OVERACTIVE BLADDER AND UNDERACTIVE DETRUSOR.pptx

A ppt on ZOAB and under active bladder

1. OVERACTIVE BLADDER AND UNDERACTIVE DETRUSOR BEDANTA PATHAK

2. DEFINITION OF OVERACTIVE BLADDER International continence society defines OAB as: The presence of “urinary urgency, usually accompanied by frequency and nocturia, with or without urge incontinence, in the absence of UTI or other pathology.” OAB is based on symptoms and is different from detrusor overactivity (DO).

3. OAB SYMPTOMS Frequency: Number of voids recorded during waking hours, including the last void before sleep and the first void after waking and rising in the morning. 8 or more visits to toilet per 24 hours. Nocturia: Nocturia is the complaint that the individual has to wake at night one or more times for voiding; each void is preceded and followed by sleep.

4. Urgency: Complaint of sudden, compelling desire to void that is difficult to defer. Urge incontinence: Involuntary leakage accompanied by or immediately preceded by urgency

5. PREVALENCE OF OAB Overall prevalence is 11.8% in adults which increases with age with similar rates in both genders. “OAB wet” is more prevalent in women due to relative weakness of bladder neck and urethral sphincter mechanism in women.

6. BLADDER NERVE SUPPLY AND RECEPTORS

7. PATHOPHYSIOLOGY AND ETIOLOGY OF OAB Etiology of OAB is complex and poorly understood. Neurological hypothesis : DO arises from generalized nerve mediated excitation of detrusor muscle. Normally bladder control is mediated in an inhibitory fashion by cerebral cortex . Damage to the brain can induce DO by reducing suprapontine inhibition Damage of the axonal pathways in the spinal cord allows the expression of primitive spinal bladder reflexes.

8. M yogenic hypothesis : Overactive detrusor contraction result from a combination of Increased spontaneous excitation within smooth muscle of bladder. Enhanced propagation of this activity to affect an excessive proportion of the bladder wall

9. MICROMOTION CONTRACTION During storage a localized micromotion contraction occur starting from an initiation point and then spreading to a limited part of bladder wall and is associated with only small fluctuation of bladder pressure. In OAB multifocal trigger points lead to continuous activity; this enhances the effect on bladder pressure and stimulates afferents by the extensive distorting movements.

10. ETIOLOGY AND ATTRIBUTABLE RISK FACTORS Idiopathic Aging Chronic bladder outlet obstruction CNS disorders Pregnancy Postmenopausal status

11. CLINICAL ASSESSMENT History: Presence and bother from each of the storage LUTS that make up OAB, other storage disorders and voiding LUTS whose presence may indicate BOO. Dysuria , haematuria . Nature and volume of fluid intake. Occult neurological disease, obstetric and gynecologic history, constipation and medication history.

12. PHYSICAL EXAMINATION : Focused physical examination should include the abdomen, pelvis, extremities, a basic neurologic examination and general assessment of cognitive and frailty. Assessment of bladder emptying by bladder scanner to measure PVR.

13. Frequency volume chart (FVC) can be informative particularly when history suggest that polyuria is responsible for urinary frequency/nocturia. In OAB pattern of voided volume is erratic.

14. PATIENT PERCEPTION OF INTENSITY OF URGENCY SCALE(PPIUS) No urgency: I felt no need to empty my bladder but did it for some other reasons. Mild urgency: I could postpone voiding for as long as necessary without fear of wetting myself. Moderate urgency: I could postpone voiding for a short while without fear of wetting myself. Severe urgency: I could not postpone voiding but has to rush to the toilet to avoid wetting myself. Urgency incontinence: I leaked before arriving at the toilet.

15. LABORATORY EXAMINATION Urinalysis is mandatory in all patients to exclude urinary tract infection, haematuria , and pyuria . Urine culture should be obtained if infection is suspected based on clinical presentation and urinalysis

16. URODYNAMIC EVALUATION It should not be used in the initial workup of uncomplicated patient It is recommended when the presence or absence of altered compliance, DO, or other urodynamic abnormalities will affect the decision to pursue or avoid an invasive, irreversible, or potentially morbit treatment. Primary aim is to reproduce patient’s symptoms and to identify additional factors likely to influence management decisions

17. The two main urodynamic diagnosis associated with OAB are DO and early and/or exaggerated filling sensation. ICS described two types of DO: Phasic : Seen in most idiopathic DO. It is characterized by contractions of increasing amplitude as the bladder volume increases. Terminal: Single involuntary detrusor contraction occurring at cystometric capacity, which causes incontinence , often resulting in complete bladder emptying.

