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.

EVAR peripheral aneurysm techniques

Parallel Grafts in the iliac bifurcation -an option at least until branched grafts become commercially available


This patient had developed metachronous common iliac artery aneurysms after aorto-bi-iliac graft placement of a AAA a decade ago. This is not infrequent occurence in a significant number of patients with aneurysmal degeneration seen in the thoracic or visceral segment abdominal aorta, iliac arteries, and popliteal arteries, years after a primary AAA repair. The patients are often older than they were at the original repair, with concomitant risk factors, and so a minimally invasive option is preferred.

Right CIAA -vulnerable tissue

saccular r ciaa

The teaching during my fellowship was that aorto-iliac bypasses for aneurysmal disease were to be taken to the iliac bifurcation to go around vulnerable tissues. These tissues vulnerable to aneurysmal degeneration were infrarenal aorta up to the renal artery origins, common iliac and internal iliac arteries, and popliteal arteries. An anastomosis to the iliac bifurcation however normal appearing may degenerate given enough time. This patient developed a saccular aneurysm on the right iliac bifurcation and a small internal iliac artery aneurysm (1.5cm).


This was treated with coil embolization and stent graft from the right iliac limb to the external iliac artery.

RCIAA treatment

This is the standard endovascular therapy for common iliac artery aneurysms, and acceptable in the setting of unilateral disease, and in a staged fashion has been considered acceptable for bilateral disease, acknowledging there is a 10-40% incidence of buttock claudication and when the contralateral hypogastric is occluded or when the patient is diabetic, the risk of buttock or colorectal necrosis is not insignificant. The patient had transiently some buttock claudication and hip and thigh neuralgia with walking but this improved in the weeks leading up to treating his left common iliac artery aneurysm.


The left common iliac artery bifurcation is sometimes challenging to access from a midline incision and exposure requiring a separate sigmoid mobilization. In men, the narrow pelvis can increase the challenge, so it is without fault that sometimes common iliac artery is left behind. This is what became aneurysmal, developing into a 3.0cm fusiform aneurysm beyond the left limb of the graft.


The internal iliac artery had a moderate 50-75% stenosis at its origin but was not aneurysmal, and I chose to revascularize this. The patient was sexually active and walked for exercise. My options included proceeding with left hypogastric embolization and stent grafting, mirroring the right but with a significant risk for buttock claudication, sexual dysfunction, and a small risk for colorectal ischemia. Other option is an external iliac or common femoral to internal iliac artery bypass which is an excellent option in good risk patients.

Endovascular options

Iliac branched stent grafts are undergoing trial. My center is participating in both available industrial FDA approval trials (disclosure, I am site PI for the Gore trial), but this patient’s presentation and anatomy exclude him from the trials. The final option is placing a parallel stent grafts -one to the internal iliac artery and the other to the external iliac artery from a large common iliac stent graft. While not ideal, until branched grafts become available, this remains a viable option. The principle is to size the grafts to minimize potential gutters between the grafts, and have long seal zones to minimize the impact of the gutters. Access from two points is required to get two grafts into position. With the acute angle of the aortobi-iliac graft, up and over access is generally not possible. The 10mm Viabahn graft that I chose to place in the hypogastric requires a 12Fr sheath, which cannot be placed from the brachial artery, so I prepped for an axillary cutdown. The left common femoral access was percutaneous.


The left CFA access allowed placement of a 16mmx10cm Excluder iliac graft limb to cover the aneurysm down to the iliac bifurcation. The left axillary arterial cutdown access allowed placement of a 12Fr sheath (Flexor) to allow access of the left internal iliac artery and safe delivery of a 10mm Viabahn stent graft. The left external iliac artery was sealed with a 13mm Viabahn stent graft that was deployed simultaneously. Ballooning was performed to both.


No leak was seen. The axillary access was repaired directly and the CFA access was repaired with two Perclose S devices.


Despite initial acceptance of bilateral hypogastric occlusion, even staged, it can be the cause of significant disability aside from buttock claudication, which sometimes does not remit with exercise. Ischemia of the pelvis can drive a plexopathy that can result in motor and sensory neuropathy and disability. Death can occur. Preserving one of the hypogastrics can go a long way to preventing these complications, and everyone eagerly awaits adding iliac branched grafts to the armamentarium.


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