Abstract
Type 2 endoleak has been proved not to significantly increase the risk of aneurysm rupture. However, it is associated with aneurysm enlargement and may require secondary interventions. Its role has been widely investigated, but a definitive consensus about its management has still not been obtained. We performed a retrospective, single-center observational study that investigates the incidence of type 2 endoleak and its implications in the long-term follow-up in all the patients who underwent endovascular aortic repair (EVAR) for abdominal aortic aneurysm from 2011 to 2016 at our institution. A total of 216 patients who underwent EVAR during the specified time period were enrolled, and 85 of them (39%) developed type 2 endoleak in their follow-up. Thirty-one of the patients who developed type 2 endoleak faced an aneurysm sac growth > 10 mm and required secondary intervention. Only nine of them showed resolution of the leak. In the long-term follow-up, patients who developed type 2 endoleak after EVAR did not show a significantly increased mortality compared with those who did not, but some of them required late open conversion due to aneurysm sac enlargement and some other developed a secondary type 1 endoleak which required correction. The management of type 2 endoleak remains debated, despite consensus exist regarding the need for intervention when a > 10-mm aneurysm sac growth is observed. Further studies are necessary to better define which are the “high-risk” type 2 endoleaks and identify the patients who would benefit more from correction.
Keywords: abdominal aortic aneurysm, endovascular repair, aneurysm, coil embolization, endograft placement, endovascular procedure, iliac artery disease
Since the introduction of aortic stent grafts, the proportion of patients with abdominal aortic aneurysm (AAA) treated with an endovascular procedure versus those treated with traditional open surgery has increased exponentially over the years. 1
In different trials, endovascular aortic repair (EVAR) showed a lower perioperative mortality and morbidity and allowed for early recovery after the procedure. 2 Given these unquestionable advantages, EVAR often also represents the treatment option preferred by the patients, who fear a longer hospitalization and the relevant perioperative pain and discomfort which follow traditional open surgery.
Nevertheless, superior outcomes of EVAR in the long term are less clear and further studies demonstrated that the mortality curve of patients treated with EVAR tend to meet and finally even overcome those treated with open surgery after a few years. Furthermore, patients treated with EVAR have a higher rate of secondary procedures. 3 One of the most common causes of reintervention after EVAR is the presence of “endoleak.”
Endoleaks have been classified into five different categories, depending on the cause of the residual aneurysm sac perfusion. Broad consensus has been achieved concerning the need to promptly treat type 1 and 3 endoleaks. They indeed determine a considerable risk of AAA rupture, due to the high pressure of the blood which still perfuses the aneurysm sac. On the contrary, the utility of treating type 2 endoleak, which is also the most frequently observed, remains less clear. 4
The European Society for Vascular Surgery guidelines indicate that a 1-cm growth of the aneurysm sac in the presence of type 2 endoleak may be considered a reasonable threshold for reintervention and they recommend endovascular techniques as the first-choice treatment modality. 5 However, many trials reported low success rate in the treatment of this type of endoleak with different endovascular techniques. 6
In this article we present the experience of our center in the management of type 2 endoleak.
Methods
We designed a retrospective, single-center observational study that received approval by the local Ethical Committee.
Inclusion criteria comprised all the patients who underwent elective EVAR for the treatment of nonruptured AAAs or aortoiliac aneurysms at our institution between January 2011 and June 2016.
The primary outcome of our study was to determine the incidence of type 2 endoleak after EVAR in our cohort of patients and to verify how it affects overall mortality.
The secondary outcome is to verify how often the presence of endoleak leads to an aneurysm sac enlargement that requires a secondary corrective procedure and also to evaluate the efficacy of secondary procedures in resolving type 2 endoleak.
A vascular surgeon and an interventional radiologist independently reviewed the clinical records, the intraprocedural angiographic images, and the entire available follow-up of all the patients enrolled in the study.
Epidemiological and anatomical baseline data were collected. We then looked for the presence of endoleak both at the intraprocedural completion angiography and during the follow-up. The presence of endoleak was detected with the use of computed tomography (CT), Doppler ultrasound, or contrast-enhanced ultrasound (CEUS). Endoleaks were classified as type 1 to 5, according to the revised classification initially proposed by White.
Postoperative follow-up was conducted according to local protocol, in line with the recommendations provided by the clinical practice guidelines.
We routinely perform a CT angiography (CTA) 1 month after every EVAR procedure and, in case of absence of complications and no evidence of endoleak, we continue the follow-up with a Doppler ultrasound performed every year thereafter. We treat type 1 and 3 endoleaks when detected, whereas we strictly monitor patients with type 2 endoleak with Doppler ultrasound and we perform CTA when we observe an aneurysm sac growth, to better define the leak and plan a treatment if we deem it is necessary. According to the guidelines we tend to treat patients in which we observe an aneurysm sac enlargement bigger than 1 cm.
