Thursday, January 7, 2010

SCIWORA (spinal cord injury without radiologic abnormality)

SCIWORA (spinal cord injury without radiologic abnormality)


http://www.orthopaedia.com/display/Main/Spinal+cord+injury (My article on ORTHOPAEDIA)
The term SCIWORA (spinal cord injury without radiologic abnormality) originally referred to spinal cord injury without radiographic or CT evidence of fracture or dislocation.However with the advent of MRI, the term has become ambiguous. Findings on MRI such as intervertebral disk rupture, spinal epidural hematoma, cord contusion, and hematomyelia have all been recognized as causing primary or secondary spinal cord injury.
SCIWORA should now be more correctly renamed as "spinal cord injury without neuroimaging abnormality" and recognize that its prognosis is actually better than patients with spinal cord injury and radiologic evidence of traumatic injury.

History

1969 : mentioned in medical literature as a unique syndrome in study of 29 children with traumatic paraplegia where 16 had no x-ray findings, done at NSIC Aylesbury, Buckinghamshire, England.
1982 : First coined by Pang and Wilberger, defined the term SCIWORA as "objective signs of myelopathy as a result of trauma" with no evidence of fracture or ligamentous instability on plain spine radiographs and tomography.

Definition

SCOWORA is defined as the occurrence of acute traumatic myelopathy despite normal plain radiographs and normal computed tomography (CT) studies.


Prevalence
  • occurs most often in pediatric population; range from birth to 16 yrs
  • a true incidence is probably close to 20% of all pediatric spinal cord injuries
    • accounts for up to 30% of severe cervical injuries in children 8 years of age and younger
    • 10% in children 9-16 yrs
    • children < 8yrs have worse prognosis.
  • cervical, thoracic SCI common, lumbar rare.
Inherent elasticity in pediatric cervical spine can allow severe spinal cord injury to occur in absence of x-ray findings due to:
  1. Extreme flexion
  2. Hyperextension
  3. Distraction of spinal column

Mechanism of Injury

  1. Direct spinal cord traction
    1. Longitudinal cord traction
    2. Root traction/avulsion
  2. Direct spinal cord compression
    1. Transient compression
      1. Ligamentous bulging
      2. Reversible disc protrusion
      3. Transient subluxation of vertebrae
    2. Persistent compression (potentially requires operative intervention)
      1. Occult fracture with cord compression
      2. Spinal epidural hematoma
      3. Persistent disc herniation
      4. Occult subluxation/instability
  3. Indirect spinal cord injury
    1. Transmission of externally applied kinetic energy to spinal cord-Spinal cord concussion (SCC)
  4. Vascular/ischemic injury
    1. Vascular occlusion, dissection, cord infarction
    2. Vasospasm
    3. Hypotension, impaired cord perfusion.
    Mainly due to MVA (motor vehicle accident) or MV - pedestrian accident, fall, or sports injury (football, diving,wrestling, gymnasts).
Mainly due to MVA (motor vehicle accident) or MV- pedestrian accident, fall, or sports injury (football, diving, wrestling, gymnasts)

Pathogenesis

  • transverse atlantal ligament injury
  • fracture through the cartilaginous end plates (which are not visualized by x-rays), may be among the causes of this injury
  • unrecognized interspinous ligamentous injury
    • in above 2 situations, flexion & extension views taken with pt awake and physician in attendance will demonstrate injury
  • adult with acute traumatic disc prolapse
  • cervical spondylosis
  • C-spine trauma occurs w/ hyperextension injury to spine w/ vertebral canal whose diameter is already comprimised by spondylosis
  • excessive anterior buckling of ligamentum flavum into canal already compromised by posterior vertebral body osteophytes probably is cause of central cord syndrome:
    • motor loss in arms > than in legs, & variable sensory loss
    • typically, pts are managed nonsurgically w/ orthosis, & their neurologic status is carefully monitored.
Diagnosis
Typical clinical history:
A two and a half year old boy presented to us with 2 day history of paucity of movement of both legs, inability to bear weight on his legs, and inability to pass urine. Previous day in the afternoon he had fallen from a tractor. There was no history of any injury to head, unconsciousness, bleeding from ear nose or throat or any seizures. Child was moving his legs after he fell and there was no deformity of legs or spine. Next day when the child woke up, the parents noted that the child was not moving his legs and was not able to sit without support. There was no history of fever or vomiting, no history of any paucity of movement or weakness in upper limbs or any history suggestive of cranial nerve involvement. There was no breathing difficulty or bowel incontinence. On general examination, there was pallor. There was no evidence of any fracture of limb bones, lacerations or deformity or tenderness over the spine. Neurological examination revealed a conscious child with normal cranial nerves and upper limbs. There was gross hypotonia in the lower limbs, 0/5 power and areflexia. Abdominal reflex, cremasteric, anal reflex were absent. Bladder was palpable and urine could be expressed out on abdominal pressure. There were no meningeal or cerebellar signs.
Neurological presentation:
  • wide spectrum of neurological dysfunction, ranging from mild, transient spinal cord concussive deficits to permanent, complete injuries of the spinal cord, incidence and severity are related to the patient's age.
    • Young children have a higher incidence of SCIWORA
    • Transient neurological deficit (i.e. paraparesis or quadriparesis), or persisting subjective symptoms (i.e. numbness or dysesthesias) would be a candidate for the diagnosis of SCIWORA.
  • Pang and Wilberger described 13 of their 24 children to have a "latent" period from 30 minutes to four days (mean 1.2 days) before the onset of objective sensorimotor deficits.
Protocols
Standards: There is insufficient evidence to support diagnostic standards.
Guidelines: There is insufficient evidence to support diagnostic guidelines.

