In this section, a selection of notable spinal traumatic conditions will be reviewed: injuries to the upper cervical spine (C1, also known as the atlas and C2, the axis); lower (subaxial) cervical injuries; thoracolumbar fractures; and osteoporotic vertebral compression fractures. Injuries to the discs (including cauda equina syndrome) and spinal sprains and strains will be covered elsewhere.
Atlas fractures are rare. They are usually caused by compression to the top of the skull, with force transmitted on the atlas into the axis. If the force causes the lateral masses to split, the injury is known as a Jefferson fracture (Figure 1). Jefferson fractures are reduced by traction and immobilized for about 12 weeks. This mechanism of injury can also cause rupture of the transverse ligament which normally prevents the atlas from slipping forward relative to the axis. In cases where the transverse ligament is ruptured, surgical arthrodesis (fusion) of C1 to C2 is indicated. If there is a dislocation of C1/C2 due to transverse ligament rupture without fracture, projection of bone into the neural canal can cause immediate death and thus are not seen clinically.
Odontoid fractures represent about 10% of cervical spine fractures and are the most common fracture of C2 itself. Odontoid fractures are seen in low energy falls in elderly patients and after high energy mechanism of injuries causing cervical hyperflexion or hyperextension in younger patients. Treatment is guided by the location of the fracture (Figure 2). Type I fractures are avulsions of the tip of the odontoid dens and are treated with a cervical orthosis. Type II fractures are at the junction of the odontoid and the body of C2. Younger patients can be treated with halo immobilization, but elderly people typically do not tolerate that and may need surgical stabilization. Surgery is more often chosen when there is comminution of the fracture or displacement or posterior angulation greater than about 5mm or 10 degrees respectively. Also, if there is a risk of poor bone healing (as suggested by a history of smoking or osteoporosis, for example) surgery may be especially indicated. Type III fractures involve the body of the axis and are treated with immobilization because the cancellous bone typically heals.
An os odontoideum is a fragment that appears like a Type II odontoid fracture; it may represent failure of fusion during growth and development or may be a residual of prior trauma. It is managed by observation, without intervention. Os odontoideum is not uncommon in patients with Downs Syndrome, and may be managed with observation or with surgery, depending upon the clinical situation.
A hangman’s fracture is a bilateral fracture of the C2 pars interarticularis with a traumatic spondylolisthesis (slippage) of C2 on C3 (Figure 3). It is the second most common fracture of the C2 vertebral body, excluding injuries to the dens. Although the name suggests a hyperextension and distraction mechanism of injury, as would be seen in a judicial execution, this injury is often seen after hyperextension with axial loading produced by motor vehicle collisions, diving or high velocity contact sports. Despite the traumatic spondylolisthesis of C2/C3, a hangman’s fracture rarely leads to spinal cord injury as the bony fractures, contrary to intuition perhaps, tend to increase the space for the spinal cord. A CT scan should be obtained to assess the fracture and MRI to assess the soft tissues. Because the vertebral artery is at particular risk for injury with a hangman’s fracture, angiography may also be needed. Nearly all cases of hangman’s fracture can be managed successfully with immobilization with a halo or collar.
Extension Teardrop Fractures
Extension teardrop fractures are small, stable avulsions that are usually not associated with cord injury (Figure 4). They are more commonly seen at C2. With forced extension of the neck, especially in the setting of stiffness caused by degenerative disease, there can be an avulsion of the anteroinferior aspect of the vertebral body with disruption of the anterior longitudinal ligament.
It is important to not conflate extension teardrop avulsion fractures with the more serious flexion teardrop fractures seen in the lower cervical spine. Both are manifest as a (teardrop-shaped) fragment fractured from the anteroinferior aspect of the vertebra. Critical differences are listed in the table below.
Cervical Facet Dislocations
Cervical facet dislocations are often caused by a combination of flexion and distraction. They are seen in younger patients after high energy trauma such as motor vehicle accidents or contact sports collisions. Bilateral facet dislocation is characterized by 50% subluxation and is often associated with significant spinal cord injury. If there is rotational force applied, it is possible to have only one facet dislocate (Figure 5). These unilateral dislocations are manifest with about 25% subluxation seen on x-ray and a single level nerve root injury (e.g., C6/7 unilateral dislocation presents with a C7 dysfunction, e.g., weakness, wrist flexion and numbness in the index and middle finger).
In addition to subluxation, there may be increased lordosis, soft tissue swelling and widening of the interspinous distance. If subluxation is seen on plain films, the bony anatomy of the injury can be confirmed with a CT scan. An MRI is used to identify disk herniation, spinal cord compression or myelomalacia, spinal cord hematoma and any disruption of the supraspinous and interspinous ligaments and facet capsules.
If there is a bilateral facet dislocation with neurological deficits, and the patient is awake and cooperative, emergent closed reduction followed by urgent surgical stabilization is indicated. Closed reduction is carried out by gradually increased axial traction applied to tongs fixed to the skull with pins. If the patient is not awake and cooperative, MRI followed by open reduction is indicated. Stable, unilateral dislocations can be treated with immobilization alone.
Cervical Body Fractures
body fractures (Figure 6) in the lower cervical vertebrae include “compression
fractures,” limited to the anterior vertebral body without retropulsion of bone
into canal, or “burst fractures” which involve the posterior aspects of the
body, with retropulsion of bone into the spinal canal and associated spinal
cord injury. (The phrase “compression fractures” is surrounded by air quotes as
it is referring to a specific pattern, as described. The mechanism of injury of
other injuries may also involve “compression,” in the general meaning of the
Flexion teardrop fractures are caused by axial/flexion forces that compress the anterior-inferior aspect of the vertebra (usually C4, C5 or C6) and push the posterior portion of vertebra into the canal. They are associated with extensive injuries to both bone and ligament and thereby produce spinal instability. Associated spinal cord injury is common.
