Chapter 94. Spine Injuries

• Management of life-threatening injuries takes priority over management of spinal injuries.
• In the multiple-trauma setting, spinal injury should be assumed to be present pending appropriate assessment.
• Spinal injuries must be considered unstable until they are evaluated thoroughly.
• Vertebral injuries must be assessed in terms of the potential to create early neurologic injury or late deformity.
• Spinal cord injury is minimized or prevented by limiting the secondary ischemic phase and maintaining appropriate spinal immobilization.
• Complete spinal cord injuries have no potential for functional recovery. Incomplete injuries have recovery potential, which must be maximized.
• Considerations in rehabilitation must be initiated at the outset.

Severely injured patients frequently require ICU admission preoperatively and more commonly postoperatively for monitoring and assessing for change that may require intervention, including surgery. It is estimated that approximately 20% of patients sustaining multiple injuries have associated spinal column trauma that may be the prime reason for ICU admission. More commonly, ICU admission is necessitated by the more immediately life-threatening injuries, and the spinal injury then could be missed or management delayed, leading to significant morbidity or even death. The intensivist plays an important role in determining outcome in these injuries by having a high index of suspicion based on awareness of the mechanisms of spinal injuries and their clinical features. This chapter reviews (1) the mechanism, classification, and clinical picture of spinal injuries and (2) the principles of management of vertebral and spinal neurologic injuries to enable the intensivist to optimize ICU management and recognize the need for early orthopedic and/or neurosurgical consultation.

It is extremely important in the management of multiply injured patients that longer-term rehabilitation considerations not be forgotten because this may result in serious chronic disability. The possibility of cervical spine injury must be considered in anyone who has suffered significant injuries to the face or head, especially those who are unconscious from trauma.1 However, patients who are at risk on the basis of preexisting abnormalities of the cervical spine (e.g., ankylosing spondylitis and congenital anomalies) may suffer serious neck injury as a result of what might appear to be trivial trauma. Knowledge of the mechanism of injury is helpful in considering the possibility of spinal injury (e.g., fractures at the thoracolumbar junction associated with falls from a height).

The vertebral column consists of three components (Fig. 94-1)2:

1. The anterior column, consisting of the anterior two-thirds of the vertebral body, disk, and annulus and the anterior longitudinal ligament

2. The middle column, consisting of the posterior one-third of the vertebral body, disk, and annulus and the posterior longitudinal ligament

3. The posterior column, consisting of the pedicles, laminae, facets, capsule, and the interspinous and supraspinous ligaments

An injury is considered to be stable if only one of the columns is involved and if the injury does not pose a risk of damage to neural structures. Any injury resulting in damage to two or more columns or risking neurologic injury (i.e., damage to the middle column) is considered to be unstable. A great variety of forces or combinations of forces may be applied to the vertebral column (e.g., flexion, extension, flexion-rotation, shear, axial load). The effect of the application of these forces to the vertebral column depends on (1) the magnitude and direction of the force and (2) the underlying anatomy.

A flexion force applied to the cervical spine may result in a pure soft tissue ligamentous injury and dislocation because of the relatively horizontal alignment of the facets. A similar force applied to the lumbar spine most commonly would result in fracture because of the vertical orientation of the facets. An exception is ankylosing spondylitis, where the force is dissipated across the vertebral column, much as it would be in a long bone.3

Cervical

Upper Cervical Spine

Because of the unique anatomy of the occipital-atlantoaxial complex, applied forces result in characteristic injury patterns, as described below.

Jefferson's Fracture

This is a four-part fracture of the ring of the atlas (C1) caused by axial loading (e.g., a fall on the vertex of the skull). If the combined lateral displacement of the lateral masses exceeds 7 mm, disruption of the transverse ligament has occurred, indicating a greater degree of instability4 (Fig. 94-2A). This injury must be differentiated on a lateral x-ray view from a stable fracture involving only the posterior arch of C1 caused by extension (see Fig. 94-2B).

