The most acute form of spinal cord compression is caused by trauma, of which 50% occurs in the cervical spine and most of the remainder at the thoracolumbar junction or in the lumbar spine. Patients are usually young males involved in road traffic accidents, falls, and occasionally sport related activities.2 The forces involved can be resolved into flexion, extension, compression, and rotation, although most patterns of fracture and subluxation seen in practice result from a combination of these forces. In approximately 10% of cases, two noncontiguous levels of the cervical spine are damaged, separated by normal segments.3

The management of acute spinal cord injury can be intimidating to those unfamiliar with this clinical problem. In fact, the major components of management of spine trauma are analogous to the management of a fracture of a long bone. The steps involved are recognition, immobilisation, investigation, reduction, fixation, and rehabilitation.

In most cases, the combination of neurological deficit and a painful, tender cervical region leads to recognition of the injury. Where the patient is unable to provide a history, for example, in the presence of an associated head injury with a decreased conscious level, it is best to presume that a spinal injury is present until proven otherwise.

The cervical spine can be immobilised easily by holding the head firmly between two hands and maintaining the cervical spine in a neutral position until better facilities are available. If the patient needs to be moved, to examine the back for example, a strict "logrolling" technique with an adequate number of personnel should be observed. Depending on the circumstances, the patient may be fitted with an appropriate sized Philadelphia style collar or be placed in cervical traction. Soft cervical collars are not adequate as they barely restrict flexion and extension movements of the cervical spine. A Philadelphia style collar supports the occiput, spreads over the shoulders, rises over the chin, and provides more effective immobilisation (Figure 10.1). Cervical tongs such as the Gardner-Wells variety may be applied in the casualty department within a matter of seconds. These require local anaesthetic and are placed 4 cm above the external auditory meatus. The pins are hand-screwed through the anaesthetised

Figure 10.1 The main points of support for a Philadelphia style collar are the occiput, shoulders, and chin

scalp into the outer skull cortex to a preset tension. The clinician then has full control of the patient's cervical spine.

Definitive investigations at an early stage must include a lateral plain radiograph of all cervical vertebrae. Some cases of missed fracture in the cervical spine are the result of inadequate radiographs that omit the lower vertebrae. Flexion/ extension views can be particularly revealing and, if carried out carefully, the patient will come to no harm even should the films show abnormal movement. These dynamic views should only be carried out under supervised conditions and after senior or specialised consultation. Cervical spine radiographs are difficult to read, especially for inexperienced junior staff, and experienced staff should be consulted before management decisions are made. More definitive investigation is carried out by CT, which almost always reveals more damage than was initially expected from plain radiographs. If C7 is not seen on ordinary radiographs it is always accessible by CT. MRI may show damage to ligaments, discs, and prevertebral tissues which have a clearly altered signal with this form of scanning, but which may not be recognised using plain radiographs4 (Figure 10.2).

At or before this stage in management, referral should be made to a specialised spinal unit, preferably an acute spinal

Figure 10.2 MRI (1-5T Siemens Magnetom, T2 weighted scan). Discoligamentous injury at C5/6 with anterior subluxation of C5 on C6. Note the altered cord signal at the level of the injury and the high signal in the interspinous ligaments posteriorly

cord injury unit. The Queen Elizabeth National Spinal Injuries Unit for Scotland receives patients with spine trauma, with and without cord injury, usually within 24 hours of injury. The pathophysiological consequences of acute spinal cord injury on cardiovascular and respiratory function and the intensive nursing requirements make early referral of these patients to an appropriate unit imperative. Spinal cord damage results in attenuated sympathetic neural control causing hypotension and bradycardia. These are "normal" for a patient who has functional cord transection and attempts at "volume loading" to elevate blood pressure are misplaced. Loss of intercostal innervation due to cervical cord trauma produces ventilatory insufficiency that is best managed in specialised units.5

Fractures, subluxations, or dislocations usually require reduction into normal alignment. This may be relatively easily brought about using simple cervical traction. In the 1970s there was a vogue for using high weight cervical traction, but this carries a risk of secondary cord damage by excessive distraction. Depending on the type and displacement of the injury, the vector of traction may need to be varied, for example by using a rolled up sheet under the shoulders to exaggerate the lordotic curve of the cervical spine. These techniques require frequent radiographic assessment and management experience and are best left to the specialist unit. Should appropriate cervical traction be unsuccessful in reducing the fracture-dislocation, the options are manipulation under anaesthesia, rarely used now, or open reduction and internal fixation. Those patients who have vertebral damage but no spinal cord injury are vulnerable to secondary injury through inadvertent or accidental mishandling of the spine and have potentially more to lose than those patients who sustain major spinal cord damage at the time of impact.

