Neurogenic Bladder in SCI

7/29/2019 Neurogenic Bladder in SCI

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Spinal Cord Injury:

Managing the Neurogenic Bladder

Kristy M. Borawski, M.D.

Assistant Professor, Division of Urology


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Disclosures/Conflict of Interest

Pfizer: speaker


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Off Label Use

Medication

Indication

Dosage


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Overview

Spinal cord injury epidemiology

Voiding physiology

Neurogenic bladder physiology Management options

Surveillance for SCI induced neurogenic bladder


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Spinal Cord Injury (SCI)

Annual incidence 40 per million population

10,000 new injuries yearly in US

200,000 living with SCI in US

4:1 male to female ratio

Average age 30.7

Bracken, et al. Am J Epi 133: 615, 1981. Jamison, et al. Cochrane Database Sys Rev 1: 2009. Linsenmeyer, et al. JSpinal Cord Med 29: 527, 2006


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Spinal Cord Injury (SCI)

Vast majority of patients with SCI haveassociated neurogenic voiding dysfunction

~11% have associated head injury

Linsenmeyer, et al. J Spinal Cord Med 29: 527, 2006


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Life Expectancy in SCI patients

Life expectancy compared to normal population

70% of normal for complete tetraplegia

86% of normal for compete paraplegia

92% incomplete lesion with motor functioncapabilities

Yeo, et al. Spinal Cord, 36: 329, 1998


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Causes of Death in SCI patients

Renal disease historically a major cause of deathin paraplegics

1940s- 1950s: Genitourinary disorders accounted for

43% of deaths

1980-1990: 10% of deaths due to GU disorders

Clemens, et al. J Urol, 184: 213, 2010. Yeo, et al. Spinal Cord, 38: 604, 2008.


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Are we really doing better?

JD Yeo, et al: Leading cause of death amongSCI patients is pneumonia

Influenza

Septicemia**

Cancer

Heart disease

Diseases of urinary system

Suicide

CVA

Yeo, et al. Spinal Cord, 38: 604, 2000.


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Are we really doing better?

Causes of septicemia

Yeo, et al. Spinal Cord, 38: 604, 2000.

Causes Number

Urinary tract 11

Pressure areas 7

Respiratory tract 5

Strangulated bowel 3

Gangrene of the leg 2

Meningitis 2

Digestive tract 1

Gas gangrene 1

Obstruction of ileal conduit 1

Cellulitis 1

Ischemic heart disease 1

Brain stem CVA 1

Chronic lymphatic leukemia 1

Total 37


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Neural Control of the Lower

Urinary Tract


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Wein, et al. Campbell-Wash Urology, Vol 3, 2007

Function of the lowerurinary tract

Fill to normal capacity atlow pressures

Store urine until sociallyacceptable time to void

Empty to completion atacceptable pressures


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Wein, et al. Campbell-Wash Urology, Vol 3, 2007

Neural Control

Three sets of peripheral nerves innervate thelower urinary tract

Parasympathetic

Sympathetic

Somatic


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Wein, et al. Campbell-Walsh Urology, Vol 3, 2007

Neural Control: Parasympathetic

Originate from sacral cord at S2-S4

Preganglionic efferent fibers travel via pelvic nervesto provide excitatory input to the bladder

Post ganglionic nerves excite bladder smooth

muscle via:

Cholinergic (muscarinic receptors)

M2/M3 exist in bladder

M3 mediate bladder contractions Non-adrenergic, non cholinergic (ATP) acting on

P2X1 purinoreceptors


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Neural Control: Sympathetic

Begins in intermediolateral gray column fromT11L2

Route to bladder

Sympathetic chain ganglia inferior mesentericganglia hypogastric nerves to pelvic ganglia

Activation results in:

Bladder relaxation: via fibers

Contraction of bladder outlet & urethra: via fibers


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Neural Control: Somatic

S2-4 motor innervation (Onufs nucleus)