Statistical Analysis
We performed a descriptive statistic of the epidemiological and anatomical baseline data of the patients enrolled in the study and we defined the incidence of type 2 endoleak, the frequency of secondary procedure performed to treat type 2 endoleak, and the success rate of these procedures.
We performed inferential statistics through Kaplan–Meier analysis to analyze the effect of type 2 endoleak on survival of patients treated with EVAR. We also used Cox regression to evaluate the correlation of age, sex, AAA dimension, and type of graft that we used with the onset of type 2 endoleak.
Results
A total of 216 patients underwent elective EVAR for the treatment AAA or aortoiliac aneurysms at our institution between January 2011 and December 2016. Among these patients, 195 were males and 21 were females. Mean age at time of intervention was 75 years.
The average maximum aortic aneurysm sac diameter of the patients that we treated was 55.5 mm (range 30–80).
Mean follow-up was 43 months.
A Gore Excluder C3 was used in 85 patients, a Medtronic Endurant II/IIS in 75 patients, a Vascutek Anaconda in 22 patients, and a Cook Zenith Alpha in 18 patients. The remaining 16 patients were treated with other types of endograft that we grouped together for the statistical analysis.
Type 2 endoleak was detected in the course of the follow-up in 85 of the 216 patients enrolled in the study (39%). In 27 patients, the type 2 endoleak was demonstrated intraoperatively at completion angiography after EVAR, whereas 58 patients developed type 2 endoleak later, in the course of the follow-up. In 47 of the latter, the leak was detected with CTA and in 11 with CEUS.
Mean time elapsed between the EVAR procedure and the diagnosis of type 2 endoleak in the 58 patients who developed the leak during the follow-up was 6.8 months (range 1–48).
Kaplan–Meier analysis did not show any significant effect of type 2 endoleak on overall survival in the long-term follow-up (log-rank p = 0.914) ( Fig. 1 ).
Fig. 1.
Kaplan–Meier survival curves of patients who did or did not develop type 2 endoleak in the long-term follow-up after endovascular aortic repair of abdominal aortic or aortoiliac aneurysms.
Cox regression demonstrated that age did not significantly affect the incidence of type 2 endoleak in our cohort of patients, neither did sex or the type of endograft that we used.
Finally, a bigger diameter at baseline of the aneurysm sac appeared to be significantly associated with a higher incidence of type 2 endoleak compared with a smaller diameter ( p = 0.019), with an odd ratio of 1.7 for every 1 cm increase.
In 38/85 patients who developed type 2 endoleak, an aneurysm sac enlargement was noticed, with a mean increase of the maximum diameter of 9.2 mm.
Thirty-one of these patients presented a > 10-mm aneurysm sac enlargement after the diagnosis of type 2 endoleak and underwent secondary intervention. A total of 46 secondary procedures were performed to treat the type 2 endoleak, with an average of 1.48 procedure per patient.
In particular, three patients underwent CT-guided translumbar percutaneous embolization with cyanoacrylate, whereas in 43 patients an endovascular approach was adopted.
Among the latter, we performed 35 percutaneous transfemoral embolizations with coils, glue, or cyanoacrylate of the inferior mesenteric artery (18 cases) ( Fig. 2 ) or of the lumbar arteries (17 cases), sometimes in association with embolization of the aneurysm sac (13 cases).
Fig. 2.
Embolization of type 2 endoleak through the superior mesenteric artery. Through right arterial femoral percutaneous access, the superior mesenteric artery is engaged with a Cobra 5 Fr catheter. A microcatheter is then used to navigate the arch of Riolan and is advanced into the inferior mesenteric artery until it reaches the aortic aneurysm sac. Angiography performed through the microcatheter demonstrates the presence of a type 2 endoleak sustained by the inferior mesenteric artery with outflow through a patent lumbar artery ( A ). Coil embolization of the inferior mesenteric artery is performed. Final angiography demonstrates interruption of the inflow of the leak ( B ).
Three further transfemoral embolization procedures failed, due to impossibility to reach the aneurysm sac through collateral vessels.
In one case, transfemoral angiography failed to demonstrate the presence of type 2 endoleak, which was still detected at the next CTA.
Embolization was performed through a transcaval puncture of the aneurysm sac in 4 patients ( Fig. 3 ).
Fig. 3.
