Neurogenic Bladder

Author(s): Philippines Cabahug, MD , Shawn Murphy, DO

Originally published:11/10/2011

Last updated:09/18/2015

1. DISEASE/DISORDER:

Definition

Neurogenic bladder is defined as bladder dysfunction resulting from a central or peripheral neurologic insult. Possible symptoms include urinary incontinence, urgency, nocturia, straining, incomplete voiding, and urinary retention.1

Initially, a functional classification was used based on cystometric findings: (1) reflex, (2) uninhibited, (3) autonomous, (4) motor paralytic, and (5) sensory. Presently, a combination of both functional and anatomic classification (based on lesion level) is used (Discussed further under Patho-anatomy/physiology).2

Etiology

Neurogenic bladder can result from nervous system disease. The location and extent of neuologic lesion will affect presentation. Suprapontine causes include stroke, traumatic brain injury, multiple systems atrophy, Alzheimer’s disease, and hydrocephalus.3

Suprasacral causes include demyelination (multiple sclerosis, transverse myelitis), spinal cord injury (SCI), vascular (arteriovenous malformations, spinal cord infarct), neoplasm, hereditary (hereditary spastic paraparesis), infectious (tropical spastic paraparesis), cervical spondylosis, and other disorders affecting the suprasacral spinal cord.3

Infrasacral (spinal root and peripheral) causes include spinal dysraphism, arachnoiditis, intervertebral disk prolapse, cauda equina lesions, diabetes mellitus, hereditary (hereditary motor sensory neuropathy), and iatrogenic (pelvic or retroperitoneal surgery).3

Epidemiology including risk factors and primary prevention

Cerebrovascular pathology, most commonly the lesions in the anteromedial frontal lobe and putamen, can cause neurogenic bladder in 20% to 50% of patients.4-6 If untreated, 20% to 30% of patients will suffer from incontinence 6-months poststroke.4

Most patients with spinal cord lesions and some patients with peripheral neuropathy will develop neurogenic bladder. Fifty percent of diabetics will develop neuropathy, with 75% to 100% of these patients developing lower urinary tract dysfunction.4

Patho-anatomy/physiology

Control of micturition is coordinated between 3 main centers:7

  1. Sacral micturition center (S2-4) ‑ (reflex center) efferent parasympathetic impulses to the bladder causes bladder contraction;
  2. Pontine micturition center ‑ coordinates relaxation of the urinary sphincter when the bladder contracts; and
  3. Cerebral cortex ‑ inhibitory to the sacral micturition center.

Voiding dysfunction can be classified according to the level of the lesion:7

  1. Suprapontine lesions cause involuntary spontaneous or induced contractions of the detrusor muscle. Urodynamic studies show detrusor overactivity without detrusor sphincter dyssynergia.
  2. Suprasacral lesions ‑ in spinal cord lesions, loss of coordinated activity results in detrusor-sphincter dyssynergia (DSD) or simultaneous contraction of the external urethral sphincter and the detrusor. This leads to incomplete bladder emptying and abnormally high bladder pressures. Urodynamics may show detrusor overactivity and DSD.
  3. Infrasacral lesions – damage at this level results in a highly compliant and acontractile bladder. Postvoid residuals (PVR) are more than 100 mL. Urodynamics may show detrusor underactivity and sphincter insufficiency.

Disease progression including natural history, disease phases or stages, disease trajectory (clinical features and presentation over time)

  1. New onset/acute: Many central neurologic disorders temporarily result in an areflexic bladder. During the spinal shock period (6- to 12-weeks postinjury), patients with SCI have a competent bladder neck, but there is detrusor acontractility/underactivity. Urinary retention is common, and incontinence occurs when there is overflow. The return of the bulbocavernosus reflex marks the recovery from spinal shock, at that time detrusor activity returns.7
  2. Subacute and chronic: Once there is recovery from spinal shock, patients with SCI develop incontinence because of involuntary detrusor contractions. Suprasacral lesions can present with high bladder pressures and PVR because of the coexistence of detrusor overactivity with dyssynergia.5

Specific secondary or associated conditions and complications

Detrusor overactivity and reduced bladder wall compliance cause increased bladder pressure, which leads to structural bladder wall changes such as trabeculations and diverticuli.6