Atlantoaxial Instability (C1 and C2)

Sagittal

A gap greater than 4 mm between the anterior arch of the atlas and the odontoid is due to insufficiency of the transverse ligament.This condition may result from trauma or inflammatory erosion (e.g., rheumatoid arthritis).

Rotational

This injury is a subluxation of variable degree, recognized by asymmetry of the gap between the lateral aspect of the odontoid and the lateral mass of C1 on each side and also a decreased joint space between the lateral masses of C1 and C2.

Fractures of the Odontoid

Shear forces in the sagittal plane cause these fractures. The level of the fracture is variable and has been classified by Anderson and D'Alonzo5 into three types (Fig. 94-3).

Hangman's Fracture

This injury is a traumatic spondylolisthesis of C2–C3. It is a bipedicle fracture of C2, usually from an extension force, with anterior displacement of the body of C2 on C3. There is a low incidence of neurologic injury.

Lower Cervical Spine

These injuries are classified on the basis of the force applied to the neck, as described below.5

Flexion

The applied force may be either compressive or distractive.

Compressive

The force acting through the anterior column results in fracture of the vertebral body. The extent of the injury varies from stable minor wedging of the anterior vertebral body only, with no neurologic loss, to marked intrusion into the neural canal, with frequent severe neurologic loss. There is usually associated facet subluxation and instability (e.g., teardrop and quadrangular fractures).

Distractive

The applied force begins posteriorly, involving the posterior ligamentous complex and, if severe, may involve all three vertebral column components. The extent of the injury varies from relatively stable subluxation through unilateral and bilateral facet dislocations to a complete vertebral body dislocation. The extent and frequency of neurologic injury usually are in proportion to the vertebral injury, but the initial displacement of the vertebrae may have been much more severe than that seen on x-ray.

Extension

The applied force may also be compressive or distractive.

Compressive

This type of force results in fractures through the laminae, which may be sheared off. These fractures can be unilateral or bilateral, and at the extreme, there may be displacement of the vertebral body anteriorly and severe instability. However, since the laminae are sheared off, there may be little intrusion into the neural canal, so the extent of neurologic injury may be less severe than the vertebral injury (Fig. 94-4).

Distractive

There is failure of the anterior column (anterior longitudinal ligament and disk) in tension, and therefore, the anterior column is usually stable in flexion. In young individuals, this condition may be missed easily clinically and radiologically and is associated with a low incidence of neurologic involvement. However, in the elderly with associated preexisting degenerative changes, there may be avulsion of bony spurs from the anterior vertebral body. The cervical spinal cord may be pinched between osteophytes on the posterior vertebral body and infolded ligamentum flavum posteriorly, typically resulting in incomplete injury (usually central cord syndrome; Fig. 94-5).

Vertical Compression

Axial load causes centrifugal displacement and intrusion into the neural canal and subsequent serious neurologic injury.

Lateral Flexion

This results in compression and fracturing of the lateral mass and also frequent contralateral ligament disruption. It is usually associated with nerve root injury on the compression side.

Thoracolumbar

Since the underlying anatomy in the thoracic and lumbar spine is similar, the mechanistic classification proposed by Denis2 is helpful.

Compression

This is usually stable and only involves the anterior column, so there is a low incidence of neurologic injury.

Burst

This condition results from axial load forces and results in major injury to the centrum of the vertebral body and intrusion of bone into the neural canal (Fig. 94-6), often associated with lateral displacement of the pedicles and a vertical fracture of the laminae. There frequently is associated neurologic injury.

Seat-Belt Type (Chance Flexion-Distraction)

This injury is caused by a severe flexion force with the axis of rotation anterior to the vertebral body, resulting in failure of all three columns in tension. The pattern can involve various combinations of bony and ligamentous injury. There is minimal encroachment into the neural canal, and the most common neurologic injury involves the nerve root exiting beneath an involved pedicle and may be unilateral or bilateral.

Fracture Dislocations

These injuries usually are caused by a combination of forces (flexion, rotation, and shear) and result in translation of the vertebrae and severe neurologic loss.