Travels to external sphincter via Pudendal nerve


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Micturition Centers

Cerebral Cortex

Inhibitory signal to thesacral micturition center

Pontine micturition center

Coordinating relaxation ofurinary sphincter whenbladder contracts

Sacral micturition center

Efferent parasym. signalscause bladder contraction

Afferent impulses provideinformation on bladderfullness


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Afferent Bladder Signals

Pelvic nerve afferents

Monitor volume of bladder & amplitude of bladdercontraction

Myelinated A and Unmyelinated C axons

C fibers are not essential for normal voiding

Wake up and respond to bladder distention & stimulate

uninhibited bladder contractions in animal models with

suprasacral spinal cord injury


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General Patterns of Neurogenic

Bladder after Neurologic Injury


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Lesions above Brainstem

Removes cerebral cortex micturition center

Detrusor overactivity

Coordinated sphincter control

Sensation may be normal or altered

Overall: urinary urgency +/- urge incontinence

Detrusor areflexia may occur initially or as permanent

dysfunction


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Suprasacral Spinal Cord Injury

Removes cerebral cortex & pontine micturition

centers

Spinal shock at first

Detrusor overactivity

No (reduced) sensation

Detrusor external (striated) sphincter dyssynergia

Present in >90% of patients with suprasacral SCI

Detrusor internal (smooth) sphincter synergia If lesion above T6, results in dyssynergic smooth

sphincter

Overall: incontinence due to detrusor overactivity

with obstruction due to DSD


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Sacral Spinal Cord Injury

Removes all micturition centers

Spinal shock at first

Detrusor areflexia

Decreased compliance may occur

Open internal (smooth) sphincter

Residual resting striated sphincter tone not undervoluntary control

Result: retention +/- incontinence


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Kaplan, et al: Urodynamic findings of 489 SCIpatients

Cervical lesion 15% detrusor acontractility

85% NDO & DSD

Thoracic

NDO with 90% showing DSD

Lumbosacral

40% detrusor acontractility

30% NDO 30% NDO and DSD

Kaplan, et al. J Urol, 1991.


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Kaplan, et al: Urodynamic findings of 489 SCI

patients Sacral level lesion

Small portion with normal urodynamics

64% with detrusor acontractility

Kaplan, et al. J Urol, 1991.


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Changes in Afferent Activity After

Spinal Cord Injury


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Changes in Afferent Activity AfterSpinal Cord Injury

Spinal Shock

Absent somatic reflex activity and flaccid muscleparalysis

Suppression of autonomic activity & somatic activity

Bladder is acontractile & areflexic

Bladder neck is usually closed (unless prior surgery)

Urinary retention is the rule Lasts 6-12 weeks

Return of reflex bladder activity occurs along withrecovery of lower extremity deep tendon reflexes


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After resolution of spinal shock, there is slow

development of autonomic micturition withneurogenic detrusor overactivity

Mediated by spinal reflex pathways

Voiding usually is inefficient due to presence of noncoordinated sphincters

Bladder contracts and external sphincter contracts rather

than relaxes detrusor sphincter dyssynergia

Yashimura, et al. Neurol Urod, 29: 63, 2010


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Afferent Changes

Recovery of bladder function after SCI isdependent on:

Plasticity of bladder afferent pathways

Unmasking of reflexes triggered by unmyelinated,capsaicin-sensitive C-fiber bladder afferent neurons

C-fiber afferents are activatedAdministering C-fiber neurotoxin capsaicin to SCI cats

blocks reflex bladder contractions

No effect in spinal cord intact cats

Yashimura, et al. Neurol Urod, 29: 63, 2010


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De Groat, et al. Exp Neurol, 2011.

