This was presented at Dia De La Patología Aortíca Marbella organized by Dr. Fernando Gallardo.
Here is the link.
This was presented at Dia De La Patología Aortíca Marbella organized by Dr. Fernando Gallardo.
Here is the link.
I recently had to remove a stent graft for infection and got to thinking about how the number of people who could comfortably and confidently manage that has thinned out in the world through the unintended consequence of the medical device market place. In every surgical specialty over the past twenty years, many open procedures were replaced with a minimally invasive option which generally involved adoption of new technology and large costs to the hospital. These newer procedures were touted as easier on the patient while being easier to perform for the average physician than the open procedure that they were replacing. That was the other selling point -that one could do several of these operations in the time it took one open procedure. In most cases, they were at best almost as good as the open procedure but at higher cost.
In the marketplace, minimally invasive always wins. In many specialties it became untenable to practice without marketing these “advanced minimally invasive” skills. Hence, the wide adoption of robotics in urology outside major academic centers -during those years of rapid adoption the surgeons would get flown to a course, work on an animal model, then for their first case a proctor would be flown out and voila -a minimally invasive specialist is born. The problem comes when learning these skills displaces the learning of traditional open surgical skills. In general surgery, it is not uncommon to hear of residents graduating without having ever having done an open cholecystectomy. It is also the case that many vascular trainees graduate with but a few if any open aortic cases. What happens when minimally invasive options run out? Who will do my carotid endarterectomy or open AAA repair?
The first case is an elderly man with an enlarging AAA sac despite having had EVAR about seven years prior. No endoleak was demonstrated but the proximal seal was short on CT. Also, it was a first generation graft which is prone to “peek a boo” endoleaks from graft junctions and stent anchoring sutures. On that last point, I use the analogy of a patio umbrella -after seven seasons, they can leak where cloth is sewn to the metal struts. It is very hard to demonstrate leak of this kind on CTA or duplex ultrasound because they are small. The patient had his EVAR because he was considered high risk for open repair at the time of his operation -moderate COPD, mild cardiac dysfunction. His sac had enlarged to over 6cm in a short time, and therefore open conversion was undertaken. No clinical signs of infection were present. A retroperitoneal approach was undertaken. After clamps were positioned, the sac was opened.
The picture does not show it, but a leak from the posterior proximal seal zone was seen with clamp off. The clamp was reapplied and the graft transected flush to the aortic neck. A bifurcated graft was sewn to this neck incorporating the main body stent graft and aortic neck in a generous running suture. The left iliac limb came out well and the new graft limb sewn to the iliac orifice, the right iliac limb was harder to clamp and therefore I clamped the stent graft and sewed the open graft to the stent graft.
The patient recovered well and went home within the week. He was relieved at no longer needing annual CT scans.
Who needs annual CT scans? Patients with metastatic cancer in remission.
The second patient was an older man referred for enlarging AAA sac without visible endoleak. The aneurysm had grown over 7cm and was causing discomfort with bending forward. He too had been deemed high risk for open repair prior to his EVAR. If he had had an early generation Excluder graft, the possibility of ultrafiltration would be more likely and relining the graft would be reasonable (link). This was again a cloth and metal stent graft which can develop intermittent bleeding from graft to stent sutures, and I don’t think relining will help.
The patient was taken for open repair (above), and on opening the AAA sac, bleeding could be seen coming from the flow divider. It stopped with pressure, but I replaced the graft in a limited fashion from the neck to the iliac limbs as in the first case. This patient did very well and was discharged home under a week.
The third patient was another fellow referred from outside who had an EVAR for a very short and angulated neck, and a secondary procedure with an aortic extension in an attempt to seal the leak had been done. This failed to seal the type Ia leak. This patient too was deemed too high risk for open surgery of what was basically a juxtarenal AAA with very tortuous anatomy.
The patient was taken for open repair, and the stent grafts slid out easily (below).
A tube graft was sewn to the short aortic neck and distally anastomosed to the main body of the stent graft -with pledgets because of the thin PTFE graft material in this particular graft. This patient did well and went home within a week.
All three cases are patients who were deemed originally too high risk for open repair, who underwent EVAR, then underwent explantation of their failing stent graft. Only one involved a patient whose graft was placed off the IFU (short angled neck), but the rationale was that he was too high risk.
What is high risk? In non-ruptured, non-infected explantation of failing stent graft, the mortality is 3% (ref 2) from an earlier series from Cleveland Clinic. With stent graft infection, the 30-day mortality of surgical management from a multi-institutional series was 11% (ref 3) when there was no rupture. From a Mayo Clinic series, stent graft resection for infection came with a 4% 30-day mortality (ref 4). These were nominally all high risk patients at the time of the original EVAR.
