Neurogenic Bladder

Neurogenic bladder is bladder dysfunction that may be either flaccid or spastic. It is caused by neurological damage. The main symptom is overflow incontinence.

Any condition that impairs bladder and bladder outlet afferent and efferent signalling can cause neurogenic bladder. Causes may involve:

• Central nervous system (CNS):
  • Cerebrovascular event
  • Spinal injury
  • Meningomyelocele
  • Amyotrophic lateral sclerosis
• Peripheral nervous system (PNS):
  • Diabetes
  • AIDS
  • Alcohol
  • Vitamin B12 deficiency neuropathies
  • Herniated disc
  • Damage due to pelvic surgery
• Mixed CNS and PNS
  • Parkinson's disease
  • Multiple sclerosis
  • Syphilis
  • Tumours

Bladder outlet obstruction often co-exists and may exacerbate symptoms.

Flaccid (hypotonic) neurogenic bladder

In this condition the bladder volume is large, pressure is low and contractions are absent.¹ It may result from peripheral nerve damage or spinal cord damage at the S2 to S4 level. After acute cord damage, initial flaccidity may be followed by long-term flaccidity or spasticity, or bladder function may improve after days, weeks or months.

Spastic bladder

In spastic bladder the volume is normal or small and involuntary contractions occur. It usually results from brain damage or spinal cord damage above T12. Precise symptoms vary by site and severity of the lesion. Bladder contraction and external urinary sphincter relaxation are typically unco-ordinated (detrusor-sphincter dyssynergia).

Mixed patterns

Mixed patterns (flaccid and spastic bladder) may be caused by many disorders, including syphilis, diabetes mellitus and brain or spinal cord tumours.

Overflow incontinence is the primary symptom in patients with a flaccid or spastic bladder. Patients retain urine and have constant overflow dribbling. Men typically also have erectile dysfunction. Patients with spastic bladder may have frequency, nocturia, and urgency or spastic paralysis with sensory deficits.

• Post-void residual volume
• Renal ultrasonography
• Serum creatinine
• Usually cystography, cystoscopy and cystometrography with urodynamic testing

Diagnosis is suspected clinically.
Usually post-void residual volume is measured, renal ultrasonography is done to detect hydronephrosis and serum creatinine is measured to assess renal function.

Further studies are often not obtained in patients who are not able to self-catheterise or able to go to the bathroom, e.g. severely debilitated elderly or post-stroke patients.

In patients with hydronephrosis or nephropathy who are not severely debilitated, cystography, cystoscopy, and cystometrography with urodynamic testing are usually recommended and may guide further therapy:

• Cystography is used to evaluate bladder capacity and detect reflux.
• Cystoscopy is used to evaluate duration and severity of retention (by detecting bladder trabeculations) and to check for bladder outlet obstruction.
• Cystometrography can determine whether bladder volume and pressure are high or low; if done during the recovery phase of flaccid bladder after spinal cord injury, it can help evaluate detrusor functional capacity and predict rehabilitation prospects.
• Urodynamic testing of voiding flow rates with sphincter electromyography can show whether bladder contraction and sphincter relaxation are co-ordinated.

General measures

General treatment includes:

• Renal function monitoring
• Control of UTIs
• High fluid intake to decrease risk of UTIs and urinary calculi (although this measure may exacerbate incontinence)
• Early ambulation/maintaining mobility
• Frequent changes of position
• Dietary calcium restriction (to inhibit calculus formation)
• Consideration of absorbent products to protect skin and clothing²
• Urethral occlusive devices (artificial devices that may be inserted into the urethra or placed over the urethral meatus to prevent urinary leakage)

Specific treatment

Cochrane reviews of this area have found little evidence to inform best practice. A review of intermittent self-catheterisation regimens found insufficient evidence to determine which catheter type or technique was best.³

• Catheterisation
• Increased fluid intake
• Surgery (as last resort)

Immediate continuous or intermittent catheterisation

This is needed for a flaccid bladder, especially if the cause is an acute spinal cord injury. Intermittent self-catheterisation is preferable to indwelling urethral catheterisation, which has a high risk of recurrent UTIs and, in men, a high risk of urethritis, periurethritis, prostatic abscesses, and urethral fistulas. Intermittent catheterisation has several advantages over other techniques, including fewer infections, reduced equipment needs and greater independence.³ However, the patient (or carer) must be able and willing to perform the procedure so it may not always be practical. Suprapubic catheterisation may be used if patients cannot self-catheterise.

Techniques to trigger voiding

For spastic bladder, treatment depends on the patient's ability to retain urine.
Patients who can retain normal volumes can use techniques to trigger voiding, e.g. applying suprapubic pressure, scratching the thighs; anticholinergics may be effective. For patients who cannot retain normal volumes, treatment is the same as that of urge incontinence and sacral nerve stimulation.

Surgery

This is a last resort. It is usually indicated if patients have had, or are at risk of, severe acute or chronic sequelae, or if social circumstances, spasticity or quadriplegia prevent use of continuous or intermittent bladder drainage:

• Sphincterotomy (for men) converts the bladder into an open draining conduit.
• Sacral (S3 and S4) rhizotomy converts a spastic into a flaccid bladder.
• Urinary diversion may involve an ileal conduit or ureterostomy.

An artificial, mechanically-controlled urinary sphincter, surgically inserted, is an option for patients who have adequate bladder capacity, good bladder emptying, and upper extremity motor skills and who can comply with instructions for use of the device; if patients do not comply, life-threatening situations (e.g. renal failure, urosepsis) can result.

Risk of serious complications, e.g. recurrent infection, vesicoureteral reflux, and autonomic dysreflexia, is high.
Common complications include:

• Recurrent UTIs and urinary calculi.
• Hydronephrosis with vesicoureteral reflux may occur because the large urine volume puts pressure on the vesicoureteral junction, causing dysfunction with reflux and, in severe cases, nephropathy.
• Patients with high thoracic or cervical spinal cord lesions are at risk of autonomic dysreflexia (a life-threatening syndrome of malignant hypertension, bradycardia or tachycardia, headache, piloerection, and sweating due to unregulated sympathetic hyperactivity). This disorder may be triggered by acute bladder distention (due to urinary retention) or bowel distention (due to constipation or faecal impaction).

Prognosis is good if the disorder is diagnosed and treated before kidneys are damaged