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Introduction

Spinal cord injury (SCI) is defined as an insult to the spinal cord resulting in an either temporary or permanent change of normal motor, sensory, or autonomic function. The extent of damage to the spinal cord depends on various factors, particularly the energy of the trauma, and may result in immediate death due to loss of respiratory function. Also depending on the extent of SCI, patients may experience sequelae such as multi-organ dysfunction, autonomic dysregulation, ventilator dependence, pressure ulcers, bowel and bladder problems, and neuropathic pain. Patients with complete spinal cord injuries have significant disability and place a great psychosocial burden on their family members and/or caretakers. Traumatic SCI remains a costly problem for society, with direct medical expenses accrued over the lifetime of one patient estimated to range from $500,000 to $2 million.1

Anatomy

The spinal cord lies within the spinal canal of the vertebrae protected by cerebrospinal fluid, meninges, ligaments, bone and muscle. It extends from the base of the medulla and most commonly ends at the level of the L1-L2 disc space with the conus medullaris. Injuries below the conus medullaris are not considered SCIs, as they affect the nerve roots of the lumbosacral plexus, known as the cauda equina.

The spinal cord is composed of 31 pairs of nerve roots: 8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal:

  • C1 to C7 exits above the corresponding vertebrae
  • C8 exits below the C7 veterbra
  • The remaining spinal nerves exit below the corresponding vertebrae
Blood Supply

The anterior and two posterior spinal arteries (vertebral artery branches) supply the anterior two thirds and posterior one third of the cord, respectively. The segmental arteries derived from the thoracoabdominal aorta supply both the anterior and posterior spinal cord. The artery of Adamkiewicz is the largest segmental artery that supplies the mid-thoracic spinal cord (T8-L1).

Function

The spinal cord serves as a relay tract for motor and sensory information.

Grey Matter (Centrally)
  • Posterior horn - Sensory fibers
  • Lateral horn - Sympathetic neurons
  • Anterior horn - Motor neurons
White Matter (Peripherally)
  • Posterior column - Primarily sensory information
  • Lateral column - Sensory and motor information
  • Anterior column - Primarily motor information
Other Fibers

Other important fibers exiting the spinal cord are the autonomic fibers:

  • Sympathetic fibers arising from the T1-L1/2 spinal cord levels (thoracolumbar outflow)
  • Parasympathetic fibers arising from CN 3,7,9,10 and S2-4 levels (craniosacral outflow)

Pathogenesis

An SCI is a dynamic process, currently accepted to occur in two steps:1

  • Primary injury - Initial mechanical injury (compression, laceration, contusion, traction) due to local deformation and energy transfer
  • Secondary injury - A phenomenon that sometimes manifest clinically by neurologic deterioration over the first 8 to 12 hours after injury, with deficits increasing 1 to 2 spinal levels. This secondary injury is a combination of a complex array of vascular, biochemical, and cellular responses, triggered by the primary injury, leading to ongoing cellular damage and cell death. Possible mechanisms include:1
    • Free radical formation
    • Ongoing ischemia
    • Hypoxia
    • Inflammation
    • Edema
    • Neurotransmitter accumulation
    • Electrolyte imbalances
    • Apoptosis

Epidemiology

The annual incidence, not including those who die at the scene of the accident, is approximately 40 cases per 1 million population in the US, or approximately 12,000 new cases each year. Most reported injuries — 81% — occur in males. The number of people alive with SCI in the US in 2010 was estimated to be approximately 265,000.2

Common causes of SCI in the US include the following:3

  • Motor vehicle accident: 40.4%
  • Falls: 27.9%; most common in people age 45 years or older
  • Violence: 15%; globally, violence as a cause of SCI is significantly higher in emerging nations
  • Sports accidents: 8%, in which diving is the most common cause
  • Other: 8.5%, including vascular disorders, tumors, infections, spondylosis, iatrogenic injuries, and vertebral fractures due to osteoporosis

Racially, SCI is most common in Caucasians (66.5%), followed by African Americans (26.8%), Latinos (8.3%), and Asians (2%). The incidence is highest in individuals age 16 to 30 years (50%), followed by those over age 60 (11.5%) and those age 15 and younger (3.5%).

