Anesthesia for Spinal Cord Injury

SPINAL CORD INJURY

The normal spine comprises three columns: ante-rior, middle, and posterior. The anterior column includes the anterior two thirds of the vertebral body and the anterior longitudinal ligament. The middle column includes the posterior third of the vertebral body, the posterior longitudinal liga-ment, and the posterior component of the annulus fibrosis. The posterior column includes the laminae and facets, the spinous processes, and the inter-spinous ligaments. Spine instability results when two or more of the three columns are disrupted. The trauma patient with a relevant mechanism of injury (typically blunt force involving acceleration– deceleration) must be approached with a high degree of suspicion for spine injury unless it has been ruled out radiographically.

A lateral radiograph of the cervical spine dem-onstrating the entire cervical spine to the top of the T1 vertebra will detect 85–90% of significant cervical spine abnormalities. Cervical spine radio-graphs should be examined for the appearance and alignment of the vertebral bodies, narrowing or widening of interspinous spaces and the central canal, alignment along the anterior and posterior ligament lines, and appearance of the spinolaminar line and posterior spinous processes of C2 through C7. The presence of one spinal fracture is associ-ated with a 10–15% incidence of a second spinal fracture.

Th oracolumbar injuries most commonly involve the T11 through L3 vertebrae as a result of flexion forces. The presence of one thoracolumbar spinal injury is associated with a 40% chance of a sec-ond fracture caudal to the first, likely due to the force required to fracture the lower spine. Bilateral calcaneus fractures also warrant a thorough thora-columbar spine evaluation due to the increased inci-dence of associated spinal fractures associated with this injury pattern.

Cervical spine injuries occurring above C2 are associated with apnea and death. Lesions of C3–5 impact phrenic nerve function, impairing dia-phragmatic breathing. High spinal injuries are often accompanied by neurogenic shock due to loss of sympathetic tone. Neurogenic shock may be masked initially in major trauma because hypotension may be attributed to a hemorrhagic, rather than a neu-rologic, cause. The presence of profound bradycar-dia 24–48 h after a high thoracic spinal cord lesion likely represents compromise of the cardioaccelera-tor function found in the T1–4 region.

The principal therapeutic objectives following spinal cord injury are to prevent exacerbation of the primary structural injury and to minimize the risk of extending neurological injury from hypotension-related hypoperfusion of ischemic areas of the spinal cord. In patients with complete spinal cord transec-tion, very few interventions will influence recovery. In patients with incomplete spinal cord lesions, careful management of hemodynamic parameters and surgical stabilization of the spine are critical in preventing extension of the existing injury.

Methylprednisolone is often administered for spinal cord injury to reduce spinal cord edema in the tight confines of the spinal canal, although there is scant evidence that this intervention improves outcomes following spinal cord injury in humans. While not considered a standard of care, it is included in the current clinical recommendations of the American Association of Neurological Surgeons as a treatment option. Maintaining supranormal mean arterial blood pressures to assure spinalcord perfusion in areas of reduced blood flow due to cord compression or vascular compromise is likely to be of more benef it than steroid administration. Hypotension must be avoided during induction of anesthesia and throughout surgical decompression and stabilization of a spinal injury.

Surgical decompression and stabilization of spinal fractures are indicated when a vertebral body loses more than 50% of its normal height or the spinal canal is narrowed by more than 30% of its normal diameter. Despite outcome studies from ani-mal models of traumatic spinal cord injury demon-strating benefit from early surgical intervention or steroid therapy, or both, current human studies have failed to demonstrate significant benefit from either intervention. Currently, the presence of a decom-pressible lesion in the area of an incomplete spinal cord transection is not an indication for early opera-tive intervention unless other, more life-threatening, conditions are present.

The elderly are at greater risk for spinal cord injury due to decreased mobility and flexibility, a higher incidence of spondylosis and osteophyte formation in the degenerative spine, and decreased intracanal space accommodating spinal cord edema following cord trauma. The incidence of spinal injury from falls in the elderly is rapidly approaching that of spinal cord injury from motor vehicle acci-dents in younger patients. Mortality following spinal cord injury in the elderly, particularly those over the age of 75 years, is higher than that in younger coun-terparts with similar injury.

The unique injury pattern of penetrating spinal cord injury warrants consideration. Unlike blunt spinal trauma, penetrating trauma of the spinal cord due to bullets and shrapnel is unlikely to induce an unstable spine. As a result, C-collar and long-board immobilization may not be indicated. In fact, C-collar placement in the presence of a cervical spine penetrating injury may hinder observation of soft tissue swelling, tracheal deviation, or other anatomic indications of imminent airway compromise. Unlike blunt trauma, penetrating injuries of the spinal cord induce damage at the moment of injury without risk of subsequent exacerbation of the injury. Like other spinal cord injuries, however, maintenance of spi-nal cord perfusion using supranormal mean arterial pressures is indicated until spinal cord function can be more fully evaluated.