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

 

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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.

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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.

External iliac remote endarterectomy restores the artery to normal, opening the way for EVAR, TAVR, TEVAR, and transplant: alternate applications of EndoRE

preop-cta

One of the nice things  about practicing at the Clinic is being able to offer unique solutions. A severely diseased or occluded external iliac artery (EIA) can be a vexing problem, particularly if bilateral, in this endovascular era. Many cardiovascular devices require femoral access that has to traverse compromised iliac arteries -those with large (>16F) delivery systems require a sufficiently wide path to get the devices to the heart and aorta. Also, living related donor kidney transplantation is predicated on minimizing risk to maximize results and having significant iliac plaque negates one as a recipient for this high stakes elective procedure. In situations where the EIA is too small to accommodate devices because of atherosclerotic plaque, the typical solution is placement of a conduit to the common iliac artery or the aorta. The practice of “endopaving” with a covered stent graft and ballooning is also described, but its long term outcomes are not reported and the internal iliac artery is usually sacrificed in this maneuver.

This patient presents with lifestyle limiting claudication and an absent right femoral pulse. ABI is moderately reduced on the right to 0.57, and he had no rest pain. CTA at our clinic revealed an occluded EIA bracketed by severely calcified and nearly occlusive plaque of the common iliac artery (CIA) and common femoral artery (CFA).

cta-preop_7
Centerline Projection

The patient was amenable to operation. Traditionally, this would have been treated with some form of bypass -aortofemoral or femorofemoral with a common femoral endarterectomy. While endovascular therapy of the occluded segment is available, one should not expect the patencies to be any better than that of occlusive lesions (CTO’s) in other arteries. Hybrid open/endovascular therapy is an option as well with CFA endarterecotmy and crossing CIA to EIA stents, but I have a better solution.

The common femoral endarterectomy rarely ends at the inguinal ligament, and is uniquely suitable for remote endarterectomy, a procedure from the early to mid twentieth century.

endoRE graphic
Steps in Remote Endarterectomy

 

The addition of modern fluoroscopic imaging and combining with endovascular techniques makes this a safe and durable operation.

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The patient was operated on in a hybrid endovascular OR suite. A right groin incision was made to expose the common femoral artery for endarterectomy and left common femoral access was achieved for angiographic access, but also to place a wire across the occlusion into the common femoral artery.

All actions on the external iliac artery plaque are done with an up-and-over wire, allowing for swift action in the instance that arterial perforation or rupture occur. This event is exceedingly rare when the operation is well planned. With this kind of access, an occlusive balloon or repairing stent graft can be rapidly delivered.

The common femoral endarterectomy is done from its distal most point and the Vollmer ring is used to mobilize the plaque. A Moll Ring Cutter (LeMaitre Vascular) is then used to cut the plaque.

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The plaque is extracted and re-establishes patency of the EIA.

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Plaque Specimen

The plaque end point is typically treated with a stent -in this  case, the common iliac plaque was also treated.

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What is nice about this approach is that this artery has been restored to nearly its original condition. I have taken biopsies of the artery several months after the procedure in the process of using the artery as inflow for a cross femoral bypass, and the artery clamped and sewed like a normal artery and the pathology returned normal artery.

This has several advantages over conduit creation which can be a morbid and high risk procedure in patients who require minimally invasive approach. A graft is avoided. The artery is over 8mm in diameter where with stenting up to 8mm with an occlusive plaque, the danger of rupture is present, and often ballooning is restricted to 6mm-7mm. This is insufficient for many TEVAR grafts and TAVR valves.

For patients being worked up for living related donor transplants who are turned down because of the presence of aortoiliac plaque, those with the right anatomy can undergo this procedure and potentially become candidates after a period of healing.

 

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.

IMG_8659

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.

 

Reversing paralysis with a bypass

Dissection CTA

The patient is middle aged and had a type B thoracic aortic dissection (TBAD) as a consequence of recreational substances that acutely raised his blood pressure. At the outside hospital, he had a CTA showing the dissection extending from his left subclavian artery and causing occlusion of his superior mesenteric artery (SMA). He developed abdominal pain and was swiftly transported to our acute aortic syndrome unit. He was taken to the operating room and underwent a TEVAR of the dissection and stenting of his SMA -this is similar to other cases I have discussed in prior posts so I am omitting the technical details. The stent covered the left subclavian artery origin to exclude the origin of the dissection. The stent was extended to the distal thoracic aorta but did not go to the celiac origin. 

