Invited commentary
Article Outline
Spinal cord ischemia (SCI) is clearly one of the more devastating complications after the repair of any thoracic pathology by any means. The multifactorial etiology of the complication has so far resulted in a variety of management strategies that have failed to garner uniform adoption. Endografting of thoracic aneurysms (TEVAR) was greeted with the expectation that this feared outcome would be diminished by avoiding aortic clamping and prolonged ischemia of the cord. This optimism appears well justified by most early published results, as SCI seems to occur in <5% of cases and mostly in aneurysmal pathology of the thoracic aorta and less so with dissection or transection.1, 2, 3, 4
In an effort to further limit the occurrence of SCI, a diligent search for predisposing risk factors has so far resulted in a myriad of associations with little consensus about the relative importance of any. Notable suspects include length of thoracic aortic coverage, left subclavian artery exclusion without reconstruction, elimination of intercostal blood supply, especially the artery of Adamkiewicz, poor lumbar and internal iliac artery collaterals, intraoperative hypotension, conduit use for access, and underlying aneurysmal pathology. The presence of a concurrent or remotely repaired abdominal aortic aneurysm (AAA) has also been repeatedly implicated, with only sparse supporting evidence.
This issue of the Journal of Vascular Surgery brings the reader two reports focusing on the risk of SCI after TEVAR in patients with AAA. The reports differ in methodology, results, patient population, and extent of use of prophylactic spinal drainage, yet are remarkably similar in the estimated risk of SCI in patients with prior AAA repair: 12.5% in a multicenter study limited to thoracic aneurysms and 14% in a single-center series with a potpourri of diagnoses. The incidence is notably the same as that reported in a smaller series by Baril in 2006.5
Despite the inherent methodologic problems of all these retrospective analyses, and other negative reports, the evidence is mounting that SCI risk is elevated after TEVAR in patients with remote aneurysm repair. The incidence of SCI seems to be significantly higher in this patient subgroup irrespective of other risk factors that may exist. The SCI hazard ratio in patients with AAA seems to range between 4 and 7.
The report from the University of Florida by Martin indicates an even more alarming SCI rate of 21% in 51 patients with untreated concurrent AAA as small as 3.0 cm in diameter, a size rarely considered an aneurysm in most clinical settings. This finding adds another dimension to the association of SCI with any current aneurysmal pathology of the abdominal aorta and clearly constitutes a cause for concern in the preoperative risk benefit assessment before TEVAR.
The rest of the information provided by these two studies is somewhat disparate due to different methodology and inclusion criteria. The multicenter study by Schlosser reports a somewhat enviable SCI rate of only 1.7% after TEVAR for thoracic aneurysms in the absence of prior AAA repair. In the absence of any abdominal aortic pathology, Martin still reports a rate of 5.6% in a more diverse group including patients with dissections, transections, and other pathologies that would have been expected to lower the incidence of this complication.
An SCI rate of >10% in the entire TEVAR series from a group with a large experience such as the University of Florida is quite sobering, pointing out that we have a long way to go before understanding all the factors that may influence the development of this debilitating complication. The contributions of emergency interventions as well as hybrid procedures to this elevated risk is not entirely clear from the data presented. Prospective focused collection of data may be required before providing guidelines for the proper selection of patients and conduct of the operation to minimize these unfortunate outcomes.
In the meantime these two studies provide a strong reminder that caution should be exercised when offering TEVAR to a large group of patients who present with remote or concurrent AAA. A careful analysis of the risk/benefit ratio under these circumstances should lead us to only offer TEVAR to patients with a higher risk profile of the underlying pathology, raising the size threshold for intervention on aneurysmal disease of the thoracic aorta.
References
- . Complications of thoracic aortic endografts: spinal cord ischemia and stroke. J Vasc Surg. 2006;43(suppl A):85A–88A
- Neurologic complications associated with endovascular repair of thoracic aortic pathology: incidence and risk factors (A study from the European Collaborators on Stent/Graft Techniques for Aortic Aneurysm Repair (EUROSTAR) Registry). J Vasc Surg. 2007;46:1103–1111
- Endovascular treatment of thoracic aortic aneurysms: results of the phase II multicenter trial of the GORE TAG thoracic endoprosthesis. J Vasc Surg. 2005;41:1–9
- . Risk factors of neurologic deficit after thoracic aortic endografting. Ann Thorac Surg. 2007;83:882–889
- Endovascular thoracic aortic repair and previous or concomitant abdominal aortic repair: is the increased risk of spinal cord ischemia real?. Ann Vasc Surg. 2006;20:188–194
PII: S0741-5214(08)01630-3
doi:10.1016/j.jvs.2008.09.047
© 2009 The Society for Vascular Surgery. Published by Elsevier Inc. All rights reserved.
Refers to article:
- Spinal cord ischemia after TEVAR in patients with abdominal aortic aneurysms , 25 November 2008
