Chapter 25

The incidence of post-traumatic deformities in patients having undergone treatment for thoracolumbar injuries is not known but is assumed to be relatively uncommon. There are ~150,000 spine fractures in North America annually with most being minor and requiring little to no treatment.1 In the young, thoracolumbar fractures are generally the result of high-energy injuries such as motor vehicle accidents, falls from heights, and penetrating trauma. In both the elderly and those with metabolic bone disease, however, low-energy mechanisms of injury are significantly more common. Thoracolumbar spine injuries occur in a bimodal distribution with the first peak in the second and third decades of life and the second peak occurring in people in their sixth decade of life. In a review of more than 1000 patients by the Scoliosis Research Society, 16% of injuries occurred between T1 and T10, 52% between T11 and L1, and 32% between L1 and L5.² The overall incidence of associated neural injury has decreased nationally as a result of the improvement in emergency medical services, on-scene immobilization and rapid transport to specialized trauma centers, as well as safer automobiles and workplace environments.³ Treatment of these injuries has been associated with complications including neurologic deterioration (1%), spinal instrument failure (2 to 8%), vascular injury, retrograde ejaculation (4% with anterior approach), deformity, chronic pain, and infection (3 to 10%).^4,5 The improvements in the acute management of polytrauma patients who have thoracolumbar spine injuries has ironically resulted in an increased incidence of post-traumatic deformity. This is due to both an increased survival rate in the setting of other associated significant injuries in addition to the presence of a complete or incomplete neurologic injury resulting in unbalanced forces on the spinal axis.⁶

♦ Anatomy

The thoracolumbar spine has several unique characteristics that make it susceptible to injury. The normal thoracic spine is surrounded posteriorly by the paraspinal musculature and laterally and anteriorly by the rib cage and sternum. As a result, the thoracic spine is significantly more resistant to both forward flexion and extension loads when compared with the lumbar spine. This relates to the coronal orientation of the thoracic facet joints that allow for lateral flexion and torsional motion while restricting forward flexion and extension.⁷ Additionally, the thoracic spine is kyphotic due to the anterior wedging of the vertebral bodies. Some have suggested that this kyphosis may predispose the thoracic spine to flexion-compression injuries, which may be further aggravated after a surgical laminectomy or traumatic posterior element disruption.8 Attainment of stability is paramount in the thoracolumbar region (T11 to L1) because of the large forces focused on this zone of transition from the stiff, kyphotic thoracic spine to the flexible, lordotic lumbar spine.¹

An anatomic factor of significance in the thoracic spine is the relatively small spinal canal. The spinal canal from T2 to T10 has the smallest ratio of canal to cord diameter of the entire neuroaxis.^9,10 This may help explain the high ratio of complete to incomplete spinal cord injuries in this region. It also emphasizes the need for adequate stability to protect the delicate neuroanatomy of the region.

♦ Clinical Presentation

If initial evaluation fails to recognize and adequately treat “at-risk” injuries or if additional trauma to the injured spinal segment occurs, patients may over time develop a slowly progressive post-traumatic deformity associated with pain and the possibility of a new onset or worsening neurologic deficit. Gradually, a progressive deformity may become evident resulting from a combination of occult instability and normal or abnormal physiologic stresses over time.^11,12

The most common presenting complaint of post-traumatic deformity is a dull, aching pain at the apex of the deformity.^13,14 Strenuous activity and prolonged sitting or standing generally aggravates the pain.¹⁵ Altered stress patterns on the adjacent vertebral column and soft tissues, as well as early degenerative changes are theorized to contribute to pain in such patients.¹⁶

Bohlman et al. have shown significant pain relief in 41 of 45 patients after late anterior decompression for chronic pain or paralysis after thoracolumbar injuries at an average of 4.5 years follow-up.¹⁷ Pain is rarely the sole criteria for surgical intervention as the majority of patients also have radiographic evidence of deformity progression, with or without a static or progressive neurologic deficit.

Malcolm and co-workers reported on 48 operatively treated patients with post-traumatic deformity of which 13 (27%) had progressive neurologic deterioration.¹⁵ Other causes of neurologic deterioration included the development of a post-traumatic syrinx or progressive post-traumatic cystic myelopathy.^18,19 These patients must also be evaluated for tethering of the spinal cord, arachnoiditis, spinal cord compression, or microcystic cord degeneration. Treatment for cystic expansile lesions of the spinal cord has had limited success with cerebrospinal fluid shunting procedures resulting in a 50% rate of shunt revision.²⁰ Nonprogressive spinal kyphotic deformity without evidence of cystic lesions of the spinal cord is also a rare cause of neurologic deterioration. Abel et al. reported on a group of 68 patients without evidence of spinal cord cystic degeneration, but who presented with symptoms of progressive neurologic deterioration in the setting of a post-traumatic deformity.⁴ They noted that the incidence of spinal cord cystic degeneration in patients with 15 degrees of kyphosis, or less than 25% spinal canal stenosis, was half that of patients with larger deformities. Neurologic deterioration was instead related to progressive deformity, stenosis, instability, arachnoiditis, and spinal cord tethering.

