AAA CTA EVAR open aneurysm surgery techniques training Uncategorized

Never Stop Following Stent Grafts -Type IV endoleak causing slow growth in 12 year old stent graft



The patient had undergone EVAR for bilateral common iliac artery aneurysm with the original Gore Excluder stent graft a dozen years before with coil embolization and extension to the external iliac on the larger side and femoral to internal iliac artery bypass on the other side. A coagulopathy, one of the clotting factor deficiencies, had made him high risk for bleeding with major open surgery. His aneurysms never shrank but remained stable and without visible endoleak by CT for a long time resulting in ever longer intervals between followup.


Between 2009 and 2013, there was subtle enlargement on the embolized side without a type I or type III leak, and the patient was brought back a year and a half later, with further growth of the sac.


This was a relatively rare type IV endoleak that was causing sac enlargement due to excessive graft porosity of the original Excluder’s graft material. Its treatment is either explantation or relining. We chose to reline the graft with an Excluder aortic cuff at the top and two Excluder iliac limbs.

2015-11-26 13_25_23

This was done percutaneously and in short followup, there has been stabilization and even some reduction in the aneurysm circumference.

CT Scans


It was long known that a certain percentage of PTFE grafts “back in the day” would sweat ultrafiltrated plasma. The relative porosity of the grafts allowed for transudation of a protein rich fluid.

Tanski W, Fillinger M. J Vasc Surg 2007;45(2):243-249.








This results in a hygroma formation. I remember seeing this in AV graft fistulae back in the 90’s -after flow was introduced, the grafts would start sweating! The newer grafts are lower porosity and this is seen very infrequently. Drs. Morasch and Makaroun published a paper in 2006 comparing parallel series of patients who received the original Gore Excluder (OGE), the currently available Excluder Low-Permeability Device (ELPD), and the Zenith device (ZEN). Sac enlargement occurred in equal measure between OGE and ZEN but zero was reported for the ELPD.

Haider S et al. J Vasc Surg 2006;44(4):694-700.

The ELPD had higher rates of sac shrinkage than the OGE, and equal rates of sac shrinkage compared to ZEN.

Haider S et al. J Vasc Surg 2006;44(4):694-700.

The diagnosis in my patient’s case came about through serial followup through a decade. While I doubt that the aneurysm would have ruptured in the same way as in a Type I, II, or III endoleak, I am sure it would have progressed to developing symptoms from aneurysmal distension or local pelvic compression.

Is it possible to visualize this kind of endoleak at the time it is suspected? I came across a case series from the Netherlands using Gadofosveset trisodium which takes longer to clear than the usual Gd-based MR contrasts and they successfully visualized transudative leaks in 3 serial patients with the original Excluder graft.

Cornelissen SA et al. J Vasc Surg 2008;47(4):861-864.

The problem is that Gd-based contrasts have toxicity, especially for patients with poor renal function. The protocol is time consuming. And I suspect that ten years out, a lot of grafts will have positive findings, especially cloth based grafts that are sutured to their supporting stents, without clinical basis for treatment as their sacs size are likely stable on a year to year basis.

That said, as we are well into the second decade of commercially available stent grafts, it is even more important than ever to continue lifelong followup even for what is assumed stable, patent grafts and anatomy.

PAD remote endarterectromy techniques

Arterial Restoration: more than just a pretty name

CTA on left shows occlusive plaque in SFA but contiguous plaque from external iliac origin into the popliteal artery. This was removed with EndoRE resulting in restoration of original artery patency -arteriogram on right. A single short stent was placed in the EIA origin and the above knee popliteal artery received a short stent as well.

This patient is a 90 plus year old man who developed ever worsening claudication to the point he was disabled and more worryingly, had developed pain over his left heel. His ABI’s were severely diminished.

preop ABI2

CTA showed that he had an occluded SFA with above knee reconstitute, but also had only single vessel runoff to the foot via a heavily diseased posterior tibial artery that had serial mild to moderate stenoses.




