Spinal Cord Trauma
Howard B. Levene
Michael Y. Wang
Barth A. Green
Timothy A. Emhoff
I. EPIDEMIOLOGY AND CLINICAL SIGNIFICANCE
A. Affects approximately 11,000 Americans per year.
B. A total of 200,000 patients living with spinal cord injury (SCI).
C. Typically affects young males (15 to 29 years), but a growing trend of middle-aged and elderly patients due to lifestyle habits and improved survivability of injuries.
D. Etiology.
1. Motor vehicle accident 47%.
2. Falls 23%.
3. Violence 14%.
4. Sports/recreation 9%.
5. Other 7%.
II. NEUROLOGIC INJURY
A. SCI can be classified by the following:
1. Mechanism (penetrating vs. blunt trauma).
2. Level (cervical, thoracic, or lumbar).
a. Designated as the lowest spinal segment with completely normal function.
3. Neurologic injury (degree of impairment), frequently designated by the American Spinal Injury Association (ASIA) grade (Table 112-1).
a. Grade A Complete: no sensory or motor function preserved in sacral segments S4-5.
b. Grade B Incomplete: sensory, but not motor, function preserved below neurologic level and extends through sacral segments S4-5.
c. Grade C Incomplete: motor function preserved below neurologic level with muscle grade less than antigravity strength.
d. Grade D Incomplete: motor function preserved below neurologic level with muscle grade greater than or equal antigravity strength.
e. Grade E Normal: sensory and motor functions normal.
B. Complete SCI.
1. No preservation of motor function and/or sensation three spinal segments below the level of injury.
2. Complete injuries above T6 can be associated with neurogenic shock (usually with cervical spine injury).
a. Hypotension from interruption of sympathetics.
b. Bradycardia from unopposed vagal (parasympathetic) output.
TABLE 112-1 American Spinal Injury Association Grading Scale for Spinal Cord Injury | ||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
c. Hypothermia: vasodilation.
d. Transient loss of all neurologic function resulting in flaccid paralysis and areflexia: spinal shock.
C. Incomplete SCI.
1. Any preservation of motor and/or sensory function three spinal segments below level of injury, including sphincter tone or sacral sensation: so-called “presacral sparing.”
2. Denotes improved likelihood of recovery of function.
D. Specific incomplete SCI syndromes.
1. Central cord syndrome.
a. Occurs in two patient populations: young athletes with congenital cervical stenosis and, more commonly, in the elderly with acquired cervical stenosis from spondylosis.
b. Hyperextension injury.
c. Upper extremity weakness out of proportion to lower extremity weakness: lower extremities recover more than upper: usually associated with residual upper extremity weakness.
d. No evidence of cervical spine fracture.
2. Brown-Sequard syndrome (usually from penetrating mechanisms).
a. Spinal cord hemisection.
b. Loss of contralateral pain and temperature sensation; ipsilateral loss of proprioception, vibratory sensation, and motor function.
3. Anterior cord syndrome.
a. Spinal cord infarction in distribution of anterior spinal artery (anterior two-thirds of cord).
b. Complete loss of motor function and loss of pain and temperature sensation, but preserved posterior column function (proprioception and vibratory sensation).
4. Conus medullaris syndrome.
a. Associated with thoracolumbar junction fracture.
b. Early loss of sexual and sphincter function.
c. Symmetric “saddle” loss of motor and/or sensory function in lower extremities.
III. PATHOPHYSIOLOGY
A. SCI is comprised of primary and secondary injury mechanisms.
1. Primary injury mechanisms.
a. Kinetic energy transferred to neural elements during trauma.
b. Compression from bone, cartilage, hematoma, or foreign bodies.
c. Results from:
i. Movement and stressing of the spine beyond its physiologic limits in hyperflexion or hyperextension.
ii. Retropulsion of bone or disc into the spinal canal.
iii. Dislocation of the spinal column.
iv. Direct laceration or transection of the cord (penetrating injury).
2. Secondary injury mechanisms.
a. Systemic hypoxia and hypotension from neurogenic shock, hypoperfusion, hypoxia, or other systemic injuries resulting in hemodynamic, pulmonary, or respiratory instabilities.
b. Local vascular insufficiency of the cord from trauma.
c. Ongoing spinal compression (herniated disk, compressive hematoma, malalignment).
d. Biochemical changes: free radicals, cytokines (see reference below).
e. Electrolyte shifts (in to/out of the damaged cord).
f. Edema.
g. Loss of energy metabolism with decreased adenosine triphosphate (ATP) production.
IV. INITIAL ASSESSMENT AND STABILIZATION
A. Primary trauma survey (Airway, Breathing, Circulation, Disability, Exposure [ABCDE]).
1. Special attention to hemodynamic stability to maintain cord perfusion and management of neurogenic shock.
a. Judicious crystalloid fluid resuscitation.
b. Search for and control of sources of ongoing hemorrhage.
c. Early use of pressors (alpha-adrenergic) to maintain mean arterial pressure (MAP) > 80 mm Hg to combat loss of sympathetic tone.
