Cervical Spine Fracture Follow-up
- Author: Moira Davenport, MD; Chief Editor: Trevor John Mills, MD, MPH more...
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 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 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 the lower extremities and more pronounced in the distal aspect of extremity.
The 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.
This syndrome involves injury to only 1 side of 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 also 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.
This syndrome manifests as ptosis, miosis, and anhydrosis.
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 them.
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. In a smaller series, 1272 patients with significant craniocerebral injury had only a 1.8% prevalence of cervical injuries. 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%. 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 that there is an increased risk (4.5% vs 1.1%) of cervical spine injury with craniocerebral (but not with facial) injuries.
Regardless of the results, none of these retrospective studies suggests decreasing standard care, such as ordering x-rays to find cervical spine injuries in trauma patients.
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