Afferent Bladder Signals:

Changes After SCI Reactivation of neonatal

perineal-to-bladder andbladder-to-bladder

excitatory reflexes Activation of C mediated

afferents

Alteration in epitheliallayer

In rat model, removingmucosa eliminated NDO

Morphological &chemical change ofafferents

Remodeling of synapsesin spinal cord

Alteration inneurotransmittermechanisms in spinalcord


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Evaluating the Neurogenic

Bladder after SCI


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Guidelines

Third International Consultation onIncontinence

Committee on neurogenic bladder management

No SCI specific protocols

European Association of Urology

Overall management recommendations for

neurogenic bladder

No SCI specific protocols

Wyndaele, et al. The 3rd International Consultation of Incontinence, 2004. Stohrer, et al. European Association ofUrology Guidelines, 2007.


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European SCI Think Tank

Defines 4 stages of management

Immediate (within first few days)

Early management (0-2 weeks)

Intermediate management (2-12 weeks)

Long term management (>12 weeks)

Abrams, et al. BJU Int, 101: 989, 2008


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Immediate management

Resuscitation time

Usually requires indwelling catheter (urethral) for

monitoring

Early management (0-2 weeks)

Remove indwelling catheter

Institute clean intermittent catheterization (CIC)



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Intermediate management (2-12 weeks)

Transition from inpatient rehabilitation home

Introduce/refer to urology

Discuss urological options

Consider obtaining baseline testing



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Baseline Interventions: 3-6 months

After resolution of spinal shock

Renal function

Serum creatinine

Creatinine clearance until muscle mass stable

Renal/bladder ultrasound

Frequency/volume bladder chartVideo urodynamics



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Urodynamics in the SCI patient

Grade A evidence to support the use of videourodynamics in patients with neurogenic lower

urinary tract dysfunction

Stohrer, et al. Eur Urol, 56: 81, 2009.


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Urodynamics in the SCI patient

Fill/Storage phase

Normal capacity

Normal compliance

>12.5mL/cmH20 No detrusor overactivity

Competent outlet

Emptying phase

Sphincter relaxation

Sustained detrusorcontraction

Minimal residual urine


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Normal Urodynamics

Filling Storage Voiding

Rectal catheter

Urethral Catheter

Detrusor Pressure = Pves - Pabd

U d i fi di h l


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Urodynamics findings that place

upper tracts at risk

Poor Compliance

High storage pressure VUR Upper tract deterioration

McGuire, et al

Storage pressure >40cmH2O associated with renal dysfunction

Detrusor leak point pressure

Ideally, would keep pressure


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upper tracts at risk Detrusor external sphincter dyssynergia

Results in high voiding pressures

Vesicoureteral reflux

Incomplete bladder emptying

Symptoms:

Weak stream

Intermittent stream

d i fi di h l


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upper tracts at riskThree types of detrusor sphincter dyssynergia

U d i fi di h l


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upper tracts at risk Neurogenic detrusor overactivity


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Options for Bladder Management


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Options for Management

Patient abilities

Tetraplegic vs. paraplegic

Concurrent head injury

Patient preference

Family support


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US Clinical Practice Guidelines

CIC is optimal option for bladder emptying

Recommend institution of CIC program prior todischarge from rehabilitation unit

Popularized by Lapides in 1972

Safe method for bladder drainage

Decreased rates of UTI, bladder stones & erosion

Numerous studies documenting patientacceptance

Kessler, et al. Neurourol & Urod, 28: 18, 2009. J Spinal Cord Med, 29: 527, 2006


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Cameron, et al: long term data available onbladder management for 12,984 SCI patients

Cameron, et al. J Urol 184: 213, 2010.


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Use of CIC drastically declined

Cameron, et al. J Urol 184: 213, 2010.


