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.

IMG_8144

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.

IMG_8151

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).

IMG_8162

IMG_8171.jpg

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.

Exovascularist’s Dilemma: Where Is Our LIMA to LAD

During our daily morning huddles, peopled by cardiologists and cardiac surgeons, one thing impresses me more than anything else. The assembled interventional cardiologists, world class and renown, they who can place a stent in any part of the body, will defer to the unassailable superiority of the LIMA to LAD bypass over any existing intervention. I am always a little sad that the analog for this, the vein bypass in the leg does not get the same love. The open surgical bypass of the leg is the great straw man at international symposia. It is fast becoming a diminishing and curious habit of a fading generation.

The acknowledged superior hemodynamics and patency of the bypass is diminished in the literature by pooling patency loss with other factors such as amputation, heart attacks, and death. Some vascular surgeons dogmatically cling to habits learned in training that favor complications, making themselves their own worst enemies both in the literature and in the marketplace. These bad habits involve long incision length, closure techniques that do not anticipate edema, and wound orientation that makes failure more likely.

Operations require far more support and resources to succeed than do interventions that soon go home. Brilliant operations alone will not heal the patient. It is pathways and postoperative care infrastructure and staff that prevent these secondary complications -the very complications that keep the leg vein bypass from being as respected, if not loved, as the LIMA to LAD.

The postoperative care of these patients devolves to management of leg edema. No medical or nursing school adequately teaches the basic science nor management of edema, which is the most common vascular condition

The incisions are too long in the classic vein bypass. When you create and then close an incision, the inflammation drives the accumulation of fluid in the extracellular space – creating edema. This postoperative edema, poorly managed, results in complications that leave the patient hobbled with time lost to healing wound complications, pain, and excess limb weight. Additionally, vein bypasses usually involve groin exposure and the delicate lymphatics that coalesce there are perturbed or destroyed during exposure. Postop, this damage and the inflammation rapidly overcomes the capacity of a lymphatic system. The traditional vein harvest also involves cutting through deep layers of fat. The fat is typically closed by broad sutures that create areas of fat necrosis -potential fodder for bacteria. The best ways the complications of long and deep incisions is to avoid them altogether. The calculus of the operative moment – “I must see the vein,” must include the vision of a patient losing months to wound therapies to heal a gaping, necrotic, infected wound. I recommend skip incisions or adopting in-situ bypass technique with endovascular management of fistulae. Or corral your cardiac PA to harvest the vein segment in the thigh after mobilizing the vein in the leg with the endoscope.

The incisions are often closed with Nylon sutures and skin clips which can become potential foci of infection. With edema, they create zones of ischemia around them, killing skin and creating entry points for skin flora as the skin expands under an unyielding clip or suture. Placed under a pannus, these sutures or clips fester in an anaerobic environment. Closure should adhere to anatomy. The body relies on connective tissue planes to keep itself together. In the groin, these are Scarpa’s layer and the dermis. They should be closed with absorbable monofilament in a buried interrupted fashion at the dermis with a final running subcuticular layer of 4-0 absorbable monofilament. Steristrips or glue at the skin finishes the job. If you use sutures, particularly at the distal anastomotic site, take care to realize that you have about 12 hours before the skin dies in the best of circumstances, and less with microangiopathy of diabetes and ESRD. Squeezing out the edema before closure with a sterile Esmarch or short counterincisions or even a large one to allow for tension free closure over an anastomosis will prevent wound complications over your graft.

The classic longitudinal groin incisions that cut across the inguinal crease divides a tension point -that crease is like a cord that supports the pannus that is slung over it and when divided and then closed with a stitch, that stitch then bears the weight of that pannus every time the patient sits up or stands. If you are observant, wound necrosis typically starts at the groin crease under a surgical clip or suture. Incisions in the groin should be obqlique and parallel to this crease, or if you can, even inside this crease. When these wounds are closed, the natural lines of tension are in line with the incision rather than orthogonal to it. The natural forces keep the wound shut.

This is only the first step. The next is keeping the wound clean and dry for at least 5 days. At the Mayo Clinic, where I trained, the nurses up on 5 Mary Brigh were trained to blow dry the groin wounds every few hours on cool setting and redressing the wound with dry gauze. You can get something close to it by ensuring the wounds painted with betadine, allowed to air dry, and dressed with dry gauze. If there is a constant leak of fluid, you have a serious problem as there is too much edema in the leg, or the wound isn’t closed, or there is a lymph leak. It needs to be actively dried out or you get a wet, macerated, infected wound like a grenade went off in the groin.