TBAD post stent

Post procedure, his lactate never rose and he was maintained on the usual post procedure protocol of keeping MAP’s (mean arterial pressure) above 80mmHg. His left subclavian artery was covered but I do not routinely bypass, especially when the left vertebral artery is at least equal in size to the contralateral one. I don’t often place spinal drains for urgent/emergent cases particularly in patients who have never had infrarenal aortic surgery and patent hypogastric arteries. He was kept sedated overnight and awoke in the morning unable to move his legs to command. He had no pain sensation up to his umbilicus.

A spinal drain was emergently placed and his blood pressure was raised to MAPs of 90+, but these failed to reverse his paralysis. After discussion among my world class partners, I chose to take the patient back for a carotid subclavian bypass which was done through a single incision with a dacron bypass graft.

Carotid subclavian bypass CTA

His paralysis resolved. He was discharged home, ambulating without assistance. Spinal cord complications are reported to occur between 1-5 percent of patients undergoing TEVAR for complicated TBAD. They were seen in 2 of 72 patients in the TEVAR arm of the INSTEAD trial (Circulation, 2009 vol. 120(25) pp. 2519-28), and was permanent in 1. While there are some who routinely place prophylactic drains, it is unclear to me that they have a significant effect if placed unselectively. I will place a Preop drain in the instance of infra renal graft, hypogastric arterial occlusive disease. In the instance of a dominant left vertebral, I will perform concomitant bypass, but just as often not. This is a gratifying and rare outcome of paralysis reversed with a carotid subclavian bypass when spinal drain and permissive hypertension did not. 

Broken Aorta, Advancing Technology

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The ligamentum arteriosum, the remnant of the ductus arteriosus between the aortic arch, tethers the arch causing a tear during sudden deceleration like hitting a steering wheel with your chest

I recently repaired a traumatic aortic dissection and was struck by how far along things had progressed since I was a resident. I remember seeing a Q&A in the mid nineties where Dr. Mattox expounded on the gold standard for diagnosing traumatic aortic injuries which at that time was contrast aortography. This caused many struggles trying to arrange for arteriography in the middle of the night (these accidents usually occur then). The repairs were open and very morbid for severely injured patients, particularly those with closed head injuries and fractures. This all changed in the early 2000’s as I had mentioned in an earlier post (link). The grafts were homemade (figure)

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and this was literal -the picture is from my kitchen back in the Bronx in 2004. The grafts were cumbersome to deploy and required long 24-28F sheaths that frequently required iliac and aortic exposures.

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The revolutionary breakthrough was the fact that thoracotomy and partial cardiac bypass could be avoided. Durability was largely assumed as these patients rarely came back for followup.

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Fastforward to 2015. CTA is done with 64 slice CT scanner with EKG and respiratory gating eliminating the artifacts that caused Dr. Mattox to assert that aortography was the gold standard. Software based image reconstruction can aid treatment planning in ways that greatly exceed the caliper and ruler methods we had in 2004.

CT_4

The grafts are currently into their second generation of development and have small profile and trackability that allows for percutaneous delivery and treatment.

aortogram trauma

The aortogram shows the tear along the inner curve. These lesions typically require coverage either partial or total of the left subclavian artery origin. This patient had a dominant right vertebral artery and I felt he would tolerate even full coverage of the left subclavian.

aortogram trauma close arch

The device, a Gore C-TAG device which has an FDA trauma indication, is clearly better than our homemade device. Deployment does not require pharmacologic or electrical bradycardia or asystole.

aortogram post stent trauma

The idea behind this design is conformability of the smaller stent elements. The aortic injury is even outlined by the stents in the aortogram above. The bird-beaking that was common to the prior generation of graft is not seen in this aortogram.

Where does this need to go next? At 18-24F access requirements need to become 12-18F and for the same reason, the grafts need to be available down to 14-18mm as trauma doesn’t just happen in middle aged men. Aside from that, it is a definite improvement over what we had in 1995 and in 2004.

Acute Aortic Syndrome Unit -TBAD with SMA Dissection and Thrombosis with Acute Mesenteric Ischemia

Figure SMA thrombus with dissection

The figure above shows the summarizes the problem that brought the patient to his local hospital and triggered his transfer to our acute aortic syndrome unit. The concept is that all chest pain of cardiovascular origin gets intake through a vast intensive care unit staffed by cardiovascular intensivists. Stabilization, workup, transfer to operating room or interventional suite all happens in an ICU that encompasses almost a city block.

The patient is an older middle aged man with sudden onset of back and abdominal pain. He was on coumadin for a prior SMV thrombosis and treatment for a ruptured appendicitis -antibiotics with plan for staged appendectomy. CT at his local hospital revealed a type B aortic dissection (TBAD) that extended into his superior mesenteric artery.

