Annals of vascular surgery
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Aortic stent-graft infection after endovascular abdominal aortic aneurysm (AAA) repair is an uncommon, but very serious complication with potentially devastating consequences.(1) Traditional open techniques of repair of AAA demonstrate an infection rate of 0.5-3%. The exact rate of infection with endovascular repair is unknown, but literature review demonstrates an overall incidence of 0.43-1.17% retrospectively.(2,3) Etiology of endovascular graft infections typically results from flora derived from the skin or gastrointestinal tract.(4)Clostridium septicum is a naturally occurring anaerobic bacterium native to the gastrointestinal tract. It is typically associated with spontaneous nontraumatic gas gangrene owing to bacteremia from the gastrointestinal tract with an incidence rate of 0.07%.(5) To our knowledge, this is the first reported case of endovascular AAA graft infection owing to Clostridium septicum species.
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The ankle--brachial index (ABI) is a simple, noninvasive, widely used test that detects peripheral arterial disease (PAD). In patients with diabetes, the ABI is notoriously unreliable and this is usually attributed to medial calcinosis, which stiffens the arteries and renders them poorly compressible. However, the distribution of atherosclerotic lesions in those with diabetes is different as well: lesions predominantly reside in below-the-knee (BTK) arteries. To what extent this contributes to the unreliability of the ABI is unknown. The aims of this study were (1) to confirm the notion that the ABI poorly predicts PAD in the diabetic foot, (2) to determine whether arterial calcifications can be blamed, and (3) to establish the role of the distribution of atherosclerotic lesions. ⋯ The ABI underestimated angiographic atherosclerotic disease in this population of patients that we thought had PAD causing tissue loss. Calcifications were frequently present and indeed can be partly blamed for the unreliability of the ABI, but the distribution of atherosclerotic disease can be held responsible as well: the ABI is hampered by design because it is meant to detect a drop in pressure caused by the additive effect of serially located lesions in the arterial tree. In the diabetic foot, where lesions tend to be situated in BTK arteries (which lie parallel to each other), the pressure measured in one distal artery is less representative of atherosclerotic disease in the lower extremity.