Thoracolumbar burst fractures (Figure 7) most commonly present with symptoms of spinal cord injury. Due to the location of the injury distal to the cervical nerve roots, only the lower extremities are affected. If the spinal canal is compromised by the retropulsion of the vertebral body, maximal compression of the spinal cord occurs at the moment of trauma. Neurologic symptoms can occur with burst fractures. In the rare cases without significant neurologic symptoms, the patient will complain of severe, focal back pain over the injured vertebrae. Mobility of the thoracolumbar junction is limited both by pain and instability.
Thoracolumbar burst fractures can be described in terms of their geographic limits: anterior, middle and posterior column injuries. Direct damage can be limited to the anterior column of the spine (anterior longitudinal ligament + anterior 2/3 of vertebral body) the anterior plus the middle column, which includes the posterior longitudinal ligament and posterior 1/3 of vertebral body; or the inclusion of the posterior column, containing the ligamentum flavum, the spinous processes, the pedicles and the posterior ligaments.
Osteoporosis and Vertebral Compression Fractures
Osteoporosis is characterized by poor bone mineral density and a propensity for so-called “fragility fractures” of the distal radius, the hip and the vertebral bodies. Of these three fragility fractures, vertebral compression fractures (Figure 8) are the most common, with an annual incidence of 700,000. It is estimated that one in four postmenopausal women will suffer a vertebral compression fracture in their lifetime. Vertebral compression fractures are responsible for more than $10 billion of health care expenditure annually in the USA and are a harbinger of increasing morbidity and mortality.
Most osteoporosis-related vertebral compression fractures are found in the thoracolumbar region (T12 to L2) in patients aged 50 to 60. (By contrast, wrist fractures are most common in the 5th decade and hip fractures are most common in the 7th decade.) In the case of a vertebral compression fracture, the onset pain is often insidious. If acute pain is noted, many patients may report that their pain started after a seemingly benign event like coughing, rolling over in bed, or lifting an object.
Physical exam for osteoporosis is unrevealing, but a secondary vertebral compression fracture can cause tenderness to palpation over the fracture level. Other signs of compression fracture include progressing loss of height, kyphotic deformity, or paraspinal muscle contraction (necessary to maintain posture).
It is unlikely that an osteoporosis-related vertebral compression fracture will cause any damage to the spinal cord. That is because the bone collapses on itself and does not create a mass effect in the central canal (as might be seen with a burst fracture of healthy bone in high energy trauma). The loss of height in the vertebral column may, however, compress the neural foramina and put pressure on exiting nerve roots.
Because vertebral compression fractures can also be caused by metastatic cancer or infection, it is important to exclude these diagnoses when the presentation is not typical for an osteoporosis-related fracture. Suspicion should be raised in patients with a known cancer history; patients under age 50, especially with no history of overt trauma; a history of weight loss, fevers, or other constitutional signs and symptoms (e.g., fever); a vertebral compression fracture located at the T5 vertebra or above; or risk factors for cancer or infection, such as smoking and immunosuppression, respectively.
A vertebral compression fracture is itself a red flag for the presence of osteoporosis, and a formal work-up (with treatment if the diagnosis is confirmed) should be initiated.
X-ray imaging of the entire spine should be performed in patients with suspected vertebral compression fractures. A 20% or 4mm loss of vertebral height is consistent with the diagnosis (see Figure 8). A CT scan may be obtained if radiography is inadequate or if there are lower extremity neurologic findings. Magnetic resonance imaging need only be performed if there is a question about the chronicity of the fracture or for further assessment of secondary spinal cord injury.
A history of at least one prior vertebral compression fracture increases risk of a future vertebral compression fractures by a factor of five. Risk of future vertebral compression fractures is 12 times greater in those with two or more previous vertebral compression fractures.
In patients with known osteoporosis of the spine, management of osteoporosis with light weight training, calcium and vitamin D supplementation, and bisphosphonate medications can reduce fracture risk by 25% to 75%.
Most patients with a vertebral compression fracture have a stable spine and thus can be treated non-operatively. Surgery is reserved for patients with continued severe back pain after six weeks of conservative therapy, although evidence of surgical intervention efficacy is limited. Operative management of a vertebral compression fracture is usually achieved with vertebroplasty or kyphoplasty (see Figure 9).
Rarely, surgical decompression and spinal stabilization with construct fixation are necessary to correct an injury to the posterior longitudinal ligament and prevent further deformity.
Vertebral compression fractures that produce kyphotic deformities can negatively impact pulmonary function by decreasing forced vital capacity when the kyphosis angle is greater than 70 degrees. This may also increase a patient’s risk of developing atelectasis and pneumonia. Kyphosis can lead to GI symptoms such as constipation, early satiety, and even bowel obstruction due to the increase in abdominal cavity pressure. Vertebral compression fractures may cause poor balance (because the patient’s center of gravity is tilted forward), leading to the potential for further falls. Loss of mobility leads to muscle atrophy and increases a patient’s risk of DVT. Overall, vertebral compression fractures increase a patient’s five-year mortality by 15%. One-year mortality for a vertebral compression fracture is 15% and 2-year mortality is 20%.