Nerve tissues can be injured by stretching, compression, and laceration. Physical disruption of the spinal cord results in complete, irreversible loss of function. However, autopsy examination of the spinal cord in patients who clinically had a complete injury showed the spinal cord frequently to be structurally intact but to exhibit fibrous and cystic degeneration resembling end-stage ischemic changes.6 Experimentally, in drop-weight tests, the initial finding is hemorrhage into the gray matter of the central cord, which may coalesce and form a central hematomyelia, surrounding edema, and increased interstitial pressure and local ischemia, as evidenced by a severe decrease in oxygen tension and an increased lactic acid concentration.

A second ischemic phase begins shortly afterward and may persist for more than 24 hours, involving both gray and white matter and spreading both proximally and distally from the site of injury.7,8 The mechanism for this secondary vascular injury may be local high concentrations of norepinephrine10–12 or other vasoactive amines. In addition to vascular injury, direct axonal injury would result in permanent functional loss due to the limited ability of central axons to recover.

It has been shown clearly that the effect of injury is directly related to the magnitude of the force and the duration of its application.13,14 Since the initial force cannot be changed, we can only prevent further force application first by immobilizing the unstable area and then by relieving the continued compression through early reduction of displaced bony fragments and disks.

Spinal Shock and Spinal Cord Injuries

The direct force applied to the spinal cord results in a physiologic block to conduction (called spinal shock), which is recognized clinically as complete cessation of all neurologic function—motor, sensory, and autonomic—below the level of the injury. In slight injuries, this phase lasts only minutes, but in more severe injuries, it may last weeks. During this phase, predictions of neurologic recovery should be avoided.

The pattern of spinal cord injury is determined clinically when the patient is out of spinal shock.

Complete Cord Injury

Clinically, in cases of complete cord injury, there is no voluntary movement and no sensation, but spinal reflexes are present or exaggerated.

Incomplete Cord Injury

Some recognized forms of incomplete cord injury are listed below.

Anterior Cord Syndrome

This syndrome is characterized by complete motor loss below the level of injury and loss of light touch sensation but preservation of position, vibration, and deep touch sensation. This pattern is caused by anterior compression of the spinal cord, which injures the lateral corticospinal and spinothalamic tracts but spares the posterior tracts.

Central Cord Syndrome

Clinically, this injury is marked by disproportionate loss of motor power in the upper extremities, with less severe loss in the lower extremities. Sensation is variably altered. This pattern is caused by central hemorrhage in the cord, which affects the lower motor neurons and decussating tracts but spares the lateral corticospinal tracts.

Brown-Séquard Syndrome

Rarely, this syndrome is seen as a pure injury with blunt trauma, but it also may be seen in penetrating injuries. Motor power is lost on the ipsilateral side, and pain and temperature sensations are lost on the contralateral side, up to one or two segments below the level of the injury.

Posterior Cord Syndrome

This rare condition results in loss of position sense.

Cauda Equina Syndrome

The degree of neurologic loss with this syndrome varies greatly, depending on the extent of nerve root damage. The motor and sensory loss is symmetric, and there may be loss of bladder and bowel control.

Root Loss

A few specific vertebral injuries are associated with loss of function of individual nerve roots. For example, a C5–C6 unilateral facet dislocation may cause ipsilateral C6 root injury. In a seat-belt injury, it is not uncommon that the nerve root exiting below the affected pedicle either unilaterally or bilaterally may be injured.

Clinical Assessment

Assessment of patients specifically for possible spinal injury begins after general assessment and resuscitative measures have been carried out. The patient must have an intact airway, adequate ventilation and circulation, and control of hemorrhage.

A history of the mechanism of injury is helpful in anticipating the type of injury. Other important information includes a history of previous neurologic abnormalities. Observations by the patient, witnesses, or the primary care giver of the occurrence of transient or persistent weakness or sensory changes or loss of bladder function related to the injury are very helpful.

