A Review of the Prevention and Management of Catastrophic Complications During Renal Artery Stenting

Introduction

Since the introduction of percutaneous transluminal renal angioplasty (PTRA) in 1978,¹ endovascular management for renovascular disease has become the standard of care with the number of renal artery interventions performed increasing annually.² Initially, endovascular treatments were limited by high restenosis rates, due to adjacent bulky aortic plaques leading to significant elastic recoil. These early limitations have been overcome with the development of a wide array of balloon expandable and self-expanding stents that are now available. In a meta-analysis by Rees et al,³ the technical success rate of PTRA is 55% for ostial lesions and 70% for nonostial lesions. With the addition of stents, the technical success rate improves to 99%. A randomized, prospective clinical trial comparing PTRA and percutaneous transluminal renal stenting (PTRS) for ostial lesions also demonstrated a significant difference in favor of stenting for immediate success rates without a significant increase in complications.⁴ The overall complication rate with renal artery stenting is reported to range from 8–36%.^5–13 Many of these complications are minor with no clinical consequence; groin hematoma and access site trauma being the most common. Fortunately, catastrophic complications during renal artery stenting are distinctly uncommon. The incidence of secondary nephrectomy is 3,10,11 Nephrectomy may be required in instances of complete renal artery occlusion from embolization or dissection that cannot be managed with endovascular techniques. Common causes of mortality with renal artery stenting include hemorrhage, acute renal failure, cholesterol embolization, sepsis, and aortic dissection.³ The overall incidence of major complications with renal artery stenting is 6–10%, and major complications may occur at any point in the procedure.^5,6,9 Manipulations with the initial catheterization can lead to dissections of the renal artery or segmental branches, which may be a cause for acute renal artery occlusion. Renal artery rupture, renal artery dissection or aortic dissection may follow stent deployment. Cholesterol embolization resulting in renal artery occlusion may occur with either the initial catheterization or the stent deployment. With meticulous technique, many of these complications can be avoided. Prevention and management of these serious complications can mean the difference between procedural success and possible catastrophe.

Renal Artery Dissection

The creation of a renal artery dissection during stenting that results in a change in management of the patient is unusual. In published series, this complication has been reported to occur in 1–18% of cases.^6,9 Beek et al report three instances of renal artery dissection, two of which were of no clinical significance, but resulted in loss of the kidney in the third.⁶ The cause for significant dissection of the renal artery is typically the subintimal passage of the guidewire during the initial catheterization. However, it might also arise from other manipulations, including predilatation prior to stent deployment, over-sizing the stent, or aggressive balloon dilatation of the stent. Regardless of the cause, dissection of the renal artery occurs more often in heavily calcified lesions. Some dissections that occur after balloon dilatation or stent placement may be beyond the physician’s control. However, technical error may be the cause when the initial guidewire placement takes a subintimal course and goes unrecognized. The resulting subintimal false channels are reported to occur in up to 18% of cases.⁶ In this situation, it is critical to identify when the wire takes this subintimal path because, if unrecognized, balloon inflation or stenting within the false channel may lead to acute renal artery occlusion or renal artery perforation. Though sometimes unavoidable, there are some techniques that may reduce the incidence of this complication.

Prevention

The key to preventing subintimal guidewire passage rests in understanding the underlying cause. When using a catheter to select the renal artery orifice, the tip of the catheter may wedge into the atherosclerotic plaque that frequently abuts the renal artery orifice. The guidewire, as it is advanced out of the catheter, then dissects underneath this plaque into the subintimal plane of the renal artery. Hydrophilic guidewires are particularly susceptible to this complication, though even “soft-tipped” guidewires may dissect if one is not careful. Some authors recommend using a reversed-curve catheter to help prevent this complication.¹⁴ When using a reversed-curve catheter, a “soft-tipped” guidewire is extended approximately one centimeter from the tip of the catheter, and the catheter is advanced cephalad while directed toward the renal ostium. This allows the guidewire to engage the renal artery orifice rather than the tip of the catheter; the catheter may then be advanced over the guidewire, rather than wedging into the plaque. Similarly, a second guidewire may be used to prevent the catheter from abutting the aortic wall, the “no-touch” technique. The renal artery orifice is gently probed with a guidewire without touching the aortic wall with the guiding catheter. This technique is discussed in more detail later in the article. If inadvertent subintimal guidewire passage occurs, early recognition is crucial in preventing a more serious complication. Relying on the course of the guidewire alone may be misleading. Typically, in the author’s experience, if the guidewire is intraluminal, it will advance with little resistance. In addition, contrast injections through a guiding catheter or sheath may help confirm whether the guidewire is intraluminal or subintimal. If a subintimal flap is raised, further attempts to catheterize the renal artery may become more difficult. In these instances, gentle probing with an angled guidewire may be the only option. If this fails, the procedure may need to be aborted and surgical revascularization may be required.

