• F Setacci, P Sirignano, G De Donato, E Chisci, G Galzerano, R Massaroni, and C Setacci.
• Vascular and Endovascular Surgery, Department of Surgery, University of Siena, Siena, Italy. setacci2@unisi.it
• J Cardiovasc Surg. 2010 Apr 1;51(2):169-76.

AbstractSpinal cord ischemia (SCI) is one of the most devastating complications undergoing surgical or endovascular repair of the thoracic aorta. The incidence of SCI after thoracic aorta open repair varies from 2% to 21%, depending on the extent of the descending thoracic aorta replacement compared with as high as 12% of cases after endovascular aortic repair. Endoluminal repair allows the avoidance of aortic cross clamping and its sequelae; however, the intercostal arteries covered by the stent graft cannot be reimplanted. Perioperative risk factors contributing to SCI have been reported to include length of aortic coverage, prior abdominal aortic aneurysm (AAA) repair, hypotension, and left subclavian artery coverage. Although the putative mechanism of loss of lumbar collateral perfusion in those who had prior aortic repairs appears reasonable, occurrence of SCI in this subset of patients has not been consistent. Spinal cord perfusion is dependent on the net pressure of the mean arterial pressure minus the mean intrathecal pressure. Systemic pressure can be maximized by volume resuscitation and vasopressors. Intrathecal spinal pressure can be minimized by drainage of the spinal cord, although this is not without its potential risks. More recently, there have been attempts at attenuating the cellular damage caused by SCI, either with systemic or intrathecal administration of pharmacologic agents, which attempt to mitigate the inflammatory response of cellular reperfusion. This is a review of the risk factors for SCI during TEVAR in patients with previous or concomitant treatment for aortic aneurysm.

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