On examination, any evidence of head or facial trauma, such as bruises, lacerations, or abrasions, can suggest the direction of an applied force. Especially important is any asymmetry of head position and tenderness along the sternomastoids. In a patient with an injured cervical cord, the arms may be held in the typical position of shoulder abduction and elbow flexion of a C5 quadriplegic. An ominous sign of neurologic loss is the presence of a paradoxical pattern of respiration. Priapism in a male patient with an injured cervical cord indicates loss of thoracolumbar sympathetic outflow. Examination of the trunk may show bruises or abrasions of the shoulders, the periscapular area, or the buttocks, suggesting a rotatory or flexion force to the spine.

A detailed neurologic examination then should be performed; it is recorded on a flow sheet to allow for serial examinations. Standardized methods of scoring for neurologic deficits have been developed that are extremely useful making neurologic assessments more consistent and reliable.15,16

The patient, wearing a cervical collar and held with gentle manual traction, may be carefully logrolled to allow examination of the back for tenderness, malalignment of the spinous processes, or a boggy gap in the supraspinous ligament, suggesting disruption of the posterior column (Fig. 94-7). While the patient is turned, sensation in the perianal area and rectal examination to include resting tone and voluntary contraction should be performed, along with testing of the bulbocavernosus reflex (Fig. 94-8).

Radiologic Examination

In multiple-trauma patients, the initial films are the scout lateral cervical spine film and an anteroposterior (AP) view of the chest and pelvis. Other, more detailed films are obtained on the basis of the clinical findings. In addition to the configuration and alignment of the vertebral bodies, the general alignment of the facets, the posterior vertebral bodies, and the interspinous distances, the specific points to observe on each film are listed in Table 94-1.

Following these x-rays, further detail may be required, and the following techniques are helpful. Since they require movement or turning of the patient, they should be done only when no instability has been demonstrated on plain films.

Cervical Spine

Swimmer's View

This view helps to visualize the cervicothoracic junction but is difficult to interpret and may show only gross malalignment.

Oblique and Pillar Views

These views are used to show the facets and lateral masses, respectively, and can be obtained with minimal movement of the patient.

Oblique Lumbar View

This view shows the lamina, pars interarticularis, and facets.

Conventional Tomography

This technique considerably improves detail and helps to show difficult areas (e.g., the cervicothoracic junction). It always should be done in two planes (AP and lateral) and requires turning of the patient; therefore, this technique is being replaced by computed tomography.

Computed Tomography

Computed tomography (CT) is a very valuable modality and requires only a single transfer of the patient, which can be done on the spine board or patient mobilizer. Routine, coronal, and sagittal reconstructions should be obtained. It is important that this examination be coordinated with other disciplines so that the patient with known or suspected spinal injury can have the appropriate areas examined at the same time as examination for other injuries (e.g., head, intrathoracic, intraabdominal).

Myelography

Myelography is indicated only under the following conditions:

1. The extent of the neural injury cannot be explained on the basis of the findings from plain films or CT.

2. Progressive neurologic loss occurs in the absence of severe encroachment on the neural canal, suggesting that the loss is ischemic in nature.

3. It is necessary to demonstrate possible dural defects or avulsed nerve roots.

Magnetic Resonance Imaging (MRI)

MRI has been used to assess the degree of soft tissue and ligamentous injury in the spine, looking for potentially unstable injury, particularly in the cervical spine. Overall, the results have not shown much advantage compared with conventional films and CT. There is a tendency to overcall significant injury. MRI does have a very high negative predictive value for significant soft tissue injury but is of uncertain positive predictive value and specificity.17 This modality offers clear imaging of the acute injury to the spinal cord as well as of late changes, such as the development of traumatic syringomyelia. Rizzolo and colleagues18 emphasized its usefulness in the unconscious or uncooperative patient in whom disk material must be removed before reduction is attempted.

