Recent advances in interventional devices and physicians' technical skills have allowed for treatment of severe peripheral arterial disease using endovascular therapy. Occlusion of the entire iliac or the superficial femoral arteries can be treated with balloon angioplasty and stenting. Bare-metal stents, either balloonexpanding or self-expanding, have been used in the past decades. However, there is decreased patency rates with the increasing length of arterial disease due to in-stent restenosis from intimal hyperplasia. Covered stents, or stent grafts, have been developed using polytetrafluoroethylene to “cover” any space between the metal struts of the bare-metal stents. This may reduce the impact of instent restenosis, and there are promising data suggesting increased patency rates for long-segment arterial disease using this “endovascular bypass.” Good technical results are achieved by treatment of all diseased arterial segments.

Preservation of the collateral vessels should be attempted whenever possible; however, good technical revascularization with coverage of all diseased segments may be more important than preservation of every collateral vessel. With coverage of these collateral vessels, there is concern that thrombosis of the stent graft may lead to acute limb ischemia and limb loss. In our experience this is rarely seen, and most patients with failed or failing endovascular intraluminal grafts present with recurrent symptoms of claudication, rest pain, or nonhealing wounds—conditions similar to those seen on initial presentation that were present prior to stent graft revascularization.

One of the failure modes for peripheral stents is occlusion caused by compromised flow through the device. Often, reduced flow leading to an occlusion is caused by progression of the disease in the native vessel proximal or distal to the treated arterial segment. For bare-metal stents, there can also be reduced flow due to a compromised stent lumen from in-stent restenosis. For stent grafts, there can be stenosis caused by intimal hyperplasia at the device edges. All of these conditions may be better characterized once flow is restored through a thrombosed stent or stent graft. These conditions must be identified and treated to maintain stent graft flow and optimize secondary patency. The treatment strategy for device occlusion is therefore two-fold: removal of thrombus within the stent or stent graft to restore flow followed by treatment of the underlying flow-limiting disease. In this article, we discuss our strategies for treating thrombosed polytetrafluoroethylene stent grafts.

TREATMENT STRATEGIES

There are a number of strategies for clearing thrombus from an occluded vessel or stent graft, from slow lytic therapy through a basic infusion catheter to more rapid removal by devices that are designed for mechanical thrombectomy. The first approach offers the advantage of reduced procedural time and cost and the theoretical advantage of a more subtle and manageable breakdown of the clot into smaller particles with less risk of distal embolization. More active clot breakdown and removal can be achieved using the mechanical thrombectomy devices, with the potential for a reduction in overall treatment time, reduced hospital stay, and less exposure of the patient to the bleeding risks associated with longterm lytic therapy.

The decision to choose slow lytic therapy versus rapid removal depends on a patient's clinical status and the duration that the stent graft has been occluded. Patients who present with clinical signs and symptoms of acute limb ischemia and threatened limbs require more rapid thrombus removal with reestablishment of distal circulation. On the other hand, patients with recurrent symptoms of chronic limb ischemia with stent grafts that have been stenosed for more than 2 weeks may have organized clots. These patients may benefit from slow lytic therapy using an infusion catheter placed in the thrombus within the stent graft for better “cleaning.” In the following sections, we describe our techniques of lytic therapy in stent grafts (Table 1).

SLOW LYTIC THERAPY

At our institution, this is the treatment of choice for treating arterial thrombosis. In most patients with thrombosed stent grafts, the clinical presentation is that of the recurrent symptoms of chronic limb ischemia that caused the patients to be treated initially. Arterial access and angiography from the abdominal aorta to the foot are performed as previously described. The thrombosed lesion is crossed and confirmed by angiography, and a wire is placed in the tibial artery that is providing the dominant outflow. Arterial access is achieved in the contralateral groin through the common femoral artery. A diagnostic flush catheter is placed in the proximal abdominal aorta. Aortography with bilateral pelvic runoff is performed to identify any proximal, in-flow–limiting arterial lesions in the abdominal aorta or the iliac arteries. The catheter is then advanced to the ipsilateral ischemic leg, using the standard “up-and-over” technique over the aortic bifurcation. Lower extremity angiography is performed from the groin to the foot. It is important that the status of the outflow in the popliteal and tibial arteries is known prior to any intervention.

For thrombosed stent grafts in the external iliac or superficial femoral (SFA) arteries, a sheath is placed upand- over the aortic bifurcation, with the tip just proximal to the stent graft or in the distal common femoral artery. For thrombosed stent grafts in the common iliac arteries, access in the ipsilateral common femoral artery may be needed, with the sheath placed just distal to the stent graft in the retrograde fashion. Using the Glidewire and Glidecath devices (Terumo Interventional Systems, Inc., Somerset, NJ), the thrombosed stent is crossed. With the catheter distal to the external iliac or the SFA stent (or the catheter in the aorta for common iliac stents), angiography is performed to confirm true luminal position of the catheter. The 0.035-inch Glidewire is then placed distally in the dominant tibial artery that provides the best outflow to the foot (Figure 1A and 1B).

The Glidecath is exchanged over the wire for an infusion catheter with the appropriate length for the thrombosed segment (5, 10, 20, or 30 cm). A Touhy- Borst side-arm adaptor is connected to the end of the infusion catheter. Tissue plasminogen activator (tPA) is diluted in a 30-mL reservoir syringe containing 5 mg of tPA and 25 mL of normal saline. This reservoir syringe is connected to a 1-mL tuberculin syringe via a threeway stop-cock. The third end of this stop-cock is then connected to the side-arm of the Touhy-Borst adaptor. Three milliliters of diluted tPA is infused immediately into the infusion catheter. The remaining tPA in the reservoir syringe is then slowly infused at a rate of 1 mL per minute. When the infusion has been completed, angiography is performed to assess the progress of thrombolytic therapy (Figure 1C). If progress is made and there is some flow of contrast in the stent graft, another infusion of 5 mg of tPA is repeated. Usually, this is not adequate for lysis of the arterial plugs at the ends of the stent graft but allows for a decrease of the thrombus load and the initiation of the lytic therapy.