Management

Early identification is crucial to the management of flow-limiting renal artery dissections. The visualization of the intimal flap on angiography may be difficult and require multiple obliquities, but may be suggested by poor flow within the renal artery. The determination of whether a dissection is flow limiting is often subjective. In circumstances, which are not clear, intravascular ultrasound may be helpful. Alternatively, hemodynamic pressure monitoring may be used: pressure wires are now available that can provide information regarding a pressure gradient across the lesion. Once it is determined that a significant dissection exists, the primary goal should be to maintain or restore patency of the renal artery. Therefore, the patient should be fully anticoagulated. It is critical to maintain guidewire access. With a guidewire in place, the dissection flap may be tacked down with prolonged balloon inflation or the placement of an additional stent. If complete thrombosis does occur, this can be managed with either local infusion of a thrombolytic or with mechanical thrombectomy. Successful use of a percutaneous rheolytic thrombectomy catheter for acute renal artery thrombosis has been reported.^15,16 In instances when flow cannot be reestablished, surgical salvage may be considered. This may consist of either surgical bypass or nephrectomy. In cases of extensive arterial dissection or irreversible ischemia, nephrectomy may be the only available option.¹⁷ One form of dissection deserves special mention is the deep dissection that results in an intramural hematoma. This typically occurs as a result of angioplasty or stent dilatation creating a focal rent in the media without a reentry point. The incidence of this lesion with renal artery stenting is uncertain: to date, there is only one known case report,¹⁸ though it has been described in up to 6.7% of patients during coronary artery angioplasty.^19,20 As many as one-third of intramural hematomas may have no angiographic abnormality;¹⁹ thus, diagnosis may require intravascular ultrasound (IVUS). When visible angiographically, the deep dissection may appear as a dissection flap with associated vessel narrowing or as a stenosis that progresses over time. With IVUS, the intramural hematoma appears as a crescent-shaped area of increased echogenicity within the media of the artery.¹⁹ The significance of this lesion is twofold: untreated, the intramural hematoma can propagate and extend distally along the renal artery. This can result in a flow limiting stenosis that may extend into the branch vessels. In addition, continued blood flow into the wall of the artery may lead to pseudoaneurysm formation, putting the patient at risk for possible delayed rupture of the renal artery. The management is similar to conventional dissections; treatment should primarily focus on sealing the entry point. This may be accomplished with prolonged balloon dilatation or placement of an additional stent; there has also been a report of the successful use of a covered stent in this situation.¹⁸

Embolization

Most ostial renal artery stenotic lesions are associated with adjacent aortic plaques. Thus, during either the initial catheterization or the subsequent angioplasty or stenting, the potential exists for embolization. A recently performed ex vivo study showed that atheroemboli were released by simply advancing the guidewire through an atherosclerotic plaque; also, every additional manipulation through the plaque resulted in additional atheroemboli.²¹ The sequela of plaque embolization may range from inconsequential to segmental infarction to complete renal artery occlusion. Clinically, this translates into injury ranging from insignificant to permanent renal impairment. The true incidence of embolization is difficult to identify because oftentimes the embolization is insignificant and unapparent on angiography. In studies using a distal protection device, debris was identified within the protection device in 65–75% of patients suggesting the incidence of embolization to be much higher than previously thought.^22,23 Major embolization occurred in 1.4% of patients in the ASPIRE-2 study.¹² In multicenter registries the incidence has ranged from 6,10