Vesicoureteric reflux (VUR) and hydronephrosis may develop with increased bladder pressures (> 40 cm H2O).1 This can lead to renal impairment and even end stage renal disease.1,6 Patients with SCI are prone to upper tract damage and renal disease.6

Genitourinary tract infections, such as cystitis or pyelonephritis, are common. Bladder stones may develop.6

2. ESSENTIALS OF ASSESSMENT

History

History should include the following: symptoms of urinary, bowel, sexual, and neurologic dysfunction and episodes of urinary tract infections (UTI) or autonomic dysreflexia (AD). In obtaining the urinary history, determine voiding pattern, bladder sensation, urinary incontinence, mode, and type of voiding (catheterization). A bladder diary should include day-time and night-time voiding frequency, volumes voided, incontinence, and urge episodes.3,6,8

Physical examination

A detailed physical exam is warranted. Inspection of the abdominal wall, prostate palpation, and observation of pelvic organ prolapse is recommended.8

Full neurologic exam should include mental status and comprehension, sensation in S2 through S5 dermatomes, reflexes, anal sphincter tone and volitional contraction, and pelvic floor function.4

Functional assessment

Assess for physical and mental conditions that could impact mobility and function. Spasticity, for example, impacts ease of care, while cognitive deficits can affect the ability to self-catheterize.8

Laboratory studies

Urinalysis is obtained when symptoms or signs of infection are present.6

Basic metabolic panel ‑ obtain baseline and follow blood urea nitrogen and creatinine concentrations.4

Imaging

Ultrasonography ‑ a portable bladder scanner can be used to determine PVR.6 Annual ultrasound should be performed to assess for renal parenchymal loss, hydronephrosis, hydroureters, or stones.5,9

Voiding cystourethrography ‑ performed if vesicoureteral reflux or urethral strictures is suspected.9

Renal scan ‑ technetium Tc 99m mertiatide nuclear renal scan provides a qualitative assessment of renal function.9

Supplemental assessment tools

Urodynamic studies assess detrusor and bladder outlet function. Uroflowmetry is a noninvasive assessment of voiding. Filling cystometry and pressure-flow studies are more invasive and measure pressure-volume relationships during bladder filling and voiding.3,4

Video-urodynamics provides the most comprehensive information for evaluating neurogenic bladder. It combines filling cystometry and pressure-flow studies with radiologic imaging.8

Electromyography of the pelvic floor muscles, urethral, and/or anal sphincters is a semiquantitative measure used to detect DSD and pelvic-floor relaxation disorders.8

Social role and social support system

Identify the patient’s goals, motivation, and available social support system since those may impact the method of bladder management selected.

3. REHABILITATION MANAGEMENT AND TREATMENTS

Available or current treatment guidelines

Goals of treatment are to protect the upper urinary tract, prevent urinary tract infection (UTI), achieve continence, and improve quality of life.Patients with neurogenic bladder are prone to develop UTI. Screening with a “dipstick test” is indicated in symptomatic patients. Asymptomatic bacteriuria is not an indication for antibiotics unless stone-forming bacteria are present (Proteus Klebsiella, and Serratia species).10 While long-term use of prophylactic antibiotics is typically not indicated, it may sometimes be used for patients with recurrent UTI in the presence of VUR and hydropnephrosis.3

Antimuscarinics are widely used for neurogenic detrusor overactivity. They decrease bladder activity and filling pressures, increase bladder capacity, and compliance. Selective and nonselective alpha-blockers are partially successful in decreasing bladder-outlet resistance. Aside from being used in the treatment of benign prostatic hypertrophy, they can relieve both voiding and bladder storage symptoms. Combination therapy of alpha-blockers with antimuscarinics may be of benefit. There is no evidence of effective drug treatment for neurogenic detrusor underactivity.8

Current pharmacologic agents for bladder management are summarized in table 1 and nonpharmacologic modalities in table 2.

Table 1. Pharmacologic Therapy for Neurogenic Bladder1,12

Medication Side Effect Comments
Antimuscarinic (anticholinergic)
Oxybutynin, tolterodine, trospium, darifenacin, solifenacin, fesoterodine
Dry mouth (most common)
Constipation Blurred vision
Drowsiness
Dry skin, mucosa
Long-term use of oxybutynin has been linked to cognitive deficits.

Newer agents have fewer side effects compared with immediate release oxybutynin.