Clearing of the Cervical Spine

Occasionally, when routine films are negative and a ligamentous injury to the cervical spine is suspected, flexion and extension films are indicated. They must be done only actively and, therefore, in an awake patient with medical supervision. Other methods for assessing the potential for unstable skeletal injuries in the unconscious patient include passive flexion extension using the image intensifier.19 This can be done by experienced personnel when good visualization of the entire cervical spine can be obtained by passively flexing and extending the patient through an arc of about 30 degrees of flexion and extension.20 MRI, when performed within 48 hours, also may be helpful.

Ankylosing Spondylitis

The fracture may not be seen initially. The patient should be managed as having an unstable injury until further investigations (tomograms, bone scan) are performed.3

Multiple Noncontiguous Injuries

It is becoming more common for patients to have more than one spinal fracture at nonadjacent levels, especially in high-velocity injuries. The primary injury is considered to be the one associated with neurologic deficit. This is most often in the upper thoracic level. When a fracture in the spine is diagnosed, the entire spine should be x-rayed.21

Unconscious or Head-Injured Patients

The absence of symptoms and/or a compromised neurologic examination in these patients makes assessment very difficult.

Immediate

Prehospital

Multiple-trauma victims and patients with spinal injuries, especially spinal injuries involving neurologic loss, should be taken directly to a level 1 tertiary care center if they are physiologically stable and if the transport time is reasonable. Major trauma-receiving centers must have a formal team designated for the management of spinal injuries.22

Priorities

The presence of a spinal injury, although serious and carrying a risk of severe late disability, does not alter the priorities of ensuring a clear airway, adequate ventilation, and adequate circulation.

Other Treatment Measures

Trauma patients with suspected or proven spinal injuries must continue to be immobilized or logrolled as indicated until definitive care is instituted. Temporary immobilization of the cervical spine is accomplished by appropriate application of a cervical collar. A long spine board should be used for transporting the patient. It is important that this initial assessment and resuscitation be expedited to avoid prolonged pressure on areas such as the occiput, sacrum, and heels.

It is imperative that adequate perfusion with well-oxygenated blood be maintained to the injured spinal cord, and therefore, supplemental oxygen is given by facemask to maintain a PaO2of at least 100 mm Hg. Other measures, as outlined below, are used to maintain a blood pressure of at least 100 mm Hg systolic.

Other general measures that should be instituted in the emergency department include insertion of intravenous lines, a nasogastric tube, and a Foley catheter.

As soon as the patient arrives in the emergency department, the spine injury team should be notified. That team then may supervise the spinal aspects of overall patient management and participate in decision making. Patients requiring manipulation for reduction of the spine should be managed where they can be monitored carefully and have easy access to x-ray facilities for serial films. Spine injury patients with other multiple trauma, all patients with high spinal cord injuries (above C5), and patients who have low cervical or thoracic cord injury as well as with significant preexisting disease are best treated initially in the intensive care setting until stabilized.23

Neurogenic Shock

Patients with neurogenic shock, particularly those with injuries above the level of T6, will be hypotensive and bradycardic owing to the combination of (1) loss of thoracic sympathetic outflow, vasodilatation, and pooling of blood and (2) relative predominance of vagal stimulation to the heart. In the absence of associated hypovolemia, the patient should be given a maintenance crystalloid infusion. If tissue perfusion is inadequate and/or the response to infusion is unsatisfactory, the patient should be investigated for concealed bleeding. Central lines are indicated, and monitoring of central venous pressure is used to gauge further fluid resuscitation. Extremes of crystalloid administration to maintain a normal pressure should be avoided, and colloids should be given as a volume expander, as repeated challenges. A persistently low perfusion pressure despite adequate fluid resuscitation warrants consideration of small doses of vasopressors.24,25