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CIC use not indicated / difficult in patients with:

Abnormal urethral anatomy

Bladder capacity


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Complications/problems associated with CIC

UTI

Bladder overdistention

Urinary incontinence

Urethral trauma with false passage

Urethral stricture

Bladder stones

Autonomic dysreflexia

Cameron, et al. J Urol 184: 213, 2010. . J Spinal Cord Med, 29: 527, 2006


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Crede Voiding / Valsalva Voiding

Application of suprapubic pressure or abdominalstraining to empty bladder

Only consider if patient has low outlet resistance

Current recommendation: Consider avoiding Crede andValsalva as primary methods of bladder emptying

Grade C recommendation

Avoid if known history of vesicoureteral reflux



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Reflex voiding into external collection device / pads

Only consider if:

Low voiding pressures on urodynamics

Low post void residualsAbsent / rare episodes of autonomic dysreflexia with bladder

filling

Rare UTIs



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Indwelling catheter (urethral / suprapubic) 23% of SCI patients are discharged from rehab units

with indwelling catheters

Higher complication rates compared to CIC

53.5% complication rate in indwelling group vs. 27% for CIC

Cameron, et al. J Urol 184: 213, 2010. . J Spinal Cord Med, 29: 527, 2006. Dmochowski, et al. J Urol, 163: 768, 2000.


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Cameron, et al. J Urol 184: 213, 2010. . J Spinal Cord Med, 29: 527, 2006, Dmochowski, et al. J Urol, 163: 768,


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Increased risk of upper tract deterioration withindwelling catheter

Low bladder compliance

Leads to increase risk of VUR pyelonephritis

Mean serum creatinine is higher

Proteinuria is greater in patients with indwelling

catheters



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Increased risk of upper tract deterioration withindwelling catheter

Addition of anticholinergic may help

Improved bladder compliance

Lowers detrusor leak point pressure

Decreased rates of hydronephrosis

No change in:

Infection rates

VUR

Serum creatinine

Renal scars

Kim, et al J Urol 159: 193, 1998. J Spinal Cord Med, 29: 527, 2006


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Increased risk of bladder cancer with indwellingcatheter

Reported incidence of squamous cell carcinoma (SCC) is

2.310% in patients with indwelling catheter 8% risk after 25 years of catheterization

Pathogenesis: chronic urothelial irritation and

inflammation leading to metaplasia neoplasia

Surveillance guidelines for cystoscopy differ

Annual surveillance for patients with indwelling catheters is

advised

J Spinal Cord Med, 29: 527, 2006. Corcos, et al. Neurourol & Uds 27: 475, 2008.


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Urethral vs. Suprapubic Catheter

Similar overall complication rates with notableexceptions

Urethral complications significantly higher in urethral

catheter group Erosion (especially in women), abscess, fistula, stricture

Slight decreased risk of UTI with suprapubic catheter

Benefit may be offset by increased risk of insertion

Recent studies using modernized techniques showimproved outcomes for indwelling catheters

J Spinal Cord Med, 29: 527, 2006. Corcos, et al. Neurourol & Uds 27: 475, 2008.


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When bladder drainage alone

is not enough

Si n /S mpt m f


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Signs/Symptom of

Insufficient Treatment

Worsening upper tracts

Hydronephrosis on RUS

Increased serum creatinine

Worsening urodynamics

Loss of compliance, elevated DLPP, increasedvoiding pressures, worsening NDO

Increased incontinence

Increased episodes of autonomics dysreflexia

Patient dissatisfaction


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Medications


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Medications

Goal of medical therapy

Improve bladder compliance

Increase bladder capacity

Decrease neurogenic detrusor overactivitydecrease incontinence

Acceptable side effects

Antim rini


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Antimuscarinics

First line agents for patients with neurogenicbladder

Some advocate starting immediately

5 muscarinic receptor subtypes; 2 in bladder

Normally, M3 receptors mediate bladdercontractions

Cameron, et al. J Urol, 182: 1062, 2009. Stevens, et al. Eur Urol 52: 531, 2007.

Antim c rinic


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Antimuscarinics

Dose requirements are usually higher than inpatients with idiopathic detrusor overactivity(Grade A)

Not all anticholinergics have data for neurogenic

population

Abrams, et al. BJU Int, 101: 989, 2008. Stohrer, et al. Eur Urol, 56: 81, 2009.