18. Non phasic changes in detrusor pressure before micturition should be regarded as changes in bladder compliance rather than as DO. Any phasic detrusor contraction during filling constitute DO, regardless of amplitude.

19. DO my be absent in many patients of OAB, but its presence is correlated with increased severity of urgency and the presence of incontinence. Where DO is absent the patient will usually report increased bladder sensation, defined as “an early and persistent desire to void”

20. It is critical to assess for the presence of BOO or inefficient bladder emptying for two reasons: OAB treatment measures that aim to improve bladder reservoir function may impair voiding, perhaps necessitating intermittent self-catheterization. Increasing severity of BOO is associated with DO, suggesting that OAB symptoms may be unlikely to improve if BOO left untreated.

21. Treatment of BOO doesn’t necessarily result in improvement of OAB symptoms. The urodynamic finding that has been most commonly associated with decreased likelihood of resolution of DO or OAB symptoms is terminal DO at diminished capacity.

22. The urodynamic report should clearly state that whether the patients symptoms were produced completely, reduced in part, or not reproduced to ensure that due caution is taken in major treatment decisions where there is diagnostic uncertainity . Ambulatory urodynamics may be considered when conventational cystometry fails to reproduce symptoms.

23. TREATMENT TREATMENT BARRIERS: Patients misconceptions and fears: Part of normal aging or everyday life. Not severe or frequent enough to treat. Too shameful to discuss. Treatment won’t help

24. FIRST LINE TREATMENT B EHAVIORAL MODIFICATION: DIETARY CHANGES AND FLUID MANAGEMENT: Weight loss in obese patient. Cessation of smoking. Avoid bladder irritant like caffeine, alcohol, spicy food, acidic food. Avoid diuretics and excessive fluid intake especially before sleep. Treat constipation .

25. In patient with lower extremity edema elevation of leg before bedtime to help to prevent nocturia . TIMED (SCHEDULED) VOIDING: Voiding by routine schedule with constant interval between void (every 2-3 hours). It will help to empty the bladder before incontinence occurs and decreased urgency and frequency. Voiding pattern may change throughout the day to match patients’ incontinence pattern.

26. BLADDER TRAINING: Gradual increase in voiding interval by 15-60 min every 1-2 weeks until an acceptable voiding interval is achieved without incontinence. Suppressing the urge using any of the following methods: Keeping the body calm until urge subsides. Taking slow deep breath. Concentration on elimination the urge by mental calculation or mental imaging.

27. After the urge subside don’t urinate until the next scheduled void. Bladder training requires a motivated patient with sufficient cognitive function. PELVIC FLOOR TRAINING ( kegel exercise): Intermittent voluntary maximal contraction of pelvic floor muscles. Set of 10 contraction 3 times per day. Continence improves after 6-12 weeks.

28. Pelvic floor training with biofeedback: A sensor is applied to vagina or rectum and measure degree of pelvic floor muscle contraction. It is better to gain voluntary control over pelvic floor muscles. Behavioral therapy is very effective for OAB as a sole method or in combination with medication.

29. SECOND LINE THERAPY Pharmacologic management: Anticholinergic agents: Oxybutynin Tolterodine Solifenacin Darifenacin Hyoscyamine Flavoxate Propiverine hydrochloride Tropsium propanthaline

30. MOA: Act by competitively inhibit muscarinic receptor in bladder wall causing reduction in detrusor over activity. Side effects: Due to inhibition of muscarinic receptor outside the bladder. Eye - blurred vision Salivary glands- Dry mouth Intestines - Constipation Heart - Tachycardia Brain - Impairment of cognition and memory (more with tertiary amines).

31. CONTRAINDICATIONS: Urinary retention Intestinal obstruction Uncontrolled narrow angle glaucoma Myasthenia gravis DURATION: symptoms improvement occurs within 1 week but maximum benefit is achieved by 3 months.

32. Propiverine hydrochloride is a new anticholinergic which is non selective. It causes detrusor muscle relaxation. Anticholinergic not recommended for treatment of OAB by International Consultation on Incontinence in 2014 are Flavoxate , Hyoscyamine , Imipramine .