Respiratory

Respiratory complications after cervical spinal cord injury occur in 60% of patients. The single most significant determining factor is the severity of the spinal cord injury.26 Respiratory complications27 are greatest in cervical cord injuries in which the patient has lost intercostal function and the abdominal muscle function needed to support a vigorous cough. The phrenic nerve is involved in lesions above C5. In lesions below C5, with a functioning diaphragm and accessory muscles and in the absence of lung injury or preexisting disease, most patients can support satisfactory ventilation. There is a tendency, even with good general care, for ventilatory function to deteriorate by the third or fourth day because of fatigue and retained secretions, and intubation and ventilation may be required early. While the patient is being ventilated, the position of the cervical vertebrae can be maintained by traction, giving access to the chest for therapy. Once the respiratory compromise has stabilized and weaning can begin, it is advantageous to immobilize the cervical spine in a halo vest (Fig. 94-9). The vest restricts access to the chest and increases chest wall stiffness. However, the upright or semiupright position facilitates diaphragmatic excursion, improving functional residual capacity,28 especially in patients lacking intercostal function. While the patient is in neurogenic shock, postural hypotension will not allow maintenance of the upright position.

Cardiac

Acute spinal cord injury may be associated with pulmonary edema. This usually occurs early, possibly owing to massive sympathetic outflow, increased afterload, and a predisposition to dysrhythmia.29,30 A persistent feature following acute spinal cord injury above the T6 level is hypotension and bradycardia, even after administration of enough fluid and colloid to fill the venous capacitance vessels. These problems may respond to atropine (0.2 to 0.4 mg); if hypotension persists, vasopressors may be required.

Gastrointestinal

Almost every patient with spinal cord injury and most patients with significant fractures of the thoracic or lumbar spine in the absence of neurologic injury will have a transient ileus, and a nasogastric tube should be inserted.

Thromboembolic Prevention

Approximately 50% of patients with spinal cord injuries develop deep vein thrombosis.31 Prophylaxis with low-dose heparin appears ineffective. Better methods include adjusted-dose heparin, low-molecular-weight heparin, low-dose heparin plus electrical stimulation of the calf, and low-dose heparin plus graduated stockings plus intermittent pneumatic compression; these measures should be continued for 6 to 12 weeks.32

Skin Care

Avoidance of decubitus ulceration depends on meticulous attention to frequent turning and protection of pressure points. This regimen is made easier by the use of special mechanized beds for turning (e.g., Stoke-Mandville bed).

Nutrition

Following acute spinal cord injury, the patient becomes catabolic.33 To minimize this effect and encourage early rehabilitation, early alimentation is encouraged as soon as the ileus resolves. If the gut cannot be used for a long period, then parenteral nutrition should be considered.

Management of the Neurologic Injury

Decision making is based on accurate neurologic assessment initially, serial examinations, and accurate documentation. In the presence of neurologic injury, the two fundamental principles of management are

1. Provision of an adequate perfusion pressure and well-oxygenated blood. The patient must not be allowed to become hypotensive or hypoxic.

2. Decompression. The degree of injury and, conversely, the ability of the spinal cord to recover vary according to the magnitude of the applied force and the duration of compression. Decompression of the injured cord must be achieved as quickly as possible, usually by reduction of displaced fracture fragments by either closed means (e.g., halo traction, postural reduction on bolsters) or open ones. The adequacy of decompression must be proven radiologically.

1. Decompression should be performed from the direction of encroachment on the neural canal (anterior or posterior).

2. The adequacy of decompression should be proven intraoperatively by direct visualization or myelography or postoperatively by CT.

3. Following decompression, a stable construct must be achieved by internal stabilization.34

Indications for surgical decompression of spinal cord and cauda equina or root injuries are as follows:

1. Progressive neurologic loss. This development is seen clinically as either an ascending level of neurologic loss or progression from incomplete to complete injury. Not infrequently, the neurologic level rises by one segment in the very early stages following injury. This event is due to ischemia, and subsequently, the neurologic loss usually recedes to the original level.

2. Failure or anticipated failure of nonoperative decompression(owing to retained bone or disk fragments). Generally, the reduction seen on plain x-rays represents the residual encroachment on the neural canal. Only in 3% of cases is there residual soft-tissue compression.