An attempt at endovascular recanalization was performed at an outside institution, but the SFA lesion could not be crossed. Bypass was not a good option -the ipsilateral saphenous vein had been harvested for CABG, and a long operation was going to have a significant impact on this patient who also had mild dementia and drank 2-3 glasses of wine a day. It is not uncommon to have a successful operation, but have the patient lose 2-3 months in recovering from the physical effects of a long operation as well as from perioperative delirium.

I felt that removing the occlusive plaque from his arteries offered a minimally invasive solution. The plaque was easily accessible via an oblique, skin line incision in the groin, and clearance could be performed from the external iliac artery origin to the planned endpoint slightly beyond Hunter’s canal. While the outflow was not perfect, in my experience, aside from a single native vein bypass, long segment restoration of vessel elasticity results in very acceptable patency rates.

endoRE graphic

Remote endarterectomy is a bit of a lost art from the early days of vascular surgery. A ring dissector (Vollmer Ring Dissector, LeMaitre Vascular) is used to liberate the plaque from the remnant adventia. A cutting device (Moll Ring Cutter, LeMaitre Vascular) shown third from left below is used to divide the plaque.


The common femoral artery plaque is usually contiguous with plaque in the external iliac artery and surgeons who perform a lot of CFA endarterectomy have various maneuvers to remove as much plaque as possible, up to stenting the end point of the plaque down to the endarterectomy patch. I have never been satisfied with this because the EIA behaves differenty than the CIA (am looking into this!) in my experience and placing stents even minimally across the inguinal ligament is not desirable. Sending the dissector up to the EIA origin frees the plaque to be removed completely with the CFA plaque. The clip below shows the Vollmer Ring dissecting plaque up to the EIA origin. I do this over a wire in the pelvis because in the rare instance of leak or rupture, rapid control is possible without having to open the abdomen.

Once freed, the cutter is used to transect the plaque and the end point is tacked down with a stent at the distal common iliac/EIA origin which is a better place for a stent than the inguinal ligament.

The PFA in this patient did not require endarterectomy and reconstruction, but if it did, I would have made the arteriotomy go onto the profunda from the CFA. The SFA plaque is then mobilized with the Vollmer ring. I don’t do this over a wire, but have a definite end point in mind based on what I see on CTA.

The CTA (images earlier) shows that the above knee popliteal artery has no significant calcified plaque. This doesn’t mean there isn’t fibrotic plaque. Cutting the plaque as in the clip below results in a coned in antegrade dissection which has to be crossed in the true lumen.

This is technically the most difficult part of the EndoRE procedure and it requires good imaging and wire skills. The trick here is that an ultrasound guided puncture of the popliteal or tibial vessel can give you distal true lumen access if needed. It was not necessary in this patient. The better maneuver is if the end point is surgically accessible is to cut down and tack down the plaque and patch the arteriotomy.

Angios -14

Angios -39

The patient regained multiphasic PT and DP signals at the end of the case, after the common femoral artery was patched and flow restored. The small groin incision was closed with a running absorbable monofilament after multilayer deep closure. The patient had a blood loss of 50mL. An ilioinguinal field block and local anesthesia provided excellent pain control. Postoperative ABI was improved to 0.82 from 0.34 and all pain was relieved. The patient felt good enough to go home on postoperative day 1.

postop PVR2

This illustrates what I feel to be a best application of both open and endovascular techniques. The above knee popliteal stent is short and in a position that is not going to result in fracture. The external iliac stent is in a protected position in the pelvis and quite large -10mm, which I expect will stay open for the life of the patient. The profunda femoral artery, the rescue artery, is widely patent, and numerous collaterals off the SFA have been restored to patency which I feel aid in maintaining the patency of this repair, along with the restored elasticity of the artery which mimics the biomechanics of autologous vein.

In most patients with compromised outflow, I start warfarin along with ASA at 81mg. Because of his age, I opted for Plavix+ASA. These fail with the development of random TASC A restenoses along the SFA which are amenable to balloon angioplasty. The role of drug eluting balloons in this situation is unknown but theoretically promising. Occlusion through thrombosis does not result in embolization and limb loss as in failure of prosthetic bypass grafts (another option in this patient), but rather leaves a situation where endovascular thrombectomy or lysis is technically feasible.