♦ Radiographic Evaluation

Plain radiographs, including long cassette 36-in standing anteroposterior and lateral radiographs, are essential in assessing the overall coronal and sagittal balance of the spine in the post-traumatic setting. Particular attention should be paid to the status of the posterior elements to evaluate for the presence of splaying of the spinous processes that is frequently associated with insufficiency of the posterior ligamentous complex. Flexion/extension and lateral bending radiographs are also useful in assessing the flexibility of the spinal deformity. Comparison of these films to the immediate postinjury and follow-up films will help clearly document changes in spinal alignment over time.¹¹

Sagittal alignment can be evaluated with the use of a plumb line dropped from the external auditory meatus. This line should pass through the anterior portion of the S1 body.¹⁸ Alternatively, this line can also be dropped from the middle of the C7 body and should fall close to the posterosuperior corner of the S1 body.²¹ Areas of kyphosis, lordosis, and scoliosis are measured by use of the Cobb technique.²² Focal kyphotic deformities are best measured using the vertebral body above and below the injury as direct measurement of the fractured vertebrae is subject to significant observer variation.^16,18

Computed tomography (CT) is an excellent imaging modality to visualize specific bony anatomy, especially the posterior elements and the posterior wall of the vertebral body, which may be difficult to accurately evaluate on plain radiographs. Obtaining 1- to 3-mm axial cuts, along with sagittal and coronal reconstructions, allows for optimum evaluation of all bony landmarks. Computed tomography can also be combined with myelography to assess the status of the neural elements, especially in situations in which MRI cannot be used or is suboptimal, such as in the postsurgical setting or in the presence of internal fixation.

Magnetic resonance imaging (MRI) is most useful in evaluating the spinal cord and soft tissues surrounding the vertebral column. It is also an excellent way to quantify neural element compression, which is critical before undergoing a surgical correction that may cause further spinal cord impingement. Subtle changes within the parenchyma of the spinal cord that may be indicative of edema, fluid collections, or scarring may also be identified. Importantly, MRI allows evaluation of the posterior ligamentous tissues of the spine that may help predict patterns of spinal instability, which is critical in preoperative planning. MRI is also invaluable in diagnosing post-traumatic syringomyelia or progressive cystic myelopathy, which has been reported to have a prevalence between 3.2% and 40% in spinal cord injury patients.^23,24

♦ Biomechanics

The majority of post-traumatic deformities of the thoracolumbar spine have misalignment of the spinal axis in more than one plane. A three-dimensional deformity involving the sagittal and or coronal plane may also be associated with a translational and or rotatory deformity. The majority of these deformities, however, are often characterized by the dominant planar deformity. It is imperative, however, for the treating physician to fully appreciate the three-dimensional nature of all post-traumatic spinal deformities.

A focal post-traumatic kyphotic deformity is generally caused by a flexion and compression type injury.25–27 The deforming force causes a loss of anterior column height and a variable loss of middle column height with or without a distraction-type injury to the posterior column. There is often a compensatory hyperextension of the adjacent spinal motion segments to correct for the altered sagittal alignment. This may result in altered facet joint function, intervertebral shear, and contracture of the posterior spinal ligaments, possibly leading to early degeneration of the adjacent motion segments.^16,18 If the posterior bony-ligamentous column is disrupted at the apex of the kyphotic deformity, the deformity may worsen with time even if properly immobilized. Injuries such as an unstable burst fracture, flexion-compression injury, or flexion-distraction injury are especially prone to post-traumatic deformity. This is especially true at the thoracolumbar junction, even in the setting of appropriate spinal immobilization.^28–31

Lordotic Deformity

A post-traumatic thoracolumbar sagittal plane lordotic deformity is relatively uncommon. Such a deformity may be seen after a primarily distraction-extension mechanism with disruption of the anterior longitudinal ligament, intervertebral disk complex, and compromise to the osseous posterior elements.

Deformity in the Coronal Plane

Scoliotic Deformity

Asymmetric lateral-flexion and compressive forces in the setting of a compromised spinal axis may lead to a post-traumatic coronal or scoliotic deformity. External compressive loads and asymmetric loss of vertebral height in the coronal plane at one or multiple adjacent levels may contribute to this deformity. Progression of post-traumatic coronal plane deformity is much more prevalent in the setting of a significant neurologic injury especially in younger age groups.^11,32,33

Additionally, the most significant factor influencing the development of scoliosis in the setting of a spinal cord injury is the age of the patient when the injury occurs. The incidence of scoliosis has been previously reported to be 100% in children with spinal cord injury below the age of 10, 19% in children between 10 and 16, and 12% in patients older than 17.^32,33

The injury pattern, the degree of skeletal maturity, and the associated neurologic deficits are not the sole causes of coronal plane deformity after a fracture of the thoracolumbar spine. Other reported etiologies include the effect of gravity, trunk muscle imbalance, osteoporosis or other metabolic bone diseases, loss of vertebral strength, hip contractures, and pelvic obliquity.^32,33

Related posts:

Flexible versus Fixed Spinal Deformity Anterior/Posterior (AP) Surgery for Spinal Deformity Principles of Sagittal Plane Deformity Technological Advances in Spinal Deformity Surgery Congenital Scoliosis Posterior Surgery for Thoracic Scoliosis

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