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Thoracolumbar Vertebral Fractures
A Review Of Litrature

*Dr. V.M Thomas,   **Dr. Arun .B,    *** Dr. Anwar. Marthya

*PG Trainee, **PG Trainee,  ***Senior Lecturer,
Department of Orthopaedics, Medical College, Calicut.

Address for Correspondence

Dr. V.M Thomas,
PG Trainee,Department of Orthopaedics, Medical College, Calicut, Kerala, India.


In the ancient Egyptian papyrus, Traumatic quadriplegia and paraplegia was considered a condition not to be treated.  Paul of Aegina (AD 625-690) was the first surgeon to do laminectomy for this condition. When the vertebral column injury occurs some degree of neurological deficit is present in significant percentage of cases.  Neurological injury occurs in 40% in the cervical vertebral injury and 15% in thoraco lumbar injury.   The outlook for patients with incomplete thoracolumbar neurological injuries has improved and can be enhanced if an optimum environment for neurological recovery is provided.  The long-term survival and the possibility of functional rehabilitation of patients with spinal cord injuries has led to increased interest in treatment of these patients.  Although corticosteroids have been shown to improve neurological recovery of patients with spinal cord injuries16, the primary treatment of patients with thoracolumbar injuries is surgical reduction, decompression, and stabilization.  Controversies regarding the classification of fractures, timing of surgical intervention and type of surgical approach exist.

J.Orthopaedics 2004;1(2)e4


Classification of thoracolumbar fracture

Spinal fracture classifications systems have been developed to aid in the understanding of fracture stability and help direct treatment.  Denis and McAfee et al described fractures based on their morphologic features.  Holdsworth and Whitesides used combinations of mechanistic and morphologic systems to classify injuries.  The McAfee system identifies six fracture types (Table 1) based on CT scan findings is currently the best classification.

Table 1: McAfee Classification of thoracolumbar spine fractures

Injury Type


Wedge-compression fracture

Isolated anterior column failure

Stable burst fracture

Anterior and middle-column compression failure, posterior column intact

Unstable burst fracture I


Compressive failure of anterior and middle columns, disruption of posterior column

Chance fracture

Horizontal vertebral avulsion injury with center of rotation anterior to vertebral body

Flexion-distraction injury

Compressive failure of anterior column, tensile failure of posterior column.  The center of rotation is posterior to anterior longitudinal ligament

Translational injuries

Disruption of spinal canal alignment in transverse plane, shear mechanism common


Neurologic classification

The American Spinal Injury Association (ASIA) defines a complete neurologic lesion as an absence of sensory and motor function below the level of injury including the lowest sacral segment2.  Although patients can be in “spinal shock”, when all reflex activities are lost, Stauffer et al have demonstrated that a bulbocavernosus reflex returns within 24 hours in 99% of patients, thus indicating the end of spinal shock.  Complete injuries have a less than 3% chance of functional motor recovery if no neurological return is seen within 24 hours and have no chance of neurological recovery after 24 to 48 hours.

A lesion is incomplete if sensory, motor, or both functions are partially present below the neurological level of injury.  Sacral sensation at the mucocutaneous junction and the presence of voluntary contraction of the external anal sphincter on digital examination should be carefully elicited as this may be the only sign of preserved function.  Patients with incomplete neurological injuries are expected to improve, with many regaining the ability to ambulate.

The level of neurological injury is graded at the lowest nerve root level that has at least antigravity strength.  Clinically recognized syndromes are given in Table 2.  Overall gross function of patients with spinal cord injuries is assessed by the Frankel classification.  This scale has recently been modified by ASIA (Table 3).