They don’t teach compression wrap techniques in medical or nursing school

The simplest thing to avoid lymph leaks is to not make them. Cutting near lymph nodes is hazardous, and once below Scarpa’s you have to orient your dissection directly over the femoral artery. Stray horizontally and you will undoubtedly cut one of the 4 to 10 invisible lymph channels.

They are invisible but detectable -after you break them, you will see a constant wetness in the wound. Think about injecting a cc or two of Lymphazurin (Isosulfan Blue, for those not allergic to Sulfa) into the intertriginous space on the same foot and you will see the lymph channel in bright blue, or stare carefully at the likely spots for a lymph leak and clip it, burn it, Ligasure or Harmonic scalpel it.

Lymph leak identified from saphenectomy incision (for CABG)

So how did we get to a rather dry discussion about edema? Wound complications are tremendously debilitating and offset any benefit from vein bypass operations. These long incisions become terrible big wounds if not prevented. It takes the concerted effort of a team and particularly nursing in actively managing edema. And at the end, the patient too must be included in this discussion. For the vein bypass of the leg to get the same respect and love as the LIMA to LAD bypass, surgical wound complications must become never events.

Water goes downhill

When both iliac systems are occluded below an abdominal aortic aneurysm: hybrid techniques on the cutting edge

preop CTA EVAR-ENDORE.jpg
AAA with iliac arterial occlusion -arrows point to right external iliac and left common iliac arterial occlusions

The patient is an 70 year old man referred for evaluation of claudication that occurred at under a block of walking. He reported no rest pain or tissue loss. He smoked heavily up to a pack a day, with congestive heart failure with an ejection fraction of 40%, prior history of myocardial infarction treated with PTCA, and pacemaker, and moderate dyspnea on exertion.

On examination, patient had a flaccid abdomen through which the AAA could be palpated, and he had no palpable femoral artery pulse bilaterally, nor anything below. He had a cardiac murmur and moderate bilateral edema. Preoperative risk evaluation placed him in the high risk category because of his heart failure, coronary artery disease, and his mild to moderate pulmonary disease.
CTA (pictured above and below) showed a 5.1cm infrarenal AAA with an hourglass shaped neck with moderate atherosclerosis in the neck, an occluded left common iliac artery with external iliac artery reconstitution via internal iliac artery collaterals, and a right external iliac artery occlusion with common femoral artery reconstitution. There was calcified right common femoral artery plaque.

Preop left and right centerlines EVAR-ENDORE.jpg

Treatment options included open surgical aortobifemoral bypass with exclusion of the AAA, total endovascular repair with some form of endo-conduit revascularization of the occluded segments of iliac artery, or a hybrid repair.

Open aortic repair in patients with heart failure and moderate COPD can be performed safely (ref 1). Dr. Hollier et al, in the golden age of open repair, reported a 5.7% mortality rate operating on 106 patients with severe category of heart, lung, kidney, or liver disease.

Typically, the hybrid repair involves sewing in a conduit to deliver the main body of a bifurcated or unibody stent graft when endovascular access is not possible. Despite techniques to stay minimally invasive -largely by staying retroperitoneal, this is not a benign procedure (ref 2). Nzara et al reviewed 15,082 patients from the NSQIP database breaking out 1% of patients who had conduit or direct puncture access.

Matched analyses of comorbidities revealed that patients requiring [conduit or direct access] had higher perioperative mortality (6.8% vs. 2.3%, P = 0.008), cardiac (4.8% vs. 1%, P = 0.004), pulmonary (8.8% vs. 3.4%, P = 0.006), and bleeding complications (10.2% vs. 4.6%, P = 0.016).

Despite these risks, I have performed AUI-FEM-FEM with good results with the modification of deploying the terminus of the stent graft across an end to end anastomosis of the conduit graft to the iliac artery (below), resulting in seal and avoiding the problems of bleeding from the usually heavily diseased artery

AUI fem fem.jpg
Aorto-uni-iliac stent graft across end to end conduit anastomosis to fem-fem bypass

The iliac limbs of some stent graft systems will have proximal flares and can be used in a telescoping manner to create an aorto-uni-iliac (AUI) configuration in occlusive disease. The Cook RENU converter has a 22mm tall sealing zone designed for deployment inside another stent graft and would conform poorly to this kind of neck as a primary  AUI endograft which this was not designed to act as. The Endurant II AUI converter has a suprarenal stent which I preferred to avoid in this patient as the juxtarenal neck likely was aneurysmal and might require future interventions

I chose to perform a right sided common femoral cutdown and from that exposure, perform an iliofemoral remote endarterectomy of the right external iliac to common femoral artery. This in my experience is a well tolerated and highly durable procedure (personal data). Kavanagh et al (ref 3) presented their experience with iliofemoral EndoRE and shared their techniques. This would create the lumenal diameter necessary to pass an 18F sheath to deliver an endograft. I chose the Gore Excluder which would achieve seal in the hourglass shaped neck and allow for future visceral segment intervention if necessary without having a suprarenal stent in the way. I planned on managing the left common iliac artery via a percutaneous recanalization.

