We need you! See something you could improve? Make an edit and help improve WikSM for everyone.

Cauda Equina Syndrome

From WikiSM
Jump to: navigation, search

Other Names

  • Cauda equina syndrome (CES)

Background

  • CES is a clinical syndrome characterized by compression of the Cauda Equina which results in progressive and potentially permanent neurological dysfunction
    • It is associated with a high risk of morbidity, mortality and litigation and thus physicians should be familiar with its presentation

History

  • Cauda equina first described by a French anatomist Lazarius more than four centuries ago[1]
  • CES first described by Mixter and Barr in 1934[2]

Epidemiology

  • The prevalence in the general population is estimated at 1 in 100,000-130,000 individuals[3]
  • According to one retrospective review, cases caused by disc herniation are 1.8 per 1 million persons[4]
  • Males and females are equally affected (need citation)

Pathophysiology

  • Caused by compression of lumbosacral nerve roots by one of the following
  • Cauda Equina Syndrome is characterized by the some combination of the following symptoms:
    • Lumbar back pain
    • Unilateral or bilateral radicular features
    • Lower extremity weakness
    • Bladder dysfunction
    • Bowel dysfunction
    • Sexual dysfunction
    • Perianal or "saddle" numbness
  • Patterns of presentation[5]
    • Type 1: Due to acute disc herniation
    • Type 2: End point of chronic back pain with or without radicular features
    • Type 3: Insidious with slow progression to neurologic dysfunction

Associated Conditions

Pathoanatomy

  • Cauda Equina
    • Means 'horses tail'
    • Represents the terminal end of the spinal cord at the end of the Conus Medullaris
    • Spinal Cord terminates between L1 and L2
    • Formed by the filum terminale and bundle of nerve roots
  • Cauda Equina particularly susceptible due to
    • No schwann cell protection
    • Relatively hypovascular in the proximal 1/3 of the nerve root

Risk Factors

  • Needs to be updated

Differential Diagnosis

Clinical Features

  • History
    • Patients may report sensory dysfunction of the perianal area
    • Bladder dysfunction typically presents with urinary retention, overflow incontinence
    • Patients may endorse sexual dysfunction (not specific)[6]
  • Physical Exam: Physical Exam Back
    • Important to check rectal tone, perianal sensation
    • Post-void residual, normal is < 200 mL
    • Loss of bulbocavernous reflex
  • Special Tests
    • Post Void Residual: Check bladder with ultrasound after micturation
    • Bulbocavernous Reflex: Stimulation of glans penis or clitoris causes reflexive contraction of anal sphincter

Evaluation

Clinical Diagnosis

  • In patients with low back pain or radicular features, the presence of one of the following suggests the diagnosis of CES
    • Saddle anesthesia
    • Recent onset of bladder dysfunction (such as urinary retention or incontinence)
    • Bowel incontinence
    • Sensory or motor weakness in either of the lower extremities
  • Clinical diagnosis has a false positive rate as high as 43% among resident neurosurgeons[7]

Radiographs

  • Standard Lumbar Spine Radiographs are often used as a screening tool
  • Not useful in detecting CES
  • May demonstrate other findings that can contribute including:
    • Degenerative changes
    • Disc space narrowing
    • Spondylolysis
  • Plain myelography has fallen out of favor due complications, availability of CT and MRI

MRI

  • Imaging modality of choice
  • Evaluates soft tissues including vertebral disc, ligamentum flavum, dural sac, and nerve roots

CT

  • Better evaluation of bone
  • Myelography is reasonable alternative when MRI is unavailable

Other Testing

  • Urodynamic testing
    • Post-void residual should be less than 200 mL
    • More than 200 mL suggests neurogenic bladder dysfunction
  • EMG/NCS
    • Can help confirm nerve dysfunction but is not required for diagnosis

Classification

Gleave and Macfarlane

  • Complete (CES-R)[8]
    • Defined as symptoms + urinary retention
    • 50-70% of patients
  • Incomplete (CES-I)
    • Defined as symptoms without urinary retention
    • 30-50% of patients

Tay and Chacha Classification

  • Type 1: Due to acute disc herniation[9]
    • Patient will have no preceding history of back pain
  • Type 2: End point of chronic back pain with or without radicular features
    • There is also an acute onset of bladder dysfunction
  • Type 3: Insidious with slow progression to neurologic dysfunction

Shephard and Kostuik Classification

  • Type I: Abrupt onset, severe symptoms[10]
    • Poor prognosis for return of bladder function
  • Type II: slower onset, charcterized by prior symptoms
    • Time intervals vary before gradual onset

Shi Classification

  • Stage I: laboratory stage or pre-clinical stage[11]
    • Characterized by no clinical symptoms while electrophysiology had changed
  • Stage II: early clinical stage
    • Characterized by decreased saddle or perianal sensation
  • Stage III: intermediate clinical stage
    • Characterized by lax anal sphincters and change in sexual function
  • Stage IV: advanced clinical stage
    • Characterized by sensory loss and sexual impotence.

