Mc. Mauney et al., PREVENTION OF SPINAL-CORD INJURY AFTER REPAIR OF THE THORACIC OR THORACOABDOMINAL AORTA, The Annals of thoracic surgery, 59(1), 1995, pp. 245-252
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.