Real world risk is a range at the intersection of patient risk and the expertise of the operating room, critical care, and hospital floor teams. The constant factor is the surgeon.
Endografts for AAA disease (EVAR, endovascular aortic aneurysm repair), makes simple work of a traditionally complex operation, the open aortic aneurysm repair. The issue has been the cost and risks of long term followup as well as endograft failure and aneurysm rupture. The Instructions For Use on these devices recommend a preop, a followup 1 month, 6 month, and 12 month CTA (with contrast) and annual followup with CTA for life. These devices were meant to treat high risk patients but high risk patients with limited life spans do not benefit from EVAR (ref 1, EVAR-2 Trial). These have lead the NHS in the UK to propose that EVAR has no role in the elective repair of abdominal aortic aneurysms in their draft proposal for the NICE guidelines for management of AAA (link). While this is a critical discussion, it is a discussion that is coming at least ten years too late. A generation of surgeons have been brought up with endovascular repair, and to suddenly announce that they must become DeBakey’s, Wiley’s, Imperato’s, and Rutherford’s is wishful thinking at best or wilful rationing of services at worst.
In 2006, Guidant pacemakers were recalled because of a 1000 cases of possible capacitor failure out of 28,000 implants for a failure rate of 3.7% -there were 2 deaths for a fatality rate of 0.00007%. EVAR-1 Trial’s 8 year result (ref 5) reported 16 aneurysm related deaths out of 339 patients (1.3%) in the EVAR group compared to 3 aneurysm related deaths out of 333 patients (0.2%) in the OPEN group.
Academic medical centers, behemoths though they are, serve a critical function in that they are critical repositories of human capital. The elders of vascular surgery, that first and second generation of surgeons who trained and received board certification, are still there and serving a vital role in preserving open aortic surgery. My generation -the ones who trained in both open and endovascular, are still here, but market forces have pushed many of my colleagues into becoming pure endovascularists. The younger generation recognizes this and last year, I sat in on an open surgical technique course at the ESVS meeting in Lyons organized by Dr. Fernando Gallardo and colleagues. It was fully attended and wonderfully proctored by master surgeons. This is of critical importance and not a trivial matter. As in the 2000’s when endovascular training was offered as a postgraduate fellowship in centers of excellence, there is no doubt in my mind that today, exovascular fellowships need to be considered and planned and that current training must reinvigorate and reincorporate their open surgical components.
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.
This was done percutaneously and in short followup, there has been stabilization and even some reduction in the aneurysm circumference.
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.
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.
The ELPD had higher rates of sac shrinkage than the OGE, and equal rates of sac shrinkage compared to ZEN.
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.
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.
The patient, an active 88 year old man, was transferred from an outside institution after a CT scan revealed a 9cm thoracoabdominal aortic aneurysm on workup of sudden onset back pain. On transfer, his blood pressure was stable but low in the 90’s. On arrival, his blood pressure dropped into the 60’s but responded to resuscitation, and after a detailed conversation with him about the risks of emergent repair, we brought him to the operating room.
The CT scan showed an 8.3cm extant III thoracabdominal aortic aneurysm which originated slightly above the diaphgragmatic hiatus and extended to the aortic bifurcation in two lobes. The larger lobe involved the visceral vessels and the infrarenal component was about 5cm.
While there was no frank rupture on the CT, the outside report mentioned haziness of the posterior wall consistent with ongoing rupture. Examination was significant for hypotension, abdominal and back pain, and a large pulsatile mass in the abdomen.
Despite the lack of contrast on this study, I was able to get a centerline reconstruction. The 3D virtual reality view then allows me to plan the operation virtually. The red and blue lines above bracket the beginning and end of the aortic aneurysm with the patient in a right lateral decubitus projection. A thoracoabdominal incision starting on the 8th rib was planned.
The patient remained stable through the intubation with a dual lumen endotracheal tube. The chest was entered and the left lung collapsed and the thoracic aorta in the chest was controlled for clamping. The retroperitoneum was dissected and the abdominal contents allowed to fall away exposing the remainder of the aneurysm. The diaphragm was taken down circumferentially. The aneurysm was leaking -not frankly but there was blood visible on the surface like a bruised, overripe plum of unusually large size.
