Injury to the thoracic region represents approximately 15 per cent of all fractures occurring in the thoracic and lumbar spine combined. Although the anatomic definition of the thoracic spine includes the level T1 to T12 we limit this discussion to T1 to T10 for reasons that will be elaborated later. The most frequent causes of thoracic trauma are motor vehicle accidents (automobile and motorcycle), falls from a height, and gunshot injuries.

Patients with thoracic spine fractures require careful evaluation and monitoring for associated trauma. Rolling the victim like a log on to a long fracture board and immobilizing them are essential measures in the early phase of evaluation and treatment. The most common associated injuries are head injuries, extremity fractures, and multiple rib fractures. A high index of suspicion should also be maintained for cardiovascular and pulmonary injuries. Routine radiographs need frequently to be supplemented with CT scans and MRI since this region of the spine is difficult, at best, to visualize on plain films.

Neurological injury occurs in 50 to 80 per cent of these patients, such injury being directly related to the low canal-to-cord ratio in this region and the presence of tenuously vascularized central nervous system tissue. Progressive neurologic loss in a cephalad direction, is ascribed to vascular insufficiency, cord oedema, and inflammatory necrosis.

The biomechanical forces most frequently implicated are axial load and flexion. Given the normal 40 to 45° of thoracic kyphosis it is easy to understand that axial force translates to a flexion/compression vector. The three most common fracture patterns encountered in the thoracic spine are the compression/anterior wedge, burst fracture, and fracture dislocations.

Axial load to the normally kyphotic thoracic spine results in force vectors creating an anterior wedge fracture. This type of fracture is commonly sustained in automobile and motorcycle accidents. Once identified on screening radiographs spot films of the injured level are obtained. Up to 25 per cent loss of anterior vertebral height is consistent with a stable injury.

Patients with loss of anterior height of 25 per cent or less may be treated symptomatically with close follow-up. The development of progressive kyphosis heralds an unstable injury with the potential for late neurological damage or painful gibbus deformity. When the anterior compression is 35 per cent or greater an unstable fracture should be suspected. This situation does not necessarily exclude orthotic treatment, but rather requires extremely well monitored follow-up. The physician should be most vigilant during the first 2 to 3 weeks after injury. During this time a comminuted vertebral body may be resorbed promoting further kyphotic angulation of the fracture and indicating the need for internal stabilization. Patients who present with 50 per cent or greater loss of anterior height should be considered for primary posterior surgical stabilization.

With sufficient force, axial loading to the thoracic spine produces failure of the posterior vertebral body wall with retropulsion of bony fragments into the canal. This fracture pattern represents failure of the anterior and middle columns. However, the kyphosis of this region naturally prevents true axial loading of the middle column. The pathognomonic sign of this fracture is widening of the interpedicular distance on the anteroposterior view compared with uninjured adjacent levels. The CT scan will demonstrate a comminuted vertebral body fracture with variable retropulsion of bony fragment into the neural canal. A 59 per cent incidence of complete neurological injury occurs when this fracture is in the thoracic spine.

Burst fractures of the thoracic spine are usually unstable. Surgical stabilization is aimed at restoring normal spinal alignment and height as well as preventing future deformity and neural injury. Some spine surgeons recommend treating these fractures with posterior distraction instrumentation (e.g. Harrington rods). As the intact posterior longitudinal ligament is stretched, theoretically the vertebral canal is cleared of the retropulsed bony fragments. An anterior approach to these injuries has been recommended citing complete clearing of the neural canal as a particular advantage to that technique.

Fracture - dislocation frequently implies that a combination of forces has acted on the spine. These combined forces produce rotation or shearing between the individual spinal segments. Motor vehicle accidents are the leading cause of fracture - dislocations. The fact that a dislocation has occurred indicates three-column instability. Furthermore, the amount of displacement seen in these injuries (which probably was greatest at the time of impact) produces rather predictable neurological damage. Hanley and Eskay report 75 per cent of patients with complete neurological deficit and only 11 per cent with normal neurological function.

The grossly unstable nature of these injuries with the associated displacement nearly always dictates surgical stabilization. If the overall condition of the patient precludes a surgical procedure then strict bed rest for 2 to 3 months may allow the fracture to heal. A certain degree of deformity will be a likely result from conservative treatment. Delayed surgical management is certainly an option; however, delaying for more than 10 to 14 days may preclude simple posterior stabilization.

Hanley EN, Eskay ML. Thoracic spine fractures. Orthopedics 1989; 12: 689 - 96.

Kostuik JP. Anterior fixation for burst fractures of the thoracic and lumbar spine with or without neurological involvement. Spine 1988; 13: 286 - 93.

Kupferschmid JP, Weaver ML, Raves JJ, Diamond DL. Thoracic spine injuries in victims of motorcycle accidents. J Trauma 1989; 29: 593 - 6.

McAfee PC, Bohlman HH, Yuan HA. Anterior decompression of traumatic thoracolumbar fractures with incomplete neurological deficit using a retroperitoneal approach. J Bone Joint Surg 1985; 67A: 89 - 104.

Meyer PR. Surgery of spine trauma. New York: Churchill Livingstone, 1989.