33. BETA 3 AGONIST : MIRABEGRON MOA : Stimulate beta 3 adrenergic receptors causing relaxation of detrusor muscle and increase bladder capacity. Adult dose is 25 to 50 mg per day. Side effects : Hypertension Headache Tachycardia Urinary retention Contraindication : Severe uncontrolled hypertension

34. Local estrogen therapy is beneficial for treatment of OAB due to direct effect on reversal of vaginal atrophy. EAU guidelines offer vaginal estrogen therapy for post-menopausal women with urinary incontinence especially if other symptoms of vulvovaginal atrophy are present

35. Role of alpha blockers: No RCT shows that they are effective for OAB Voiding symptoms in women with functional outflow obstruction, were successfully treated with an alpha blocker (Robinson et al.) In men with BPH combination of alpha blocker and anticholinergic has significant improvement in voiding symptoms ( Casabe et al.)

36. THIRD LINE THERAPY Botulinium A- toxin intravesical injection: Inhibits detrusor contraction by inhibiting release of Ach at neuromuscular junction. FDA approved in treatment of OAB refractory to antimuscarinic medications. Side effects are increased risk of UTI and urinary retention that require catheterization. Contraindications are UTI, pregnancy, myasthenia gravis.

37. Administration of Botulinium toxin: For OAB without neurological disorder- 100 units/10ml injected into 20 sites avoiding trigone . For incontinence with neurologic disorder- 200 units/30ml injected at 30 sites avoiding trigone . Causes improvement in 2 weeks but repeated injections are required .

38. Tibial nerve stimulation: Less invasive way of sacral nerve roots stimulation Electrical stimulation of tibial nerve transmitted to S3- modification of voiding reflex Weekly sessions for 12 months

39. SACRAL NEUROMODULATION Modifies voiding reflex by direct electric stimulation of s3 afferent nerve. Effectively suppresses the hyperactivity of detrusor muscle. Indicated in patients who fail or cannot tolerate conservative treatment

40. It consist of two stages: Percutaneous nerve evaluation (PNE) which determine if the patient is candidate for SNM, done as OPD procedure. Permanent implantation done if patient shows 50% or greater improvement of symptoms after 3-5 days.

41. SURGICAL TREATMENT Indicated in OAB refractory to less invasive treatment and reduced bladder capacity causing incontinence. Types: augmentation cystoplasty autoaugmentation urinary diversion as ileal conduit, catheterizable stoma

42. UNDERACTIVE DETRUSOR ICS defines detrusor underactivity (DUA) on the basis of urodynamic study as “a contraction of reduced strength and/or duration, resulting in prolonged bladder emptying and/or failure to achieve complete bladder emptying within a normal time span” If no contraction occurs the term acontractile detrusor is used

43. Underactive bladder is characterized by a slow urinary stream, hesitancy, and straining to void, with or without a feeling of incomplete bladder emptying, sometimes with storage symptoms

44. EPIDEMIOLOGY Population prevalence is not known DUA affects 9-28% of men under age 50 and 48% in those over 70 years undergoing urodynamic study. In women DUA is found in 12-45% undergoing urodynamic study.

45. Detrusor hyperactivity impaired contractility (DHIC): DUA with concomitant DOA DUA often coexists with other LUT dysfunctions in the elderly; BOO in males and Urodynamic SUI in females.

46. ETIOPATHOGENESIS No obvious cause in majority May occur commonly due to age related changes and decline in detrusor function. More pronounced decline in detrusor contraction in men because of bladder wall changes occurring as a result of BOO.

47. MYOGENIC FACTORS Alteration in normal structure and function of detrusor or ECM may result in diminution of transmitted contractile force. Intrinsic ability of detrusor muscle cells to contract compromised by cellular dysfunction. Axonal degeneration and widespread disruption of detrusor myocytes .

48. NEUROGENIC FACTORS Brain circuits: CNS control mechanism governing micturition reflex: perception and integration of storage and voiding, if disturbed, may result in DUA. Bladder efferent pathway: Interruption or impairment of efferent signaling in sacral cord, sacral roots, and pelvic nerves- absent or reduced detrusor contraction.

49. An impairment in afferent function (from bladder or urethra) reduce or prematurely end the micturition reflex, leading to impairment or loss of voiding efficiency. Normal aging is associated with a decline in sensory function in the lower urinary tract.

50. Sequence of events leading to DUA in BOO: Increased bladder outlet resistance- compensatory hypertrophy and hyperplasia- blood supply also increases (contractile protein is almost normal; bladder in compensated stage)- slowly detrusor contraction declines and bladder emptying is hampered, marking the decompensation phase.

51. DUA IN DIABETES May impair detrusor function through a combination of myogenic and neurogenic mechanism:- Diabetes-induced bladder dysfunction (DBD) or diabetic cystopathy . DBD temporal theory: Osmotic diuresis by hyperglycaemia - increased bladder wall pressure due to stretching-compensatory hypertrophy- oxidative stress-bladder decompensation - poor bladder sensation and impaired voiding function.

