Southern Association for Vascular surgery
October 15, 2007

Spinal Cord Ischemia after TEVAR in Patients with AAA

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Daniel J Martin, Robert J Feezor, Tomas D Martin, Philip Hess, Thomas M Beaver, Charles T Klodell, Thomas S Huber, James M Seeger, W. Anthony Lee
University of Florida, Gainesville, FL

Background: We examined the incidence and anatomic factors that may contribute to spinal cord ischemia (SCI) in patients with a history of abdominal aortic aneurysms (AAA) after thoracic endovascular aortic repair (TEVAR).
Methods: The medical records, CT angiograms, and a prospectively maintained clinical database of all TEVAR patients at a single institution between 2000 and 2007 were reviewed. Variables specific to the preoperative abdominal aortoiliac anatomy were examined.
Results: Of the 261 patients who underwent TEVAR, 27 developed SCI (10%). 13 (5%) of these were completely reversed with spinal drainage, and 14 (5%) were permanent. Compared to those who did not have SCI, patients with SCI were older (73+/-9.0 vs. 66+/-15.0 yrs, p=.02), had greater proportion of men (89% vs. 65%, p=.02), and had a higher ASA classification (Class IV: 89% vs. 60%, p=.03). The distribution of aortic pathologies was similar: 57% descending TAA, 28% dissection, 15% penetrating ulceration. 28% (n=73) of patients undergoing TEVAR had an AAA or a previously repaired AAA. Among those with SCI, 55% had a history of AAA as compared to 25% of patients without SCI (p=.002). In the subset of 37 of 73 patients with unrepaired AAA, those that developed SCI had 4.7+/-2.8 patent lumbar arteries vs. 7.4+/-1.4 in those without SCI (p=.0004), despite similar size of the aneurysms in both groups (42+/-11 vs. 43+/-9 mm, p=.78). Hypogastric artery patency was similar between the 2 groups. All patients with SCI and unrepaired AAA had at least one patent hypogastric vessel and 78% had both, similar to the non-SCI patients (96% and 93%, respectively).
Conclusions: Although the causes of SCI after TEVAR are multifactorial, abdominal aortic anatomy appears to be associated with development of this complication. Patients with either prior AAA repair or those with unrepaired AAA but decreased number of patent lumbar arteries appear to be at increased risk for SCI than those without a history of AAA.


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