Urodynamics and Bladder Outlet Obstruction

1. Urodynamics and Bladder Outlet Obstruction Hann-Chorng Kuo Department of Urology Buddhist Tzu Chi General Hospital

2. Bladder Outlet Obstruction • BOO occurs in both women and men • The most frequent clinical problem in aging males • BOO can be progressive, results in bladder irritation, compensation,and decompensation

3. Benign prostatic enlargement

4. Storage and Empty Symptoms related to BOO • Bladder dysfunction or outlet obstruction • Increased frequency day or night • Urgency or urge incontinence • Hesitancy and reduced urinary stream • Intermittency and postvoid dribbling • Urinary retention • Upper tract dilatation, bladder stone, uremia • Urinary tract infection

5. Detrusor Changes after BOO • Irritative stage: detrusor hypertrophy, uninhibited detrusor contractions • Compensation stage: Detrusor hypertrophy, trabeculation, pseudodiverticulum, increased urethral resistance, increased residual urine, stenosis at UVJ, bilateral hydroureter and hydronephrosis • Decompensation stage: overdistended, over-flow incontinence, renal function is decreased

6. Bladder Filling Phase • Laplace’s law: T = Pdet R (Tension= detrusor pressure x radius of bladder) • Low frequency micromotion of detrusor exist in bladder • Regional spontaneous contractions cause only slight changes of stress in bladder wall • Bladder filling at 0.5-1ml/min (F.S. 300ml) • Rapid stretch (i.e. diuresis) can cause a sensation of fullness at a small volume (F.S. 150ml)

7. Rhythmic Detrusor Contractions after Resiniferatoxin treatment

8. Voiding Phase • Voiding process starts from relaxation of external sphincter followed by detrusor contraction • At the opening pressure, flow starts • Urethral compliance allows increased flow through increasing Pdet • Urethral obstruction reduces compliance and reduces flow increase

9. Initiation of VoidingThe Relationship of Q and Pdet

10. Initiation of VoidingActive relaxation of External sphincter

11. Initiation of VoidingPassive opening of urethral wall

12. Urethral Compliance • Not constant during voiding • Passive viscoelastic property of urethral wall • Active properties of urethral smooth muscle and periurethral external sphincter • Pdet= Puo + Q2 / c c= coefficient of urethral compliance

13. Bladder Pressure • Intravesical pressure (Pves) = intra-abdominal pressure (Pabd) + detrusor pressure (Pdet) • Patients may use mainly Pabd to void • Pdet depends on intravesical volume • Pdet decreases at decreasing volume during voiding phase • Isovolumetric contraction (Piso) occurs when flow is suddenly interrupted (stop test)

14. Reduced Pdet at decreasing intravesical volume

15. Iso-volumetric Detrusor Contraction at Stop Test

16. Pressure Flow Relations • I: Isometric contraction of detrusor • II: Detrusor pressure further increases activation, flow continues to increase until maximal activation of detrusor reaches • III: Decrease in bladder volume and decreasing pressure and flow

17. Relationship of Pressure & Flow

18. Passive Urethral Resistance Relation • Schafer proposed PURR, a straight line is drawn through two values read from recording, the pressure at maximal flow rate and the lowest pressure at which actual flow occurs (Pmuo) • Griffiths used value of opening pressure (URA) for passive urethral resistance

19. The Abrams-Griffiths Plot

20. The Schafer Nomogram

21. The Contraction Power • WF is the power developed by detrusor contraction per unit of area • During voiding, WF initially increases and reaches a plateau value, then decreases • Classification of obstruction by obstructive grades and contractility

22. Decrease in Contractile Velocity in Bladder Outlet Obstruction

23. Constrictive vs Compressive Pressure Flow Plots

24. Obstruction • Urethral resistance increases & flow decreases • Residual urine increases as detrusor decompensation occurs • Obstructive symptoms are unreliable • Bladder trabeculaion, thickened, impaired voiding may be aging, neuropathic, musculogenic, increased urethral resistance or in combination • Both filling and empty phases should be investigated for voiding dysfunction

25. Confirmation of Increased Urethral Resistance • Measuring detrusor pressure at peak flow • Using A-G number by ICS nomogram • Urethral resistance R = Pdet / Qmax 2 • Catheter of different size may interfere urethral resistance • Bladder dysfunction and increased urethral resistance may coexist

26. Pressure Flow Plot for Diagnosis of Obstruction

27. Abrams Griffiths Number • AG number = Pdet.Qmax – 2 x Qmax • Obstruction AG> 40 • Nonobstruction AG<20 • Equivocal 20<AG<40

28. Constrictive Obstructionin Urethral Stricture • A normal or high opening pressure and a constant flow rate although Pdet increases during voiding • Bladder trabeculation and large residual urine may develop

29. Constrictive Obstruction in Female Urethral Stricture

30. Constrictive Obstructionin Anterior Urethral Valve

31. Compressive Obstructionin BPH Obstruction

32. Compressive Obstructionin Dysfunctional Voiding

33. Constrictive Obstruction in Urethral Stricture

34. Obstruction in Detrusor External Sphincter Dyssynergia (DESD)

35. Bladder Outlet Obstruction in Women • No definite criteria for BOO in women • A sustained voiding pressure and a low flow rate, moderate residual urine, and radiological evidence of infravesical narrowing during voiding • Primary bladder neck obstruction, urethral stricture, dysfunctional voiding, cystocele, post-incontinence stricture are most common

36. Post-incontinence surgeryBladder neck obstruction

37. Spastic Urethral SphincterCompressive Obstruction

38. Decompensation of Detrusor • Acute urinary retention develops when intra-urethral resistance increases combined with an increase of sympathetic tone due to bladder distension • Relief of bladder distention may reverse acute retention with the aid of alpha-blocker • Decrease in detrusor tone may occur during acute retention

39. Low Contractility Force in BPH Obstruction

40. BPH with Acute Urinary Retention

41. Decompensation of Detrusor • Contractility is reduced as the length of smooth muscle is beyond an optimal amount • Increased upper tract pressure as intravesical pressure is increased • Reverse of detrusor contractility takes time depending on the duration of detrusor decompensation

42. Post-prostatectomy Low Detrusor Contractility

43. Chronic urinary retention • No detrusor contractility • Patients use abdominal straining to void • Overflow incontinence • Small voiding amount • Resistance at ureterovesical junction is increased • Upper tract dilatation and azotemia

44. Poor bladder compliance and low contractility after prostatectomy

45. Detrusor Overactivity • No correlation of detrusor instability with severity of infravesical obstruction • Aging process • Poor cortical perfusion • Changes of vasoactive intestinal polypeptides or neurotransmitters • Occult neurological lesion

46. Detrusor overactivity and Pseudodyssynergia in CVA

47. DESD with incontinence & Bilateral vesicoureteral reflux

48. Impaired Detrusor Contractility • Decrease in either contraction force or velocity in about 40% • Wide spread degeneration of muscle cells • Degeneration of axons • Reduction of intermediate cell junctions • Collagenosis between individual muscle cells with myohypertrophy

49. Partial Bladder Outlet Obstruction and Energetics • Decrease in glucose oxidation by 30% • Decrease in creatine phosphate in rabbit • Less creatine phosphate and ATP in obstructed bladder, which returned to normal after relief of obstruction • Acute initial mitochondrial damage produced by obstruction in rabbit

50. Origins of Hesitancy • Time delay between start of voiding and effective flow • Increased initial opening pressure related to compressive obstruction • Possibly due to delay in relaxation of external sphincter • No correlation with detrusor contractility