Superficial Femoral Artery Stent Fracture that Led to Perforation, Hematoma and Deep Venous Thrombosis

Superficial Femoral Artery Stent Fracture that Led to Perforation, Hematoma and Deep Venous Thrombosis
Superficial Femoral Artery Stent Fracture that Led to Perforation, Hematoma and Deep Venous Thrombosis
Superficial Femoral Artery Stent Fracture that Led to Perforation, Hematoma and Deep Venous Thrombosis
Superficial Femoral Artery Stent Fracture that Led to Perforation, Hematoma and Deep Venous Thrombosis
Superficial Femoral Artery Stent Fracture that Led to Perforation, Hematoma and Deep Venous Thrombosis

Steve Lewitton, MD and Anvar Babaev, MD, PhD

Author Affiliations:
From the New York University School of Medicine, Department of Medicine, Division of Cardiology, New York, New York.
The authors report no conflicts of interest regarding the content herein.
Manuscript submitted April 15, 2008, provisional acceptance given June 6, 2008, and accepted June 11, 2008.
Address for Correspondence: Anvar Babaev, MD, PhD, NYU Cardiac Catheterization Laboratory, 550 First Avenue, New York, NY 10016.

ABSTRACT: We describe the case of a 70-year old male with total occlusion of the left superficial femoral artery (SFA) treated with percutaneous implantation of a self-expanding nitinol stent. The patient’s course post-stent implantation was complicated by the development of stent fracture with SFA perforation and a large, compressive  intramuscular hematoma with deep venous thrombosis (DVT). The patient returned to the catheterization laboratory where the fracture and perforation were successfully treated by the deployment of another stent across the fracture site. The DVT was initially treated with an inferior vena cava filter until anticoagulation could safely be instituted.

J INVASIVE CARDIOL 2008;20:479–481

Stent fracture is a rare complication following revascularization and stenting of the superficial femoral artery (SFA). Stent fracture is most often asymptomatic, but has been associated with an increased risk of restenosis. We report a case of stent fracture following treatment of an SFA occlusion complicated by SFA perforation and intramuscular hematoma that led to deep venous thrombosis.

Case Report. A 70-year-old male with hypertension, hyperlipidemia, peripheral arterial disease (PAD) and coronary artery disease was referred to our institution for the evaluation of severe claudication and intermittent rest pain of the left leg.

Magnetic resonance angiography of the lower extremities demonstrated a total occlusion of the left SFA and a severe mid-popliteal artery stenosis. The patient refused bypass surgery.

The patient underwent angiography of the left-lower extremity using a contralateral approach. Angiography confirmed a total occlusion of the mid-to-distal left SFA approximately 15 cm in length (Figure 1). The distal SFA reconstituted via collaterals from the deep femoral artery. The findings also confirmed the severe popliteal artery lesion.

After discussion with the patient, a decision was made to attempt percutaneous revascularization of the left SFA. After the use of multiple wires and support catheters, the total occlusion was crossed with a Miracle Bros 6 0.014 inch wire (Abbott Vascular, Abbott Park, Illinois) advanced subintimally to the distal reconstitution site. An Outback Re-Entry Catheter (Cordis Corp., Miami Lakes, Florida) was used to re-enter the true lumen of the distal SFA.

The lesion was dilated with a 3.5 mm x 120 mm Amphirion balloon (ev3, Inc., Plymouth, Minnesota) and stented with 2 overlapping 6.0 mm FlexStar self-expanding stents (Edwards Lifesciences, Irvine, California). There were areas within the stents that appeared underexpanded and these were treated with a 5.0 mm Submarine Plus balloon (ev3) inflated to a maximal pressure of 10 atm. The mid-popliteal artery lesion was treated with a SilverHawk LS atherectomy device (FoxHollow Technologies, Inc., Redwood City, California) with a good angiographic result.

The final angiogram demonstrated good stent apposition with brisk antegrade flow and no evidence of stent fracture (Figure 2). The patient was observed overnight and discharged home the following morning on dual antiplatelet therapy of aspirin 325 mg and clopidogrel 75 mg daily.

The patient returned to the hospital in the evening of the following day after developing acute and severe pain as well as swelling of the left lower thigh while changing position from seated to upright. Physical examination demonstrated a tender, swollen and painful thigh, intact distal pulses and a warm foot. Laboratory values were significant for a fall in hemoglobin from 11.8 (at discharge from the hospital) to 8.8 g/dL.

A computed tomographic scan (CT) of the lower extremity demonstrated edema and a hematoma in the left biceps femoris muscle extending from the groin to the junction of the mid and distal thirds of the thigh, with thrombus found within the left popliteal vein extending into the peroneal vein consistent with deep venous thrombosis (DVT), presumably due to external venous compression by the hematoma.

The patient returned to the catheterization laboratory for angiography which demonstrated two fractures (proximal and distal) within the distal SFA stent. Upon injection of contrast dye, the distal fracture site (Figure 3) had extraluminal extravasation of dye into the adjacent tissue (Figure 4). The diagnosis was made of stent fracture with perforation of the distal SFA and active bleeding into the adjacent soft tissue.

