History and Physical Exam
Common presentations of cervical spine fracture include the following:
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Posterior neck pain on palpation of spinous processes
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Limited range of motion associated with pain
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Weakness, numbness, or paresthesias along affected nerve roots
Clinical evaluation of the cervical spine in a patient with blunt trauma is unreliable. In a study of surgical residents' ability to predict cervical injuries on the basis of clinical examination alone, sensitivity and specificity were 46% and 94%, respectively. Because of these limitations and the potential for catastrophic morbidity if injury is missed, most patients with complex blunt trauma seen in the ED undergo radiographic evaluation before clearance, with some exceptions.
Common findings on physical examination in cervical spine injury include the following:
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Spinal shock
Flaccidity
Areflexia
Loss of anal sphincter tone
Fecal incontinence
Priapism
Loss of bulbocavernosus reflex
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Neurogenic shock
Hypotension
Paradoxical bradycardia
Flushed, dry, and warm peripheral skin
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Autonomic dysfunction
Ileus
Urinary retention
Poikilothermia
Causes
Motor vehicle collisions and falls account for 50% and 20% of cervical spine injuries, respectively. Studies have shown that the impact velocity at the time of a motor vehicle collision, [29, 30] airbag deployment on unrestrained drivers, [31, 32] drivers aged 65 years or older, and rollover mechanisms [33] all significantly increase the likelihood of a cervical spine injury.
Sports-related activities account for 15%. The remaining injuries are attributed to interpersonal violence. The following athletic activities have the highest incidence of associated cervical spine injuries. Participants in these events should be considered at high risk:
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Diving
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Equestrian activities
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Football
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Gymnastics
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Skiing
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Hang gliding
Penetrating trauma rarely causes cervical spine fracture but may result in significant neurologic deficits. [34] In one study of 144 cervical gunshot wounds, 40 were associated with neurologic deficits. [35]
Complications
Spinal shock
Severe spinal cord injury may cause a concussive injury of the spinal cord termed spinal shock syndrome.
Spinal shock manifests as distal areflexia of a transient nature that may last from a few hours to weeks. Initially, the patient experiences a flaccid quadriplegia along with areflexia. Segmental reflexes start to return usually within 24 hours as spinal shock starts to resolve. At that point, flaccid quadriplegia changes to spastic paralysis.
Eventually, total resolution can be expected.
Neurogenic shock
Neurogenic shock is spinal shock that causes vasomotor instability because of loss of sympathetic tone.
Patients with neurogenic shock are hypotensive but have paradoxical bradycardia.
Flushed, dry, and warm peripheral skin (in contrast to findings with hypovolemic or cardiogenic shock) may be present. Other signs of autonomic dysfunction include ileus, urinary retention, and poikilothermia.
Loss of anal sphincter tone with fecal incontinence and priapism suggest spinal shock. Return of the bulbocavernosus reflex heralds resolution of spinal shock.
Complete and incomplete cord syndromes
Besides spinal shock, complete and incomplete spinal cord syndromes may occur.
Spinal shock mimics a complete spinal cord lesion. Emergency physicians should wait until spinal shock resolves to make an accurate estimate of the patient's prognosis.
Incomplete cord syndromes are described and include anterior spinal cord syndrome, central spinal cord syndrome, Brown-Séquard syndrome, and less frequent cord syndromes at high cervical levels (ie, Horner syndrome, posteroinferior cerebellar artery syndrome).
The prognosis of a patient with a complete lesion, after spinal shock subsides, is permanent paraplegia.
Patients with an incomplete lesion (partial motor or sensory function) can expect to regain some degree of function.
Anterior spinal cord syndrome
Anterior spinal cord syndrome involves complete motor paralysis and loss of temperature and pain perception distal to the lesion. Since posterior columns are spared, light touch, vibration, and proprioceptive input are preserved.
This syndrome is caused by compression of the anterior spinal artery, which results in anterior cord ischemia or direct compression of the anterior cord. It is associated with burst fractures of the spinal column with fragment retropulsion caused by axial compression.
Central spinal cord syndrome
This syndrome is caused by damage to the corticospinal tract.
It is characterized by weakness, greater in the upper extremities than in the lower extremities and more pronounced in the distal aspect of the extremity.
This syndrome usually is associated with a hyperextension injury in patients with spondylosis or congenital stenosis of the cervical canal.
Extension of the cervical spine, causing buckling of the ligamentum flavum into the spinal cord, is believed to cause central spinal cord syndrome.
Brown-Séquard syndrome
This syndrome involves injury to only 1 side of the spinal cord.
It causes paralysis, loss of vibration sensation, and loss of proprioceptive input ipsilaterally, with contralateral loss of pain and temperature perception because of involvement of posterior columns and spinothalamic tracts on the same side.
