractory OAB• Distressing symptoms continue despite conservative & drug therapy

• INTRAVESICAL THERAPY- • Temporary effect & risk of voiding difficulties• Capsaicin (in neurogenic DOA), • Resiniferatoxin, • Botulinum Toxin (idiopathic DOA)

• NEUROMODULATION- • Peripheral – using posterior tibial nerve (similar effect as

antimuscarinics)• Sacral neuromodulation- expensive, invasive• Cutaneous sacral neuromodulation- less invasive

• SURGERY-Denervation (interrupt nervous pathway)Augmentation & clam cystoplasty (increase bladder capacity)Urinary diversion (ileal conduit)Detrusor myectomy

• RECENT DEVELOPMENTS-Oxybutinin patch, gelMirabegron – β3 agonist Solabegron – also in Irritable Bowel Synd , produces visceral analgesia by releasing somatostatin & adipocytes

• THANK YOU..