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SCI after trauma affects some 10,000 Americans each year.[120] Blunt trauma accounts for most cases of SCI: 40% from motor vehicle collision, 20% from falls, and the remainder as the result of penetrating trauma (14%).[160] Complete neurologic deficit occurs in approximately 3500 patients a year and partial deficit in an additional 4500.[161] The health care cost of SCI is staggering: $5.6 billion in direct and indirect costs to the government each year for medical care, rehabilitation, and lost wages.[162] Cervical spine injuries occur in 1.5% to 3% of all major trauma patients. Within this group, those involved in head-first falls and high-speed motor vehicle accidents have about a 10% incidence of cervical spine fracture, and victims of trauma by these two high-risk mechanisms should always be closely examined for this injury. The incidence of cervical spine injury in head trauma victims is low, only 1% to 3% in adults and 0.5% in children. Advances in the management of patients with SCI, including pulmonary care, nutrition, and rehabilitation, coupled with an improved understanding of the pathophysiology of SCI, have reduced the mortality of isolated SCI to 5% to 7% in the first year.[163]
The mechanical patterns of SCI are often predictive of the resulting deficit. The four major patterns of injury are distraction, compression, torsion, and penetration. Distraction of the spinal cord occurs whenever the bony spine is hyperextended, as in hangings, or when the head or face incurs a significant impact while the body is moving rapidly (as seen in ejected motor vehicle operators, motorcyclists, struck pedestrians, or falls from a height). Compression of the bony spine is caused by axial loading in a fall or by sudden deceleration during a motor vehicle collision. Torsional injuries can occur after falls or high-energy motor vehicle collisions and may directly tear the tissue of the spinal cord. Though comparatively rare, penetrating trauma to the spinal cord can occur with stab or gunshot wounds at any level.
Most spinal injuries are found in the lower cervical spine, just above the thorax, or in the upper lumbar region, just below the thorax. Blunt SCI is most common in regions of the cord that are most flexible, especially at the junctions between flexible and inflexible segments. SCI at midthoracic levels is less common because the rib cage and intercostal musculature provide rotational stabilization. Because of the rapidly fatal nature of neurologic injury in the upper cervical spine, the true incidence of SCI at these levels is not known.
SCI is commonly accompanied by radiographically visible injury to the bony spine and concomitant disruption of the muscles, ligaments, and soft tissues that support it. However, clinically significant injury to the cervical spinal cord can occur in the absence of visible skeletal injury. This phenomenon, known as SCIWORA (spinal cord injury without radiographic abnormality), is more common in children and is presumably the result of a temporary hyper-distraction or torsion of the neck insufficient to disrupt the bony skeleton.[164]
Primary injury to the spinal cord sustained at the moment of trauma may be exacerbated by a number of secondary factors ( Fig. 63-12 ). Extrication from the scene of the injury and initial medical treatment (including
SCI includes sensory deficits, motor deficits, or both. Incomplete deficits may be worse on one side than the other and may improve rapidly in the first minutes after injury. Complete deficits—representing total disruption of the spinal cord at one level—are much more ominous, with generally little improvement seen over time. Cervical spine injuries causing quadriplegia are accompanied by significant hypotension because of inappropriate vasodilatation and loss of cardiac inotropy (neurogenic shock). Functioning of lower cord levels will gradually return, with restoration of normal vascular tone. Autonomic hyperreflexia develops in 85% of patients with a complete injury above T5 because of excessive sympathetic response to stimuli below the level of injury, absent the brain's normal damping effect.[166]
Determining cervical spine stability can be difficult. The Eastern Association for the Surgery of Trauma has published guidelines regarding which patients require cervical spine radiographs, which views and studies should be
Figure 63-12
Mechanisms of spinal cord injury. Mechanical trauma
to the spinal cord is exacerbated by systemic hypoperfusion or hypoxia. (Redrawn
from Dutton RP: Spinal cord injury. Int Anesthesiol Clin 40:109, 2002.)