Table 2: Incomplete cord syndromes



Anterior cord

A lesion that produces variable loss of motor function and of sensitivity to pain and temperature, while preserving proprioception


A lesion that produces relatively greater ipsilateral proprioceptive and motor loss and contralateral loss of sensitivity to pain and temperature

Central cord

A lesion, occurring almost exclusively in the cervical region, that produces sacral sensory sparing and greater weakness in the upper limbs than in the lower limbs

Dorsal cord (posterior cord)

A lesion occurring almost in the dorsal sensory column mainly affecting proprioception 

Conus medullaris

Injury of the sacral cord (conus) and lumbar nerve roots within the neural canal, which usually results in an areflexic bladder, bowel, and lower limbs.  Sacral segments may occasionally show preserved reflexes. E.g., bulbocavernosus and micturition reflexes.

Cauda equina

Injury to the lumbosacral nerve roots within the neural canal resulting in areflexic bladder, bowel and lower limbs.

 Table 3: ASIA impairment scale




Complete: No sensory or motor function below level of neurologic deficit level.  Sacral sparing is absent.


Incomplete.  Sensory but not motor function is preserved below the neurologic deficit level


Incomplete.  Motor function is preserved below the neurologic deficit level, and the majority of key muscles below the neurologic deficit level has a muscle grade lower than 3


Incomplete.  Motor function is preserved below the neurologic deficit level, and the majority of key muscles below the neurologic deficit level, has a muscle grade higher or equal to 3.


Sensory and motor function is normal


Neurological injury of spinal cord

Primary injuries – which occur at the time of injury. 





Secondary injury – which occur later as the result of


Swelling that accompany all spinal injuries

Late sequelae

Chronic pain

Delayed neurological deterioration due to spinal deformity, residual spinal compression, scar formation and post traumatic Syringomyelia

Pathophysiology of neurologic injury

Neurologic injuries result from two basic mechanisms, compression or traction.  Traction injuries in the thoracolumbar area frequently arise from seat-belt-type accidents  Traction injuries to neurologic structures have a poor prognosis for recovery.  Compressive injuries cause neurologic injury from crushing and then from persistent compression on the cord and nerve roots.

The effects of the duration and magnitude of compression and contusion on neurologic recovery have been studied in animal experiments.  Bohlmann et al developed an anterior cervical spinal cord injury model in dogs.  He demonstrated differences in neurologic recovery between compression and contusion injuries.  Animals that had contusion injuries recovered fully over time; however, those animals with persistent compression achieved full recovery only after decompression.  No correlation between the neurologic function of the animals and the extent of histopathologic damage was found.  Using a rat model, Rivlin and Tator found that the clinical consequence of cord compression was inversely related to the duration of cord compression.  Similarly, Dolan et al found that increasing the force and the duration of spinal cord compression was directly proportional to a reduction in neurological recovery.  Delamarter et al showed that a 50% compression of the Cauda equina led to significant neurophysiologic and electrodiagnostic changes in dogs.  A 75% compression of the Cauda equina resulted in permanent paraplegia.

More recently, Delamarter et al created spinal cord injuries at L5 and L6 just above the conus in dogs using constriction bands.  The animals underwent “decompression” immediately, and at 1,6, and 24 hours.  Those animals that had decompression immediately and at 1 hour were clinically and electrophysiologically normal at 6 weeks, although histologically gray matter necrosis was noted.  The animals “decompressed” at 6 hours or later did not make significant neurologic recovery.

The intrinsic mechanisms occurring during cord injury have been extensively investigated.  The initial phase is characterised by hemorrhage into the cord and formation of edema at the injured site and surrounding region.  Local spinal cord blood flow is diminished and can be further compromised by extension of edema.  A secondary tissue degeneration phase begins within hours of injury due to release of membrane-destabilizing enzymes, mediators of inflammation, and disturbance of electrophysiological coupling by disruption of calcium channel pathways.  Lipid peroxidation and hydrolysis appears to play a major role in the secondary phase of spinal cord injury.  Current pharmacologic intervention, such as methylprednisolone, gangliosides, and lazaroids, aims to suppress the secondary cell destruction phase on a biochemical basis.  Bracken et al16 reported the results of a randomized double blind study in patients with spinal cord injuries.  High doses of methylprednisolone, naloxone, or a placebo were administered to 487 patients.  The patients given methylprednisolone had statistically significant improvement of motor and sensory scores compared with the two other groups.  To be effective, the drug had to be administered within 8 hours of injury.  Methylprednisolone was administered as a 30mg/kg loading dose and as a continuous 5.4mg/kg/hr dosage for 23 hours. 