Transcaval embolization of a type 2 endoleak. Through right venous femoral percutaneous access, a transcaval puncture of the aortic aneurysm sac is performed with the use of a TIPS (transjugular intrahepatic portosystemic shunt) needle. A hydrophilic guidewire is inserted through the needle and is used for introducing a 5-Fr catheter in the aneurysm sac. Angiography is performed through the catheter and confirms the presence of a type 2 endoleak sustained by several patent lumbar arteries ( A ). The leak is embolized by injecting cyanoacrylate in the aneurysm sac through the catheter. Final control shows the presence of radiopaque cyanoacrylate in the aneurysm sac right where the presence of type 2 endoleak was previously demonstrated ( B ).
The management of patients with type 2 endoleak and a > 1-cm aneurysm sac growth is summarized in Fig. 4 .
Fig. 4.
Management of patients with type 2 endoleak and a > 1-cm abdominal aortic aneurysm (AAA) sac growth.
In only 9/31 patients who underwent secondary procedures, we achieved resolution of the leak. In particular, the leak resolved in 8 of them after a single secondary procedure that consisted in transfemoral embolization of the inferior mesenteric artery (IMA) or of the lumbar arteries. In the remaining one, we could appreciate extinction of the leak only after four corrective procedures. More into detail, we first made two attempts to embolize the IMA and the lumbar arteries with a transfemoral approach. We then made a third attempt to embolize the leak with direct CT-guided percutaneous translumbar puncture of the aneurysm sac and finally we obtained resolution of the leak by mean of transcaval embolization of the aneurysm sac.
Type 2 endoleak persisted in the remaining 22 patients and we decided to perform late open conversion in two of them, due to continuous growth of the aneurysm sac. Both the conversions had regular postoperative course. The remaining 20 patients with persistent type 2 endoleak were managed conservatively, whether because they did not show a significant further growth of the aneurysm sac or because they were deemed to be at high risk for surgical conversion. None of them faced aneurysm-related mortality in the next follow-up.
Interestingly, spontaneous resolution of type 2 endoleak was not uncommon, as it was observed in 14 patients. In two of them, it occurred after both the patients had previously undergone two ineffective endovascular corrective procedures; in the remaining 12 patients no previous attempt to correct the leak had been performed because of no evidence of significant aneurysm sac growth.
Noticeably, eight patients with type 2 endoleak developed a late type 1 endoleak, at a mean follow-up of 50.5 months.
Five of them presented type 1A endoleak. Among these, one underwent proximal extension of the endograft with deployment of an aortic cuff and three underwent open conversion with removal of the endograft and surgical repair. The last refused further procedure and was then lost at follow-up.
Three patients showed a type 1B endoleak. Two of them underwent endovascular effective repair with deployment of an iliac extension of the endograft, and a 91-year-old patient was not considered eligible for repair due to his age and general condition but was still alive at his last follow-up.
In none of the patients with type 2 endoleak who developed late type 1 endoleak a > 1-cm aneurysmal sac growth was noticed prior to the detection of late type 1 endoleak. On the contrary, a > 1-cm sac growth was observed in 4 of them after the type 1 endoleak was diagnosed.
Discussion
The role of type 2 endoleak after EVAR is still not well understood and, despite the rapid progress in the endovascular techniques, it continues to represent a pitfall in the treatment of AAAs. In the EUROSTAR registry, correction of type 2 endoleak demonstrated no significant reduction of the risk of aneurysm rupture compared with a conservative approach. 7
However, it was associated with a higher risk of enlargement of the aneurysm and reinterventions. 8
The incidence of type 2 endoleak varies greatly in the literature and the one that we report in our article is quite high compared with other centers.
It is possible that this is because we do not routinely put into action preventive maneuvers.
Indeed, preventive intraprocedural aneurysm sac embolization has been described, 9 10 as well as preventive selective embolization of the patent IMA or of the main lumbar arteries. 11 In some papers these measures proved to be effective in reducing the incidence of type 2 endoleak, but broad consensus about their employment is still not established. 12
Endovascular aortic sealing was introduced with the Nellix endograft, manufactured by Endologix. In the early experience this device showed promising results. 13 However, the long-term failure rate was demonstrated to be high. 14
We think that a strict follow-up is the key not to miss a large number of endoleaks that could otherwise be unrecognized. The aneurysm sac, even after being excluded by the bloodstream with an EVAR procedure, remains a dynamic environment. Thrombus modifications as well as spontaneous onset or extinction of leaks are not uncommon and can be observed even after many years.