This is followed by a slow, long-term infusion of tPA. The Glidewire is exchanged for an infusion wire, with its tip in the tibial artery that has the best outflow to the foot for simultaneous administration of tPA into the best outflow tract. The long-term infusion is partitioned into a portion for lysis of the lesion via the infusion catheter and a portion through the infusion wire to deliver lytic agent downstream to break down any potential distal embolization that may occur. We use an infusion rate of 30 mL per hour for the system: 20 mL per hour through the infusion catheter and 10 mL per hour through the distal infusion wire. After overnight infusion, angiography is performed to assess the progress of thrombolysis (Figure 1D). Additional therapy using slow, long-term infusion can be provided if there is residual thrombus present.

Once the thrombus has been removed from the stent graft, the next step is to identify and treat the lesion that caused the stent graft to thrombose. If the offending lesion is not treated, the stent graft will likely thrombose again. The lesion could be in the native artery distal or proximal to the stent graft (caused by the natural atherosclerotic process). The lesion could also be at either end of the device (caused by intimal hyperplasia). These lesions are usually amenable to endovascular treatment options, such as percutaneous transluminal angioplasty, cutting-balloon angioplasty, bare-metal stents, or stent graft extension (Figure 1E and 1F).

Occasionally, in patients with chronic stent graft thrombosis, there is minimal residual thrombus after the initial lytic therapy with 10 mg of tPA (Figure 2A through 2F). This thrombus and the arterial plugs can be removed with the AngioJet catheter (Bayer Radiology and Interventional, Indianola, PA), using the mechanical thrombectomy mode as later described. The underlying cause is then treated (Figure 2G through 2K). This option allows for 1-day treatment and avoids the risk of bleeding from long-term thrombolytic therapy.

RAPID PHARMACOMECHANICAL THROMBECTOMY

Rapid thrombectomy is recommended for patients who have acute limb ischemia with impending limb loss. In these cases, rapid removal of thrombus from the stent graft with reestablishment of distal perfusion to preserve the limb is of the essence. Patients are taken emergently for arteriography and intervention. Ten mg of tPA is ordered from the pharmacy for thawing. Arterial access and angiography from the abdominal aorta to the foot are performed as previously described. The thrombosed lesion is crossed and confirmed by angiography, and a wire is placed in the tibial artery providing the dominant outflow.

A distal protection filter can be placed at the discretion of the interventionist. The AngioJet system is prepared according to the manufacturer's guideline, and the device is placed into the thrombosed stent graft. Ten mg of tPA is diluted into a 100-mL normal saline bag. Using the Power Pulse mode (this allows for infusion but not concurrent aspiration), the AngioJet catheter is advanced along the entire length of the clot to infuse the 10 mg of tPA. We wait 30 minutes to allow the thrombolytic process to take place. The AngioJet is changed to mechanical thrombectomy mode (simultaneous saline hydrolization of thrombus and aspiration of debris), and the catheter is advanced back and forth along the entire length of the thrombosed stent graft. It is important that the AngioJet catheter is used to treat the arterial plugs that are present at the proximal and distal end of the stent graft.

Arteriography is performed to assess the progress of thrombectomy. If contrast is not visualized within the stent graft, it is possible that the arterial plug is still present even though the thrombus has been removed from the stent graft. To visualize the lumen of the stent graft, a Glidecath device is advanced over the wire and placed within the proximal 1 or 2 cm of the stent graft. The Tuohy-Borst adapter is connected to the Glidecath device, and contrast is injected from the side-arm of the adapter. Any thrombus or arterial plug that is still present is treated with the AngioJet as needed until the maximum volume is reached according to the manufacturer's recommendations.

Once the result is adequate, the underlying disease is treated. This treatment paradigm offers the potential for complete treatment in the same day. Although the approach described in this article is not the standard protocol suggested by the manufacturer, this stage-wise approach has been effective at our institution.

CONCLUSION

Stent graft thrombosis can be effectively treated using the methods of thrombolysis described in this article. When the thrombus is cleared from the stent graft, the underlying disease process that caused the stent graft to fail can be treated. This treatment restores flow in the stent graft to original treatment conditions after the stent graft was initially placed for de novo disease, and may lead to similar outcomes that are seen from the de novo treatment. Additional studies are needed to evaluate the long-term outcomes of these approaches to maintaining secondary patency in stent grafts, although initial data from our institution appear promising.

Charlie C. Cheng, MD, is Assistant Professor, University of Texas Medical Branch at Galveston in Texas. He has disclosed that he has no financial interests related to this article. Dr. Cheng may be reached at cccheng@utmb.edu.

Lorraine Choi, MD, is with the University of Texas Medical Branch at Galveston in Texas. She has disclosed that she has no financial interests related to this article.

Zulfiqar Cheema, MD, is with the University of Texas Medical Branch at Galveston in Texas. He has disclosed that he has no financial interests related to this article.

Michael B. Silva Jr, MD, FACS, is The Fred J. and Dorothy E. Wolma Professor in Vascular Surgery, Professor of Radiology, Chief of the Division of Vascular Surgery and Endovascular Therapy, and Director or Texas Vascular Center, University of Texas Medical Branch at Galveston in Texas. Dr. Silva has received lectureship honoraria and institutional training grants from Gore & Associates. Dr. Silva may be reached at (409) 772-6366; mbsilva@utmb.edu.