Recovery of neural function may be further influenced by the vascular supply to the spinal cord.  The thoracic spinal cord has relatively poor vascular supply as opposed to the cervical spinal cord and the conus medullaris, which have a more abundant collateral network.  Additionally, after injury, the spinal cord loses its ability to autoregulate, and, therefore, spinal cord blood flow becomes directly related to blood pressure.

These studies support the basic principles of immobilization, fracture reduction, stabilization and decompression in patients with spinal cord injuries.  The concept of early decompression is supported by human and animal studies; however, some neurologic recovery can be gained by late decompression.

Patient evaluation

Resuscitation of patients with spinal cord injuries follows the principles established by the American College of Surgeons.  Further diagnostic and therapeutic measures are dictated by the presence of concomitant injuries, which occur in 47% to 60% of patients with spinal injuries.  Hypertension associated with bradycardia may be secondary to neurogenic shock and often is present in patients with thoracolumbar spinal cord injuries.  The presence of protracted neurogenic shock in the absence of other sources of volume loss should be treated with vasopressors to avoid over infusion and possible development of pulmonary edema.

After resuscitation, the patient is rolled to allow inspection and palpation of the spinal column.  Areas of localized tenderness, gaps between spinous processes, swelling, and gibbous deformities are elicited.  Persistent localized tenderness despite normal radiographs is associated with occult fractures in more than 30% of our patients.

Muscle strength is measured by systematic evaluation of all muscle groups of the extremities and the anal sphincter.  Sensory examination includes testing of proprioceptive and pain temperature pathways.  Presence and quality of deep tendon reflexes and long tract signs are evaluated in all extremities.  Because the prognosis of a patient with an incomplete neurologic deficit may be considerably altered by an appropriate intervention, it is imperative that this neurologic examination is recorded in the patient’s chart.  Preservation of perianal pin prick sensation, voluntary rectal tone, and great toe flexion are considered signs of sacral sparing and may be the only remaining neurologic function in some patients with incomplete spinal cord injuries.  The presence of sacral sparing implies at least some structural continuity of the long tracts and should lead to timely attempts at optimizing chances for neural recovery.

Radiological assessment

Anteroposterior and lateral radiographs are obtained in patients with suspected spinal injuries.  If one spinal fracture is detected, a complete spine series is required, because noncontiguous spine fractures occur in 10% to 30% of patients.

CT has enhanced the understanding of mechanisms of neurologic injury and fracture morphology.  The middle column and subtle posterior injuries can easily be diagnosed with.  To allow accurate fracture classification and to help direct treatment, we recommend CT examination in the majority of patients with thoracolumbar fractures.

Magnetic resonance imaging (MRI) can demonstrate spinal cord pathology and the presence of neural compression.  Other soft tissue injuries and the state of the intervertebral disk can be identified.  Cotler et al reported that MRI can predict neurologic recovery based on T2 weighted images.  MRI is indicated in patients with progressive neurologic deterioration, incongruous neurologic and skeletal injury, and unexplained neurologic deficit.  Also, MRI can be used to assess the status of the posterior ligamentous complex.  Myelography has little role in the evaluation of patients with acute neurologic injury, unless MRI is not available.

Emergency treatment

Prior to definitive treatment, patients are rolled every 2 hours to prevent decubitus ulcers.  Considerable fracture site motion can occur with this technique; therefore, we believe truly unstable fractures require surgical stabilization.

All patients with spinal cord injuries presenting with in 8 hours from injury should receive high doses of methylprednisolone as specified previously.

