Neuropathic Bladder. Magda Kujawa Consultant Urologist Stockport NHS Foundation Trust 12/03/2014

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Transcription:

Neuropathic Bladder Magda Kujawa Consultant Urologist Stockport NHS Foundation Trust 12/03/2014

Plan Physiology- bladder and sphincter behaviour in neurological disease Clinical consequences of Symptoms Bladder management techniques Managing Incontinence MS/ Parkinsons/ CVA/ Congenital disorders

Neuropathic Bladder To understand pathophysiology must understand normal physiology Storage Voiding Co-ordination of these phases Impact on upper tracts

Function Can be split into 2 main phases 1. Storage/ Filling (99%) 2. Voiding (1%)

Storage Bladder filling occurs without rise in pressure Compliance Passive elastic properties of bladder wall Ability of smooth muscle to maintain constant tension while stretching Spinal reflexes controlling tension while bladder filling Urethra and sphincteric mechanism closed

Voiding Urethral Relaxation precedes detrusor contraction Simultaneous relaxation of pelvic floor Funnelling of bladder neck to facilitate flow into proximal urethra Detrusor contraction to forcefully expel urine

Neuronal Control Complex series of peripheral and central neuronal pathways Co-ordinate the activities of the bladder and the urethra/sphincter mechanisms Control compliance (receptive relaxation) Sense bladder fullness Maintain continence Initiate voluntary voiding

Neuronal Control

Involuntary Storage Reflexes Lumbo-sacral spinal cord Increasing bladder fullness increases activity Sympathetic nerves bladder relaxation urethral contraction Pudendal nerve pelvic floor contraction Inhibits parasympathetic (bladder contraction) Guarding reflex

Desire to void Conscious act co-ordinated in mid brain and pons (pontine micturition centre) Causes switch from storage to voiding phase when bladder full and appropriate to void Many other areas in brain impact upon the pontine micturition centre Involved with delaying micturition, inhibiting premature contraction, appropriate voiding NB Dementia!

The control of the urethral sphincter Superior Hypogastric plexus (sympathetic) Spinal Cord Detrusor Detrusor Pelvic nerve (parasympathe tic) Pudendal nerve (somatic) External urethral sphincter Internal urethral sphincter

Micturition Cycle Mediated by complex coordination Sacral micturition centre Receptive relaxation Reflex bladder contraction Pontine micturition centre Co-ordination Filling/voiding

Bladder and sphincter behaviour in neurological disease Bladder control is complex There are many sites where disease or injury can have impact Not always predictable Complete vs Incomplete

Bladder and sphincter behaviour in neurological disease Abnormal or neuropathic behaviour may affect bladder +/- sphincter Activity of bladder and sphincter Overactive bladder is one that intermittently contracts during bladder filling Neurogenic detrusor overactivity in context of neurological disease Previously detrusor hyperreflexia Bladder where pressure rises progressively during filling = poorly compliant Bladder unable to store urine at low pressure

Detrusor Overactivity on Urodynamics

Detrusor Overactivity on Urodynamics

Poor Compliance

Bladder and sphincter behaviour in neurological disease Other end of spectrum is underactive bladder or areflexia Low pressure during filling and voiding

Detrusor Areflexia

Bladder and sphincter behaviour in neurological disease Overactive sphincter generates high pressure while filling but also voiding when it should be relaxed Detrusor sphincter dyssynergia Can be seen during electromyographical recording of sphincter Activity seen in sphincter during voiding when it should be relaxed and inactive

DSD and EMG activity during void

Bladder and sphincter behaviour in neurological disease Over time neurogenic detrusor overactivity can lead to Trabeculated bladder If sphincter is also dyssynergic Incomplete bladder emptying Raised intravesical pressure Hydronephrosis Chronic urinary tract infection Vesico ureteric reflux Pyelonephritis Stone formation Ultimately renal failure

Bladder and sphincter behaviour in neurological disease The bladder is an unreliable witness Many different pathological entities that translate to same symptoms Frequency, nocturia, urgency, urge incontinence and stress incontinence and UTI

Bladder and sphincter behaviour in neurological disease Better understanding of these conditions Continued assessment Advances in management Reduction in incidence of death from consequences for those particularly with Congenital neuropathic bladder Spinal cord injury

Assessment Presence and Severity of symptoms Assessment of bladder emptying MSSU Check electrolytes May require flexible cystoscopy Urodynamic assessment is cornerstone

Urodynamic assessment in neuropaths- Indications New onset of incontinence or change in incontinence patterns or voiding pattern Recurrent UTI? New onset Development of upper tract dilatation (loss of renal function) Prior to reconstructive surgery

Urodynamics

Urodynamic assessment in neuropaths Video or standard? Allow time? Hoist required Staffing Presence of urine infection Fill on top of residual Avoid rapid filling- ideally 10-30mls per min