Anticholinergics


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Anticholinergics

Muscarinic Receptor Subtypes

Subtype Distribution Role

M1 Brain (cortex, hippocampus), Salivary

gland

Cognitive function, memory; saliva

secretion

M2 Heart, brain, smooth muscle Regulation of heart rate & HRvariability; behavioral flexibility

M3 Smooth muscle, glands, eye Smooth muscle contraction, iriscontraction, gland secretion

M4 Brain (forebrain, striatum) Dopamine dependent behaviors

M5 Brain (substantia nigra), eye Regulation of striatal dopamine release

Anticholinergics


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Anticholinergics

Antimuscarinics & M3 Receptor Selectivity

Anticholinergics


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Anticholinergics

Antimuscarinics & Side Effects

Dry mouth

Constipation

Blurred vision

Anticholinergics


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Anticholinergics

Constipation Dry Mouth

Enablex 7.5mg 14.8% 20.2%

15mg 21.3% 35.3%

Vesicare 5mg 5.4% 10.9%

10mg 13.4% 27.6%Sactura XL 60mg 8.5% 10.7%

Detrol LA 4mg 7% 35%

Toviaz 4mg 4.2% 18.8%

8mg 6% 34.6%

Anticholinergics:


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gCognitive Side Effects

Merchant, et al.

Prevalence of cognitive impairment more thandoubled with the use of drugs with anticholinergic

activity in community dwelling older persons

CNS Penetration


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CNS Penetration

Entry into the brain via BBB by passivediffusion dependent on:

Molecular size, polarity, lipophilicity

Highly lipophilic, non polar small molecules willmore readily cross the BBB by passive diffusion

Oxybutynin: 357kDareadily passes BBB

Darifenacin, solifenacin, tolterodine, fesoterodine all

>475kDa unlikely to pass via passive diffusion

Tropsium (Sancura) hydrophilic, polar compound,

428kDa low propensitiy for BBB penetration

Cognitive Impairment &


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g pReceptor Selectivity

M1 & M2 receptors are important in cognitivefunctioning and memory & behavioral flexibility& learning

More data that central blockade of M1 receptors has

a key functional role in cognitive impairment

Less M3 selectivity may be associated with increasedrisk of cognitive impairment


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Sanctura (tropsium): although relatively non-selective, low BBBpenetration should have low potential for cognitive risk as longas BBB integrity is not compromised

As of now, best evidence is with darifenacin (enablex): 3 trials

Alpha Blockers


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Alpha Blockers

Detrusor has 2 types 1 adrenergic receptor

1/3: 1-d 2/3: 1-a

Bladder neck, prostate: predominantly1-a

Sundin, et al: Increase in adrenergic receptor sites anda switch to -adrenergic contractive function from thetypical -adrenergic relaxation function during bladderfilling

Tamsulosin (flomax) RCT: no significant increase inbladder capacity

Cameron, et al. J Urol, 182: 1062, 2009.

Tricyclic antidepressants (TCAs)


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Tricyclic antidepressants (TCAs)

Imipramine has been shown to suppress bladder

overactivity by various mechanisms Muscarinic receptor antagonist

Direct smooth muscle inhibitor

Blocks reuptake of serotonin reduces bladder overactivity

Also shown to stimulate fibers at dome resulting in

improved bladder compliance

TCAs (Imipramine) have been shown to increase

compliance in the pediatric neurogenic population No RCT supporting their use

Cardiac side effects use with caution


Combination therapy


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py McGuire, et al: retrospectively evaluated group of

patients initially on no medications or antimuscarinics

only

No initial medications

2 medications (n=22)

Mean bladder pressure at capacity decreased 52% (36

17cmH20) Mean compliance increased 5-fold (11.3 56.3 mL/cmH20)

3 medications (n=28)

Bladder pressure decreased 67% (35.9 11.9cmH20)

Compliance increased 9.7 fold (7.2 69.6mL/cmH20)

Initial antimuscarinics 3 drug therapy (n=27)

Bladder pressure decreased 60% (27.2 10.9 cmH20)

Compliance increased 3-fold (18.4 54.3 mL/cmH20)


Combination therapy


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py Other studies support the use of combination therapy

Gossl, et al: 41 children with MMC treated with oraloxybutinin

40% increase in capacity

158% increase in compliance

Swierzewski, et al: added terazosin (alpha blocker) toexisting CIC + anticholinergic therapy

Compliance increased by 73%

Capacity increased by 157mL

Bladder pressure decreased by 36cmH20

Results reversed when medication stopped

Cameron, et al. J Urol, 182: 1062, 2009. Swierzewski, et al. J Urol, 151: 951, 1994.