Surgical treatment

We currently recommend early surgical treatment for patients with thoracolumbar fracture for complete and incomplete spinal cord injury.

Goals of surgery

The goals of surgery are to reduce fracture and dislocations, stabilize the injured segment and decompress the neural elements.  Injuries of the cervical spine can usually be reduced quickly using skeletal traction.  Fracture reduction results in an indirect decompression of the neural elements and may lead to improved neurologic recovery.  Because nonoperative means usually fail to achieve an anatomic fracture reduction in the thoracolumbar spine, we, therefore, recommend early surgical treatment in patients with partial defects.  Unfortunately, surgical treatment for complete paraplegic patients does not result in significant neurologic recovery.  Early surgical care in patients with complete paraplegia does decrease the rate of complications, hospitalization time, and overall costs, however.  Other indications for emergent surgical care are patients with progressive neurologic deficits, open spine fractures, and burns of the torso with concomitant unstable spine fractures.

Timing of surgery

Timing of surgical intervention and the effect on neurologic outcome remain controversial.  The only accepted indication for emergent surgical treatment in a  patient with a thoracolumbar fracture is progressive neurologic deterioration.  This complication is rare, seen in 1% t0 2% of cases and may be secondary to fracture displacement, expanding epidural hematoma, spinal cord edema, or infarction.  Immediate spinal realignment and decompression of the neural elements has been shown to consistently reduce permanent neurologic sequelae in several animal investigations.  There appears to be a small window of time below 4 hours, when spinal cord decompression can result in reversal of neurologic deficits.  We have observed this phenomenon in three patients with bilateral cervical facet dislocations who had reduction within 2 hours of injury.  After reduction, these patients felt an immediate return of sensation, and the rapid return of motor function over the next 24 hours.

Krengel et al evaluated efficacy of surgical decompression within the first 24 hours in patients with incomplete spinal cord injury secondary to fractures between T3 and T11.  Thirteen patients presented with Frankel B or C paraplegia.  The average improvement in Frankel score was 2.2 grades, with 11 of 13 regaining the ability to ambulate.  These results exceeded outcomes reported for other treatment methods, including nonoperative treatment, delayed posterior instrumentation, or late anterior decompression.  No patients developed neurologic worsening as a result of early treatment.


Non operative management

Postural reduction for the treatment of spinal cord injuries was developed by L.Guttman at the Stoke Mandeville Hospital.  The treatment methods consisted of rotating beds supplemented by pillows and rolls placed under the patients’ backs to support a reduced position.  Duration of  recumbency averaged 10 to 13 weeks followed by a supportive plastic jacket for several weeks.

A long term outcome of closed treatment in neurologically intact patients with thoracolumbar burst fractures was recently reported by Mumford et al.  They found that 66% of patients had good or excellent results at a follow-up an average of 2 years later.  Only one patient developed neurologic deterioration (2.1%).  Radiagraphic follow-up of these patients revealed an average increase of kyphosis of 30 and an improvement of the canal compromise from an initial average of 37% (16% to 66%) to 14% (3% to 40%) secondary to remodelling.

Jacobs et al compared recumbent treatment and posterior instrumentation in patients with incomplete thoracolumbar cord lesions.  They documented a 44% incidence of improvement in the non operative treatment group compared with a 53% improvement in the Harrington rod group.  The group treated with Harrington rods had better fracture reduction, fewer complications, and spent less time for rehabilitation than the recumbent treatment group.  Burke and Murray, however, found no significant differences in their comparison of nonoperatively and operatively treated patients with injuries between T2 and T11 and initial Frankel grades B and C.

In the majority of comparison studies between surgical and non surgical treatment, it appears that neurologic recovery is enhanced in surgically treated patients.

