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overactive bladder
- 1. Practical Approaches to TheManagement of Overactive Bladder DR. Talal Ballout Urologest
- 2. Bladder Properties • Bladderis one of the most compliant organs of the body • Should provide perfect continence • Voluntary and efficient emptying at low pressure
- 3. Micturition Cycle • Filland store • Empty completely - simple but important phases - important to help classify and treat disorders of micturition
- 4. Bladder Filling andStorage • Accommodates large volumes of urine - maintains low intravesical pressure (< 12 cm water) - sustains sensation that is appropriate • No involuntary contractions - hyperreflexia, overactivity, reflex contractions or instability • Maintain a closed and continent outlet at rest even with sudden intra-abdominal forces
- 5. Bladder Emptying • Bladdercontraction - adequate magnitude - sustained to empty • Coordinated urethral relaxation - bladder neck and proximal urethral smooth muscle - striated external urethral sphincter • No anatomic obstruction
- 6. Parasympathetic Muscarinic Receptors •M1- neuronal, brain • M2- cardiac, detrusor • M3- detrusor, gastrointestinal smooth muscle, salivary glands • M4 + M5 • M3 receptors (20%) responsible for smooth muscle contraction • M2 receptors (80%) responsible for inhibition of smooth muscle relaxation
- 7. Overactive Bladder • Clinicalterm used to describe symptoms of frequency, urgency, +/- urge incontinence - term used without knowing specific cause of symptoms (eg, detrusor overactivity) • ICS 2002–Urgency with or without urge incontinence, usually with frequency and nocturia - absence of pathologic or metabolic conditions that might explain these symptoms
- 8. Overactive Bladder Pathophysiology •Multifactorial disorder • A constellation of functional abnormalities • 90% of cases idiopathic • Can be caused by: - neurologic defects - myogenic defects
- 9. Overactive Bladder NeurologicDefects • CVA • Dementia (eg, vascular disease, Alzheimer’s, encephalitis) • Cerebral palsy • Brain tumor • Parkinson’s disease • Multiple sclerosis • Shy-Drager syndrome
- 10. Overactive Bladder andSpinal Cord Injury • Complete suprasacral lesions above T7 - detrusor hyperreflexia - smooth sphincter dyssynergia - striated sphincter dyssynergia - no sensation • Complete suprasacral lesions below T7 - detrusor hyperreflexia - smooth sphincter synergy - striated sphincter dyssynergia - no sensation
- 11. Overactive Bladder PatientEvaluation • History • Physical • Urodynamics • Cystoscopy
- 12. History • Urologic • Ob/Gyn •Neurologic • Medical/surgical • Social/psych • Radiation • Pelvic trauma
- 13. Incontinence History • Characterizationof incontinence • Length and severity of symptoms • Impact on quality of life • Associated bowel problems
- 14. Physical Exam Women •Systematic vaginal and pelvic exam - condition of mucosa - urethral mobility (Q tip test) - demonstration of continence (CST) - vaginal prolapse (anterior wall, posterior wall, apical) - bimanual exam
- 15. Physical Exam • Men–DREand urogenital exam • Neurologic exam - mental status - mobility - lumbar and sacral sensory and motor eg, BC reflex, anal wink, knee and ankle DTR’s
- 16. Ancillary Tests • Voidingand intake diary - Extremely important especially in cases of overactive bladder • Incontinence diary • Urine analysis - urine culture and cytology when indicated • Post void residual • Pad test
- 17. Role of Cystometry •Defining underlying pathophysiology - bladder filling - involuntary detrusor contractions - low bladder compliance - urethral obstruction - impaired detrusor contractility • Directing treatment
- 18. Pharmacologic Treatment ofBladder Overactivity • Decrease detrusor activity - abolish involuntary detrusor contractions - increase volume at which they occur - increase compliance • Increase bladder capacity • Commonly used agents focus on inhibition at the end organ level
- 19. Pharmacologic Agents Bladder Overactivity •Antimuscarinics • Muscle relaxants • Mixed action drugs • Tricyclic antidepressants • Alpha blockers • Beta agonists • Vasopressin analogues
- 20. Antimuscarinics • Antimuscarinics (anticholinergic)drugs have been the mainstay of medical therapy for bladder overactivity • Have been somewhat limited by the high incidence of side effects and lack of selectivity
- 21. Mechanism of Actionof Antimuscarinics • Inhibit bladder contraction - ACh from cholinergic nerves stimulate muscarinic receptors - block stimulation of muscarinic receptors
- 22. Antimuscarinic Agents ofCommon Side Effects • Dry mouth • Constipation • Drowsiness/somnolence • Blurred vision/dry eyes
- 23. Antimuscarinics 2007 • OxybutyninIR BID-TID • Oxybutynin ER QD • Oxybutynin TDS BIW • Tolterodine IR/ER BID/QD • Tropsium BID • Solifenacin QD • Darifenacin QD
- 24. What is theDifference? • Efficacy - no great differences - dose-dependent • Tolerability • Safety • Clinical effectiveness–different for different patients depending on expectations
- 25. Imipramine • Prominent systemicanticholinergic effects • Weak antimuscarinic effects on the bladder • Strong direct inhibitory effect on bladder smooth muscle which is not anticholinergic or adrenergic • Decreases contractility/increases outlet resistance • Effects on lower urinary tract are additive to those of atropine-like agents; useful in combo with other anticholinergics • Most common side effects - anticholinergic effects, weakness, fatigue, sedation
- 26. Combination Pharmacotherapy • Combinationtherapy–combining 2 drugs that have different actions, eg, anticholinergic and tricyclic • Intravesical instillation of Oxybutynin - works best in cases where oral form is effective but patients can’t tolerate side effects - requires self-catheterization
- 27. Evaluation of Refractory OveractiveBladder • Post void residual • Comprehensive urodynamic testing • Cystoscopy • Urine cytology • Upper tract study - renal ultrasound - CT/MRI - IVP • Neurological evaluation, if necessary
- 28. Refractory Detrusor Overactivity •Intravesical instillations–Capsaicin • Botulinum-A Toxin • Neuromodulation - efficacy in neurogenic overactivity not universally accepted • Urinary reconstruction - augmentation - diversion
- 29. Conclusion • Improved understandingof pathophysiology • Contribution of alternate neural receptors • Better understanding of receptor action and interaction • Mechanism of action of antimuscarinics and side effects