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Failure Despite Maximal Medical

Therapy


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Historically, progressed to surgical managementor an indwelling catheter

Sphincterotomy

Bladder Augmentation

Ileovesicostomy

Urinary Diversion

Botox


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Botulinum Toxin A

Isolated in 1897 by van Ermengem 150-kD amino acid di-chain

Mechanism of action

Binds to pre-synaptic nerve endingsof cholinergic neurons

Enters neuron via endocytosis

Cleaves SNAP-25 protein that isneeded for synaptic vesicle fusion

Results in inhibition of acetylcholinesecretion

Karsenty, et al. Eur Urol 53: 275, 2008. Reitz, et al. Eur Urol 45: 510, 2004.

B


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Botox

Increasing evidence of increased activity

Inhibits release of acetylcholine, adenosinetriphosphate and several neurotransmitters

(substance P) Down-regulates expression of purinergic & capsaicin

receptors on afferent neurons in the bladder

Botox can treats neurogenic detrusoroveractivity via motor & sensory pathways

Karsenty, et al. Eur Urol 53: 275, 2008.

Botulinum toxin


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o u u o

Seven distinct structurally similar serotypes ofbotulinum toxin (BTX)

BTX-A & BTX-B have been used in variousneurological disorders

BTX-A (Botox, Allergan, Inc) approved for use in USby FDA for strabismus, blepharospasm, hemifacial spasm& cervical dystonia


Botulinum toxin: update!!


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p

August 24, 2011

BOTOX (onabotulinumtoxinA) Receives U.S.

FDA Approval For The Treatment Of Urinary

Incontinence In Adults with Neurological

Conditions Including Multiple Sclerosis AndSpinal Cord Injury


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Significant improvement incontinence rates

Significant improvement in QOLparameters


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Significant improvement of maximum detrusor pressure

RCT Botox vs. Placebo for NGB


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Herschorn, et al. J Urol, 2011.

Secondary to SCI/MS

Herschorn, et al. RCT comparing 300 Units or placebo

30 injection sites

Trigone sparing


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Herschorn, et al. J Urol, 2011.Adverse Events

Ideal Dosage for Botox Still Unknown


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Cruz. Eur Urol, 2011.

Improvement with 200 & 300 units in


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p

SCI population

Improvement with 200 & 300 units in


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p

SCI population

Slight increase in SE for 300 Units


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Slight increase in SE for 300 Units

Long Term Data


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Pannek, et al. BJU Int 104: 1246, 2009.

Multiple studies document long term success

despite the need for repeat injections 4-9 months

Pannek, et al: declining results with repeated

injections 1 in 4 subjects required surgical intervention

Are the Results Sustainable?


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Are the Results Sustainable?

Giannantoni, et al

Giannantoni, et al. 2009 Eur Urol; 55: 705-712

Improvement in QOL index

Repeated Injections


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Treatment resistance or lack of response

Antibody formation a concern for repeated injection No formal studies documenting the presence of antibodies in

non responders in urologic literature

In cervical dystonia: subjects with antibodies required shorter intervals

between injections and required larger doses Schulte-Baukloh, et al

Of 25 subjects who received BoNTA, 4 tested + forantibodies & 4 were borderline

Only 3/8 were considered treatment failures

Dowson, et al. 2010 Nat Rev Urol; 7: 661-667.

Side Effects


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Pannek, et al. BJU Int 104: 1246, 2009. Karsenty, et al. Eur Urol 53: 275, 2008.