The aorta was clamped in the chest after giving the patient 5000 units of heparin -I often don’t if there is a lot of blood loss and I anticipate factor depletion. The transdiaphragmatic aorta was controlled and the celiac axis (CA), superior mesenteric artery (SMA), and left renal artery were controlled with vessel loops. The aortic bifurcation was controlled as well after I considered anastomosing to the narrow segment of aorta around the renal arteries. While saving the infrarenal aneurysm for later has an appeal, I feel that if you cut the graft and start sewing to the aorta and find that it is not of good quality, you have wasted time. The aortic clamp was moved down from the chest to the transdiagphragmatic aorta which was now mobilized. This avoided for me some spinal cord ischemia but can be a risky move because the aorta was not healthy even in the nonaneurysmal segments. A 32mm Dacron graft what had 4 branches was brought into the field and anastomosed proximally with 4-0 polypropylene suture.
I picked up using narrow gauge suture for aortic anastomoses from my cardiothoracic surgery confreres at the Clinic (Eric Roselli, MD). They will use 5-0 polypropylene with the idea that the smaller needles result in smaller needle holes. I used to use 2-0 suture with an MH needle and have seen my partners be successful at it, often buttressing the anastomosis with a gusset (Dan Clair), but this patient had the tensile strength to take suture well so I went with the smaller SH needle and smaller gauge suture. Other maneuvers include sewing to a strip of Teflon, or in the case of terrible aortic tissues, using interrupted sutures which give some added stability but at the cost of time (credit to Tom Bower).
Time is the killer. While cell salvage gives you some margin for blood loss, this is lost with coagulopathy and hypothermia. The grafts to the viscera were sent from distal to proximal -I feel this greatly eases wire access if needed from a femoral access. There can be a problem with twisting, and I avoid this two ways -by allowing for generous length with looping around the main graft to create forgiveness -closing the retroperitoneum inevitably twists the graft -this I credit to my former partner Pat O’Hara who retired last year. The right renal artery received the first graft while cold saline was given to the left renal artery which was revascularized last. Neither had ostial lesions which I have learned to stent with a bare metal stent directly with the artery open -this I credit to Jeanwan Kang, MD, one of my current partners. The CA graft resulted in great back bleeding from the SMA. The SMA graft and left renal artery grafts completed the visceral segment of the case.
The distal anastomosis was challenging because the bifurcation was heavily calcified. I have to say, the distal often will give me fits when the proximal does not because of the calcium. I generally do perform an endarectomy, but this often results in very poor remnant adventitia. The advice here is be prepared to go distally, but consider that it may add time to the case.
The hemostasis was obtained -the most important factor in hemostasis is early and successful repercussion. The wound was restored with repair of the diaphragm, closure of the chest over two chest tubes and closure of the abdomen.
The success of these patients only begins with the operation which I cannot do without the active participation of our cardiac anesthesia, nursing, and trainees -our fellow Eric Shang did his work competently. I am fortunate to have strong help in our vascular intensive care unit. There, my patient was actively resuscitated with blood product, stabilized, and weaned off the ventilator within 2 days. Fortunately, he was not paralyzed by this operation which can happen in up to 10% of patient. Also, his renal function stabilized and he never required dialysis. He was eventually discharged to rehab in under 2 weeks. He returned to my office about a month after the rupture, walked in, accompanied by his family. He was making progress with his rehab, and his wounds had healed well.
Various indices are formulated to predict outcome, which traditionally are viewed as poor for open repair on octogenarians. I am still old fashioned and rely on the “eyeball” test. Several risk stratifying schemes have been published. Most recently, the group from Harborview (link, another link) published a simple stratification scheme for infrarenal AAA rupture. Garland et al (in press) found that having combinations of the following factors predicted mortality well for ruptured AAA including:
If this was a ruptured infrarenal AAA, the patient had two of the risk factors -age>76 and BP<70mmHg, which conferred a risk of 80% mortality for open repair, which translates to a higher number for thoracoabdominal aortic aneurysm repair.
One of our recent aortic fellows, Muhammad Aftab, published the Baylor experience on open repair of TAAA when he was there and found that for open repair, rupture conferred an independent risk for death with a OR of 5.7.
Despite the dismal statistics, several intangibles did favor survival in the patient. He was at 88 still a working professional. He exercised everyday and was fit. He did not drink to excess and never smoked. And he had complete understanding during our preoperative conversation and had a strong grip. And he survived waiting several hours at his hospital for workup and eventual transfer which is a stress test. This last factor accounts for the higher mortality rates for rupture that occurs in hospitals and in places like Seattle where the EMS transport is highly efficient, and better mortality rates at rural referral centers like Mayo where the filtering effect of time leaves a greater proportion of patients likely to survive an operation for rupture.
Aftab et al. J Thorac Cardiovasc Surg 2015;149:S34-S41