Guideline 5 is controversial, and some trauma centers will maintain cervical spine immobilization devices on any patient who cannot receive an adequate neurologic examination. Unfortunately, no commonly used device sufficiently limits neck mobility to prevent aggravating ligamentous cervical spine injuries if the patient is sufficiently active.[168] Rigid cervical collars also hinder patient hygiene and may lead to occipital decubitus ulcers.
Because the spinal cord is susceptible to secondary injury in the same way that brain tissue is, early treatment of a patient with SCI is focused on preservation of adequate perfusion. Hypoxemia must be avoided at all costs, and MAP should be maintained at a normal to high level. These goals may be difficult to achieve in a patient with acute SCI because airway management will be significantly complicated by the presence of an unstable spinal injury and support of perfusion pressure will depend on reversing the negative inotropy and inappropriate vasodilatation caused by neurogenic shock. Emergency intubations are performed as described earlier, with inclusion of manual in-line axial stabilization. In the acute setting (less than 24 hours from the moment of injury), succinylcholine can be safely used in patients with SCI.[169] A patient with progressive respiratory failure but adequate oxygenation may more appropriately tolerate an awake bronchoscopic intubation.
After successful control of the airway, adequacy of the circulation becomes the next priority. Hypotension from neurogenic shock is commonly manifested as bradycardia rather than tachycardia (because of loss of cardiac accelerator function and unopposed parasympathetic tone), but it may be difficult to distinguish from hypotension caused by acute hemorrhage. A hypotensive trauma patient is always assumed to be bleeding until this possibility is definitively ruled out by diagnostic investigation of the chest cavity, abdomen, retroperitoneum, and long bone compartments. Fluid administration is indicated, subject to the end points of resuscitation outlined earlier. Once hemorrhage has been ruled out or treated, some data support maintenance of MAP at greater than 85 mm Hg for 7 days after injury, although this approach is highly controversial.[170] Fluid administration will help expand vascular volume and counter the effects of inappropriate vasodilatation, but it may produce an added strain on the heart. In any patient with a poor response to initial volume loading, pulmonary artery catheterization is indicated as a guide to subsequent resuscitation.[171]
Circulatory management is followed by a glucocorticoid steroid bolus, administered to any patient with a complete or partial neurologic deficit. A bolus dose of 30 mg/kg of methylprednisolone, followed by a maintenance infusion of 5.4 mg/kg/hr, is given if the patient is less than 8 hours removed from the time of injury. This infusion is continued for 24 hours if started within 3 hours of injury and for 48 hours if started 3 to 8 hours after injury. High-dose glucocorticoid therapy demonstrated a small, but statistically significant improvement in neurologic level after SCI in two large multicenter trials: the National Acute Spinal Cord Injury Study (NASCIS) II and III.[172] [173] Methylprednisolone improves spinal cord blood flow, reduces intracellular calcium influx, and mitigates the formation of free radicals in ischemic spinal cord tissue. The NASCIS results have been challenged for several reasons.[174] [175] [176] The positive benefits seen with high-dose steroid administration were driven by results in a few subpopulations and were not present in most patients. The improvement in spinal level seen after steroid administration has not been shown to lead to increased survival or improved quality of life, and the results have not been reproducible in other studies of acute SCI. Despite these faults, most practitioners choose to follow the given recommendations because of the devastating nature of SCI and the absence of other therapies.
A number of investigational pharmacologic therapies to minimize secondary injury have been studied. NASCIS II[172] found no benefit from the administration of large-dose naloxone, an opioid antagonist, whereas NASCIS III[173] found no benefit from the administration of tirilazad, an inhibitor of free radical formation. Monosialotetrahexosylganglioside (GM1 ganglioside) has been shown to improve functional recovery when administered in animal models of acute SCI.[177] Despite study in a number of human trials, with suggestive results, it is not yet confirmed as effective and is therefore not commercially available in the United States. More recently, the sodium channel blocker riluzole has been found to reduce the extent of spinal cord damage and enhance the rate of recovery after acute SCI in a rat model. [178] This drug has not been tested in humans with SCI.