Side effects are usually mild

Injection site pain

Procedure-related UTI (2-23%)

Mild hematuria (2-21%)

Elevated PVR

De novo need for CIC (6-88%) Localized muscle weakness reported

Documented reports of generalized weakness / fatiguefollowing Botox injections

Warn patients about black box warning with BoNTA

Potential to spread beyond treatment area & producedifficulty swallowing and breathing

Contraindications


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Pregnancy category C

Relative contraindication in patients with neuromusculardisease

Use caution with certain medications that can potentiate

the results of BoNTA Aminoglycosides

Clindamycin

Succinylcholine

Gomez, et al. 2010 Curr Urol Rep; 11: 353-359.


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Sacral Neuromodulation

Sacral Neuromodulation: Interstim


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Complete spinal cord injury

Poor outcomes reported with use of Interstim Incomplete injuries

Limited data available that appears to support its use

Lombardi, et al. Spinal Cord, 47: 486, 2009.

Early Sacral Neuromodulation(SNM)?


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(SNM)?

Could early neuromodulation prevent theplasticity that results in a neurogenic bladder?

Sievert, et al: 10 patients received bilateral SNM

6 who refused served as controls

All were complete SCI above T12

Prior to intervention, UDS confirmed areflexia duringspinal shock period

Time to SNM implantation: 2.9 months (0.84.5months)

Sievert, et al. Ann Neurol, 67: 74, 2010


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Sievert, et al. Ann Neurol, 67: 74, 2010

SNM group

Control


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How should we monitor the SCI

patient?

How should we monitor the SCIpatient?


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patient?

US Practice Guidelines No definitive

recommendations

Upper & lower tract

evaluation annually

How should we monitor the SCI patient?


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Veterans Affairs Health Care policyAnnual UA, C&S

Annual BUN, serum creatinine

Annual anatomical exam (renal US / CT) Urodynamics should be performed when objective

information on voiding function is needed

Cystoscopy every 10 years in patients with indwellingcatheters or who use tobacco products



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Proposed European Guidelines

Annual urodynamics for high risk group (detrusor overactivity,low bladder compliance, reflex voiding, Crede voiding)

Biannual urodynamics for low risk group



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Prior guidelines recommended annual UDSevery 5 years & then with symptom / uppertract change

Nossier, et al: 3/80 patients did not requiretreatment modification (mean f/u 67 months)

If UDS were repeated based on symptom/upper

tract findings only, 68% of treatment failure (i.e.those needing treatment modification) would nothave been identified

Nossier, et al. Neurourol Urodyn 26(2): 228, 2007.


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Other Considerations

Bladder Cancer


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Relative risk of bladder cancer 1628 timesthat of the normal population

Recent review of 1319 spinal cord patients

32 developed cancer

46.9% SCC, 31.3% TCC, 9.4% adenocarcinoma,12.5% mixed SCC/TCC

Bladder management: 44% urethral catheter, 48%

external catheter, 8% CIC 42% found on screening cystoscopy

Kalisvaart, et al. Spinal Cord, 48: 257, 2010. Goath, et al. Arch Phys Med Rehabil, 83: 346, 2002.

Bladder Cancer


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Causes of increased bladder cancer

Chronic irritation

Recurrent UTI

Bladder stones

Indwelling catheterAlteration in bladder urothelial due to interaction of

bladder mucosa with high volume of urine

Average time from injury

bladder cancer dx 34 years


Cystoscopy Recommendations


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With symptoms

Hematuria

Recurrent UTI

Any significant change in urinary habits

Annual

Consider in indwelling catheter group

Consider in high risk patients (recurrent UTI,

bladder stones, tobacco use, etc..)


Conclusion


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SCI associated with significant GU dysfunction

Prompt referral to center of excellence for SCIpatients is preferred

Early & lifelong GU involvement

If you care for SCI patients, ensure that they arereceiving urologic care.

Documents

Neurogenic Bladder in SCI