Urodynamic assessment in neuropaths Key questions In storage/filling phase Normal sensation Evidence of phasic detrusor overactivity Evidence of continued increase in pressure with filling(poor compliance) When does leakage occur Is there reflux (video or ultrasound) In voiding phase?any dyssynergia? emptying

General priniciples of Management Protect upper tracts and preserve renal function Improve symptoms Tailor management to patient s medical, functional status and expectations Conservative Individualize

Medical management Behavioural measures Control UTI Anticholinergics Β-3 agonists CISC Sheath Indwelling catheter Urethral Suprapubic

Surgical Management Intravesical botox injections 200-300u Temporary benefit duration often dose dependent Can be performed under local anaesthetic Effectively paralyses muscle to reduce compliance and detrusor overactivity Protects upper tracts

Technique for 200 units 20 injection sites 4 lines of 5 around lateral and posterior wall bladder air

Surgical management Bladder reconstruction Need commitment to ISC Clam cystoplasty Mitrofanoff Urinary Diversion

Clam Cystoplasty

Mitrofanoff Principle

Urinary Diversion Still a very useful procedure MS patients High spinal injury

Multiple Sclerosis De-myelination of nerves of brain and spinal cord Plaques or sclerosis in different areas at different times Nerve transmission affected 4 main types Benign Relapsing remitting Primary progressive Secondary progressive 20-40 years 2:3 male to female

Typical symptoms of MS 75% of MS patients have spinal cord involvement Frequency, Nocturia, Urgency and Urge incontinence due to neurogenic detrusor overactivity Incomplete bladder emptying due to dyssynergic sphincter UTI secondary to incomplete bladder emptying Rarely have upper tract problems Mobility problems and poor hand function have big impact on management

Investigation History/ Type of their MS MSSU Post void scan Flexible cystoscopy if haematuria/ recurrent UTI Upper tract imaging

Management If incomplete bladder emptying and hand function allows teach intermittent self catheterisation? Home best Use anticholinergics to treat detrusor overactivity If using variable dose preparation such as oxybutynin,darifenacin solifenacin or fesoterodine often the higher dose will be required Reassessment If no benefit then urodynamics

Next step Overactivity not controlled? Intravesical botox injections 200u/300u Not able to manage ISC Carer to perform Indwelling catheter Better is supra-pubic catheter Easier to change Avoids patulous urethra/ acquired hypospadias Urinary diversion

Cerebrovascular accident 3 mechanisms Reduced cortical inhibitory control of the micturition reflex leads to detrusor overactivity commonly causes symptoms of frequency urgency urge incontinence and nocturia Cognitive, functional and language deficits, normal bladder function but still incontinent Detrusor areflexia (underactive bladder) because of concomitant neuropathy or medication Upper tract problems are unusual as Pons intact

Cerebrovascular accident Assessment Management of detrusor overactivity Compromised by other neurological deficit and co-morbidities Use of other continence aids

Parkinson s Disease Progressive loss of Dopa producing cells of the substantia nigra of the basal ganglia Located near and has effect upon Pons of brainstem Frequency, nocturia, urgency and urge incontinence exacerbated by the movement disorder of Parkinsons Often have concomittant bladder outflow obstruction which may be prostatic or may be sphincter related (bradykinesia) Treat overactivity with anticholinergic in first instance Trospium Chloride (Regurin) does not cross blood brain barrier

Parkinson s Disease Treat obstructive symptoms with α blocker +/- 5ARI Urodynamics can be helpful in establishing contribution of overactivity and obstruction to symptoms Video urodynamics can help establish if obstruction at bladder neck or external sphincter However poorer outcome with TURP well established Often end up with indwelling catheter

Urodynamic example

Multiple System Atrophy Formerly known as Shy-Drager Syndrome Parkinsons plus autonomic neuropathy Younger males affected Incontinent because of deficient sphincter Surgery should be avoided

Congenital cord lesions

Congenital cord lesions Normal Spina Bifida Occulta Meninogocele Myelomeningocele

Spina Bifida

Congenital cord lesions Pattern of dysfunction depends on level of abnormality and whether complete or incomplete lesions Eg Thoracolumbar and lumbar myelomeningocele tend to be complete Lumbar and lumbosacral can be incomplete At or below L3 can be ambulant

Congenital cord lesions Clinical effects then Neurogenic detrusor overactivity +/- sphincter weakness Acontractile bladder +/- sphincter weakness Main concern is loss of upper tract function and so investigation and management geared to surveillance for this Combination of poor compliance, detrusor sphincter dyssynergia and lack of sphincter weakness and elevated leak point pressures are strong risk for upper tract deterioration Sphincter weakness can help preserve upper tracts in this situation.

Congenital cord lesions Symptoms are frequency, nocturia,urgency,urge incontinence and leakage without obvious preceeding urgency or increased intraabdominal pressure Urodynamics essential with upper tract imaging Measurement of detrusor leak point pressure

Conclusions Clear idea of pathophysiology Understand patterns of symptoms and potential consequences of various conditions Not everyone has read the textbook Aware of red flag symptoms