Endoleak Following AAA Repair

Problems detected during follow-up affect treatment durability and success.


To view the table that corresponds to this article, please refer to the print version of our November/December issue, page 45.

As the prevalence of endovascular aneurysm repair (EVAR) increases, so does our understanding of the benefits and limitations of this technology. Initial clinical trials have reported high success rates for endovascular exclusion of AAAs,1-4 but problems detected during follow-up care leave the long-term durability and success of this treatment yet to be determined.5-7 A recent review of ruptures after endograft placement for AAA exclusion noted that 44 out of 47 known ruptures showed previous evidence of an endoleak (the persistence of blood flow around the endograft within the aneurysm sac).8 White et al originally classified endoleaks,9 and this classification system has recently been updated (Table 1).10

The presence of an endoleak can expose an aneurysm sac to systemic arterial pressure after EVAR.11,12 This persistence of pressure (or reintroduction of pressure after the sac has collapsed, in the case of late endoleaks) may be the cause of endoleak-related rupture. However, most endoleaks found in early follow-up do not lead to rupture, and the presence of an endoleak is not a predictor of mortality.3

A great deal of controversy persists regarding the most appropriate diagnostic and treatment modalities for an endoleak from various endografts. Between 20% and 40% of patients undergoing EVAR experience an endoleak at some point after endograft deployment.4,11,13 Consequently, the detection and treatment of endoleaks has become a major consideration in endovascular surgery.

Most surgeons agree that patients should be evaluated with a high-quality CT scan using intravenous contrast within 1 month after EVAR, and then again at 6 months if there are any problems detected at the first postprocedure scan. If no problems are detected, future scans can be performed on a yearly basis. The following summary provides information on the various types of endoleaks, with evaluation and treatment recommendations for each type.

A type I endoleak comprises a failure to seal the attachment sites of the endograft to the native vessels. These are widely recognized as the endoleaks most closely linked to rupture and are the most aggressively treated.8,13 Type I endoleaks can occur at proximal or distal attachment sites, and have been correlated to short aneurysm neck, large vessel diameter, aneurysm neck angulation, and tortuosity of the iliac arteries.14,15

Type I Endoleak in Unsupported Grafts
The characteristics of a type I endoleak vary by the type of endograft involved; subsequent treatment should be individualized with the particular device in mind. For example, proximal (type IA) endoleaks detected intraprocedurally with the Ancure endograft seem to have a more benign clinical course than others.16 A review of cases at the University of Pittsburgh showed that 7% of patients who underwent EVAR with Ancure grafts had an intraprocedural proximal endoleak after graft deployment and ballooning of the attachment site. At 1-month follow-up, a CT scan showed resolution of 82% of these leaks. The subsequent clinical outcome of these patients is essentially the same as those who never had a proximal endoleak. Figures 1 and 2 demonstrate an intraprocedural type IA endoleak and its spontaneous resolution on the 1-month follow-up CT scan.

The Ancure graft has a proximal low radial force and a sharp change in compliance between the attachment system and the unsupported graft. This combination of features may make the graft vulnerable to early endoleaks that resolve subsequently during remodeling of the proximal attachment site. Therefore, we feel comfortable observing small type IA leaks around Ancure grafts for at least 1 month after placement; if there is no sac enlargement, we continue the observation for 6 months. If a leak is still present at 6 months, the physician should investigate the problem angiographically and provide treatment.

Unsupported grafts do not demonstrate the same pattern of spontaneous resolution of distal (type IB) endoleaks. Many early Ancure ruptures were linked to type IB endoleaks seen with first-generation tube grafts.8 Due in part to this problem, bifurcated or monoiliac grafts are now the standard of care. It is imperative to create an adequate distal seal between the graft and iliac artery; type IB endoleaks can be a persistent problem with unsupported grafts, and the majority require reintervention.11 Late endoleaks can occur at the distal attachment site when the length of the seal is short. We have recently encountered two patients at 4 and 5 years post-EVAR with late type IB endoleaks in aorto-monoiliac devices; these leaks resulted in rupture. Many distal endoleaks can be avoided by selecting patients with suitable iliac anatomy or by placing limb extenders at the time of EVAR deployment. If the interventionalist finds a type IB endoleak at the time of deployment of an unsupported graft, it should be treated at that point. Coils have been successfully used to obliterate the space between a vessel wall and graft, but this strategy is primarily used for type II endoleaks.

Type I Endoleak in Supported Grafts
Fully supported grafts such as the AneuRx (Medtronic, Minneapolis, MN) and the Excluder (W.L. Gore and Associates, Flagstaff, AZ) perform differently than nonsupported grafts when associated with type I endoleaks. Type IA endoleaks seen in this setting rarely exhibit spontaneous resolution and may lead to rupture.8 Therefore, these should be treated at the time of implantation. Treatment of type IA endoleaks most often involves ballooning the site; if a leak persists, additional stents or extension cuffs can be deployed over the attachment areas. Type IB endoleaks in fully supported grafts are generally easily treated with modular extensions.

Any type I endoleak that arises during follow-up of a previously excluded AAA is probably due to aneurysm remodeling and possible graft kinking with a loss of seal between the graft and vessel. These endoleaks should be promptly treated.