Alpha-blockers
Terazosin, alfuzosin, doxazosin, tamsulosin, silodosin, alfusozin
Nasal congestion
Abnormal ejaculation (tamsulosin)
Dizziness
Postural hypotension
Terazosin and doxazosin may lead to postural hypotension.
Beta-agonists

Mirabegron

Hypertension, urinary retention, headache, tachycardia Contraindicated in patients with uncontrolled hypertension

 

Table 2. Nonpharmacologic Treatment of Neurogenic Bladder3,7,11

Conservative Comments
Behavioral
Fluid, caffeine regulationTimed voiding, bladder retraining, prompted voiding
Adjust fluid intake if catheterized volumes > 500 mL.

Adapted to patient’s voiding diary, fluid intake, PVRs, and urodynamics parameters.

Techniques to facilitate bladder emptying

Triggered reflex voiding

Crede (bladder compression) and Valsalva (abdominal straining)
Catheterization
Intermittent catheterization

Indwelling catheterization

Not recommended: risk further elevating bladder pressures.Creates high bladder pressures; avoid in reflux, urethral pathology, and UTI.
Consider in lower motor neuron injuries (areflexic bladders) or those who had sphincterotomy.Safe and effective; perform 4-6 x/day with goal catheterized volumes < 500 mL.
Needs sufficient hand skills or willing caregiver.
Avoid in urethral pathology; high fluid intake regimen; bladder capacity < 200 mL; development of AD with bladder filling in spite of treatment; poor cognition, motivation, and compliance.Consider in patients with poor hand skills, high fluid intake, cognitive impairments, elevated detrusor pressures, or need for temporary management of vesicoureteral reflux.Transurethral: use if no blockade or urethral/bladder neck erosion.Suprapubic: use if urethral pathology/catheter obstruction is present or for difficult catheter insertion.
External appliances Condom catheters and pads to achieve social continence.
Surgical
Endourethral stents or transurethral sphincterotomy

 

Bladder augmentation

 

Continent urinary diversion
Electric stimulation and posterior sacral rhizotomy

 

Sacral (InterStim) Neuromodulation

For patients with DSD who want to reflex void but have insufficient hand skills or caregiver assistance.
Patients with overactive detrusor.
Consider if bladder augmentation not feasible or failure of all other treatment.
Cutaneous ileovesicostomy: variant of urinary diversion; ileum connected to bladder and brought to abdominal wall.
Consider in patients with high PVRs, chronic or recurrent UTIs, reduced bladder capacity, and compliance.Most commonly used non-pharmacological modality for overactive bladder symptoms, can also be used for non-obstructive urinary retention; remove prior to getting MRI or turned off in pregnancy
Other interventional procedures
Percutaneous tibial nerve stimulation (PTN)
Botulinum Toxin Type A
Minimally invasive, useful in medically refractory overactive bladder

For overactive bladder/detrusor overactivity

Coordination of care

Multidisciplinary: adopt a comprehensive approach to managing the patient’s urologic, neurologic, functional, and social issues. Maintain regular interaction and consultation between the patient, caregivers, physicians (general practitioner and/or a specialist experienced in neuro-urology, eg, a physiatrist/urologist/neurologist), nurses, and members of the rehabilitation team (physical and occupational therapy). Nurses can evaluate continence needs, trial and adaptation of catheters, and ensure education and follow-up. The therapist can evaluate for barriers to following a catheterization program, such as spasticity, sensory-motor deficits, and cognitive/behavioral issues. They can assess the need for appliances to facilitate catheterization and home modifications.3

Patient & family education

Patients and caregivers have an active role in the management of bladder dysfunction. Specifics have been described earlier.

Translation into practice: practice “pearls”/performance improvement in practice (PIPs)/changes in clinical practice behaviors and skills

A detailed history and physical examination, bladder diary, and PVR measurements are essential in evaluation of neurogenic bladder. Urodynamics are useful in initial evaluation and follow-up.

Urine is not routinely tested unless patients are symptomatic (eg, fever, malaise, increased tone/spasms).

Clean intermittent self-catheterization is the preferred method to facilitate bladder emptying when feasible.