Life expectancy of persons with an SCI continues to increase, but it is still below the general population. Mortality rates are significantly higher in the first year than during subsequent years. Leading causes of death include:4

  • Pneumonia
  • Pulmonary embolism
  • Septicemia
  • Heart disease
  • Subsequent trauma
  • Suicide
  • Alcohol-related

Prognosis

Predictors of early hospital death include increased age, level of injury, Glasgow Coma Scale score, medical co-morbidities, severe systemic injuries, and associated traumatic brain injury (TBI).5,6 For example, patients with lesions at C1-C3 have a 6.6 times higher mortality rate than the mortality rate for those with paraplegia.1

Prognostic factors associated with recovery include the following:

  • Cord compression, spinal cord hemorrhage, and cord swelling are associated with a poor prognosis for neurologic recovery.7
  • Incomplete injuries exhibit the largest degree of improvement compared to complete injuries.8
  • Between 10% and 15% of patients with complete injuries convert to incomplete injuries.9
  • Approximately 5% of those with complete paraplegia walked at 1 year following injury, compared to 46% of those with incomplete tetraplegia and 76% of those with incomplete paraplegia.

Most patients regain some functions between 1 week and 6 months after injury, but the likelihood of spontaneous recovery diminishes after 6 months.7 Of note, patients with persistent complete spinal cord injury for longer than 24-48 hours have a poor prognosis for recovery.10

Clinical Presentation

A meticulous neurologic assessment, including evaluation of motor function, sensory function, and deep tendon reflexes, is crucial and required to establish the presence or absence of a SCI and to further classify the lesion. Isolated SCI are said to occur in only 20% of cases, while 20-57% have other significant injuries, such as TBI or major chest injuries.1

Important definitions:

  • Complete injury - Absence of sensory and motor functions in the segments below the level of the lesion. In the acute setting, reflexes are absent, there is no response to plantar stimulation, and muscles are flaccid. Urinary retention and bladder distension usually occur. Cord transection above C3 causes apnea, resulting in mechanical ventilator dependence in surviving patients.
  • Incomplete injury - Preservation of sensory or motor function below the level of injury, including the lowest sacral segments (Table 1)
  • Tetraplegia - Cervical region injury with associated loss of muscle strength in all extremities. Most common level is C5
  • Paraplegia - Injury to the cord in the thoracic, lumbar, or sacral region, including the cauda equina and conus medullaris. Most common level T12

Table 1. Incomplete Spinal Cord Syndromes

Syndromes

Injury

Presentation

Anterior Cord Syndrome

Acute disc herniation
Anterior spinal artery occlusion

No motor, pain, or temperature sensation below level of injury
Intact touch, proprioception and vibration

Posterior Cord Syndrome

Hyperextension injuries with fractures of posterior elements of vertebrae

Diminished proprioception and light touch

Brown-Sequard Syndrome

Hemisection of cord due to penetrating injuries or lateral mass fractures

Ipsilateral loss of proprioception and motor function
Contralateral loss of pain and temperature sensation

Central Cord Syndrome

Injury to central cord due to neck hyperextension; commonly seen in older patients with cervical spondylosis

Significant weakness of the upper extremities and to a lesser extent the lower extremities
Sacral sensory sparing; variable sensory loss, likely to lose pain and/or temperature sensation than proprioception and/or vibration

Conus Medullaris

Injury to the sacral cord with or without lumbar nerve roots

Areflexia of the bladder, bowel, and lower limbs
Knee jerk usually preserved
Motor and sensory loss in the lower limbs variable

Spinal Cord Concussion

Characterized by a temporary neurologic deficit originating from the spinal cord that fully recovers without any evidence of structural damage

 

Shock Syndromes

Injury

Spinal Shock

Injury involving the lower thoracic cord. Transient loss of all neurologic function, including reflexes and rectal tone, below the level of the injury with associated autonomic dysfunction.

Neurogenic Shock

Injury above T6 which results in severe autonomic dysfunction with hypotension, bradycardia, and peripheral vasodilation. Hypothermia is also characteristic.