Bovine arch in 3DVR view on TeraRecon Aquarius reconstruction.
Bovine arch and TBAD in 3DVR view on TeraRecon Aquarius reconstruction.
The aortic dissection terminated in the infrarenal aorta. The celiac and SMA had true and false lumen perfusion, the right kidney was perfused through the false lumen, the left through the true. Both legs received true lumen flow.

Figure Centerline true lumen compression

The dissection started at the left subclavian artery origin. The false lumen compressed the true lumen up at the proximal descending thoracic aorta. This is an important finding because in this configuration with much of the filling of the dissection from the distal reentry sites, the false lumen acts like a pressurized, compressive lesion. With time, the adventitia around the false lumen may become aneurysmal if the false lumen fails to thrombose or obliterate. When the dissection is acute, the flap may cause a direct obstruction to flow or a dynamic one that depends on the pressure difference between true and false lumen.

Figure SMA thrombus with dissection

In this patient, thrombosis occured in the SMA beyond the origin due to dissection and decreased flow. This was consistent with the patient’s complaint of generalized abdominal pain and examination findings of pain out of proportion to the exam, indicating acute mesenteric ischemia.

His laboratory findings were within normal ranges, indicating this was early in the process. It is important to remember that no lab value correlates with acute mesenteric ischemia except very late in the process, and acute mesenteric ischemia remains a clinical diagnosis (reference 1) that is associated with a high mortality rate.

He was taken to the hybrid operating room. Right groin access was achieved and wire access to the arch was achieved. IVUS (Intravascular ultrasound, Volcano) was used to confirm the location of the wire -I believe this is an important adjunct as simply passing the wire doesn’t guarantee travel up the true lumen.

IVUS confirming true lumen access, and dissection flap compressing SMA origin
IVUS confirming true lumen access, and dissection flap compressing SMA origin
A conformable TAG endograft (CTAG, Gore) was delivered through a 24F sheath into position. Two devices were used to cover the thoracic aorta from the left subclavian artery to a position immediately above the celiac axis. The left subclavian was partially covered -the bare stents covering the rest.

Before deploying CTAG

Partial coverage of the left subclavian artery confirmed by persistence of strong left brachial artery pulse
Partial coverage of the left subclavian artery confirmed by persistence of strong left brachial artery pulse

Post Deployment of two 40mmx20cm CTAG (Gore) endografts
Post Deployment of two 40mmx20cm CTAG (Gore) endografts
This excluded the proximal entry tear of the TBAD. IVUS (image below) showed improved lumenal diameter of the true lumen into the SMA.

After stent graft placement in the thoracic aorta, the true lumen into the SMA expands
After stent graft placement in the thoracic aorta, the true lumen into the SMA expands
Once this was done, wire access into the SMA was achieved. This was technically challenging from the groin, and the backup plan was access from the left brachial artery which had been prepped. With patience, 6French access into the SMA was achieved. The origin was stented with a balloon expandable 8mm x3cm stent -sizing was based on IVUS and CT. This creates an alarming arteriogram as the stent appears oversized on subsequent runs -it is important to remember that the false lumen still takes up space beyond. Arteriography located the thrombosed segment and the reconstituted SMA beyond.

SMA beyond occlusion

Wire access was achieved across the thrombus. At this point, I had a range of options for thrombectomy including simply aspirating which retracting a catheter. This was not optimal as I could lose subsequent wire access or reenter the false lumen. The other option was an open thrombectomy and patch angioplasty -the thighs were prepped in case we had to harvest vein. Again, in the setting of dissection and going into the mesentery, an open revascularization while feasible, is challenging.

Thrombectomy catheters like Angiojet were available, but I chose to try the Export aspiration catheter (Medtronic). It is simple to set up and goes over a 0.14 wire. It is designed for the coronaries which have a similar lumenal diameter as the SMA. It worked well in this setting in retrieving thrombus which had a pale element that may have indicated some chronicity.

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The completion arteriogram was satisfying.

Post thrombectomy SMA

The SMA completely filled as did the celiac axis and both renal arteries. I opted not to treat the right renal artery as we had given 250mL of contrast, and it was filling well without intervention. The patient was making excellent urine and his blood pressure had been maintained with mean arterial pressures above 70mmHg. At this point, IVUS confirmed good deployment of the stent.

IVUS after SMA stent

The sheath was removed and the access site repaired. The general surgeons explored the patient and found all the bowel to be well perfused with pulsatile flows seen in the mesenteric arcade. The appendix was removed.

