Neurogenic Bladder - Saudi Urology Group

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Transcript Neurogenic Bladder - Saudi Urology Group

Prepared by
Dr. Abdullah Ghazi (R4)
Supervised by
Dr. Ali Binmahfooz
1/12/2010 KFSH&RC
 Anatomy and physiology
 Classification of neurogenic LUTS.
 Evaluation.
 Management.
Anatomy and Physiology
Bladder - Anatomy
Neuroanatomy of Voiding
Neuroanatomy of Voiding
 Frontal lobe
 Micturition center
 Sends inhibitory signals
 Pons (Pontine Micturition Center)
 Excitatory center
 Coordinates urinary sphincters and the bladder
 Spinal cord
 Intermediary between upper and lower control
Peripheral Nervous System
 Somatic (S2-S4)
 Pudendal nerves
Excitatory to external
 Parasympathetic (S2-S4)
 Pelvic nerves
Excitatory to bladder,
relaxes sphincter
 Sympathetic (T10-L2)
 Hypogastric nerves to
pelvic ganglia
 Inhibitory to bladder,
excitatory to urethra
Normal Voiding
 SNS primarily controls bladder and the IUS
 Bladder increases capacity but not pressure
 Internal urinary sphincter to remain tightly closed
 Parasympathetic stimulation inhibited
 Somatics (pudendal N) regulate
 External urinary sphincter
 Pelvic diaphragm
 Immediately prior to PNS stimulation, SNS is suppressed
 Stimulates detrusor to contract
 Pudendal nerve is inhibited  external sphincter opens 
facilitation of voluntary urination
Pathophysiology of Voiding
 Brain lesion above pons destroys master control center
 Stroke (35%)
 Brain tumor (24%).
 Hydrocephalus (22%).
 CP (35%).
 Mental retarted (50%)
 Basal ganglia pathology (40%)
 Result :
 urge incontinence.
 night incontinence.
 coordinated sphincter
Pathophysiology of Voiding
 Spinal cord.
 Spinal cord lesion (95%).
 Myelomeningocele (50%DSD).
 Multiple Sclerosis (70%).
 Result:
 Detrusor hyperreflexia &
spastic bladder.
 Detrusor Sphincteric Dyssynergia.
 Some: Areflexic bladder
Pathophysiology of Voiding
 Lumbosacral spinal lesion
 Spinal tumor.
 Herniated disc (50%).
 Lumbar laminectomy (50%).
 Radical hysterectomy.
 Pelvic trauma
 Result – areflexic bladder
Pathophysiology of Voiding
 Peripheral nerve injury
 Diabetes (50-25%).
 Polio.
 Alcohol abuse
 GBS.
Classification (Madersbacher)
 General history
 Specific history
 Urinary history
 Bowel history:
 Sexual history
 Neurological history
 Sensation S2-S5 on both sides of the body
 Reflexes
 Anal sphincter tone
 Urinalysis
 Blood chemistry
 Voiding diary
 Residual urine (UFM).
 Quantification of urine loss by pad testing if
 Urinary tract imaging studies
 Urodynamic study.
Finding at Urodynamic
 Filling phase
 Hyposensitivity or hypersensitivity
 Vegetative sensations
 Low compliance
 High capacity bladder
 Detrusor overactivity, spontaneous or provoked
 Sphincter acontractility.
Finding at Urodynamic
 Voiding phase
 Detrusor acontractility
 Non-relaxing urethra
 Non-relaxing bladder neck
 Urodynamic investigation is necessary to document the
dysfunction of the LUT (A).
The recording of a bladder diary is advisable (B).
Non-invasive testing is mandatory before invasive
urodynamics is planned (A).
Video-urodynamics is the gold standard for invasive
urodynamics in patients with NLUTD. If this is available,
then a filling cystometry continuing into a pressure flow
study should be performed (A).
A physiological filling rate and body-warm saline must be
used (A).
Specific uro-neurophysiological tests are elective
procedures (C).