Imaging and Diagnostic Studies

The primary goal of imaging studies is to promptly identify injuries that may be life-threatening or placing the spinal cord at risk. A study by the National Emergency X-Radiography Utilization Study Group (NEXUS)11 found that patients with blunt trauma who meet the following five criteria can be classified as having a low probability of injury (with NPV = 99.8%):

  • No midline cervical tenderness
  • No focal neurologic deficit
  • Normal alertness
  • No intoxication
  • No painful, distractive injury

Although this tool may decrease the number of unnecessary images, it should be used with care and should not replace clinical judgment.12

Plain X-rays

Trauma patients with suspected SCI should have a complete plain radiographic evaluation of the cervical spine views (AP, lateral, and open-mouth odontoid views), and the lateral view must visualize the C7-T1 junction to be considered adequate. A swimmers view can be ordered if the C7-T1 is not satisfactorily imagined. Flexion and extension views are not recommended in the acute injury period, and are of limited clinical value due to patient splinting from pain. Patients with any suspected SCI should have imaging of the entire spinal column because the frequency of noncontiguous spinal injuries have been reported to be as high as 10.5% of patients.13,14 The presence of a spinal cord injury clearly warrants additional imaging studies with CT and/or MRI.

Computed Tomography

There is increasing evidence that computed tomography (CT) scans are more sensitive than plain radiography in detecting spinal fractures.15-18 The use of spiral CT traumagram is indicated in a blunt trauma patient who is unconscious or unable to provide a reliable clinical exam due to altered mental status or distracting injuries. Spiral CT of the spine has been found to identify 99% of all fractures of the cervical, thoracic, and lumbar spine and to provide more accurate assessment of bone injury and spinal canal compromise when compared to plain radiographs.15-17

Antevil et al18 reported on the use of CT to evaluate cervical spine injury, and found 100% sensitivity, versus 70% sensitivity using plain radiographs. They also noted significantly shorter mean time for initial radiologic evaluation for CT (1 hour) versus plain films (1.9 hours). Computed tomography of the chest, abdomen, and pelvis has also been highly effective in recognizing thoracic and lumbar spine trauma, with reported 100% sensitivity and 97% specificity compared to plain radiographs, which had 73% sensitivity and 100% specificity.16

If a spine fracture is identified with routine spiral CT traumagram or on plain radiographs, the entire spine CT scan should be carefully reviewed or obtained due to the high incidence of additional, non-contiguous spinal column fractures, which has been reported to be from 10-20%.13,14

Magnetic Resonance Imaging

Magnetic resonance imaging (MRI) is useful in evaluating the integrity of the spinal cord and surrounding soft tissues for injuries. MRIs can be time consuming, have decreased sensitivity when identifying early cord damage (edema), and are contraindicated in patients with metallic foreign bodies or cardiac devices.

Spinal cord injury without radiographic abnormalities (SCIWORA) originally described injuries without X-ray or CT evidence of pathology. However, with the increased use of MRIs, other causes have been recognized. SCIWORA is currently a diagnosis of exclusion, which is most commonly seen in the pediatric population.

Computed Tomography Myelogram

This imaging technique is rarely used due to the availability of MRI. However, if an MRI is not available or contraindicated, a computed tomography myelogram may be used as an alternative to evaluate the spinal canal.

Classification

The widely used American Spinal Injury Association (ASIA) Impairment Score is based on a careful neurologic assessment that includes evaluation of pin-prick and light-touch sensory function, motor function of 10 key muscles on each side of the body, perianal motor and sensory function, and the bulbocavernosus reflex (Figure 1).

  • A = Complete. No sensory or motor function preserved in the sacral segments S4-S5.
  • B = Sensory Incomplete. Sensory but not motor function below level of the injury, including the sacral segments S4-S5.
  • C = Motor Incomplete. Motor function below the neurological level with muscle function below injury level grade < 3.
  • D = Motor Incomplete. Motor function below the neurological level with muscle function below the injury level grade > 3.
  • E = Normal. Normal sensation and motor in a patient with prior deficits.

A detailed ASIA Impairment Score evaluation performed between 24 to 48 hours may be unreliable due to the presence of spinal shock. Therefore, a patient with an SCI should have a repeat assessment after 72 hours to determine the patient’s ASIA Impairment Score.

