A lot of people can put in a stent graft, unfortunately only a few can take them out.

 

IMG_8167
Drs. Roy Miler and Xiao Yi Teng performing anastomosis on open coversion of an aortic stent graft, now graduated and in practice. A significant part of their open aortic experience is in addressing failing stent grafts.

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.

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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.

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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.

IMG_6528

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).

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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.

References

  1. Lancet 2005;365:2187–92.
  2. J Vasc Surg. 2009 Mar;49(3):589-95.
  3. J Vasc Surg. 2016 Feb;63(2):332-40.
  4. J Vasc Surg. 2013 Aug;58(2):371-9.
  5. Lancet 2005;365:2179–86.

Moneyballing a Type II Thoracoabdominal Aortic Aneurysm


The innovation of sabremetrics in baseball management and finance as described in Michael Lewis’ wonderful book Moneyball wasn’t just the ability to quantify skill to predict outcomes, it was the ability to assemble that skill without overpaying. For a baseball team on a budget, spending all your payroll on a superstar makes no sense when you can get equivalent quants of skill in a statistical aggregate of no-name players with proven metrics. Rather than pay for an A-Rod, you can recruit, and pay for, 5 players that in aggregate, statistically achieve what you would get with a healthy A-Rod, so the thinking goes. How does this translate into vascular surgery? Can we arbitrage complication rates?

The open repair of type II thoracoabdominal aortic aneurysms is a heroic endeavor, putatively best done by surgeons wearing cowboy boots, and classically comes with sobering complication rates that exceed 20% for death and paralysis. Is it possible to reduce this risk by subdividing this most enormous of cardiovascular operations into component parts?

The patient is a middle aged man in his 50’s who presented with a type B aortic dissection. His dissection flap spanned from his left subclavian artery to the infrarenal aorta. He was a long time smoker and had hypertension that was difficult to control, made much worse after his dissection. He had a moderate dilatation of his thoracic aorta, maximally 36mm and tapering to 35mm in visceral segment. There was a 4.9cm infrarenal AAA where the dissection terminated.

CTA at presentation

His chest pain resolved with blood pressure control and he was discharged, but in followup his thoracic aortic segment grew and his blood pressure worsened, never getting below a 150mmHg systolic despite multiple agents. CTA two months after presentation, showed growth of his TAA to 44mm from  36mm in two months  and the visceral segment showed that his dissection flap impinged on flow to the right renal artery. His AAA remained the same. He continued to have bouts of chest pain related to hypertension.

CTA at 2mo post presentation

Twenty years ago, the board answer would have been to replace the whole aorta. In young, otherwise healthy man who had been working in road construction up to the dissection, he would have been considered a candidate for a direct open repair of the type II thoracoabdominal aortic aneurysm. From the landmark paper out of Houston by Dr. Svensson in 1993, open type II TAAA repair was associated with about a 10% death rate and 30 percent paralysis rate. Waiting a few months for the aneurysms to grow further in this patient, in the 90’s this patient would probably have ended up with an open TAAA repair. Good thing we have better options.

The goals of modern therapy are to treat the urgent indication while holding off repair of less critical segments of the aorta, and to do so in a way that each operation builds on the previous one.

This patient needed a left subclavian artery debranching and then TEVAR of his dissecting thoracic aortic aneurysm, and intervention on his right renal artery. We did this in one setting performing first a left carotid subclavian artery transposition and then percutaneous TEVAR from the left common carotid artery origin to the supraceliac abdominal aorta.

TEVAR with carotid SCA transposition

completion TEVAR.png

The completion aortography showed good deployment of the CTAG device from the left common carotid artery origin to the celiac axis origin. The false lumen was no longer visualized. The right renal artery which was narrowed was treated with a balloon expandable stent.

The distal thoracic aorta, the true lumen was constrained by a chronic dissection flap. It is here I gently dilate the distal thoracic stent graft with the hopes of eliminating the distal false lumen. This is different from the acute dissection where I rarely balloon.

The TEVAR was done percutaneously, minimizing the overall time in the operating room. The technical details of the transposition can be found in the excellent paper by Dr. Mark Morasch.