Fixation of the cervical spine may be carried out using external orthotic supports such as a halo fixator which is particularly useful for high cervical fractures. Even in this device a small range of flexion and extension can still occur. Methods of internal fixation have evolved and improved, especially in recent years. In the cervical spine, plate or rod and screw constructs are increasingly replacing sublaminar wires and laminar clamp devices. Internal fixation enables the patient to begin mobilisation and rehabilitation at an earlier stage.6 For thoracic and lumbar fractures the use of pedicle screw fixation reduces the number of vertebral levels permanently immobilised and allows intraoperative fracture reduction and restoration of alignment.7 Malalignment of the spinal column is reduced using internal fixation, but long term stability only comes through bone union. There is continued debate among specialists over the merits, demerits, and appropriate timing of surgical intervention in spinal injury. It is clear that in selected circumstances internal fixation and fusion does have a role to play and does impart advantages to patients, allowing earlier mobilisation for rehabilitation and conferring better long term stability. There is no evidence, however, that surgical intervention improves neurological outcome. Despite anecdotal reports, there is no recognised causal association between surgical decompression and fixation and neurological recovery in patients with acute spinal trauma.8

Enthusiasm for the use of high dose methylprednisolone in acute spinal trauma, especially in North America, followed the publication of the second national acute spinal cord injury study (NASCIS 11).9 This prospective, randomised trial showed statistical improvement in limb function where the steroid was administered as a bolus infusion of 30 mg/kg given over 15 minutes and, after a 45 minute pause, followed by an infusion of 5 4 mg/kg per hour over 23 hours. This statistical improvement, however, was mainly sensory so that it did not result in any clear functional or clinical gain by the patient. The steroid treated group had a higher rate of infectious complications. For these reasons, this practice has not become established in the United Kingdom. Methylprednisolone is not given routinely at the Queen Elizabeth National Spinal Injuries Unit for Scotland.

More recently, substantial concern has been raised about the methodology of the study and of the subsequent NASCIS III trial.10 Coleman et al. questioned the appropriateness of generalising results from a trial population that included individuals with minor cord injury to the more severely injured population and pointed out a concern that the positive result of the trial could be a statistical artefact. The placebo group treated before eight hours did poorly not only when compared to the group that received steroids but also when compared to the second placebo group, treated after eight hours, suggesting that the early placebo group was perhaps more severely injured than either of the other two groups. Finally, a concern that the primary data from NASCIS were not publicly available even nine years after completion of the trial means that reporting of these studies does not meet standards required for FDA approval.11

Hurlbert called the use of methylprednisolone in spinal cord injury "an inappropriate standard of care" and raised further concerns that half of the data from the trials (all observations on the left side of all patients) were excluded from analysis.12 The primary outcome analysis was negative and despite more than 60 post hoc tests, no correction for multiple comparisons was provided. He analysed six other studies of steroids in spinal cord injury demonstrating that the results are not reproducible, and offered compelling arguments and an analysis of the available data supporting the view that methylprednisolone should be considered an investigational agent with an unproven role in spinal cord injury. The handicap posed to future studies in neuroprotection if this status is not recognised is also highlighted.13 Although the NASCIS trials were prospective and randomised, well designed, and well executed, they do not provide compelling data, appropriate analysis, or evidence of clinically meaningful outcomes. The results are not reproducible and thus they fall well short of criteria for Level I evidence (evidence sufficient to support a standard of care). The use of steroids in spinal cord trauma should be considered unproven and experimental.

As in severe head injury, the primary traumatic event in spinal cord injury is followed by microvascular and biochemical changes that compound the original injury. It may be possible to block or attenuate some of these changes pharmacologically. For example, the action of the excitotoxin glutamate, released following trauma to central neural tissue, can be modified using N-methyl-D-aspartate receptor blockade in experimental models. Although considerable attention has been focused on biochemical methods of preventing or modifying the secondary damage produced following brain and spinal cord injury/4 none are yet proven in clinical trials. A randomised controlled trial of ganglioside GMI (Syngen) failed to show a benefit of the drug in a primary efficacy analysis. It did suggest, however, an earlier recovery in the treated group and that further studies of the drug in incomplete injuries should be undertaken, as these patients showed a trend to improvement that did not reach significance due to small numbers of patients. The hope that effective pharmacological neuroprotective agents may be found thus persists though it is as yet unrealised.15

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