The 5 Minute Urology Consult 3rd Ed.

SPINAL CORD INJURY, UROLOGIC CONSIDERATIONS

Jessica Wetterlin, MD

Derek Matoka, MD

BASICS

DESCRIPTION

• Spinal cord injury (SCI) may result from damage to the spinal column secondary to trauma, vascular injury, infection, or disc prolapse

• SCI can impact lower urinary tract and sexual function and varies based on level and completeness of injury

• Upper and lower urinary tract dysfunction due to SCI can lead to significant morbidity/mortality

– Increased risk for renal failure, UTI (urinary tract infection), renal/bladder calculi, and malignancy

EPIDEMIOLOGY

Incidence

40 cases per million in US; 12,000 new cases per year (1)

Prevalence

• 270,000 people alive in US in 2012 with SCIs

• Extent of lesion

– SCI are graded using the ASIA scale (American Spinal Injury Association)

– 45% of injuries are neurologically complete (ASIA grade A), 55% incomplete (ASIA B-D)

• Age: SCI previously affected young adults with most injuries occurring between the ages of 16 and 30. Since 2005, the average age of injury is 41 yr

• 53% tetraplegia, 46% paraplegia, and less than 1% experience complete neurologic recovery

• Gender: 80.6% of spinal cord injured patients in US are male

• Race/ethnicity: Since 2005, 66% of SCI patients are Caucasian, 26.2% African American, 2.1% Asian, and 0.9% Native American

RISK FACTORS

• Trauma

– Since 2005, motor vehicle accidents account for nearly 40% of SCI cases, followed by falls and acts of violence (primarily gunshot wounds)

• Vascular injury

• Disc prolapse

• Spinal cord tumors

Genetics

Congenital malformations (myelodysplasia)

PATHOPHYSIOLOGY

• Spinal control of micturition is located at the S2–S4 level of the spinal cord

• The sacral cord begins at spinal column level T12–L1. The cord terminates in the cauda equina at approximately spinal column level L2

• Spinal shock = a period of decreased excitability of spinal cord segments at or below the level of the lesion

– Involves suppression of autonomic and somatic activity resulting in an acontractile, areflexic bladder

– Bladder neck (smooth sphincter) generally remains competent/closed

– Urinary retention is generally the rule

– Generally lasts 6–12 wk after injury

• A significant association exists between the level of a spinal cord lesion and the corresponding bladder and sphincter behavior

• Most patients with complete SCI show clinical signs and symptoms of bladder dysfunction; incomplete SCI demonstrates variable function

– Suprasacral lesions generally result in an upper motor neuron deficit with NDO (neurogenic detrusor overactivity) with or without DSD (detrusor sphincter dyssynergia)

– Sacral lesions generally produce a lower motor neuron deficit with resulting detrusor areflexia

• NDO: Involuntary detrusor contraction during the filling and storage phase

– Symptoms: Urinary urgency, frequency, incontinence

– Can lead to upper tract damage due to detrusor hypertonicity, high voiding pressures, high-pressure reflux, recurrent UTIs and their sequelae

• DSD: Abnormal reflexive sphincter contraction during involuntary detrusor contraction

– Causes bladder outflow obstruction, increased post void residuals (PVRs) and elevated intravesical pressures

– Can lead to damage to upper tracts, UTIs, urolithiasis

– Intravesical pressure >40 cm H2O is responsible for sequelae of NDO-DSD

– DO (detrusor overactivity) must be present for DSD, but NDO may occur without DSD

– 10–20% of patients have internal (bladder neck) sphincter dyssynergia with external sphincter dyssynergia

• Detrusor areflexia

– Results from damage to sacral reflex arc which results in absent detrusor contraction

– Results in low-pressure storage (volumes up to 500 mL)

– Decreased risk of upper tract damage

ASSOCIATED CONDITIONS

Arachnoiditis, Guillain–Barré, multiple sclerosis, spinal stenosis, transverse myelitis, tumor, or malignancy

GENERAL PREVENTION

• Drive safely, wear seatbelt, prevent falls

• Prevent secondary complications of SCI

DIAGNOSIS

HISTORY

• Onset, duration, etiology of injury

• Voiding symptoms

– Irritative or obstructive

– Incontinence: Stress, urge, overflow

• Method of urinary management

– Voluntary voiding, clean intermittent catheterization (CIC), indwelling catheter or Credé/Valsalva voiding with or without external catheter