The stent fractures and SFA laceration were treated with 6.0 mm Viabahn heparin-coated self-expanding stents (W.L. Gore & Associates, Inc., Flagstaff, Arizona) deployed across the fracture sites. The stents were postdilated with a 6.0 mm balloon (ev3) with complete resolution of dye extravasation (Figure 5). There was an excellent angiographic result with no compromise of distal runoff.

The patient was not anticoagulated for the DVT out of concern that anticoagulation would increase the risk of further bleeding. Instead, we elected to treat him with ongoing dual antiplatelet therapy and place an inferior vena cava (IVC) filter to prevent embolization of the DVT.

Warfarin therapy was started 5 days after the procedure. Arterial and venous ultrasound was performed every 2 weeks. Four weeks after the procedure, vascular ultrasound demonstrated complete resolution of the venous thrombus and patent SFA stents. Swelling and tenderness of the left thigh had resolved as well. Six-month follow up demonstrated no evidence of in-stent restenosis and normal ankle-brachial indexes.
Discussion. In recent years, rapid developments in endovascular therapies for PAD and patient preferences have led to a shift in revascularization strategies from open surgical techniques to lower-morbidity endovascular approaches.1

Successful revascularization of SFA lesions depends upon the durability and longevity of the treatment. A meta-analysis has demonstrated better long-term patency rates at 3 years in patients treated with stents rather than with angioplasty alone. This finding was primarily driven by those patients with critical ischemia or occlusion.2 Subsequent studies have confirmed better long-term results with nitinol stent implantation and a low rate of stent fracture (2%).3

With the use of stents in the SFA, the risk of stent fracture has been increasingly recognized. The superficial course of the vessel and the mechanical force exerted by surrounding musculature expose the artery (and the implanted stent) to significant external forces that may cause stent compression or fracture. Both are significant risk factors for restenosis, making them clinically important even in patients who do not initially manifest symptoms. Mild stent fracture may be benign; however, severe stent fracture is associated with an increased incidence of restenosis or reocclusion.4

Initial experience with SFA stenting suggested that fracture was a rare event, primarily seen after implantation across flexion points. However, subsequent studies utilizing routine angiographic follow up after long-segment SFA stenting with conventional or sirolimus-eluting self-expanding nitinol stents demonstrated an incidence of up to 18.2%. In this study, none of the patients had any significant clinical symptoms.5

Subsequent studies suggest that newer self-expanding nitinol stents are associated with a lower incidence of stent fracture than first-generation self-expanding or balloon-expandable stents.5 This is likely a result of enhanced stent flexibility resulting from characteristics of the nickel titanium (nitinol) alloy and newer segmental stent designs.

Scheinert et al conducted a systematic radiographic follow up of all patients at one center who underwent implantation of a self-expanding nitinol stent into the SFA and explored the incidence of stent fracture. At an average of 10.7 months’ follow up, the investigators noted a stent fracture rate of 37.2% and they reported that the incidence of fracture increased with the length of the stented segment and the number of stents implanted. The lowest fracture rate was seen in segments less than 8 cm and the highest in segments greater than 16 cm.6

The Resilient II trial randomized patients to implantation of nitinol FlexStar self-expanding stents (Edwards Lifesciences) in the SFA similar to that used in our patient. In that trial, the fracture rate was 2.9% (9 fractures) between 0- to 12-month follow up, and none of those fractures were associated with restenosis at 12 months.7 Based on this study, it seems that this stent has one the lowest fracture rates compared to other available stents on the U.S. market. However, our case demonstrates that even this stent can fracture and lead to a major complication.

Stent fracture leading to laceration of the treated vessel is an uncommon event, and persistent bleeding is even more rare. However, stent fracture within peripheral arteries is not only associated with an increased risk of restenosis, but has also been found to predispose patients to serious vascular complications.

Babalik et al reported a patient with stent fracture in the popliteal artery presenting with acute occlusion requiring surgical intervention for limb salvage.8 There have also been case reports of stent fracture with formation of a pseudoaneurysm at the site of fracture.9

To the best of our knowledge, our report appears to be the first of stent fracture leading to perforation of the stented vessel. In this case, vascular damage and bleeding caused the development of a large hematoma in the thigh. This hematoma was large enough to cause external compression of the adjacent veins with resulting formation of a DVT. These were successfully treated with covered stents and an initial strategy of vena cava filter with subsequent (delayed) warfarin therapy. This led to complete resolution of claudication symptoms and DVT.

Patients who undergo implantation of a peripheral stent should be notified that all stents carry a certain fracture rate. We hope that the future development of new, more flexible or bioabsorbable stents will limit the likelihood of stent fracture. To aid in the recognition of stent fracture, in addition to general post-stent implantation instructions, all patients should be notified that the development of acute pain or swelling should prompt immediate medical evaluation. The evaluation of a patient who has developed pain or swelling after stent implantation should include an assessment for stent fracture.

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