Treatment Priority
1. Protection of the upper urinary tract
2. Improvement of urinary continence
3. Restoration of (parts of) the LUT function
4. Improvement of the patient’s quality of life.
Goal of Treatment
 In patients with high detrusor pressure (detrusor
overactivity, low detrusor compliance, DSD, other
causes of bladder outlet obstruction).
 Aim to conversion high-pressure bladder into a passive
low-pressure reservoir despite the resulting residual
Non-invasive Conservative Treatment
 Assisted bladder emptying, Credé, Valsalva.
 Lower urinary tract rehabilitation
Behavioural modification techniques
Pelvic floor muscle exercises
Pelvic floor electrostimulation
 Drug treatment
Anticholinergic agents
Phosphodiesterase inhibitors, desmopressin.
Cholinergic drugs (bethanechol chloride).
Increasing bladder outlet resistance (no puplish).
 Electrical neuromodulation
 External appliances
 The first aim of any therapy is the protection of the
upper urinary tract.
 The mainstay of treatment for overactive detrusor is
anticholinergic drug therapy (A)
 Lower urinary tract rehabilitation may be effective in
selected cases.
 Condom catheter or pads may reduce urinary
incontinence to a socially acceptable situation.
 Any method of assisted bladder emptying should be
used with the greatest caution (A).
Minimal Invasive Treatment
Intravesical drug treatment
Intravesical electrostimulation
Botulinum toxin injections in the bladder
Bladder neck and urethral procedures
 Botulinum toxin sphincter injection
 Balloon dilatation
 Sphincterotomy
 Stents
 Bladder neck incision
 Increasing bladder outlet resistance
 Intermittent catheterization is the standard treatment for
patients who are unable to empty their bladder (A).
Patients should be well instructed in the technique and risks of
Aseptic IC is the method of choice (B).
The catheter size should be 12-14 Fr (B).
The frequency of IC is 4-6 times per day (B).
The bladder volume should remain below 400 mL (B).
Indwelling transurethral and suprapubic catheterization should
be used only exceptionally, under close control, and the catheter
should be changed frequently. Silicone catheters are preferred
and should be changed every 2-4 weeks, while (coated) latex
catheters need to be changed every 1-2 weeks. (A).
 Botulinum toxin injection in the detrusor is the most
effective minimally invasive treatment to reduce
neurogenic detrusor overactivity (A).
 Sphincterotomy is the standard treatment for DSD
 Bladder neck incision is effective in a fibrotic bladder
neck (B).
Surgical Treatment
 Urethral and bladder neck procedures
 Urethral sling
 Artificial urinary sphincter
 Functional sphincter augmentation (gracilis m)
 Bladder neck and urethra reconstruction (Extrophy)
 Detrusor myectomy (auto-augmentation)
 Denervation, deafferentation, neurostimulation,
 Bladder covering by striated muscle (rectus m)
 Bladder augmentation or substitution
 Urinary diversion (continent diversion, incontinent
 Detrusor
 Overactive
Detrusor myectomy is an acceptable option for the treatment
of overactive bladder when more conservative approaches
have failed. It is limited invasive and has minimal morbidity
- Sacral rhizotomy with SARS in complete lesions and sacral
neuromodulation in incomplete lesions are effective
treatments in selected patients (B).
Bladder augmentation is an acceptable option for decreasing
detrusor pressure whenever less invasive procedures have
failed. For the treatment of a severely thick or fibrotic bladder
wall, a bladder substitution might be considered (B).
 Detrusor
 Underactive
SARS with rhizotomy and sacral neuromodulation are
effective in selected patients (B).
Restoration of a functional bladder by covering with striated
muscle is still experimental (4).
 Urethra
 Overactive (DSD): like minimal invasive treatment
 Underactive
The placement of a urethral sling is an established procedure
The artificial urinary sphincter is very effective (B).
Transposition of the gracilis muscle is still experimental
(Level of evidence: 4).
 European Association of Urology 2010
M. Stöhrer, B. Blok, D. Castro-Diaz, E. Chartier-Kastler,
G. Del Popolo, G. Kramer, J. Pannek, P. Radziszewski,
J-J. Wyndaele