Surgical treatment

            The choice of surgical approach and instrumentation requires a thorough understanding of fracture type, injury level, and degree of neural injury.  Patients who have a distractive injury of the posterior elements that occurs in flexion-distraction injuries, Chance-type injuries, and fracture-dislocations are best treated with posterior instrumentation.  Patients with unstable burst injuries and incomplete paraplegia associated with high-grade spinal canal stenosis may benefit in the long term from immediate anterior decompression.  Patients with unstable burst fractures and lesser degrees of canal stenosis are treated by posterior instrumentation.

Principles of surgical care

For posterior approaches, the patient is placed prone using a Stryker frame.  A transverse pelvic roll increases lordosis, thus reducing the deformity.  The use of succinylcholine is contraindicated in patients with neurologic injury because it can lead to an uncontrolled release of potassium and ventricular fibrillation.

 Early surgical treatment of thoracolumbar fractures may be associated with extensive blood loss; however, induced hypotension is contraindicated because this can lead to a decrease in spinal perfusion because of the loss of spinal cord autoregulation.  To limit transfusion requirements, we routinely collect blood in the cell saver device.

After surgery, the patient is casted in the operating theatre for a custom-molded orthosis.  This step allows for earlier patient ambulation and decreases hospitalization time.  The orthoses is worn for 3 to 4 months.

Posterior Surgical Treatment of Unstable Burst Fractures

In unstable burst-type fractures, the spinal deformity consists of a loss of vertebral body height, kyphotic angulation, and retropulsion of bone into the spinal canal.  Posterior instrumentation restores vertebral body height via distraction forces.  Additionally, the anterior and middle columns are restored to normal length during correction of the kyphosis.  The spinal column assumes the contour of the rods, resulting in correction of the kyphotic deformity.  This correction is facilitated by using Harrington rods with square-ended hooks or rod sleeves.  Newer systems reduce deformity by in situ rod contouring or allowing rotation of hooks and pedicle screws about vertical bars or rods.

The techniques of posterior instrumentation for thoracolumbar burst fractures have been studied extensively.  In simple rod-hook systems at least two levels above and below the injury should be spanned to provide sufficient leverage to achieve and maintain fracture reduction.  The use of instrumentation systems that allow for rod contouring is essential.  Indirect spinal canal decompression is thought to be achieved by development of tension in the posterior longitudinal ligament, which then pushes the retropulsed bone fragments forward.  This process has been termed ligamentotaxis. Crutcher et al found posterior distraction instrumentation to reduce canal compromise by only 50% of the initial occlusion, leaving an average of 32% canal compromise.

Edwards et al developed rod sleeves that are centered over the pedicle of the fractured vertebrae.  They act to push the vertebrae forward, thereby reducing the kyphotic deformity.  To use these rod sleeves, the posterior neural arch must be intact, otherwise iatrogenic neurologic injury can result.  Edwards et al found excellent maintenance of alignment in terms of kyphosis, vertebral body height, and translation in their review of 122 patients.  The spinal canal area was improved by 32% (from 55% patency to 87%) if the rod-sleeve construct was inserted within 2 days of injury.  Between 3 and 14 days, they found a 23% improvement in canal deviance (range, 53% to 76%).  Little improvement was found with surgery after 14 days.  An average of 64% recovery of original neurologic function occurred in incomplete thoracolumbar fractures.

Dick described the “fixateur interne”, which uses 5mm Schantz pins linked to 7mm threaded rods.  The Schanz pins are placed into the pedicles of the vertebrae above and below the injured level.  The long lever arms of the Schanz pins allow excellent control of the unstable spine.  Satisfactory reduction of kyphosis and neurologic recovery occurred in 52% of patients with a Frankel score of A through C.  All patients with Frankel D had at least partial recovery.

Short segment fixation using Cotrel-Du-bousset (CD) instrumentation has had poor outcome as reported by McLain et al.  They reviewed 19 patients and found vertebral collapse, vertebral translation, or hardware failure in 10 patients.  The primary cause for failure was attributed to the fixation device.  Outcome studies using newer systems such as the Texas Scottish Rite Hospital or ISOLA® Spinal Systems in trauma applications have been good.  Moss Miami posterior spinal instrumentation is a new spinal instrumentation introduced, which is a hybrid system using pedicular screws, rods, laminar hooks and pedicular hooks.  It is easy to apply.

