Presentation
A patient with no significant past medical history presented with symptoms of progressive right lower extremity (RLE) claudication. Initial ankle-brachial indices (ABIs) were 0.76 (R) and 1.17 (L).
Patient Data
Complete absence of the right common iliac and common femoral arteries. The right superficial femoral artery (SFA) can be visualized with some calcified and noncalcified plaque. The right SFA is a direct branch of the right profunda femoris artery, which is receiving supply from hypertrophied lumbar, rectal, and pelvic collaterals.
The left common iliac artery continues off the aorta. The left common femoral artery, profunda femoris, and SFA are patent.
Case Discussion
Our patient presented with symptoms of progressive RLE claudication and was found to have congenital atresia of the right common iliac artery on CT. After diagnosis, she underwent left to right femoral-femoral bypass by vascular surgery with initial improvement in her ABIs but presented again with symptoms of right-sided thigh pain and claudication 8 months later. CT at this time revealed thrombosis of the bypass graft and she underwent catheter-directed thrombolysis with atherectomy, balloon angioplasty, and stent deployment within the bypass graft anastomotic site. Since then she has had repeated episodes of graft thrombosis requiring thrombolysis. She is following up closely with our interventional radiology department.
Congenital vascular malformations of the iliofemoral arteries are rare and are usually either detected incidentally or cause symptoms related to chronic limb ischemia (1). Generally, congenital malformation of the external iliac arteries can be classified into three groups: anomalies in the artery’s origin or course, aplasia or hypoplasia accompanied by a compensating persistent sciatic artery, and isolated aplasia or hypoplasia (2). Complete common iliac artery atresia is extremely rare with only 13 other reported cases since 1964 (3). In fact, most of these cases were found incidentally and were asymptomatic at the time of diagnosis. The postulated mechanism for this is adequate collateral vessel development in the embryo which supplies blood to the affected lower extremity (3). In our patient, the SFA arose from the profunda femoris which was supplied by hypertrophied lumbar, rectal, and pelvic collaterals, potentially delaying the onset of her symptoms.
Acknowledgments: Dr. Hashir Saeed, MD, and Dr. Tim Whitehead, MD, contributed to the diagnosis of this patient.
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