Download Figure 1, ASIA Impairment Score

Treatment

Pre-hospital Management
  • Standard Advanced Trauma Life Support (ATLS) protocol
  • Stabilize and immobilize to prevent further injury with hard backboard, semi-rigid cervical collar, and lateral support devices during transport to the hospital19
  • Immediately remove from hard backboard to prevent pressure ulcerations
  • Intubation and ventilation support may be necessary if the patient exhibits signs of impending respiratory failure due to loss of phrenic nerve function (C3-5), decreased mental status, or other associated thoracic injuries8
  • In the patient with hypotension following trauma, hemorrhage should be ruled out before assuming neurogenic shock, which is caused by the loss of sympathetic cardiovascular tone
  • When an SCI is suspected , the mean arterial blood pressure should be maintained at 80 to 100 mm Hg to improve spinal cord perfusion20
  • Severe bradycardia may require the use of an external pacemaker or atropine
  • If not contraindicated, insert Foley catheter to avoid bladder trauma due to distension
  • H2-blocker to prevent stress or steroid-induced gastrointestinal ulcers
Pharmacologic Therapy: Methylprednisolone

High-dose methylprednisolone has been postulated to be beneficial in reducing secondary injury due to anti-inflammatory properties, and remains a controversial topic. The National Acute Spinal Cord Injury Studies (NASCIS) II trial21 reported no significant benefit of methylprednisolone administration within 24 hours of injury, and in fact found a negative effect on the primary outcome of motor and sensory recovery. However, post hoc subset analysis demonstrated a small but statistically significant motor and sensory improvement following administration of methylprednisolone within 8 hours of injury at 30 mg/kg bolus followed by 5.4 mg/kg per hour for 23 hours.

This study was followed by NASCIS III,22 which evaluated administration of methylprednisolone within 8 hours of injury, and the researchers also found a negative impact on the primary outcome measure. However, post hoc subset analysis found methylprednisolone treatment initiated between 3 and 8 hours after injury and administered for 48 hours resulted in a statistically insignificant (p=0.08) improvement in functional independence measures and motor recovery compared to 24 hours of treatment. Unfortunately, the increase to 48 hours of treatment resulted in a higher incidence of wound infection, pulmonary embolism, severe sepsis, and pneumonia.

Despite positive findings, the NASCIS studies have been criticized due to the post hoc nature of the data analysis, the small effect sizes, and concerns about complications arising from treatment. Additionally, other randomized trials have failed to show the benefit of methylprednisolone, but have further highlighted the concern for complications. The American Association of Neurological Surgeons (AANS) guidelines23 recommend the 24- or 48-hour steroid therapy protocol as an option in the treatment of SCI and not the standard of care because the current evidence suggests the harmful side effects may outweigh the clinical benefits of treatment.

Operative Treatment

Goals of operative treatment include optimizing neurologic outcome and allowing early rehabilitation. This can be performed through decompression of the neural elements and, in certain cases, preventing further spinal cord injury from mechanical instability.

Closed Reduction of Cervical Spinal Fracture/Dislocation
Despite the AANS stating there are insufficient data to support treatment guidelines/standards, the organization recommends early closed reduction for restoration of anatomic alignment in awake patients without additional rostral injuries. Patients, who cannot be examined, ie, obtunded, should undergo MRI prior to attempted reduction. The presence of significant disc herniation is a relative indication for ventral decompression prior to reduction. In a patient with a worsening neurologic exam or in failed closed reductions, MRI studies are recommended

When performing this technique, use a halo or skull tongs to increase axial traction gradually (5-pound increments) while performing serial lateral X-rays and neurologic exams.

Surgical Decompression
Indications for cervical decompression include the following:

  • Spinal cord compression with progressive neurologic degeneration or instability
  • Patient not a candidate or not responding to closed reduction
  • Penetrating injuries for surgical exploration and debridement

Indications for thoracolumbar decompression include the following:24

  • Results of Thoracolumbar Injury Severity Score
    • Variables scored: morphology of injury, neurologic involvement, integrity of posterior ligament complex
    • If score < 4, non-operative
    • If > 4, operative
    • If = 4, at surgeon's discretion

Although the Thorocolumbar Injury Severity Score is the best decision-making algorithm currently recommended, there is a need for higher-quality studies to further evaluate its effectiveness.

