PREVENTION OF SPINAL-CORD INJURY AFTER REPAIR OF THE THORACIC OR THORACOABDOMINAL AORTA

Spinal cord injury occurring as the result of surgical repair of thora cic and thoracoabdominal aortic disease remains a devastating complica tion. The incidence of postoperative neurologic deficits varies from 4 % to 38%. Factors associated with a greater risk for injury include th e presence of dissection or extensive thoracoabdominal disease, and a prolonged cross-clamp time. Spinal ford ischemia initiates a deleterio us cascade of biochemical events that ultimately result in an increase d intracellular calcium concentration. Calcium-activated proteases, li pases, and nucleases mediate the processes that cause cell injury. The accumulation of oxygen-derived free radicals and the occurrence of hy peremia during reperfusion are also contributing causes of spinal cord injury. Increasing the spinal cord blood now with shunts, oxygenated bypass circuits, cerebrospinal fluid drainage, the intrathecal adminis tration of vasodilators, and the reattachment of intercostal arteries has been tried in an effort to increase spinal cord perfusion. Pharmac ologically based measures to prevent spinal cord injury have been purs ued, and these have consisted of hypothermia, anesthetic agents, calci um channel blockers, free radical scavengers, and immune system modula tion. However, no single technique has proved to be consistently effec tive in preventing ischemia-induced spinal cord injury.