Femoral Artery Dissection and Occlusion

A 62-year-old woman presented with a painful, cold, pulseless right lower extremity after a diagnostic heart catheterization 4 days earlier and percutaneous transluminal coronary angioplasty 2 days thereafter. Each procedure was performed through right femoral artery access and closed with an Angio-Seal™ Vascular Closure Device (St. Jude Medical, Inc.; St. Paul, Minn). Computed tomographic angiography showed occlusion of the right common femoral artery and 80% stenosis of the left external iliac artery without evidence of retroperitoneal hematoma (Fig. 1). Operative exploration revealed a focal dissection originating at the site of 2 contiguous percutaneous closure devices, complete false-lumen compression of true-lumen flow, and no atherosclerotic plaque. Components of the percutaneous closure devices were found within the false lumen (Fig. 2). After the removal of those components, débridement of the contiguous vessel wall, and resection of the dissection flap by means of endarterectomy, a thrombectomy and Dacron-patch angioplasty resulted in the restoration of the patient's pulses.

Fig. 1 View of the aorta and lower-extremity runoff (computed tomographic angiographic 3-dimensional reconstruction) shows occlusion of the right common femoral artery at the level of the inguinal ligament (arrow) with distal reconstitution through collateral vessels; 80% stenosis of the left external iliac artery; and 50% stenosis of the right popliteal artery.

Fig. 2 Photograph of specimen that includes soft tissue, an excised segment of the right common femoral arterial wall, and foreign bodies representing residual components of previously placed Angio-Seal devices. The “anchor” component was obtained from the space between the dissection flap and vessel wall.

Comment

Percutaneous closure devices are an alternative to manual compression after endovascular procedures, offering improved patient satisfaction and reduction in the time to full ambulation.^1,2 The Angio-Seal consists of 3 bioabsorbable, radiolucent components, including a polymeric (polylactic and polyglycolic acid) anchor placed against the inside of the vessel wall, a collagen plug placed atop the arteriotomy in the tissue tract, and a polyglycolic acid suture that clinches the anchor and collagen together to form a seal.¹ Complete bioabsorption occurs within 60 to 90 days.

In this case, the intraoperative finding of a percutaneous closure device anchor component within the dissection's false lumen strongly supports the hypothesis that the presence of a “semi-rigid tissue sandwich,” before bioabsorption, causes a dissection either during repeat vascular access or percutaneous closure device deployment. This could occur by different mechanisms. If a focal dissection caused by initial access is successfully tethered by a percutaneous closure device, repeat contiguous access or percutaneous closure device deployment might tear the flap tissue, propagating dissection. Alternatively, in the presence of normal vascular-wall tissue, the semi-rigid sandwich might serve as a fulcrum that would compromise the compliance of the contiguous vessel wall, affect the passage of the wire and sheath, and initiate a dissection during repeat access that would be exacerbated by deployment of the percutaneous closure device anchor component. We conclude that repeating the use of percutaneous closure devices in a given vessel without allowing time for biodegradation is contraindicated.