Controversy - Timing of Decompression Surgery

Emerging evidence suggests that early decompression may enhance recovery after cervical SCI and has acceptable safety; however the clinical evidence is variable.

  • In the only prior randomized controlled trial, Vacarro (1997) showed no significant neurologic benefit with early (< 72 hours) compare to delayed (> 5 days) cord decompression.25
  • A review article by Fehling et al (2010) indicated that early decompression (< 24 hours) should be considered in any SCI patient, particularly in cases of cervical SCI.26 Additionally, they suggested that very early decompression (> 12 hours) should be consider in patients with incomplete cervical SCI, except in the case of patients with central cord syndrome.26
  • The STASCIS multi-centered, international, prospective cohort study (2012) had the following findings:27
    • N=313, early (< 24 hours) = 182, late (> 24 hours) =131
    • At 6 months post-injury, odds ratio = 2.8 of at least 2 grade AIS improvement with early surgery vs late
    • No significant difference in mortalities and complications
    • Limitations:
      • Early group with slightly lower mean age and greater proportion of more-severe degree of initial injury
      • 27% of patients lost to follow up

Rehabilitation

Due to prolonged survival of patients with SCI, rehabilitation has an increasingly important role. The primary goals are to prevent secondary complications, maximize physical functioning, and reintegrate the patient into the community. This task is most effectively accomplished with a multidisciplinary, team-based approach. Early transfer to a specialized SCI center is recommended as there is evidence that it decreases overall length of stay, mortality, and the number and severity of complications.28

Complications

Complications associated with management of an SCI include the following:

  • UTIs or urinary incontinence
  • Syringomyelia, spinal cord tethering, progressive spinal deformity
  • Bowel incontinence
  • Pressure sores
  • Lung infections
  • Sepsis
  • Thrombotic disease
  • Muscle spasms
  • Chronic pain
  • Depression
  • Neurologic deterioration
  • Steroid-associated risk of infections, sepsis, avascular necrosis