Unfortunately, despite we are in possession of the accurate preoperative baseline measurements of the AAA diameters of all the patients enrolled in the study, as it is routinely measured by means of multiplanar reconstructions of the CTA and registered in the clinical records at our institution, we could not have access to the preoperative CT scans of 71 patients. Furthermore, medication reconciliation at admission was not sufficiently accurate for some of them. Thereby, we could not include some relevant information in our study, such as the number of patent lumbar arteries originating from the aneurysm sac, neither we know exactly how many of our patients were taking oral anticoagulants before and after the EVAR procedure. This might represent a weakness of our study, as these two factors were demonstrated to affect the incidence of type 2 endoleak in previous researches. Older age was not associated with an increased risk of type 2 endoleak in our cohort of patients. This correlation was reported in other previous papers, despite a clear explanation for it is still not provided. 15
In our experience none of the patients who developed type 2 endoleak faced aneurysm-related death and this may seem to suggest that type 2 endoleak is a relatively nonthreatening condition. On the other hand, interestingly, in 8 patients with type 2 endoleak included in our experience we observed the onset of late type 1 endoleak and 3 of them required open conversion. We think that this is a very important finding, as it suggests that type 2 endoleak can sometimes represent a dangerous entity. However, we have no data that demonstrates a causal correlation between the type 2 endoleak and the late onset of type 1 endoleak. We can only speculate on the fact that type 2 endoleak might have induced thrombus modifications or dilation of the aortic neck or of the iliac landing zones that allowed for AAA reperfusion by a late type 1 endoleak.
The guidelines suggest intervening with a secondary procedure in case of type 2 endoleak and a concomitant > 1 cm aneurysm sac growth, but the level of evidence supporting this behavior is not high. 5 Other factors in addition to the sac growth might play a role in determining the risk of aneurysm rupture due to type 2 endoleak, such as the residual intrasac pressure. 16
Treatment of type 2 endoleak requires an experienced multidisciplinary team capable to carry out CT-guided percutaneous punctures and familiar with the use of microcatheter and material for endovascular embolization such as coils, glue, or cyanoacrylate.
Despite good local expertise, secondary procedures for the treatment of type 2 endoleak showed poor results in our experience. The particularly low success rate that we report compared with other series looks somehow unexpected and we do not have a clear explanation for it. However, it is consistent with other experiences reported in the literature. In a systematic review and meta-analysis published in 2018, it was emphasized that clinical success rate (resolution of type 2 endoleak at follow-up) was often significantly lower than technical success rate (absence of residual type 2 endoleak at the end of the procedure) after secondary procedure for the treatment of type 2 endoleak, and some of the paper included in the analysis reported rate of type 2 endoleak resolution even lower than the one we observed at our institution. 17
Conclusion
Type 2 endoleak remains one of the biggest pitfalls in the endovascular repair of AAAs. Despite its implications have been investigated in several trials, its ideal management is still not well established. Effort must be put into developing new materials and into coming up with preventive operative strategies that can be used to reduce its incidence and also to treat this condition more effectively compared with the options that are currently at our disposal.
Funding Statement
Funding None.
Footnotes
Conflict of Interest None declared.
References
- 1.Boyle J R, Mao J, Beck A W et al. Editor's Choice - variation in intact abdominal aortic aneurysm repair outcomes by country: analysis of International Consortium of Vascular Registries 2010 - 2016. Eur J Vasc Endovasc Surg. 2021;62(01):16–24. doi: 10.1016/j.ejvs.2021.03.034. [DOI] [PubMed] [Google Scholar]