Prevention

Prevention of embolization during renal artery stenting has been aided in recent years by the development of low-profile stent delivery platforms. The new low-profile stent delivery systems are available in 0.014-inch and 0.018-inch profiles for either mono-rail or over-the-wire delivery. These have low crossing profiles of 0.066-inch for the 6mm Genesis stent (Cordis, Miami, Florida) as opposed to a crossing profile of 0.080-inch for 0.035-inch systems.²⁴ The lower crossing profile may reduce the degree of embolization during stenting. In two studies evaluating the use of low-profile stent platforms, there was no direct evidence of embolization during the procedure.^24,25 However, in one of these studies, two patients did go on to thrombose the stent within one week of placement. The authors postulated that this was due to cholesterol embolization.²⁵ In order to reduce the risk of embolization, one must reduce the manipulations through the bulky aortic and renal ostial plaques responsible for the majority of cases of atherosclerotic renal artery stenosis. Two technical modifications may aid in this objective: the “no-touch” technique and direct renal artery stenting. The “no-touch” technique was first described by Feldman et al in 1999 as a technique to reduce the incidence of atheroemboli from catheter manipulations in the aorta.²⁶ The technique is relatively straightforward. The initial guiding catheter or sheath is advanced over a 0.035-inch J-tipped guidewire to the level of the renal arteries. The J-tipped guidewire is advanced above the renal arteries. This acts as a support to prevent direct contact between the guide and the aortic wall. The guiding catheter or sheath is used to cannulate the target vessel. Once this cannulation is successful, the lesion is crossed with a 0.014-0.035 inch steerable guidewire. After the second guidewire is in place, the placement of the stent is performed according to conventional techniques. The development of low-profile systems and premounted balloon expandable stents has made it possible in many instances to perform direct stenting of the renal artery. When using this technique, the lesion is not predilated with a small diameter balloon. Rather, after successfully passing a 0.014-inch or 0.018-inch guidewire, a low-profile stent is placed across the lesion and deployed. This reduces two potential causes of atheroemboli: the initial advancement of a catheter or sheath across the lesion and predilatation with a small diameter balloon. In a study performed by Cremonesi et al, this technique was combined with the “no-touch” technique to perform renal artery stenting in 99 patients.²⁷ They reported 100% technical success with only two complications. One patient had a renal artery dissection treated be the placement of an additional stent, and one patient developed a localized aortic dissection. There was no evidence for distal embolization either angiographically or clinically. Because of concern over the impact of atheroemboli on renal function, there is increasing interest in the use of distal protection devices. In an early study, Henry et al treated 32 lesions using the PercuSurge (Medtronic Inc., Minneapolis, Minnesota) device.²⁸ This device consists of an occlusion balloon that is inflated during the stent placement. After stent deployment, the debris is aspirated through a 5.2 Fr catheter before the balloon is deflated. In all cases, visible debris was aspirated following stent placement, and there were no device related complications. Other devices that have been used include the Angioguard system (Cordis Corp., Miami Florida) and the FilterWire EX (Boston Scientific, Natick, Massachusetts).^22,23 Using the Angioguard system, Holden et al treated 46 renal arteries. The distal protection baskets contained debris in 65% of cases. None of the patients had acute decline in renal function when treated using distal protection. There are potential drawbacks to the use of distal protection devices in the renal arteries. As shown in the carotid arteries, there is dislodgement of debris with the placement of the distal protection device.²⁹ In high-grade stenosis, predilatation with a small diameter balloon may be required in order to pass the device: this may also be a source for embolism. In instances of early branching of the renal artery, it may not be possible to protect the entire kidney, and difficult renal artery anatomy may prohibit placement of a distal protection device. In one study, the device could not be placed in 2 of 5 renal arteries due to vessel tortuosity or early bifurcation.²² Nonetheless, in studies in which the distal protection device has been used, the associated complication rates are low. Although there is potential for significant reduction in atheroemboli with distal protection devices, there is currently little evidence to support this assertion. For this reason, the use of distal protection devices is being incorporated in a large multicenter trial investigating renal artery stenting.^30,31 This trial will help establish whether the reduction of atheroemboli translates into reduction in renal failure following stenting with improved mortality rates.

Management

The key to management of embolization is prevention. However, when embolization does occur, the management should be based on the clinical situation. With complete renal artery occlusion, prompt revascularization should be the goal. The kidney can only tolerate 60–90 minutes without blood flow, though there are reports of complete recovery of renal function when flow is restored in up to 3 hours.³² Restoration of flow may be achieved with a combination of pharmacologic and mechanical tools. The patient should be fully anticoagulated; consideration may be given to the use of antiplatelet agents, though their efficacy in this situation has not been determined. There are several reports of using catheter directed thrombolysis as an effective means for reestablishing flow.^5,33 In addition, several mechanical thrombectomy devices are available that might be useful. At least one, the Angiojet (Possis, Minneapolis, Minnesota) has been used successfully in the renal artery.¹⁶ There are also several reports of catheter thromboaspiration that have also shown to be effective even when thrombolysis fails.^34,35 With this technique, a 6–8 Fr guiding catheter is advanced to the level of occlusion. Using a 60-ml syringe, a vacuum suction is applied. The catheter is removed and flushed with saline. By using a Tuohy-borst Y-adaptor, this can be performed while maintaining guidewire access. When these techniques fail, consideration should be given to emergent surgical revascularization or nephrectomy.