The great thing is that this is by far superior to stenting of a TASC D femoral arterial lesion.


Type II Endoleak –Iliolumbar Access

The patient had undergone an uneventful EVAR, but in followup had developed AAA sac growth. Pictured above are the post deployment CT’s from 1 month and 6 months. Reviewing the original aortogram, you can see that there was flow into the sac very late via an iliolumbar collateral.

Plan was made for arteriography and intervention. As discussed in an earlier post, 3D VR was very helpful in planning access to the type II endoleak, particularly in plotting C-arm angles and access vessels.

The 3D-VR image view on Aquarius Intuition (TeraRecon) predicts a camera angle of 50 degree LAO to see the branch leaking to the lumbar vessel causing the leak.

Initial aortography confirms the absence of a type I or III leak in early phase.

Later in the phase, the endoleak can be well seen, corresponding to the CTA.

I do an intraoperative transabdominal duplex of the aorta. I have submitted this technique for presentation and eventual publication, but briefly, using an abdominal probe on the abdomen, the sac and endoleak can be readily visualized, and the source of the leak confirmed.

The inferior mesenteric artery which is so often involved is not in this case, and can be easily seen with duplex in patients who are NPO and under general anesthesia. I perform these studies myself, as they are far less challenging than when a patient is awake.

Selection of the branch vessel is straightforward as the CTA well illustrates the course of the source iliolumbar vessel. The CTA even showed the loop that was challenging to traverse. The sequence of access involved IIA, branch access with a glide catheter, placing a Rosen wire for anchorage, and pushing the sheath over the glide catheter into the branch vessel, giving stability. Further access into and across the loop was then possible with superselective catheters based on an 0.18 wire system.

Once access into the AAA sac was achieved, coil embolization of the leak cavity chased by glue (NBCA) allowed for obliteration of the endoleak.

Duplex ultrasound confirmed effective closure, with absence of perigraft flow.

Using duplex in this fashion adds another dimension to the treatment imaging and has the potential for reducing radiation dose and contrast volume.

The patient in followup has shown sac shrinkage. The other treatment options are: direct lumbar puncture, open surgery with sac marsupialization and oversewing of leaks, and laparoscopic ligation of lumbar arteries. I have tried all of these, but this went as easy as could be expected and I credit the ability to visualize the entry path in 3 dimensional virtual reality. The toughest part was negotiating the loop, but a shaped 0.18 glide wire simplified this.

In 2006, Sheehan et al [J Vasc Surg 2006;43:657-61] reviewed an 7 year experience from 5 academic centers. 1909 patients had EVAR with various endografts, and there was an overall 15% rate of type II endoleak. Most resolved within the first year. No significant variation by endograft design appeared to correlate with type II endoleak, which makes sense, although TALENT graft had the highest rate. Spontaneous resolution was common. Late endoleaks were frequent. No conversions were due to type II endoleak. Higashiura, Greenberg et al [J Vasc Interv Radiol 2007;18:975-981] reviewed the CCF experience with the Zenith graft and type II leaks. Of 204 patients with suitable followup, there was a 17% rate of early type II endoleak. Of these, only a 7 of 18 patients with persistent leak developed sac enlargement. Most type II endoleaks spontaneously resolved in followup. No variables could predict persistence of type II endoleak. Treatment prevented sac enlargement.

Silverberg, Marin et al [J Vasc Surg 2006;44:453-59] found similar rates of type II endoleaks -16%, in a study group of 965. Spontaneous resolution occurred in 36% in a mean time of 14.5 months. Treatment was reserved for sac enlargement. 8.4% of those with type II endoleaks experienced sac enlargement greater than 5mm. The vast majority of patients had a benign course. Regression analysis revealed cancer, CAD, COPD were associated with earlier spontaneous closure of type II endoleaks.

Ruptures can occur with persistent type II endoleak [Jones, Cambria et al. J Vasc Surg 2007;46:1-8]. Selective treatment of those with persistent leak and sac growth >5mm seems to be a safe and cost effective approach [Steinmetz, Sicard et al. J Vasc Surg 2004;39:306-13].

Link to type II endoleak papers