4. CUTTING EDGE/EMERGING AND UNIQUE CONCEPTS AND PRACTICE

Cutting edge concepts and practice

Botulinum neurotoxin (BoNT) injections are an alternative treatment for detrusor/bladder overactivity and DSD. Injections can decrease urethral outlet resistance. BTX causes a reversible chemical denervation that lasts approximately 9 months. The dosage injected into the detrusor depends on the preparation used. Loss of efficacy is not reported with repeated injections. No ultrastructural changes are seen on histologic studies. An occasional adverse effect is generalized muscle weakness.4 It is reported to improve incontinence and increase functional bladder capacity in SCI patients.11 In a recent evidence based review, Level A recommendations support the use of onabotulinumtoxinA (A/Ona) for DSD and neurogenic/idiopathic detrusor overactivity.13 However, a standardized dose and injection protocol remains to be established.5 For neurogenic detrusor overactivity, effective doses were 200-300 units of (A/Ona) into 20-30 sites.13 Intravesical therapies with capsaicin (CAP) and resiniferatoxin (RTX) are used to decrease detrusor overactivity. CAP and RTX act on vanilloid receptors, which desensitizes C-fibers. However, these agents have limited clinical efficacy compared with BTX injections.1

Sacral posterior root rhizotomy with sacral anterior root stimulation can be done to manage refractory involuntary detrusor contractions and underactive detrusor.5,8

5. GAPS IN THE EVIDENCE-BASED KNOWLEDGE

Gaps in the evidence-based knowledge

Additional research is needed to identify optimal measures to prevent complications of neurogenic bladder.

REFERENCES

  1. Cameron AP. Pharmacologic therapy for the neurogenic bladder. Urol Clin North Am. 2010;37:495-506.
  2. Cardenas D, Chiodo A, Samson G. Management of bladder dysfunction. In: Braddom RL, Chan l, Harrast MA, et al, eds. Physical Medicine & Rehabilitation. 4th ed. Philadelphia, Pa: Saunders Elsevier; 2011:604.
  3. Panicker JN, de Seze M, Fowler CJ. Rehabilitation in practice: neurogenic lower urinary tract dysfunction and its management. Clin Rehabil. 2010;24:579-589.
  4. Stohrer M, Blok B, Castro-Diaz D, et al. Guidelines on neurogenic lower urinary tract dysfunction. March 2008. Available at: http://www.uroweb.org/gls/pdf/Neurogenic%20LUTS%202010.pdf. Accessed April 19, 2011.
  5. Jeong SJ, Cho SY, Oh SJ. Spinal cord/brain injury and the neurogenic bladder. Urol Clin North Am. 2010;37:537-546.
  6. Panicker JN, Fowler CJ. The bare essentials: uro-neurology. Pract Neurol. 2010;10:178-185.
  7. Consortium for Spinal Cord Medicine. Bladder management for adults with spinal cord injury: a clinical practice guideline for health-care providers. J Spinal Cord Med. 2006;29:527-573.
  8. Stohrer M, Blok B, Castro-Diaz D, et al. EAU guidelines on neurogenic lower urinary tract dysfunction. Eur Urol. 2009;56:81-88.
  9. Kaynan AM, Perkash I. Neurogenic bladder. In: Frontera WR, Silver JK, Rizzo TDJ, eds. Essentials of Physical Medicine and Rehabilitation: Musculoskeletal Disorders, Pain, and Rehabilitation. 2nd ed. Philadelphia, Pa: Saunders Elsevier; 2008:736.
  10. Favazza T, Midha M, Martin J, Grob BM. Factors influencing bladder stone formation in patients with spinal cord injury. J Spinal Cord Med. 2004;27:252-254.
  11. Lamin E, Smith AL. Urologic agents for treatment of bladder dysfunction in neurologic disease. Curt Treat Options Neurol. 2014; 16:280
  12. Wyndaele JJ, Kovindha A, Madersbacher H, et al. Neurologic urinary incontinence. Neurourol Urodyn. 2010;29:159-164.
  13. Chancellor MB, Elovic E, Esquenazi A, Naumann M. Evidence-based review and assessment of botulinum neurotoxin for the treatment of urologic conditions. Toxicon. 2013; 67: 129-140.

Original Version of Topic

Philippines Cabahug, MD , Shawn Murphy, DO. Neurogenic Bladder.  2011/11/10.

Author Disclosure

Philippines Cabahug, MD
Nothing to Disclose

Shawn Murphy, DO
Nothing to Disclose

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