- 2.Dutch Randomized Endovascular Aneurysm Management (DREAM)Trial Group . Prinssen M, Verhoeven E L, Buth J et al. A randomized trial comparing conventional and endovascular repair of abdominal aortic aneurysms. N Engl J Med. 2004;351(16):1607–1618. doi: 10.1056/NEJMoa042002. [DOI] [PubMed] [Google Scholar]
- 3.OVER Veterans Affairs Cooperative Study Group . Lederle F A, Kyriakides T C, Stroupe K T et al. Open versus endovascular repair of abdominal aortic aneurysm. N Engl J Med. 2019;380(22):2126–2135. doi: 10.1056/NEJMoa1715955. [DOI] [PubMed] [Google Scholar]
- 4.ENGAGE investigators . Dijkstra M L, Zeebregts C J, Verhagen H JM et al. Incidence, natural course, and outcome of type II endoleaks in infrarenal endovascular aneurysm repair based on the ENGAGE registry data. J Vasc Surg. 2020;71(03):780–789. doi: 10.1016/j.jvs.2019.04.486. [DOI] [PubMed] [Google Scholar]
- 5.Esvs Guidelines Committee . Wanhainen A, Verzini F, Van Herzeele I et al. Editor's Choice - European Society for Vascular Surgery (ESVS) 2019 clinical practice guidelines on the management of abdominal aorto-iliac artery aneurysms. Eur J Vasc Endovasc Surg. 2019;57(01):8–93. doi: 10.1016/j.ejvs.2018.09.020. [DOI] [PubMed] [Google Scholar]
- 6.Hajibandeh S, Ahmad N, Antoniou G A, Torella F. Is intervention better than surveillance in patients with type 2 endoleak post-endovascular abdominal aortic aneurysm repair? Interact Cardiovasc Thorac Surg. 2015;20(01):128–134. doi: 10.1093/icvts/ivu335. [DOI] [PubMed] [Google Scholar]
- 7.van Marrewijk C, Buth J, Harris P L, Norgren L, Nevelsteen A, Wyatt M G. Significance of endoleaks after endovascular repair of abdominal aortic aneurysms: the EUROSTAR experience. J Vasc Surg. 2002;35(03):461–473. doi: 10.1067/mva.2002.118823. [DOI] [PubMed] [Google Scholar]
- 8.EUROSTAR Collaborators . van Marrewijk C J, Fransen G, Laheij R J, Harris P L, Buth J. Is a type II endoleak after EVAR a harbinger of risk? Causes and outcome of open conversion and aneurysm rupture during follow-up. Eur J Vasc Endovasc Surg. 2004;27(02):128–137. doi: 10.1016/j.ejvs.2003.10.016. [DOI] [PubMed] [Google Scholar]
- 9.Mascoli C, Freyrie A, Gargiulo M et al. Selective intra-procedural AAA sac embolization during EVAR reduces the rate of type II endoleak. Eur J Vasc Endovasc Surg. 2016;51(05):632–639. doi: 10.1016/j.ejvs.2015.12.009. [DOI] [PubMed] [Google Scholar]
- 10.Fabre D, Fadel E, Brenot P et al. Type II endoleak prevention with coil embolization during endovascular aneurysm repair in high-risk patients. J Vasc Surg. 2015;62(01):1–7. doi: 10.1016/j.jvs.2015.02.030. [DOI] [PubMed] [Google Scholar]
- 11.Manunga J M, Cragg A, Garberich R et al. Preoperative inferior mesenteric artery embolization: a valid method to reduce the rate of type II endoleak after EVAR? Ann Vasc Surg. 2017;39:40–47. doi: 10.1016/j.avsg.2016.05.106. [DOI] [PubMed] [Google Scholar]
- 12.Biancari F, Mäkelä J, Juvonen T, Venermo M. Is inferior mesenteric artery embolization indicated prior to endovascular repair of abdominal aortic aneurysm? Eur J Vasc Endovasc Surg. 2015;50(05):671–674. doi: 10.1016/j.ejvs.2015.06.116. [DOI] [PubMed] [Google Scholar]
- 13.Nellix Investigators . Carpenter J P, Cuff R, Buckley C et al. One-year pivotal trial outcomes of the Nellix system for endovascular aneurysm sealing. J Vasc Surg. 2017;65(02):330–3.36E6. doi: 10.1016/j.jvs.2016.09.024. [DOI] [PubMed] [Google Scholar]
- 14.Singh A A, Benaragama K S, Pope T et al. Progressive device failure at long term follow up of the Nellix EndoVascular Aneurysm Sealing (EVAS) system. Eur J Vasc Endovasc Surg. 2021;61(02):211–218. doi: 10.1016/j.ejvs.2020.11.004. [DOI] [PubMed] [Google Scholar]
- 15.Vascular Study Group of New England . Lo R C, Buck D B, Herrmann J et al. Risk factors and consequences of persistent type II endoleaks. J Vasc Surg. 2016;63(04):895–901. doi: 10.1016/j.jvs.2015.10.088. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 16.Dias N V, Ivancev K, Malina M, Resch T, Lindblad B, Sonesson B. Intra-aneurysm sac pressure measurements after endovascular aneurysm repair: differences between shrinking, unchanged, and expanding aneurysms with and without endoleaks. J Vasc Surg. 2004;39(06):1229–1235. doi: 10.1016/j.jvs.2004.02.041. [DOI] [PubMed] [Google Scholar]
- 17.Ultee K HJ, Büttner S, Huurman R et al. Editor's Choice - systematic review and meta-analysis of the outcome of treatment for type II endoleak following endovascular aneurysm repair. Eur J Vasc Endovasc Surg. 2018;56(06):794–807. doi: 10.1016/j.ejvs.2018.06.009. [DOI] [PubMed] [Google Scholar]