On waking, the patient was noted to not move his legs. A spinal drain was expertly placed by our cardiac anesthesia staff and his blood pressure was raised to MAP’s above 80. He recovered motor function in his legs soon after. I usually don’t place preop CSF drains in this scenario in the presence of good pelvic circulation, no history of infrarenal aortic interventions, and patency of the left subclavian artery. That said, with TEVAR of TBAD, there is a small incidence of paraplegia (1-5%) which I emphasize in my preoperative discussion.

He was started on heparin anticoagulation postop because of his history of SMV and now SMA thrombosis, interrupting it briefly to remove the CSF drain. A CTA was obtained to confirm absence of bleeding showing obliteration of the dissection in the aorta and good patency through the true lumen of the SMA.

CT before and after

pre and pos t SMA

Most importantly, he had complete relief of his abdominal pain.

The treatment of acute mesenteric ischemia has greatly evolved since I presented my paper in 2002. While open revascularization remains a gold standard, it is becoming increasingly apparent that good to better results may be obtained with an endovascular approach. Dan Clair, our chair, has made the comment that early revascularization with endovascular technique is analogous to emergent PTCA in occlusions of the coronary system and that re-establishing flow is a critical first step.

Open exploration still is the mainstay of managing acute mesenteric ischemia, but laparoscopic exploration remains feasible. This patient underwent open conversion after an initial laparoscopic exploration to remove a ruptured retrocecal appendix that had been treated for over a month on antibiotics. Without bowel necrosis, a second look is usually unnecessary, but is critical when threatened bowel is left behind.

Reference

  1. Park WM et al. J Vasc Surg. 2002 Mar;35(3):445-52.

External iliac remote endarterectomy in lieu of a conduit for TEVAR

IMG_1281

The patient had diffuse atherosclerosis with small luminal area even in areas without calcified plaque. It predicted inaccessibility for the 22 French sheath required to deliver the 32mm C-TAG device to be placed for a symptomatic type B thoracic aortic dissection associated with a small but expanding proximal aneurysm.

IMG_1277

My options included direct aortic puncture, an aortofemoral conduit, or an endoconduit. The aorta was heavily calcified and the bifurcation was narrowed by circumferential plaque down to 6-7mm at its narrowest and the left iliac had a severe narrowing due to this plaque. The common femoral artery was severely diseased with a lumen diameter of 4mm due to heavily calcified plaque.

I have come to favor direct aortic puncture over conduits, but the heavily calcified aorta and the absence of safe areas to clamp made me think about other options. My experience with endoconduits has been limited to revising problems of endoconduits from elsewhere, but others report it as a feasible option.

The problem with a long artery narrowed with irregular plaque and even intimal thickening is that it will readily expand to accommodate a large sheath but removing it involves the frictional resistance of the whole artery and typically the “iliac on a stick” avulsion involves the whole length of external iliac artery, likely because the common iliac is anchored by the aortoiliac plaque, the smaller diameter of the EIA, and the longer more tortuous path offering greater resistance in the EIA compared to the aorto-common iliac segment.

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Remote endarterectomy, a technique involving endarterectomizing an artery through a single arteriotomy, offers the possibility of increasing the lumen of even a mildly diseased artery and reducing the frictional coefficient, assuming the remnant smooth adventitia is less resistant than rough irregular intimal plaque.

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The plan was to expose the right common femoral artery and endarterectomize it and gain wire access from the R. CFA. A wire would be placed on the left iliofemoral system to protect it for later kissing iliac stents. A right EIA remote endarterectomy would be performed, and then the right aorto-common iliac segment would be balloon dilated to 8mm.

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The operation went as planned. The external iliac plaque was removed in a single piece from the EIA origin.

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Arteriography showed the right EIA to be free of intimal disease, and dilators and ultimately the 22F sheath went in easily.

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The TEVAR also went uneventully -the left subclavian which had a prior common carotid to subclavian bypass, was covered and the aneurysm and flap were excluded from the left CCA to the celiac axis.

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The most difficult part of the operation was removing the sheath, as is usually the case with a tight iliac, but the friction point was largely at the common iliac and not the external iliac. No artery could be seen extruding with the sheath at the groin while steady tension was applied to the sheath under fluoro. The aortic bifurcation was repaired with kissing iliac stent. The patient recovered well and her chest pain resolved.

I have done this for EVAR, including reopening occluded external iliac arteries, and even for a 26F access for TAVR, avoiding the need for placement of a conduit in selected patients.

Addendum: in followup, I had the chance to check up on the repair -the EIA remained large and patent.

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