3. Incomplete cord and/or cauda equina lesions with residual compression.

In the following situations, surgical decompression will be of no benefit or may even be harmful:

1. A complete spinal cord lesion in a patient out of spinal shock

2. Progressive neurologic loss due to ischemia, with no blockage or significant residual compression, as seen on myelography

Techniques of Spinal Cord Decompression

Anterior decompression of the cervical spinal cord35 is the technique of choice in the following injuries:

1. Axial load (burst) fractures

2. Cervical disk injuries

3. Distractive extension injuries with residual neural canal encroachment by posterior vertebral body osteophytes

Extremely complex patterns of fractures and fracture dislocations (e.g., quadrangular,36 teardrop,37 compressive extension) may be treated by a combination of anterior and posterior approaches.

The most common type of injury to the upper thoracic spine that may require decompression is a fracture dislocation that is extremely unstable and difficult to reduce nonoperatively. When decompression is indicated, the reduction can best be performed posteriorly, followed by stabilization using a segmental spinal instrumentation technique. New developments in instrumentation such as hook rods, pedicle screws, cages, and anterior plating systems have made it possible to achieve neural decompression, as well as a high degree of stability and correction of deformity, while also limiting the extent of the fusion.

For fracture dislocations, surgical decompression can be performed by laminectomy, clearing residual bone from within the neural canal followed by reduction and stabilization using pedicle screw or hook rod systems.

Burst fractures of the thoracolumbar spine usually can be decompressed posteriorly by pedicle screw distraction (ligamentotaxis) if done within 4 to 5 days of the injury. Anterior corpectomy and reconstruction are another option in the situation of severe canal encroachment or if residual neural compression persists after a posterior procedure.38

Adjunctive Techniques to Reduce Spinal Injury

The secondary ischemia following initial spinal cord injury is a major contributor to further neurologic damage and functional loss. Attention has been paid to understanding the pathophysiology of this process in order to identify ways to minimize its effect.39 Despite initial enthusiasm, many modalities, such as spinal cord cooling, hyperbaric oxygen, mannitol, and dimethylsulfoxide (DMSO), have not been shown to be effective.

Steroids

The glucocorticoids (e.g., dexamethasone) are presumed to act by decreasing the effect of norepinephrine, stabilizing cell membranes, preventing release of lysosomal enzymes, inhibiting complement activation, and reversing the sodium and potassium electrolyte imbalance that results from tissue edema and necrosis.40 Experimentally, controversy exists regarding the effectiveness of steroids. Clinically, Bracken and colleagues41 have indicated that the administration of methylprednisolone, 30 mg/kg within 8 hours of injury, followed by infusion of 5.4 mg/kg per hour for 23 hours resulted in improvement in neurologic function. A further study42 suggested that there was improved motor outcome when methyprednisolone was initiated earlier than 3 hours and for 24 hours or between 3 and 8 hours for 48 hours. However, functional outcome was not improved. Review of the data leaves unsolved issues.43–45

Since complications may be associated with the use of steroids,46 administration of these agents on an ad hoc basis is discouraged. The spine injury team should adopt a policy with respect to the use of steroids, standardizing dosage, time of administration, and duration of treatment.

When considering the bony injury, the principles of fracture management (reduction, maintenance, and mobilization) apply. These goals may be accomplished nonoperatively. With failed closed reduction, inability to maintain position, or the desire for early mobilization, an open reduction and internal stabilization are indicated. Stable fractures of the cervical or thoracolumbar spine can be mobilized early with limited use of an orthosis for pain relief.

In the cervical spine, unstable fractures that do not require reduction may be managed in an orthosis only (e.g., a nondisplaced type III fracture of the odontoid), but careful monitoring is necessary to demonstrate that the position is maintained. When a reduction is necessary, halo traction should be used so that once the fracture is reduced, the patient can be mobilized in a halo vest (see Fig. 94-9). The initial enthusiasm regarding the ability of the halo vest to control unstable cervical injuries has been challenged.47 Patient selection criteria for halo vest management are outlined in Table 94-2.