It is associated with hemisection of the spinal cord from penetrating trauma; however, it can be caused by a lateral mass fracture of a cervical vertebra.
High cervical spinal cord syndromes
These syndromes are associated with damage to the spinal tract of the trigeminal nerve in the high cervical region.
A characteristic onion-skin pattern of anesthesia in the face may occur.
Horner syndrome
Horner syndrome manifests as ptosis, miosis, and anhidrosis.
It results from damage to the cervical sympathetic chain.
Posteroinferior cerebellar artery syndrome
A diverse constellation of symptoms, including dysphagia, dysphonia, hiccups, vertigo, vomiting, or cerebellar ataxia, may occur.
Any of the high cervical cord syndromes may result from direct injury to the upper cervical level and/or cervicomedullary junction.
Vertebral artery occlusion from dislocation or hyperextension of the cervical column also can produce these syndromes.
Craniofacial injuries
An association between significant craniofacial injuries and cervical spine fractures seems intuitively logical, yet several retrospective series do not support this assumption.
A retrospective review of 2555 patients with significant facial injuries found that only 1.3% had concomitant cervical spine injury. [36] In a smaller series, 1272 patients with significant craniocerebral injury had only a 1.8% prevalence of cervical injuries. [37] A review of 1050 patients admitted with facial fractures found only a 4% prevalence of an associated cervical injury, even though the prevalence of associated head injuries was 85%. [38] These and other series indicate that closed head injuries and facial fractures may not significantly increase the risk of concomitant cervical spine injury.
A larger retrospective study suggests there is increased risk (4.5% vs 1.1%) of cervical spine injury with craniocerebral (but not with facial) injuries. [39]
Regardless of the results, none of these retrospective studies suggests decreasing standard care, such as ordering radiographs to find cervical spine injuries in trauma patients.
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Odontoid fractures. (A) Type I odontoid fracture represents an avulsion of the tip of the dens at the insertion site of the alar ligament. Although mechanically stable, it is associated with life-threatening atlanto-occipital dislocation. (B) Type II odontoid fracture is a fracture at the base of the dens. This is the most common type of odontoid fracture. (C) With type III odontoid fracture, the fracture line extends into the body of the axis.
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(A) Simple wedge fracture with a flexion mechanism of injury is stable. (B) Flexion teardrop fracture with a flexion mechanism is unstable.
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Anterior subluxation with a flexion mechanism is stable in extension but potentially unstable in flexion.
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Bilateral facet dislocation with a flexion mechanism is extremely unstable and can have an associated disk herniation that impinges on the spinal cord during reduction.
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Clay shoveler fracture. (A) Lateral view of this fracture caused by a flexion mechanism shows that it is stable and represents an avulsion fracture of the base of the spinous process near the supraspinous ligament. (B) Anteroposterior view shows the vertically split appearance of the spinous process.
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Unilateral facet dislocation. (A) Lateral view of this fracture caused by a flexion-rotation mechanism shows that it is stable. Anterior displacement of spine is less than one half of the diameter of a vertebral body. (B) Anteroposterior view shows disruption of a line connecting spinous processes at the level of the dislocation. (C) Oblique view shows that the expected tiling of the laminae is disrupted, and the dislocated superior articulating facet of the lower vertebra is seen projecting within the neural foramina.
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Hangman fracture caused by an extension mechanism is unstable. Fracture line is evident in the lateral projection extending through pedicles of C2, along with disruption of the spinolaminar line. Sometimes, this fracture is associated with unilateral or bilateral facet dislocation, which makes it highly unstable.
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(A) Fracture of the posterior arch of C1 fracture caused by an extension mechanism is stable. Lateral projection shows a fracture line through the posterior neural arch without widening predental space. An odontoid view must be obtained to differentiate this benign fracture from a Jefferson fracture. (B) Jefferson fracture caused by a vertical (axial) compression mechanism is unstable. This fracture of all aspects of the C1 ring is associated with possible disruption of the transverse ligament of the atlas. Lateral projection may show a widened predental space and a fracture through the posterior arch of C1. Odontoid view shows displacement of the lateral masses of C1, allowing distinction of this fracture from a simple fracture of the posterior neural arch of C1.
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Burst fracture of vertebral body caused by a vertical (axial) compression mechanism is stable mechanically and involves disruption of the anterior and middle columns, with variable degree of protrusion of the latter. This middle column posterior protrusion may extend into the spinal canal and be associated with an anterior cord syndrome.
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(A) Normal lateral projection shows the relationships of anterior, posterior, and spinolaminar lines and prevertebral spaces. (B) Normal oblique projection shows the normal appearance of the laminae as shingles on a roof forming a regular elliptical curve with equal interlaminar spaces.