52. NEUROLOGIC DISEASE OR INJURY CVA- neurogenic DOA is most common, 75% acontractile detrusor & AUR due to cerebral shock. Multiple sclerosis- DUA in 20% cases. Parkinsons disease-DUA is far less common than DOA.

53. DIAGNOSIS Only accepted diagnostic modality is invasive urodynamic study. No universal diagnostic criteria

54. Detrusor Contraction Strength : Current methods of estimating detrusor voiding function almost exclusively focus on detrusor contraction strength. Detrusor contraction speed : A bladder that contracts more slowly could in theory result in clinical symptoms, although this is not part of ICS definition. Detrusor contraction duration : A detrusor contraction of reduced duration is suggested by ICS definition.

55. Bladder sensation: Assessment of bladder sensation is relevant to DUA evaluation as afferent nerves play a central role in the initiation and maintenance of a detrusor contraction. Most commonly undertaken using patient’s perceptions of bladder feeling (first sensation, first desire, strong desire and capacity)

56. Ambulatory urodynamic study: Failure to void during UDS- anxiety or so called bashful bladder; arises due to poor pelvic floor relaxation reflex detrusor inhibition, or true DUA or acontractile detrusor Careful history and ambulatory UDS are useful.

57. MANAGEMENT GOALS: To reduce symptoms and improve QOL. Reduce risk of complications of impaired emptying viz. UTIs, bladder stones, ureteric reflux leading to back pressure on upper urinary tract, and skin damage from overflow urinary incontinence associated with chronic retention

58. Lack of effective treatments to improve detrusor function. Thus management entails bladder drainage techniques (catheterization) or therapies aimed at reducing bladder outlet resistance, for example, by relaxing the external urethral sphincter mechanism.

59. INITIAL ASSESSMENT Routine urologic evaluation (bladder diary, DRE, urinalysis, uroflowmetry , PVR using USG) Neurologic assessment ( sacral dermatome anal tone, bulbocavernosal reflex, lower limb reflexes). Neurologic deficits require further specialist evaluation. MRI spine to assess lumbar spinal cord and cauda equina

60. Careful drug history to identify medications that impair bladder contractility (agents with anticholinergic or opioid effects) or that increase bladder outlet resistance (e.g., alpha adrenergic agonist). Fecal impaction/constipation may contribute to poor bladder emptying by a direct obstructive effect.

61. CONSERVATIVE MANAGEMENT Scheduled voiding to increase the voiding frequency in patients with sensory impairment. Double voiding to improve bladder emptying may help reduce bothersome frequency. Bladder expression technique such as valsalva voiding or crede maneuver used only in very specific neurogenic situations (DUA with incompetent sphincter); otherwise not recommended due to risk for generating high intravescical pressure causing VUR.

62. Pelvic floor physiotherapy and biofeedback to successfully treat children and adults with dysfunctional voiding. CISC is preferred method of establishing bladder drainage which is safe and effective with lower rates of infection than with indwelling catheter. A suprapubic catheter is the best long-term option in patients unwilling or unable to perform CISC.

63. PHARMACOTHERAPY Parasympathomimetics : Used with the aim of increasing bladder contractility. Bethanechol and carbachol , most common compunds used. More likely to be effective if the problem is reduced or absent contractile stimulus. Less likely to be effective if underlying problem is reduced responsiveness to stimulus Combination of alpha adrenergic antagonist and a parasympathomimetic has been considered a therapeutic possibility.

64. ELECTRICAL STIMULATION Sacral nerve root stimulator Intravesical electrotherapy (IVE) Sacral neuromodulation : Good efficacy in non-obstructive urinary retention and DUA. SNM inhibits urethral afferent signals and allows restoration of normal afferent flow to the brain and resumption of normal bladder sensation and detrusor contractions.

65. Botulinium neurotoxin A injected into urethral sphincter reduces outlet resistance and improves bladder emptying in DSD. Short lived action, hence not licensed now.

66. Bladder outlet surgery: Compared to conservative treatment, outlet surgery confers no significant improvement in symptoms or urodynamic parameters in DUA. Predictors of poor outcome: Low voiding pressure (<45 cm of water) Older age (>80 years) High residual volume>1500 ml

67. Resection or incision of bladder neck in women with DUA is not recommended, because this may lead to incontinence or bladder neck stenosis Urinary diversion if CISC not possible and patient wishes to avoid SPC: Catheterizable stoma Ileal conduit

68. Reconstructive surgery: Latissimus dorsi detrusor myoplasty

69. THANK YOU