Aortic Dissection

Aortic dissection is a rare, but potentially serious, complication of renal artery stenting that occurs with reported incidence of up to 2.2%.⁹ Though the precise cause of the development of aortic dissection in this situation is not known, it is postulated to be a consequence of the application of multidirectional forces on the aortic wall at the level of the renal ostium.³⁶ Prevention may not always be possible, but it does seem likely that overdilating a stent within the renal artery orifice may be a contributing factor. This is illustrated in a recently reported case where a dissection of the perirenal aorta developed after increasing the diameter of a balloon expandable stent from 6–7 mm while treating a renal ostial stenosis.³⁷ At the time of the second balloon dilatation, the patient complained of severe chest and back pain, and the diagnosis of aortic dissection was confirmed during aortography. The diagnosis of aortic dissection should be considered whenever a patient develops severe chest, back or abdominal pain following renal artery stent placement.³⁶ This may be confirmed angiographically or the patient may be sent for cross-sectional imaging. Any imaging should include the thoracic aorta to determine the extent of the dissection, specifically whether it has extended into the chest to involve the aortic arch. Management will be similar to the management for an idiopathic aortic dissection. Pharmacologic management should be promptly instituted; if the blood pressure is elevated, it should be aggressively lowered. The patient should be closely monitored for signs of propagation of the dissection flap or the development of visceral ischemia.

Renal Artery Rupture

Renal artery rupture is one of the most feared, though fortunately, rare complications with renal artery stenting with a reported incidence of only 0–1.7%.¹⁰ The clinical manifestation is often not subtle: there is immediate back or flank pain with bleeding into the retroperitoneum. The patient may become hypotensive and tachycardic. Contrast extravasation into the retroperitoneum is visible with angiography, evident by an amorphous collection of contrast emanating from the renal artery. Rarely, renal artery rupture may present several hours after the procedure.³⁸

Prevention 

enal artery rupture is usually secondary to either balloon dilatation in the subintimal plane or balloon dilation of a heavily calcified plaque. Anatomic factors may be present that are out of the control of the interventionalist. However, careful selection of balloon size will reduce the risk of arterial perforation. Calibration may be performed using either a marker catheter or with a known sheath diameter. The artery should be measured in a segment in which the vessel walls are roughly parallel, beyond any area of post stenotic dilatation.

Management

Early recognition and immediate management are the keys to successful management of renal artery perforation. Ideally, this complication will be recognized prior to removal of the guidewire. Often, reversal of anticoagulation and prolonged balloon inflation will be all that is required to control the hemorrhage. If heparin has been administered, its effect may be reversed with the administration of intravenous protamine. The angioplasty balloon is replaced across the site of perforation and gently inflated such that wall apposition is achieved. Contrast may be injected through the guiding catheter or sheath to ensure the absence of flow. The balloon is initially left inflated for three to ten minutes. Once the balloon is deflated, the artery is reassessed for continued extravasation. If the extravasation persists, repeat balloon inflation for a longer duration may be attempted or a covered-stent may be placed. The increasing commercial availability of covered stents has made this an attractive solution for renal artery perforations that do not respond to prolonged balloon tamponade. Though there are no large series looking at the used of covered stents in the renal arteries, there are several published reports of the successful use of covered stents in treating a renal artery rupture. In one of the largest series, Gaxotte et al implanted 13 Jostent stentgrafts (Jomed International AB, Helsingborg, Sweden) in 12 renal arteries for a variety of indications.³⁹ Two of the patients in this cohort were treated for acute renal artery rupture. In both cases, the covered stent was successful in achieving hemostasis. In all patients, at 6 months the only reported complications were two cases of restenosis (8.3%) successfully treated with balloon dilatation. Nonetheless, continued or delayed flow around the covered stent that goes unrecognized may place the patient at risk for developing a pseudoaneurysm or delayed rupture. Therefore, either follow-up cross sectional imaging or angiography is recommended in these patients. Using these techniques, the majority of renal artery ruptures may be managed with endovascular means. In a review by Morris et al, five patients had renal artery ruptures with renal artery stenting.³³ All five patients were managed nonoperatively: four out of five patients were successfully treated with prolonged balloon tamponade, and the fifth patient was treated with a homemade covered stent. In circumstances in which prolonged balloon inflation is unsuccessful and stent grafts are not available, the angioplasty balloon should be left inflated across the perforation in preparation for emergent surgical repair.

Summary

Serious complications with renal artery stenting are fortunately rare; however, the effects can be devastating. Renal artery dissection or plaque embolization may lead to acute occlusion of the renal artery, while rupture may lead to catastrophic hemorrhage. Prevention, early recognition and prompt management are the keys to preserving renal function and reducing patient morbidity and mortality ensuring that the benefits of renal artery stenting will continue to outweigh any potential risks.