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 Voiding The Relationship of Q and Pdet

10. Initiation of Voiding Active relaxation of External sphincter

11. Initiation of Voiding Passive 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 Obstruction in 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 Obstruction in Anterior Urethral Valve

31. Compressive Obstruction in BPH Obstruction

32. Compressive Obstruction in 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 surgery Bladder neck obstruction

37. Spastic Urethral Sphincter Compressive 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

51. Poorly Relaxed Urethral Sphincter Hesitancy Intermittency

52. Origins of Frequency Urgency Urge incontinence Nocturia
Attributed to detrusor instability
Correlated with small voided amount and large residual urine
DI increases with age, decreased after prostatectomy,not correlated with detrusor pressure
Not absolutely caused by obstruction

53. Poor Stream & Dribbling in Obstruction
Poor stream indicates either increased passive urethral resistance (BPO), decreased detrusor contractility force, or in combination with active urethral resistance (spastic urethral sphincter)
Terminal dribble may result from obstruction, evacuation of urine from urethra,or after-contraction

54. Low detrusor contractility and Poor stream in woman

55. Post-micturition Contraction Residual urine sensation