We appreciate the comments from Dr. Gaylis concerning our article.1Dietzek AM Goldsmith J Veith FJ Sanchez LA Gupta SK Wengerter KR Interruption of critical aortoiliac collateral circulation during nonvascular operations: a cause of acute limb-threatening ischemia.J Vasc Surg. 1990; 12: 645-653Abstract Full Text Full Text PDF PubMed Scopus (35) Google Scholar Two of the four patients we reported required coronary artery bypass grafting, one for unstable angina and one for new ischemic electrocardiographic changes, one patient had moderate claudication and required a radical cystoprostatectomy, and one patient had no vascular symptoms and required a colectomy for colon carcinoma. In these patients, treatment of any lower extremity vascular problems before the procedures they had would have been inappropriate. We agree with Dr. Gaylis that a variety of established causes are known to precipitate thrombosis in major arteries affected by atherosclerosis. Alternatively, when these etiologic factors are eliminated as potential reasons for acute postoperative lower extremity ischemia, as they were in the four patients presented in our article, one must look for other less common and well established antecedents. Furthermore, in all four patients, preoperative pulse examinations and in the second patient a CT scan of the abdomen, revealed that the major supply arteries to the affected extremities were already either occluded or severely stenosed before the nonvascular procedure. Limb viability was therefore known to be dependent on collateral circulation. We speculate that the most important collateral pathways were unfortunately not recognized at the time of the nonvascular operations and were disrupted. Although the specific initiating factors for the growth or dilation of collateral circulation are not fully known, the development of these collateral pathways is in response to a critical diminution in blood flow through major supply arteries, most often as a result of stenoses or occlusions from advanced atherosclerosis. If limb viability is to be maintained as a result of these collateral pathways then they must be relatively free of significant atherosclerotic disease. It is possible that thrombosis of collateral pathways could result in critical ischemia; however, it is unlikely that this would occur in these relatively undiseased vessels in the absence of severe hypotension. Although it was not mentioned in our article, a significant amount of collateral circulation remained and was visualized on the arteriograms of all four patients obtained after the onset of postoperative acute lower extremity, ischemia. It is improbable that this resulted from thrombosis that was limited to only those collateral arteries that were crucial. Rather, it is much more plausible that ischemia in these patients was a consequence of surgical disruption of what are known to be important collateral pathways given the occlusive patterns described in each patient. We believe that Dr. Gaylis is correct in his statement that the cause of postoperative arterial thrombosis is multifactorial. In the four patients we presented, however, we feel that arterial thrombosis was not the cause of their acute lower extremity ischemia. Albeit a rare occurrence, ligation of collateral arteries to an ischemic limb may in fact be an important cause of limb-threatening ischemia.