Patients with bony injury to the spinal cord will require surgery based on their neurologic symptoms and the anatomic stability of the injury. MRI is indicated to assess ligamentous and soft tissue injury in any patient with a bone fracture or neurologic deficit. Surgery is more commonly required for cervical lesions, whereas supportive bracing or extension casting of the torso may be used for thoracic and lumbar fractures. Early intubation is almost universally required for patients with cervical spine fracture and quadriplegia. Ventilatory support is absolutely required for patients with a deficit above C4 because they will lack diaphragmatic function. Patients with deficits from C4 to C7 will still need support, however, because of lost chest wall innervation, paradoxical respiratory motion, and an inability to clear secretions. Because these patients will need to be kept flat and often in cervical traction until definitive surgical stabilization, atelectasis will develop quickly and may lead to rapid, progressive desaturation. Early intubation is recommended and can often be accomplished by awake fiberoptic bronchoscopy before hypoxia renders the patient anxious and uncooperative. Spontaneous ventilation and extubation are possible after surgical stabilization and resolution of spinal shock, although pneumonia is a common and recurrent complication that frequently necessitates tracheostomy to facilitate pulmonary toilet. SCI patients are at great risk for decubitus ulcer formation and skin breakdown secondary to the rigid cervical collar and will thus require meticulous nursing care. Deep venous thrombosis formation is a serious risk, and all SCI
A patient about to undergo surgical reduction and fixation of a spinal column fracture poses a number of challenges for the anesthesiologist. First and foremost is the need for intubation of the trachea in a patient with a known injury to the cervical spine. Direct laryngoscopy with in-line stabilization is appropriate in the emergency setting and in unconscious, combative, or hypoxemic patients when the status of the spine is not known.[179] In the OR, an awake, alert, and cooperative patient can be intubated by a number of different methods known to produce less displacement of the cervical spine and presumably less risk of worsening an unstable SCI. The most common technique in current clinical practice is awake fiberoptic intubation. Although the nasal route is associated with an easier path to intubation in most patients, it can lead to an increased risk of sinusitis in the ICU if the patient is not extubated at the conclusion of the procedure. Oral intubation is likely to be more challenging technically, but it will be of greater value if the patient remains intubated. Blind nasal intubation, transillumination with a lighted stylet, the use of an intubating LMA or Bullard laryngoscope, and any of a variety of other instrument systems for indirect laryngoscopy are acceptable. The clinician is advised to use the equipment and techniques that are most familiar. The important concept is to successfully achieve tracheal intubation while minimizing motion of the cervical spine and preserving the ability to assess neurologic function after positioning.
Quadriplegic and paraplegic patients may have underlying hemodynamic instability as a result of spinal shock at the time of surgery. In most spinal fixations, especially those in the cervical region, blood loss is not substantial. Indeed, the major blood loss comes from harvesting the iliac crest bone graft, if needed for the procedure. Arterial pressure monitoring is indicated, and any pressor or inotropic drugs in use when the patient arrives at the OR should be continued throughout the procedure. The anesthesia provider should not have to increase these drugs in response to intraoperative hypotension unless the response to fluid administration is poor. Thoracic and lumbar fractures can bleed more readily, particularly if multiple levels are involved or the surgeon will be performing a corpectomy of one or more vertebral bodies. Elderly patients and those who have had significant hemodynamic lability before surgery may require more intensive hemodynamic monitoring with a pulmonary artery catheter.
In the case of a multiply injured patient who comes to the OR for nonspinal surgery (in the presence of a known spinal injury), the management principles are similar to those outlined earlier. In addition to managing the case at hand, particular attention to airway management, patient positioning, and hemodynamic support is needed. Like patients with TBI, patients with SCI also suffer from impairment of autoregulation in the region of the injury, thus making close attention to adequate perfusion of critical importance.
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