When open reduction and internal stabilization are indicated, the fracture pattern must be analyzed carefully in preoperative planning to make sure that the force causing the injury will be neutralized so that sufficient stability will be achieved that minimal, if any, external support will be required. Using modern implant techniques, this result is for the most part achievable.48,49

In fractures of the thoracic and lumbar spine, similar principles may be applied. Unstable fractures not requiring reduction may be treated with bed rest and logrolling for 2 to 3 weeks, followed by a well-fitted, rigid polypropylene brace. Closed postural reduction of some minimally displaced thoracolumbar fractures can be achieved by positioning the patient on corrective bolsters and careful logrolling until sufficient bony healing has occurred to allow mobilization in an orthosis. However, this approach requires skilled personnel in specialty units. With the advent of much-improved techniques of stabilization, there is an increased emphasis on health care costs and earlier mobilization, and thus there is an increasing trend toward early surgical stabilization.50,51 However, careful attention must be given to achieving sufficient stability to allow early mobilization.52–54

Hypothermia

Hypothermia is a particularly important problem in patients with cervical or high thoracic cord injuries. The patient is unable to produce vasoconstriction because of loss of the thoracic sympathetic outflow and also is unable to shiver to maintain core temperature. This results in hypotension and bradycardia. The temperature must be monitored carefully, and the patient must be kept covered or warmed by radiant heaters.

Autonomic Dysreflexia

This potentially dangerous complication occurs in patients with spinal cord injuries above the T6 level at any time after the stage of spinal shock. The presenting symptoms are quite variable, the most consistent being hyperhidrosis, headache, and vasodilatation above the level of the neurologic loss with nasal stuffiness. Paroxysmal hypertension is the cardinal sign; bradycardia is present inconsistently. The usual precipitating events are distention or manipulation of the bladder or rectum or intraabdominal pathology. These stimuli result in massive reflex sympathetic outflow, causing hypertension and reflex bradycardia and vasodilatation in the part of the body above the level of the spinal cord lesion. Immediate management should consist of placing the patient in an upright position and removing the stimulus, e.g., by bladder decompression. Vasodilator therapy may be required for severe hypertension.55

The Swollen Limb

The neurologically impaired patient may present at any time after the injury with a painless swollen limb. The differential diagnosis includes fracture, venous thrombosis, and myositis ossificans. Myositis ossificans is a frequent occurrence in association with spinal cord injury. In total joint arthroplasty, the use of indomethacin may decrease the occurrence and severity of this complication, but the usefulness of this agent is unproven in spinal injuries. Physiotherapy to maintain range of motion should be reduced but probably not discontinued.

Many assessment tools are available for documenting neurologic status after acute spinal cord injury, such as the Frankel scale and the American Spinal Injury Association (ASIA) scale. A practical method of determining function is incorporated in the Functional Independent Measure (FIM), which is a combination of a neurologic assessment and an assessment of the ability to perform various self-care activities. Restoration of the highest possible level of function in the patient with a spinal injury begins with initial management. Since function is related directly to the level of neurologic injury, preservation of even a single nerve root or segment, especially in the cervical cord, may make the difference between independence and the need for attendant care. For example, a C7 quadriplegic with strong active elbow extension can do transfers from bed to chair and chair to toilet and can live independently with some assistance at home. A C6 quadriplegic with good shoulder muscles and some active wrist extension is capable of independent feeding and grooming because of a fairly strong tenodesis grip. The patient can turn independently in bed, assist with transfers, operate a regular wheelchair, and even operate a car with hand controls. By contrast, a patient with a C5 injury is capable of very limited self-care, cannot turn in bed, and can only use an electric wheelchair.

Maintaining range of movement of joints that can be moved actively is essential to achieving maximum function. This is also important in joints that have lost active movement because flexion contractures of hips and knees interfere severely with independent transfers.

In some instances, it may be advantageous to leave an imbalance of certain muscle groups in order to facilitate function. For example, some tightness of the long finger flexors will improve the grip in patients dependent on the tenodesis effect for grasping objects.

Active therapy must begin during the phase of spinal shock and continue as the patient passes into the stages of spasticity.