Management

Prognosis

  • Overall prognosis is weighted on multiple factors including etiology, speed of onset, duration of compression, degree of neurological deficit, symptoms and signs, and levels of spinal involvement[12]
  • Intervention within 48 hours of symptoms appears to produce better outcomes than delayed intervention[13]
    • Subgroup analysis suggests within 24 hours is better
    • 87% of patients recovered normal bladder function when operated on under 24 hours, those more than 24 hours only had 43% recovery[14]
    • This is the most widely cited study among spinal surgeons
  • Whether outcome is related to timing of surgical intervention is debated
    • Two UK studies found outcome is independent of timing[15]
  • Incontinence at presentation is a poor prognostic indicator[16]

Nonoperative

  • Recommend emergent evaluation and surgical consultation in the setting of suspected CES
  • If pursuing non-operative management, can try several things
  • Vasodilatory agents
    • Prostaglandin E1 improved local blood flow in animal studies[17]
  • Anti-inflammatory agents

Operative

  • Timing
    • Urgency of surgery remains controversial
    • Often difficult to determine time of onset of symptoms
    • Debate of incomplete vs complete CES
  • Indications
  • Technique
    • Ultimately, technique is aimed at underlying etiology, most commonly a disc
    • Discectomy - surgical decompression at the level of the herniation
    • Laminectomy

Rehab and Return to Play

Rehabilitation

  • Needs to be updated

Return to Play

  • Needs to be updated

Complications

  • Need for repeated surgery
  • Chronic pain
  • Chronic neurological deficits

See Also

References

  1. ↑ by a French anatomist Lazarius more than four centuries ago
  2. ↑ by a French anatomist Lazarius more than four centuries ago
  3. ↑ Mooney V. Differential diagnosis of low back disorders: principles of classification. In: Frymore JW, eds. The adult spine. New York: Raven Press; 1991: 1559–1560.
  4. ↑ Podnar S. Epidemiology of cauda equina and conus medullaris lesions. Muscle Nerve 2007;35:529-31.
  5. ↑ DeLong WB, Polissar N, Neradilek B. Timing of surgery in cauda equina syndrome with urinary retention: meta-analysis of observational studies. J Neurosurg Spine 2008;8:305-20.
  6. ↑ Tay EC, Chacha PB. Midline prolapse of a lumbar intervertebral disc with compression of the cauda equina. J Bone Joint Surg Br 1979; 61: 43–46.
  7. ↑ Bell DA, Collie D, Statham PF. Cauda equina syndrome: what is the correlation between clinical assessment and MRI scanning? Br J Neurosurg 2007;21:201-3.
  8. ↑ Gleave JR, Macfarlane R. Cauda equina syndrome: what is the relationship between timing of surgery and outcome? Br J Neurosurg 2002; 16: 325–328.
  9. ↑ Tay EC, Chacha PB. Midline prolapse of a lumbar intervertebral disc with compression of the cauda equina. J Bone Joint Surg Br 1979; 61: 43–46.
  10. ↑ Shephard RH. Diagnosis and prognosis of cauda equina syndrome produced by protrusion of lumbar disk. Br Med J 1959; 2: 1434–1439.
  11. ↑ Shi JG, Jia LS, Yuan W, Ye XJ, Chen DY, Ni B, et al. Clinical stages and early diagnosis of cauda equina syndrome due to lumbo-sacral nerve injury. Orthop J Chin (Chin) 2005; 7: 491–493
  12. ↑ Della-Giustina. Emergency department evaluation and treatment of back pain. Emerg Med Clin North Am 1999; 17: 877–893.
  13. ↑ Ahn UM, Ahn NU, Buchowski JM, Garrett ES, Sieber AN, Kostuik JP. Cauda equina syndrome secondary to lumbar disc herniation: a meta-analysis of surgical outcomes. Spine 2000;25:1515-22.
  14. ↑ Jerwood D, Todd NV. Reanalysis of the timing of cauda equina surgery. Br J Neurosurg 2006;20:178-9
  15. ↑ McCarthy MJ, Aylott CE, Grevitt MP, Hegarty J. Cauda equina syndrome: factors affecting long-term functional and sphincteric outcome. Spine 2007;32:207-16.
  16. ↑ Qureshi A, Sell P. Cauda equina syndrome treated by surgical decompression: the influence of timing on surgical outcome. Eur Spine J 2007;16:2143-51.
  17. ↑ Yamamoto T, Shimoyama N, Asano H, Mizuguchi T. OP-1206, a prostaglandin E1 derivative, attenuates the thermal hyperesthesia induced by constriction injury to the sciatic nerve in the rat. Anesth Analg 1995; 80: 515–520.
Created by:
John Kiel on 14 June 2020 20:50:04
Authors:
Last edited:
5 October 2022 23:57:46
Categories:

Retrieved from "https://wikism.org/w/index.php?title=Cauda_Equina_Syndrome&oldid=18040"