An alternative to the arthrodesis of long segments is to limit the fusion to the level of injury and remove the rods about 1 year later to regain motion of the instrumented but not fused segments.  Kahanovitz et al found evidence of articular cartilage degeneration of unfused but instrumented levels in animal and human studies.  Dekutoski et al documented good clinical results and radiographic return of motion in unfused levels in patients with the rod long-fuse short technique.

Posterior treatment of flexion-distraction and Chance-Type Injuries

Flexion-distraction and Chance-Type injuries are associated with neurologic deficit in 10% of cases.  Anderson et al reported on the complete neurologic recovery in all patients with incomplete impairment who were treated with posterior instrumentation.  Patients may present with complete spinal cord injuries at higher levels than the bony injury because of traction spinal cord injuries.  Unfortunately, the prognosis for neural recovery is extremely poor.

Posterior instrumentation is indicated in patients with Chance-type injuries and flexion distraction injuries who have ligamentous injuries, kyphosis of more than 100, or associated abdominal trauma.  Reduction is achieved with lordotic positioning and placement of an interspinous wire.  Flexion-distraction injuries require neutralization using either a rod-hook sleeve or pedicle screw system.  Chance-type injuries can be treated with compression instrumentation.  During reduction, patients should be assessed for displacement of the intervertebral disk into the canal as has been reported by Levine et al and others.

Posterior Treatment of Fracture Dislocations

Patients with facet fracture-dislocations and anterior vertebral body translation usually present with complete paraplegia, although they may rarely present with incomplete neurologic impairment or intact.  These patients are treated posteriorly with segmental instrumentation.  Unchecked distraction can result in excessive lengthening of the spinal column because these injuries may be associated with complete ligament disruption.  Krengel et al reported anatomic reduction after Harrington rod distraction instrumentation in 9 of 10 patients with fracture dislocations of the thoracic spine.  For patients with fracture-dislocations of the lumbar spine, we recommend the use of pedicle screw systems.

Posterior Decompression

Laminectomy is indicated for depressed fractures of the posterior elements, epidural hematoma, and dural lacerations with cerebrospinal fluid leak.

Flesh et al described the posterolateral decompression technique that allows forward impaction of the retropulsed bone and disk fragments, thus decompressing the ventral side of the neural tissues.  This technique is facilitated by removal of the facets or pedicles.  Manipulation and medial retraction of the neural elements in the injury zone and copious epidural bleeding are potential drawbacks of this approach.  

Anterior Decompression and Fusion

Spinal cord injury results in permanent loss of cell nuclei and axonal tracts; however, some viable neural tissue may remain, which may be prevented from recovery because of persistent cord compression.  Anterior decompression has been shown to increase axoplasmic flow, decrease ischemia, and lead to improvement of neurolgic function.

Anterior decompression and strut grafting of the acute burst fracture causes a significant increase of instability and the possible development of a progressive deformity and graft dislodgement.  Anterior instrumentation has been developed to minimize this complication.  The Kaneda device uses threaded rods that rigidly connect to screws placed transversely across the vertebral body.  Distraction or compression can then be applied.

A potential cause of anterior device failure is the settling of the anterior strut graft that occurs during healing.  This settling increases bending on the screws and couplings.  Carl et al found that 3mm of bone graft settling occurred if a strut graft was placed on the bleeding subchondral with keyed-in grafts.  Based on their findings, the authors recommended a dynamized anterior CD instrumentation.  This implant system, however, allowed an average of 80 loss of reduction. 


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 This is a peer reviewed paper 

Please cite as :

V.M Thomas,
Thoracolumbar Vertebral Fractures
A Review Of Literature    
J.Orthopaedics 2004;1(2)e4





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