The patient’s right common femoral artery was exposed in the usual manner. Wire access across the occluded external iliac artery was achieved from a puncture of the common femoral artery. Remote endarterectomy (EndoRE) was performed over a wire from the common femoral artery to the external iliac artery origin (pictures below).

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External iliac to common femoral artery plaque removed with Moll ring cutter (LeMaitre Vascular) over a wire

The 18F sheath went up with minimal resistance, and the EVAR was performed in the usual manner. The left common iliac artery occlusion was managed percutaneously from a left brachial access. The stent graft on the left was terminated above the iliac bifurcation and a self expanding stent was used to extend across the iliac bifurcation which had a persistent stenosis after recanalization.

The patient recovered well and was sent home several days postprocedure. He returned a month later with healed wounds and palpable peripheral pulses. He no longer had claudication and CTA showed the aneurysm sac to have no endoleak (figures below).

post CTA EVAR-ENDORE

postop centerline EVAR-ENDORE
Composite imaging showing normal appearing right iliofemoral segment (EIA + CFA) and patent left common iliac artery.

Discussion
I have previously posted on using EndoRE (remote endarterectomy) for both occlusive disease and as an adjunct in EVAR. Iliofemoral EndoRE has excellent patency in the short and midterm, and in my experience has superior patency compared to the femoropopliteal segment where EndoRE is traditionally used. This case illustrates both scenarios. While the common iliac artery occlusions can be expected to have acceptable patencies with percutaneous interventions, the external iliac lesions typically fail when managed percutaneously especially when the stents are extended across the inguinal ligament. The external iliac artery is quite mobile and biologically, in my opinon, behaves much as the popliteal artery and not like the common iliac. Also, the common femoral arterial plaque is contiguous with the external iliac plaque, making in my mind, imperative to clear out all the plaque rather than what can just be seen through a groin exposure.

On microscopy, the external iliac artery is restored to a normal patent artery -I have sent arterial biopsies several months after endarterectomy and the artery felt and sewed like a normal artery and had normal structure on pathology. This implies that the external iliac can be restored to a near normal status and patients that are turned down for living related donor transplantation of kidneys can become excellent recipients. In this case, this hybrid approach effectively treated his claudication but also sealed off his moderate sized AAA while not precluding future visceral segment surgery or intervention with a large suprarenal stent.

 

Reference

  1. Hollier LH et al. J Vasc Surg 1986; 3:712-7.
  2. Nzara R et al. Ann Vasc Surg. 2015 Nov;29(8):1548-53
  3. Kavanagh CM et al. J Vasc Surg 2016;64:1327-34

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.

 

When Better is Better Than Good

original bypass

The dictum that better is the enemy of good is one of the old chestnuts carried around surgery training forever. It is an admonition against an unhealthy perfectionism that arises from either vanity or self doubt, and in the worse cases, both. The typical scenario is a surgeon trying to make a textbook picture perfect result and finding the patient’s tissues lacking, will take down their work to make it better, and repeat this process while the patient and everyone else in the room lingers.

Trying to avoid this, many surgeons will try to avoid any difficulties -the bad patch of scar tissue, irradiated body parts, areas of prior infection. But the mental contortions involved in avoiding “perfect” can result in actual physical contortions that in the end don’t pay off in good enough. I have not been immune to this, and I don’t think any physician or surgeon can honestly say they haven’t experienced some variation on this.

This patient is a younger middle aged man who in his youth experienced a posterior dislocation of his left knee, resulting in an arterial transection. This was repaired with an in-situ graft. Subsequently, he had complications of osteomyelitis and had his knee fused after resection of his joint. He did well with this bypass for several decades, but it finally failed several years ago, and a new one was created (image above).

Rather than directing the graft in line as in the previous one, this was was taken from a medial exposure of the femoral artery and tunneled superficially around the fused knee to coil lateral, ending in the anterior tibial artery.

This graft in turn thrombosed and was lysed by the outside surgeons and underwent serial interventions of proximal and distal stenoses at the anastomoses. The patient, when I met him, was contemplating an above knee amputation as a path to returning to work as a nurse in a rural hospital.