Type II endoleaks are a result of retrograde flow from small arteries such as the lumbars or the inferior mesenteric artery (IMA). Detection of a type II endoleak is accomplished by routine duplex ultrasound, but is more commonly performed by CT scanning. Both methods have some disadvantages; however, the most serious problem is related to CT scanning. The timing of contrast injection during the CT scan will determine whether a type II endoleak is visible. Due to the nature of retrograde flow, these can be very low-flow systems. Delayed films may be necessary to assess late perfusion within the sac and should be performed with any suspicion of type II endoleak.

Interventionalists debate the significance of type II endoleaks, as many of these leaks will spontaneously resolve, regardless of graft type. Additionally, some patients will demonstrate stability or even shrinkage of the aneurysm sac in the presence of a patent type II endoleak.17 Current treatment of type II endoleaks is based on the behavior of the aneurysm sac, most of which can be safely observed for 6 months. However, if the sac expands during this time or at a later date, there is little doubt that the patient should undergo angiography and treatment usually in the form of embolization of feeding and draining vessels. Figure 3 illustrates successful coil embolization of a type II leak. Occasionally, a presumed type II endoleak is actually noted at angiography as a type I requiring prompt treatment.11

More controversy surrounds the best course of action when a type II endoleak is detected without an increase in sac size during follow-up. I favor an aggressive approach to treating all persistent endoleaks at 6 months and would consider further conservative treatment only when a type II endoleak is difficult to treat and the aneurysm sac is shrinking in size. The lessons learned through patients lost to follow-up and returning with rupture are difficult to ignore.

It is important to remember, however, that most type II endoleaks have a benign course and aggressive treatment should not involve excessive patient morbidity. In this setting, successful embolization performed via transarterial or translumbar techniques can be technically demanding, and should not be attempted by a beginning interventionalist. A recent comparison of the two techniques found that a significantly higher percentage of the translumbar embolizations resulted in durable exclusion of perigraft flow.18

There has been an interest in pre-EVAR embolization of patent lumbar arteries and IMA in an effort to prevent type II endoleaks,19 and also in laparoscopic ligation of patent lumbars and/or IMA.20 Currently, this is not the standard of care and preprocedural ligation of potential feeding vessels has not resulted in a significant decrease in type II endoleaks.

As with type I endoleaks, the surgeon should promptly evaluate and treat any new type II leak arising in a previously excluded aneurysm sac, as these may be more serious endoleaks appearing as type II. This is particularly important in modular grafts that may develop late type III endoleaks.

Type III endoleaks arise from a defect within the graft. This flaw can be a disjunction between modular components (type IIIA), or a hole in the fabric of the graft (type IIIB). Type III endoleaks are very graft-specific and can be serious because they are invariably associated with a sudden elevation of intrasac pressure.

All type III defects should be repaired as soon as they are detected. The interventionalist can successfully correct most of these defects with a modular extension or covered stent.

Type IV endoleaks are caused by fabric porosity and subside within 30 days. No specific treatment is necessary.

No Demonstrable Endoleak
Occasionally, the patient’s aneurysm sac will increase in size without a demonstrable endoleak. If the aneurysm is large and the increase in sac size is significant (>5 mm), the physician should perform an angiographic evaluation. An endoleak detected on angiography should be treated. Difficulty arises when no endoleak can be found on either CT scan or angiogram, and the aneurysm sac continues to expand. At this point, the physician can assume that the aneurysm is pressurized either from an unapparent endoleak or from endotension.

The term endotension was initially coined to refer to continued pressure within an aneurysm sac, with or without demonstrable flow. This term, however, has now evolved to mainly represent the concept of a pressurized aneurysm sac without apparent endoleak. Possible sources of this pressure include transmission through clots from side branches, attachment sites, or porosity of ultrafine graft fabric.21 Although most leading endovascular surgeons agree that an embolized or spontaneously thrombosed endoleak is no longer problematic,10 the true nature and clinical consequence of endotension is unknown. In this situation, the interventionalist should consider performing a second endograft within the first, or converting to open surgical repair.

Endoleaks are intrinsic to EVAR and require clear methods of evaluation and treatment. CT scans should be performed shortly after EVAR, and then yearly if there are no abnormalities detected. Any abnormalities (including sac expansion) demand intensive investigation. From the first mention of EVAR as a treatment option, physicians should clearly explain to patients the need for frequent evaluation and the possibility of further intervention.

Recommended treatments
Type IA endoleaks should be repaired in the operating room if fully supported grafts are used. Unsupported (Ancure) grafts have a high rate of spontaneous closure of type IA endoleaks and can be observed for up to 6 months if no sac expansion is noted. Type IB leaks should be repaired at the time of detection.

Type II endoleaks noted on the first postoperative CT scan can be safely observed for 6 months if there is no sac expansion. Further observation is appropriate only in the presence of sac shrinkage.
Type III endoleaks are seen with modular grafts and should be treated at the time of detection.

Ellen D. Dillavou, MD, is a Vascular Fellow at the University of Pittsburgh in Pittsburgh, Pennsylvania. Dr. Dillavou may be reached at (412) 648-8420; dillavoued@msx.upmc.edu.

Navyash Gupta, MD, is Assistant Professor at the University of Pittsburgh in Pittsburgh, Pennsylvania. Dr. Gupta may be reached at (412) 648-9012; guptany@msx.upmc.edu.

Michel S. Makaroun, MD, is Professor and Chief in the Division of Vascular Surgery and Director of Endovascular Surgery at the University of Pittsburgh in Pittsburgh, Pennsylvania. Dr. Makaroun may be reached at (412) 648-9015; makarounms@msx.upmc.edu.

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