The management of type II endoleak provoked a whole host of opinions among experts at CX35 yesterday. Are type II endoleaks benign, or not? Are “dangerous” type II endoleaks really misdiagnosed type I or type III endoleaks? Do type II endoleaks need treatment (and how), or is leaving them akin to “leaving a baby on a railway line”? Experts taking part in a panel discussion about the management of type II endoleaks following endovascular aneurysm repair (EVAR) did not agree

According to Hence Verhagen (Rotterdam, The Netherlands), type II endoleaks by themselves are benign and there is no proof that type II endoleaks cause type I or type III endoleaks. He said: “With a type II endoleak, it may be the outflow vessel that you are looking at instead of the inflow vessel [ie, it is the result of a type I or type III endoleak].”

Verhagen claimed that there “was no need to worry” about the treatment of type II endoleaks because they were associated with low pressure. He added that even if they were treated, there was little evidence that treatment would be effective—“In 100 patients with a type II endoleak, only two to five have a growing sac. Of these, only 30% will be successfully treated and that is the rate reported with experienced centres; therefore, only one of 100 patients will benefit from treatment.

However, Jean-Pierre Becquemin (Créteil, France) disagreed and commented: “I am really convinced that sometimes if you wait for more than five years to intervene, that type II endoleaks will lead to sac enlargement and maybe a type 1 endoleak.”

Becquemin argued that certain patterns of type II endoleaks were not benign and “must be treated by all appropriate means before catastrophe occurs”. He explained that he and his colleagues, in a recent study published in Journal of Vascular Surgery, reviewed the long-term outcomes of consecutive patients who had undergone EVAR for atherosclerotic infrarenal aortic or aortoiliac aneurysms between June 1995 and May 2010 at their centre (Henri Mondor Hospital, Creteil, France). 

After a mean follow-up period of 31.3 months (range 12.4–61.4 months), 201 patients (of 700 overall) had at least one type II endoleak and these patients were at higher risk of sac growth and re-intervention compared with patients without a type II endoleak. Additionally, persistent (p<0.001) and recurrent (p=0.008) type II endoleaks were both highly predictive of sac growth as were type II endoleaks that were associated with a type I or type III endoleak (p<0.001). Becquemin reported that mortality was not increased in patients with type II endoleaks but added: “Type II endoleaks did not kill these patients because these endoleaks were treated.” Concluding the results of study, Becquemin said: “Believing type II endoleaks are benign is like believing leaving a baby on a railway line is fine”—ie, there is no immediate danger, but danger may be approaching.

In the ensuing discussion, Becquemin acknowledged that type II endoleak were not necessarily the problem per se, and that it might actually be sac growth that was the main issue. “But you cannot neglect type II endoleaks. That is my strong feeling,” he said.

Matt Thompson, London, UK, claimed that there was not a “one size fits all” answer regarding whether or not type II endoleaks were benign. He said: “I am a pretty firm believer that some type II endoleaks are dangerous and that they are going to lead to aneurysm problems with the endograft, but I think the vast majority are benign.” He added that, probably, the “biggest problem” with type II endoleaks was that some endoleaks were labelled as type II endoleaks when “in reality”, they were actually a high-pressure type I or type III endoleak. “I think that is where the confusion comes from”, he commented. In his view, multi-imaging modality was “very important” to prove that sac growth was really being caused by a type II endoleak rather than a type I or type III endoleak.

Thompson also claimed that his experience with open aneurysm repair indicated that some type II endoleaks could lead to sac expansion. CX35 programme chairman Roger Greenhalgh (Imperial College, London, UK), who was chairing the session, commented that he had also seen open surgery cases that had showed type II endoleaks to be the cause of sac expansion.

He said: “Years after a perfectly good Dacron replacement by my predecessor, an apparent second rupture occurred. When I got it controlled and opened the sac, the whole thing was being driven by what today we would call a type II endoleak, with a massive lumbar, which was forcing the sac and I had to tie it.” He added that while not all type II endoleaks would lead to rupture, he was concerned about the possibility of type II endoleaks driving sac expansion.

In his presentation, Thompson also gave an update about the Nellix technology (Endologix) for EVAR. He said that, at present, there was not much long-term data for the technology but the data so far did indicate it could represent a “paradigm shift” in treatment because of its apparent ability to reduce complications and endoleaks.

Although the panel discussion did not reach a consensus, there was a clear message from the audience—nearly 80% of delegates voted against the motion that “Type II endoleaks without sac expansion of more than 5mm per year needs intervention”. Greenhalgh commented: “By implication, some of you believe that type II endoleaks do need intervention if there is sac expansion greater than 5mm.”

Apples and oranges

Robert Morgan (London, UK) said that type II endoleaks were “heterogeneous” and that comparing the different types of type II endoleak was like “comparing apples and oranges. Some type II endoleaks are ‘more benign’ than others.” He added that in type II endoleaks, absence of mural thrombus, the size of the endoleak nidus, the presence of inflow and outflow vessels, and the size of lumbar arteries or the inferior mesenteric artery were all factors in predicting future sac enlargement.

However, he claimed that studies had indicated that type II endoleaks were associated with a low rate of rupture.

Morgan also reviewed the treatment of type II endoleaks, stating that there was not enough data to determine the direct sac puncture embolisation technique was the preferred option to the transarterial technique approach. He said: “In practice, there are enthusiasts for either technique. Logistics [in my view] favour a transarterial technique.” 

According to Paolo Frigatti (Udine, Italy), preventing—rather than treating—type II endoleaks might be a valid strategy. He said that previous reports had shown: “Injection of fibrin glue alone or in association with microcoils in the aneurysm sac during EVAR can facilitate sac thrombosis and reduce the incidence of type II leaks during follow-up.”

Imaging for type II endoleaks needs improvement

Frans Moll (Utrecht, The Netherlands) said that imaging needed to be improved to detect more type II endoleaks. Improved imaging would also detect more feeding vessels for better embolisation. He said that MRI with blood pool contrast agent might give the needed improvement. However, he added: “Not all patients and stent grafts are MRI compatible and nothing of the effect of this better imaging on the outcome of EVAR is proven yet.”

Taking into account the diverging views on the management of type II endoleak, Greenhalgh said: “I wish I could say to the audience that the speakers today have made it easier, but perhaps it has been true to say, it is has been made more difficult for you. But one thing always to remember is that if you do not know the answer, clock that you don’t know the answer—so that you try to harder to find an answer.”

CX35 type II endoleaks survey

Delegates were invited to be part in a CX35 survey about the management of type II endoleaks yesterday. Please visit the BIBA MedTech Insights stand (Gallery Level) if you would like to participate.