Options:
  • Plain spinal radiographs of the region of injury and CT scan with attention to the suspected level of neurological injury to exclude occult fractures are recommended.
  • MR of the region of suspected neurological injury may provide useful diagnostic information.
  • Plain radiographs of the entire spinal column may be considered.
  • Neither spinal angiography nor myelography is recommended in the evaluation of patients with SCIWORA.
Diagnosis of exclusion:
  • MRI may give a more anatomic diagnosis by showing hemorrhage or edema of the spinal cord;
  • pseudosubluxation: anterior displacement may be up to 4 mm;
  • SSEPs: Somatosensory Evoked Potentials, are electrophysiologic response of nervour system to sensory stimulation, used not diagnostically, but to test neurologic function, can relate any decrease or absence of impulse transmission through the spinal cord, obtained within 24 hrs of admission and compared in follow up analysis.

Differential diagnosis

  • Traumatic compressive myelopathy (compression by fractured vertebrae, disc herniation etc)
  • Acute disseminated encephalomyelitis
  • Transverse myelitis

Treatment

Spine is immobilized for one to three weeks;
Standards: There is insufficient evidence to support treatment standards.
Guidelines: There is insufficient evidence to support treatment guidelines.
Options:
  • External immobilization is recommended until spinal stability is confirmed flexion and extension radiographs.
  • External immobilization of the spinal segment of injury (collar or a more rigid brace) for up to 12 weeks may be considered.
  • Avoidance of "high-risk" activities for up to six months following SCIWORA may be considered.
  • Hard collar immobilization for patients with cervical level SCIWORA for 12 weeks
    • avoidance of activities that encourage flexion and extension of the neck for an additional 12 weeks has not been associated with recurrent injury.
  • Once deficits have resolved range of motion is gradually increased.
    • To avoid the risk of recurrent injury, activity should be strictly limited for at least 3 months.
  • High dose steroids
    • Methylprednisolone bolus of 30 mg/Kg iv within 8 hr s of injury, followed by infusion at 5.4 mg/Kg/hr for the next 23 hrs is beneficial in improving the outcome.
    • When given over 48 hrs outcome at 6 wks and 6 months was better in a recent study.
    • Role of stem cell transplant is emerging.
Nursing Management:
  • spine stabilization,
  • patient & parents counseling & explanation,
  • regular neuro assessment;
  • caution in turningpositioning,
  • suctioning,
  • prevention of complications like pressure sore, pulmonary side effect, contractures.

Prognosis

Standards: There is insufficient evidence to support prognostic standards.
Guidelines: There is insufficient evidence to support prognostic guidelines.
Options: MRI of the region of neurological injury may provide useful prognostic information about neurological outcome following SCIWORA.
Two greatest dangers:
  1. delay in onset or deterioration of neurologic symptoms
  2. recurrent injury

References

1. Bracken MB, Shepard MJ, Collins WF, Holford TR, et al: A randomized trial of methylprednisolone or naloxone in the treatment of acute spinal cord injury: Results of the second National Acute Spinal Cord Injury Study (NASCIS II). N Engl J Med 322:1405-1411,1990.
2. Davis PC, Reisner A, Hudgins PA, Davis WE, O'Brien MS: Spinal injuries in children:Role of MR. AJNR 14:607-617-1993.
3. Dickman CA, Zabramski JM, Hadley MN, Rekate HL, Sonntag VKH: Pediatric spinal cord injury without radiographic abnormalities. J Spinal Disorders 4:296-305,1991.
4. Eleraky MA, Theodore N, Adams M, Rekate HL, Sonntag VKH: Pediatric cervical spine injuries: report of 102 cases and review of the literature. J Neurosurg (Spine) 92:12-17, 2000.
5. Grabb PA, Pang D: Magnetic Resonance imaging in the evaluation of spinal cord injury without radiographic abnormality in children. Neurosurgery 35:406-414, 1994.
6. Hadley MN, Zabramski JM, Browner CM, Rekate H, Sonntag VKH: Pediatric spinal trauma. J Neurosurg 68:18-24,1988.
7. Hamilton MG, Myles ST: Pediatric spinal injury: review of 174 hospital admissions. J Neurosurg 77:700-704, 1992.
8. Osenbach RK, Menezes AH: Spinal cord injury without radiographic abnormality in children. Pediatr Neurosci 15:168-175, 1989.
9. Osenbach RK, Menezes AH: Pediatric spinal cord and vertebral column injury. Neurosurgery 30:385-390, 1992.
10. Pang D, Wilerger JE: Spinal cord injury without radiographic abnormalities in children J Neurosurg 57:114-129, 1982.
11. Pang D, Pollack IF: Spinal cord injury without radiographic abnormality in children-The SCIWORA syndrome. J Trauma 29:654-664, 1989.
12. Pollack IF, Pang D, Sclabassi R: Recurrent spinal cord injury without radiographic abnormalities in children. J Neurosurg 69:177-182, 1988.
13. Rathbone D, Johnson G, Letts M: Spinal cord concussion in pediatric athletes. J Ped Orthop 12:616-620, 1992.
14. Ramon S, Dominguez R, Ramirez L, Paraira M, Olona M, Castello T, Garcia-Fernandez L: Clinical and magnetic resonance imaging correlation in acute spinal cord injury. Spinal Cord 35:664-673, 1997.
15. Rossitch E, Oakes WJ: Perinatal spinal cord injury. Pediatr Neurosurg 18: 149-152, 1992.
16. Ruge JR, Sinson GP, McLone DG, Cerullo LJ: Pediatric spinal injury: the very young. J Neurosurg 68:25-30, 1988.
17. Turgut M, Akpmar G, Akalan N, Ozcan OE: Spinal injuries in the pediatric age group. EurSpine J 5:148-152, 1996.