While there should be no reason long bypasses should do any less better than short bypasses, I do have to say these things about this patient’s bypass:

  1. No vein is perfect and the longer your bypass, the more chances you will have that a segment of bad vein will end up in your bypass
  2. Turning flow sharply can cause harsh turbulence. Turbulence can cause transition of potential energy into kinetic energy which acts to damage intimal, resulting in intimal hyperplasia.
  3. Thrombosis is a sure sign that your graft is disadvantaged, and the longer the period of thrombosis, the longer the intima “cooks” in the inflammatory response that accompanies thrombosis, making the vein graft even more vulnerable to subsequent intimal hyperplasia, thrombosis, or stricture.
  4. A high flow, small diameter vein graft entering a larger, disease free bed results in more turbulence but also Bernoulli effects that cause the graft to close intermittently, vibrating like one of those party favors that make a Bronx Cheer (a Heimlich valve). This is the cause I think of the distal long segment narrowing on this graft.

This patient was decided on amputation when our service was consulted, and after reviewing his CTA, I offered balloon angioplasty as his symptoms were primarily of paresthesia and neuropathic pain. I used cutting balloons and got angiographically satisfactory results.

intervention

The patient, although he admitted to feeling much better, was sad. He relayed that he had felt this way several times before, only to have his life interrupted by pain and weakness signaling a restenosis.

 

A direct graft would require about 10 centimeters of vein
 
It was only a month later when I heard the patient had returned with the same symptoms. He wasn’t angry nor full of any “I told you so” that frankly I was muttering to myself. Reviewing his CTA, he had restenosed to a pinhole. The vein, to use a scientific term, was “no good.”

The other interesting finding was that he had an abundance of very good vein. Following surgical dictum, his original and subsequent surgeons had used his vein from his contralateral saphenous vein. His right leg, fused at the knee, lacked a good calf muscle pump action. While there were no varicose veins, the greater and lesser saphenous veins were large and generous conduits, at least by 3DVR imagery, confirmed on duplex (image below, white arrows).

veins
3DVR showing presence of potential conduit

The extant arteries were smooth and plaque-free. I decided to harvest his lesser saphenous vein and through the same incision expose his distal superficial femoral artery and tibioperoneal trunk. While I anticipated some scarring, I was confident that the sections of artery I wanted to expose were easy to access because of some distance from the fused knee.

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On left short saphenous vein was harvested then same exposure used to expose TP Trunk

The picture shows the exposure and reversed vein graft in-situ, using the segment of lesser saphenous vein. As in prior experience in redo surgery, you can never know if a dissection will be easy or hard simply based on fear or concern for breaking something. It’s not until you start bushwacking –carving through scar and dealing with extraneous bleeding will you learn whether it was easy or hard. You can only be certain it was necessary. The only hitch was the femoral artery while well exposed, was buried in scar, and I chose not to get circumferential control as I was fairly deep, and had avid backbleeding from a posteriorly oriented collateral that required a mass clamp of the deep tissues.

Will this work better? Don’t know but it has a good chance, and I think a better chance. It is a large vein oriented in a straight path over a short distance going from good artery to good artery. This is better theoretically than a long meandering bypass with smaller vein. 

VESS Meeting -Vail, CO 2015

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VESS is a special medical society whose mission is to foster academic activity and collegiality among young vascular surgeons. Dr. Vikram Kashyap, the outgoing president, gave an engaging talk about changing with the times, referencing three powerhouse rock groups -Rush, The Police, and the Red Hot Chili Peppers, three of my favorite groups.

Dr. Max Wohlauer presented our case report on “Osteosarcoma masquerading as an axillary artery pseudoanuerysm.”

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The case report ended the Friday morning session and was well received.

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Dr. John Weber opened the Friday afternoon session with “Median arcuate ligament syndrome is not a vascular disease.” Shown above prepping for the talk, he is also in the conference dress code of being ready for the slopes.

The talk was also well received and not surprising to most who agreed. In a conversation I had with Dr. Kenneth Cherry, he mentioned that he and Dr. Jeb Hallett had concluded as much decades ago.

The scuttlebutt in the conference was about the NY Times article about the scandalous overuse of femoral stents by some physicians. It is a matter of course that the first line of therapy for mild to moderate claudication is a combination of risk factor modification and exercise therapy -something not mentioned by the writers as something emphasized by Vascular Surgeons who as a rule are against plying stents on asymptomatic or mildly symptomatic patients.

The other thing was the tremendous demand for vascular surgeons, and the success of the 0-5 training programs which represent the future of vascular surgery. Dr. Karl Illig professed as much in the Q&A of a report from Wake Forest. Surprisingly the majority (100%) of 0-5 graduates in 2013 went into academic practice.