 

renal PTAS

When I do this procedure for acute dissection, I quote the patient a general risk of stroke, paralysis of about 2-5% and death of 1-2 percent for someone with low cardiopulmonary risk like this patient had. He recovered rapidly and went home post op day 5.

 

Followup post TEVAR

He at 6 month post TEVAR followup, CTA showed stablility in his thoracic aorta. in infrarenal AAA grew from 5.0 to 5.7cm between the 1 month CT and the 6 month CT.

6 month CTA imaging

The terminus of the stent graft excluded the false lumen in the thoracic aorta but also resulted in filling and pressurization of the false lumen beyond and can be seen as a 44mm lateral dilation of the visceral segment of the aorta which had developed in the 6 month interval since the TEVAR.
The infrarenal neck continued the dissection and had dilated to about 36mm, but was parallel for a good length above the AAA. I decided to treat the inrarenal aorta with direct transabdominal repair. This would allow me to fenestrate the aorta, and possibly prevent further growth of the viseral segment while reserving the retroperitoneum for the visceral segment repair if it came to it. The neck diameter was 36mm.

tube graftHis operation was performed via an anterior approach with the patient supine. A tube graft repair was performed expeditiously and included resecting the dissection flap up to the clamp. Care was taken to avoid injury to the renal stent. The proximal anastomosis went well – the dilated aorta yet had strong tissue strength. A felt strip was used to buttress the aortic side of the anastomosis. The estimated risk of paralysis was less than 1% and risk of death was less than 2%. The patient recovered uneventfully and went home on POD 5.

He did well in subsequent followup, having successfully quit smoking. He retired early on disability and was becoming more active, but the visceral segment dilatation was concerning. At 6 months post infrarenal AAA repair, he underwent CTA and it showed patent thoracic stent graft and infrarenal abdominal graft. The intervening visceral segment continued to enlarge and was now 46mm. The decision was to wait another interval 9 months to see if this would stabilize. The segment grew some more and was 49mm. He wanted to give it another 6 months and at that time, CTA showed further growth over 5cm, and he had developed some abdominal discomfort. He was taken to the operating room.

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A four branch repair of the visceral segment thoracoabdominal aortic aneurysm was performed. The diaphragm was taken down and the stent graft was clamped as was the infrarenal tube graft. A premade Coselli graft was used to bypass to the right renal, SMA, celiac, and left renal in those order. The patient had a CSF drain for the case which was removed on postoperative day 2. He recovered rapidly and went home on postoperative day 6. His estimated risk of paralysis was about 2-5%, mitigated by a protocol centered on CSF drainage and blood pressure control. His risk of death was 5%. Telephone followup reveals the he is pain free at a month out and functional nearly at baseline.

This illustrates the notion that three smaller operations in an aggregate over three years achieved the equivalent of the single big open type II TAAA repair.

equivalence
Illustration on left from Svensson et al.

The idea is to make each step achievable -like coming down a mountain taking three days on well marked paths rather than base jumping off the summit.

Clearly, the patient was younger and a fast healer, and credit must also be given to the anesthesia/critical care team who see high acuity cases in volume every day and not every patient can expect to have such short stays and excellent outcome, but these are far more likely if operations are planned out in such a manner.

Reference

Svensson LG, Crawford ES, Hess KR, Coselli JS, Safi HJ. Experience with 1509 patients undergoing thoracoabdominal aortic operations.  J Vasc Surg 1993;17(2):357-36.

 

Ruptured Thoracoabdominal Aortic Aneurysm In 88 Year Old -a survival

TAAA

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.

centerline

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.

centerline 3D

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.

Version 2

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:

  1. Age >76
  2. preop Cr>2.0mg/dL
  3. BP<70mmHg at any point
  4. arterial pH<7.2
Mortality risk based on number 1-4 of positive risk predictors
Mortality risk

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.

rupture risk table from AFTAB paper

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.

Reference

Aftab et al. J Thorac Cardiovasc Surg 2015;149:S34-S41