• Urinary tract infection (UTI)

– Associated symptoms, severity, and frequency of recurrence

• Urolithiasis episodes, interventions, calculus composition

• Erectile dysfunction

PHYSICAL EXAM

• Temperature, blood pressure

• Palpable flank mass/tenderness

• Suprapubic fullness: Distended bladder

• Evaluate incontinence; spontaneous or with stress maneuvers

• GU exam for testicular or prostate abnormality

• Complete Neurologic exam: Sensation, tone, and sphincter control

• Bulbocavernosus reflex: Contraction of anal sphincter with stimulation of glans penis/clitoris

DIAGNOSTIC TESTS & INTERPRETATION

Lab

• Blood studies:

– Serum chemistry: Basic metabolic panel (BMP) (assess renal function and acidosis), CBC

– Urinalysis

Imaging

• Renal US (ultrasound): To screen for calculi, hydronephrosis, masses

• VCUG (voiding cystourethrogram)

– Trabeculation, diverticulum, incomplete emptying, vesicoureteral reflux

• Nuclear medicine renal scan:

– Performed to evaluate for compromised function or presence of obstructive element

Diagnostic Procedures/Surgery

• PVR: To ensure complete bladder emptying

• Video urodynamics: Essential to assess and follow bladder dynamics and anatomical changes so that effective urologic management can be tailored appropriately

Pathologic Findings

Bladder wall thickening and fibrosis common

DIFFERENTIAL DIAGNOSIS

• Infection

• Intervertebral disc disease

• Malignancy (metastasis)

• Spinal cord vascular disease

• Traumatic

• Vertebral body injury

TREATMENT

GENERAL MEASURES

• Goal of treatment: Optimize intravesical bladder pressures to protect upper urinary tract

• Spontaneous voiding with continence

• Indwelling catheterization should be avoided when possible to avoid complications (urethral strictures, UTIs, calculi, malignancy)

– Indwelling urethral catheter or suprapubic tube (SPT)

• Intermittent self-catheterization: Most effective treatment, requires manual dexterity

– If unable to self-catheterize urethra

Males: External catheter, outlet obstruction procedure, urinary diversion, or creation of continent catheterizable stoma

Females: Urinary diversion or creation of continent catheterizable stoma

– Incontinence between catheterizations may suggest elevated intravesical pressure due to poor compliance or DO

Reduce storage pressure: Increase frequency of catheterizations, anticholinergics, or augmentation cystoplasty

• Lower urinary tracts that cannot be reconstructed require urinary diversion with or without cystectomy

– Incontinent urostomy

– Continent urinary reservoir

MEDICATION

First Line

• Anticholinergics improve urinary storage pressure and decrease involuntary contraction

– Oxybutynin 5 mg PO BID–TID

– Tolterodine 2 mg PO BID, others

• α-adrenergic blockers: Decrease internal sphincter function, lower voiding pressures; ineffective for DSD

– Agents include: doxazosin 1–8 mg PO QD, terazosin 1–10 mg PO QHS, tamsulosin 0.4 mg PO QD

Second Line

Botulinum toxin injected into detrusor

SURGERY/OTHER PROCEDURES

• Sphincterotomy: Requires external catheter

• Augmentation cystoplasty: Use of intestinal segment to enlarge the bladder, increasing bladder volume to decrease intravesical pressure

– Usually requires clean intermittent catheterization (CIC)

• Ileovesicostomy

– Useful for those unable to perform CIC

• Sacral neuromodulation

– Deafferentation with dorsal rhizotomy abolishes spontaneous detrusor contraction, improving urinary storage

– Nerve root stimulation allows for control over detrusor contraction

ADDITIONAL TREATMENT

Radiation Therapy

N/A

Additional Therapies

Sacral nerve root stimulator

Complementary & Alternative Therapies

Vanilloid agents (capsaicin and resiniferatoxin) suppress uninhibited detrusor contraction

ONGOING CARE

PROGNOSIS

• Proper urologic care improves morbidity, mortality, and quality of life in SCI individuals

