Autonomic dysfunction - neurogenic bladder

Description

Bladder dysfunction from a neurological lesion. The level of the lesion predicts the pattern - this is the whole examinable structure

Lesion level	Pattern	Clinical
Suprapontine (stroke, PD, dementia, MS)	Detrusor overactivity with synergic sphincter	Urgency, frequency, urge incontinence. Emptying preserved
Suprasacral spinal (cord injury, MS, transverse myelitis)	Detrusor overactivity + detrusor-sphincter dyssynergia	Urgency, incomplete emptying, high storage pressures -> upper tract damage. The dangerous group
Sacral / infrasacral (conus, cauda equina, diabetic neuropathy, pelvic surgery)	Detrusor areflexia + open or fixed sphincter	Painless retention with overflow incontinence, poor stream, no sensation of fullness

The kidney, not the continence, is what determines prognosis - high detrusor pressure causes reflux, hydronephrosis and renal failure

Spinal cord injury: ~80-90% have neurogenic bladder
Multiple sclerosis: ~75% over the disease course
Parkinson disease ~40-70%; stroke ~30-50% in the first month
Diabetes: cystopathy in ~40-80% of those with established autonomic neuropathy
Spina bifida - the commonest paediatric cause; renal failure was historically the leading cause of death, now largely preventable

Normal control

Phase	Innervation	Effect
Storage	Sympathetic - hypogastric nerve (T10-L2)	Beta-3 relaxes detrusor; alpha-1 contracts internal sphincter
Storage	Somatic - pudendal nerve (S2-4, Onuf nucleus)	Contracts external sphincter
Voiding	Parasympathetic - pelvic nerve (S2-4)	Detrusor contraction is mediated mainly by acetylcholine acting on M3 muscarinic receptors

Coordination by the pontine micturition centre (Barrington nucleus)
- -> a lesion above the pons removes cortical inhibition but preserves coordination = overactivity with synergy
- -> a lesion between the pons and the sacral cord disconnects the coordinating centre = dyssynergia
- -> a lesion at or below S2-4 removes the efferent limb = areflexic, atonic bladder

Consequences of dyssynergia

Detrusor contracts against a closed sphincter
- -> inc intravesical pressure -> bladder wall trabeculation and diverticula
- -> vesicoureteric reflux -> hydronephrosis -> CKD
- -> incomplete emptying -> recurrent UTI, stones

History

Storage symptoms (urgency, frequency, nocturia, incontinence) vs voiding symptoms (hesitancy, poor stream, straining, incomplete emptying)
Awareness of bladder filling - lost in sacral lesions
Bowel and sexual function, saddle sensation - cauda equina red flags
Fluid intake, drug review (anticholinergics, opioids, alpha-agonists, diuretics)

Examination

Perineal sensation (S2-4), anal tone, bulbocavernosus and anal wink reflexes
Palpable bladder; lower limb neurology; spinal examination

Investigations

Bladder diary - the single most informative and most neglected investigation
Post-void residual by bladder scan (>100-150 mL is significant)
MSU; UEC and eGFR
Renal tract ultrasound - to detect hydronephrosis, stones and bladder wall thickening
Urodynamics with video - the definitive study
- Measures detrusor leak point pressure; >40 cmH2O predicts upper tract deterioration
- Essential in all suprasacral spinal lesions
MRI spine if the neurological diagnosis is unknown

Two goals, in order: protect the kidneys, then achieve continence.

A. Storage failure (detrusor overactivity)

Timed voiding, fluid management, pelvic floor training
Antimuscarinics - oxybutynin, solifenacin, darifenacin, trospium
- Cognitive impairment is the limiting adverse effect - avoid oxybutynin in the elderly and in PD/dementia; trospium and darifenacin cross the blood-brain barrier least
Mirabegron (beta-3 agonist) - preferred where anticholinergic burden matters
Intradetrusor botulinum toxin A - highly effective for refractory neurogenic detrusor overactivity
- Warn about the need for intermittent self-catheterisation afterwards
Augmentation cystoplasty for refractory high-pressure bladders

B. Emptying failure (areflexia, retention, dyssynergia)

Clean intermittent self-catheterisation is the standard of care - 4-6 times daily
- Lower infection and upper tract risk than an indwelling catheter
Indwelling urethral catheter is a last resort - stones, urethral erosion, chronic infection, squamous cell carcinoma of the bladder with long-term use
- Suprapubic catheter is preferable if long-term drainage is unavoidable
Alpha-blockers for bladder neck/sphincter relaxation
Sphincterotomy or urethral stent in selected men with dyssynergia
*Do not use bethanechol - ineffective and poorly tolerated*

C. Protect the upper tracts

Keep detrusor pressures low and residual volumes small - this is the whole point
Surveillance renal ultrasound and UEC (annually in high-risk lesions), periodic urodynamics
Treat reflux and stones

D. Infection

Treat symptomatic UTI only. Do not treat asymptomatic bacteriuria - universal in catheterised and CISC patients, and treating it selects resistance
Symptoms may be atypical: increased spasticity, autonomic dysreflexia, malaise, incontinence

E. Autonomic dysreflexia - the emergency

Lesions at or above T6: noxious stimulus below the lesion (usually a blocked catheter or full bladder) -> unopposed sympathetic surge
- Severe hypertension + bradycardia + pounding headache + flushing and sweating above the lesion, pallor below
- -> sit the patient upright, remove the stimulus (unblock or drain the bladder, check for faecal impaction), then GTN or nifedipine
- Can cause intracerebral haemorrhage and death. It is a bladder problem masquerading as a hypertensive crisis

Renal failure was historically the leading cause of death in spinal cord injury; systematic urological surveillance has largely eliminated it
Risk of upper tract damage tracks detrusor leak point pressure >40 cmH2O and residual volume, not symptoms
Long-term indwelling catheter: stones, recurrent infection, and squamous cell carcinoma of the bladder after ~10 years
Incontinence is a major driver of social isolation, skin breakdown and pressure injury

Monitor

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