Urodynamics and Bladder Outlet Obstruction

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Urodynamics and Bladder Outlet Obstruction

• Hann-Chorng Kuo
• Department of Urology
• Buddhist Tzu Chi General Hospital

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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

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Benign prostatic enlargement
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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

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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

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Bladder Filling Phase

• Laplaces 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)

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Rhythmic Detrusor Contractions after
Resiniferatoxin treatment
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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

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Initiation of VoidingThe Relationship of Q and
Pdet
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Initiation of VoidingActive relaxation of
External sphincter
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Initiation of VoidingPassive opening of urethral
wall
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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

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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)

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Reduced Pdet at decreasing intravesical volume
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Iso-volumetric Detrusor Contraction at Stop Test
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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

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Relationship of Pressure Flow
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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

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The Abrams-Griffiths Plot
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The Schafer Nomogram
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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

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Decrease in Contractile Velocity in Bladder
Outlet Obstruction
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Constrictive vs Compressive Pressure Flow Plots
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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

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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

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Pressure Flow Plot for Diagnosis of Obstruction
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Abrams Griffiths Number

• AG number Pdet.Qmax 2 x Qmax
• Obstruction
• AGgt 40
• Nonobstruction
• AGlt20
• Equivocal
• 20ltAGlt40

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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

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Constrictive Obstruction in Female Urethral
Stricture
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Constrictive Obstructionin Anterior Urethral
Valve
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Compressive Obstructionin BPH Obstruction
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Compressive Obstructionin Dysfunctional Voiding
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Constrictive Obstruction in Urethral Stricture
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Obstruction in Detrusor External Sphincter
Dyssynergia (DESD)
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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

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Post-incontinence surgeryBladder neck obstruction
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Spastic Urethral SphincterCompressive Obstruction
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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

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Low Contractility Force in BPH Obstruction
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BPH with Acute Urinary Retention
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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

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Post-prostatectomy Low Detrusor Contractility
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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

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Poor bladder compliance and low contractility
after prostatectomy
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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

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Detrusor overactivity and Pseudodyssynergia in CVA
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DESD with incontinence Bilateral
vesicoureteral reflux
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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

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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

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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

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Poorly Relaxed Urethral Sphincter Hesitancy
Intermittency
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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

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Poor Stream Dribblingin 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

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Low detrusor contractility and Poor stream in
woman
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Post-micturition ContractionResidual urine
sensation