• Early data suggested renal disease was major cause of death in the paraplegic patient. However more recent data has revealed that pneumonia, septicemia, heart attack, accidents, and suicides are now leading causes of morbidity (2)

COMPLICATIONS

• UTI/sepsis (3)

• Urolithiasis

– Due to urinary stasis, chronic infection, acidosis associated with immobility, bladder calculi related to chronic indwelling catheters

• Upper urinary tract deterioration

– Hydroureteronephrosis due to elevated intravesical pressure

• Lower urinary tract deterioration

– Detrusor hypertrophy, decreased compliance

– Urethral erosion, fistula with chronic catheterization

• Autonomic dysreflexia

– Can occur with SCI at T6 level or higher, with complete/incomplete spinal cord lesions

– Triggered by a noxious stimuli below the level of the lesion; bladder and bowel manipulation are the most common causes

– Unopposed sympathetic activity results in vasoconstriction and HTN (hypertension)

– HTN sensed by baroreceptors in carotid and aortic arch activating parasympathetics above lesion to counter the sympathetic response. However, the SCI inhibits parasympathetic activity below the level of the lesion

– Signs and symptoms include HTN, headache, bradycardia, flushing, diaphoresis, blurred vision

Treatment: Remove offending stimuli

Address HTN with rapid onset/short duration agent (nifedipine, captopril, hydralazine)

• Neoplastic transformation

– Associated with chronic catheter

• Depression

• Skin complications (related to incontinence)

FOLLOW-UP

Patient Monitoring

• UTI screening: Routine urine cultures are unnecessary in healthy, asymptomatic individuals.

• UDS: Completed periodically. However, no consensus exists regarding frequency. Obtain UDS after resolution of spinal shock and every 5 yr in stable patients. If a change in bladder-related symptoms (incontinence) is noted, UDS should be repeated to evaluate for change in bladder dynamics.

• Renal US: Useful, noninvasive screening method to monitor upper and lower tracts.

– Recommended initially and annually for 5–10 yr, then every other year.

• Basic metabolic panel: Biennially.

• Renal function scan: In setting of progressive hydroureteronephrosis on renal US.

• Bladder cancer surveillance: Cystoscopy is recommended annually for patients with chronic indwelling catheters or augmentation cystoplasty.

Patient Resources

None

REFERENCES

1. National Spinal Cord Injury Statistical Center. Spinal cord injury facts and figures at a glance. J Spinal Cord Med. 2013;36(1):1–2.

2. Cameron AP, Rodriguez GM, Schomer KG. Systematic review of urological follow-up after spinal cord injury. J Urol. 2012;187:391–397.

3. Patki P, Woodhouse J, Hamid R, et al. Lower urinary tract dysfunction in ambulatory patients with incomplete spinal cord injury. J Urol. 2006;175:1784–1787.

ADDITIONAL READING

Tapia C, Khalaf K, Berenson K, et al. Health-related quality of life and economic impact of urinary incontinence due to detrusor overactivity associated with a neurologic condition: A systematic review. Health Qual Life Outcomes. 2013;11:13.

See Also (Topic, Algorithm, Media)

• Autonomic Dysreflexia

• Bladder Areflexia (Detrusor Areflexia)

• Detrusor-Sphincter Dyssynergia (DSD)

• Neurogenic Bladder, General

• Neurogenic Detrusor Overactivity (NDO)

• Spinal Cord Injury, Urologic Considerations Images

• Urodynamics, Indications and Normal Values

CODES

ICD9

• 586 Renal failure, unspecified

• 599.0 Urinary tract infection, site not specified

• 952.9 Unspecified site of spinal cord injury without evidence of spinal bone injury

ICD10

• N19 Unspecified kidney failure

• N39.0 Urinary tract infection, site not specified

• S34.109A Unsp injury to unsp level of lumbar spinal cord, init encntr

CLINICAL/SURGICAL PEARLS

• Suprasacral lesions generally result in an upper motor neuron deficit with NDO.

• Sacral lesions generally produce a lower motor neuron deficit with resulting detrusor areflexia.

• UDS should be obtained at least 6 wk after injury and repeated when appropriate.



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