References

  1. Sekhon LH, Fehlings MG. Epidemiology, demographics, and pathophysiology of acute spinal cord injury. Spine (Phila Pa 1976). Dec 15 2001;26(24 Suppl):S2-12.
  2. National Spinal Cord Injury Statistical Center Spinal Cord Injury Facts and Figures at a Glance (Fact sheet). NSCISC February 2011.
  3. Ackery A, Tator C, Krassioukov A. A global perspective on spinal cord injury epidemiology. J Neurotrauma. Oct 2004;21(10):1355-1370.
  4. Annual Report for the Spinal Cord Injury Model Systems. NSCISC 2010.
  5. Claxton AR, Wong DT, Chung F, Fehlings MG. Predictors of hospital mortality and mechanical ventilation in patients with cervical spinal cord injury. Can J Anaesth. Feb 1998;45(2):144-149.
  6. Varma A, Hill EG, Nicholas J, Selassie A. Predictors of early mortality after traumatic spinal cord injury: a population-based study. Spine (Phila Pa 1976). Apr 1 2010;35(7):778-783.
  7. Waters RL, Adkins RH, Yakura JS, Sie I. Motor and sensory recovery following incomplete tetraplegia. Arch Phys Med Rehabil. Mar 1994;75(3):306-311.
  8. Stevens RD, Bhardwaj A, Kirsch JR, Mirski MA. Critical care and perioperative management in traumatic spinal cord injury. J Neurosurg Anesthesiol. Jul 2003;15(3):215-229.
  9. Yakura, Joy S. Recovery following spinal cord injury. The Free Library 22 December 1996. 17 April 2012.
  10. Cortez R, Levi AD. Acute spinal cord injury. Curr Treat Options Neurol. Mar 2007;9(2):115-125.
  11. Hoffman JR, Mower WR, Wolfson AB, Todd KH, Zucker MI. Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National Emergency X-Radiography Utilization Study Group. N Engl J Med. Jul 13 2000;343(2):94-99.
  12. Furlan JC, Noonan V, Singh A, Fehlings MG. Assessment of impairment in patients with acute traumatic spinal cord injury: a systematic review of the literature. J Neurotrauma. Aug 2011;28(8):1445-1477.
  13. Vaccaro AR, An HS, Lin S, Sun S, Balderston RA, Cotler JM. Noncontiguous injuries of the spine. J Spinal Disord. Sep 1992;5(3):320-329.
  14. Henderson RL, Reid DC, Saboe LA. Multiple noncontiguous spine fractures. Spine (Phila Pa 1976). Feb 1991;16(2):128-131.
  15. Brown CV, Antevil JL, Sise MJ, Sack DI. Spiral computed tomography for the diagnosis of cervical, thoracic, and lumbar spine fractures: its time has come. J Trauma. May 2005;58(5):890-895; discussion 895-896.
  16. Berry GE, Adams S, Harris MB, et al. Are plain radiographs of the spine necessary during evaluation after blunt trauma? Accuracy of screening torso computed tomography in thoracic/lumbar spine fracture diagnosis. J Trauma. Dec 2005;59(6):1410-1413; discussion 1413.
  17. Sanchez B, Waxman K, Jones T, Conner S, Chung R, Becerra S. Cervical spine clearance in blunt trauma: evaluation of a computed tomography-based protocol. J Trauma. Jul 2005;59(1):179-183.
  18. Antevil JL, Sise MJ, Sack DI, Kidder B, Hopper A, Brown CV. Spiral computed tomography for the initial evaluation of spine trauma: A new standard of care? J Trauma. Aug 2006;61(2):382-387.
  19. Nockels RP. Nonoperative management of acute spinal cord injury. Spine (Phila Pa 1976). Dec 15 2001;26(24 Suppl):S31-37.
  20. Blood pressure management after acute spinal cord injury. Neurosurgery. Mar 2002;50(3 Suppl):S58-62.
  21. Bracken MB, Shepard MJ, Collins WF, et al. A randomized, controlled trial of methylprednisolone or naloxone in the treatment of acute spinal-cord injury. Results of the Second National Acute Spinal Cord Injury Study. N Engl J Med. May 17 1990;322(20):1405-1411.
  22. Bracken MB, Shepard MJ, Holford TR, et al. Administration of methylprednisolone for 24 or 48 hours or tirilazad mesylate for 48 hours in the treatment of acute spinal cord injury. Results of the Third National Acute Spinal Cord Injury Randomized Controlled Trial. National Acute Spinal Cord Injury Study. JAMA. May 28 1997;277(20):1597-1604.
  23. ANNS guidelines. Hadley M, Walters B, Grabb P, et al. Guidelines for the management of acute cervical spine and spinal cord injuries. Rolling Meadows (IL): American Association of Neurological Surgeons: Section on Disorders of the Spine and Peripheral Nerves; 2007.
  24. Vaccaro AR, Lehman RA, Jr., Hurlbert RJ, et al. A new classification of thoracolumbar injuries: the importance of injury morphology, the integrity of the posterior ligamentous complex, and neurologic status. Spine (Phila Pa 1976). Oct 15 2005;30(20):2325-2333.
  25. Vaccaro AR, Daugherty RJ, Sheehan TP, et al. Neurologic outcome of early versus late surgery for cervical spinal cord injury. Spine (Phila Pa 1976). Nov 15 1997;22(22):2609-2613.
  26. Fehlings MG, Rabin D, Sears W, Cadotte DW, Aarabi B. Current practice in the timing of surgical intervention in spinal cord injury. Spine (Phila Pa 1976). Oct 1 2010;35(21 Suppl):S166-173.
  27. Fehlings MG, Vaccaro A, Wilson JR, et al. Early versus delayed decompression for traumatic cervical spinal cord injury: results of the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS). PLoS One. 2012;7(2):e32037.
  28. Parent S, Barchi S, LeBreton M, Casha S, Fehlings MG. The impact of specialized centers of care for spinal cord injury on length of stay, complications, and mortality: a systematic review of the literature. J Neurotrauma. Aug 2011;28(8):1363-1370.


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