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.

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

Arterial Restoration -Something New, Something Old

Something that I recently promised Dr. James S.T. Yao, I will be working to publish on my stent removal and extended remote endarterectomy cases and techniques. Meanwhile, here is a talk.

Nutcracker Syndrome: The Renal Vein Transposition

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Case Report

Patient is a 43 year old woman who had been having bouts of severe left sided abdominal pain for several years with worsening episodes of nausea and vomiting resulting in several visits to the emergency room. She has also had microscopic hematuria. Gastrointestinal workup including gastric emptying study, esophagogastroduodenoscopy and colonoscopy were negative, as was a workup for kidney stones. Eventually she was referred to my clinic for management of nutcracker syndrome. She denied lower abdominal pain nor excessive menstrual bleeding.

On examination, she was tender over the left kidney and flank. Laboratory examination was positive for microscopic hematuria. CT venography (below) showed an obstruction of her left renal vein by the superior mesenteric artery. Drainage via gonadal vein was not demonstrated, and no pelvic varices or complex of retroperitoneal veins was apparent.

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Duplex showed the narrowing in the left renal vein and spectral Doppler showed elevated velocities across the compression caused by the superior mesenteric artery (below). The collecting system was not obstructed.

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Treatment options included endovascularization with a large stent in the left renal vein, left renal vein transposition to a lower position on the inferior vena cava, left renal autotransplantation, and left nephrectomy. Stent placement comes with a degree of risk for cardiopulmonary embolism which may require a sternotomy to fish out an errant stent. The risk for this in the US is because the largest nitinol stents available are 14mm in diameter which might result in undersizing in a vein that could easily dilate to well over 20mm. Larger nitinol stents for venous applications are available in Europe but currently are not approved in the US (yet). Wall stents, while certainly wide enough, have the problem of being long and stiff when not fully deployed. A 22×35 Wall stent may be 50mm long if deployed inadvertently into a tributary vein or contrained at the narrowing. Because it slides easily, passing balloons in or out can cause it to slip out of position. Because this stent elongates when compressed and packed, deployment is challenging and it is prone to “watermelon seeding,” a set up for embolism. It does have the virtue of easy reconstraining.

My friend and recent host for Midwest Vascular Surgery Society Travelling Fellowship, Dr. John V. White, in Chicago, seems to have solved this problem by a multistep process of predeploying a temporary suprarenal IVC filter, deploying a stent (whatever fits), leaving the filter as a protection against stent migration for 4 weeks until the stent permanently seats itself through scarring/intimal ingrowth, then removing the filter.

I chose to perform venography and renal vein transposition. The patient was placed in a supine position on a hybrid angiographic operating room table and her right femoral vein was accessed. She was placed in 15 degrees reverse Trendelenberg which is about the upper limit possible. Venography below.

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Arrow points to left ascending lumbar vein which is taking most of the reflux. It drains the left kidney across the midline via retroartic channels to the IVC
The films showed left renal vein compression by the superior mesenteric artery with outflow via the ascending lumbar vein, both supra and infrarenal tributaries. A midline exposure was performed and the retroperitoneum opened as in an transabdominal aortic exposure. The vena cava was exposed, and the left renal vein was mobilized by ligating and dividing its tributaries. A point 5cm below the tributary point was marked on the IVC, and this was the target for transposition.

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After heparinizing and clamping, the renal tributary was taken with a 5mm cuff –this would ensure proper length without narrowing the IVC.

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The vein was anastomosed and flow was excellent by pulse Doppler.

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She recovered well but had a longer stay because of an ileus, being discharged on day 5. Because she lived at a distance, and came back for followup the following week prior to boarding a plane for home. She no longer had the left sided abdominal pain and there was no hematuria. CT showed excellent drainage through the transposed vein.

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Followup will be periodic (6 monthly) renal venous duplex from home. Given that there was minimal tension on the repair, I expect this to do well.

Discussion:

Nutcracker syndrome is one of the many unfortunate consequences of our bipedal lifestyle. The small intestines hang like baggy sausages off the branched stems of the superior mesenteric artery (SMA), and in some individuals, the SMA compresses the left renal vein against the aorta. The left renal vein receives up to 12-15% of cardiac output via the left kidney, and with outflow obstruction, drains the blood through small collaterals. The renal venous hypertension results in swelling of the left kidney with subsequent left renal colic -with flank and abdominal pain, nausea, and vomiting. There is hematuria which can be gross or microscopic. With drainage via an incompetent gonadal vein, varicoceles can occur with discomfort in men and pelvic varices with pelvic congestion syndrome can occur in women.

Diagnosis is challenging because it is one of the relatively rare non-gastrointestinal causes of abdominal pain (table).

  1. Mesenteric ischemia
  2. Median arcuate ligament syndrome
  3. Nutcracker syndrome
  4. Neuromuscular
  5. Urolithiasis
  6. Inflammatory aortitis/arteritis
  7. Hypersplenism
  8. Portal hypertension
  9. Arterial aneurysm
  10. Infections
  11. Pelvic Congestion Syndrome
  12. Endometriosis
  13. Hernias 

A history of left sided abdominal pain, flank pain, nausea, vomiting, associated pelvic pain, and episodes of hematuria are diagnostic. Examination is typically positive for left renal tenderness and flank tenderness. Laboratory examination include urinalysis for hematuria. Duplex, while technically challenging, will show renal venous compression with velocity elevation or loss of respirophasicity, CTA will typically show obstruction of the left renal vein with filling of collaterals, as will MRV.

Venography should be done in a stepwise manner (White protocol) to fully demonstrate the maldistribution of blood. That is the key word, maldistribution. I learned from my fellowship with Dr. White that performing venography in as upright a position as possible recreated the pathophysiology, the physics, particularly for pelvic congestion and nutcracker. Remember, this is a disease of bipedalism, of upright posture. Many negative studies done supine become positive, as the contrast will fall to where it prefers to go. As I have stated in the past, on the venous side, demonstrating drainage has different imaging needs than demonstrating flow. Pathologic venous drainage has three characteristics:

  1. Varicose veins develop as an end stage process
  2. Reversal of flow or reflux is demonstrated, particularly into small tributary veins
  3. The midline is crossed in these usually small, now larger, collateral veins

While pressure gradients are nice if they are large, they are difficult to assess when they narrow to 1-2mmHg, particularly if they vary with cardiac cycle and respiration. Because we are assessing drainage, the distribution of contrast and the direction it goes is particularly important, and far more sensitive than pressure measurements.

Venography was done per a modification of Dr. White’s protocol for pelvic congestion:

  1. Steep reverse Trendelenberg
  2. Hand injection 10mL half diluted contrast, gently as to not create false reflux
  3. Runs with catheter in left EIV, right EIV, left renal vein, right renal vein
    1. With pelvic congestion workup, add selective bilateral gonadal and internal iliac veins.

 

I have started transposing gonadal veins when they have enlarged from chronic reflux (link, ref 2). Renal vein transposition was chosen because her ovarian vein was competent and too small to transpose (ref 1-3). While the patency rate of stents in veins seems to be acceptable, long term data is unavailable. Also, venographic appearances are deceiving -see the in-vivo measurement of the left renal vein after dissection:

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Left renal vein at widest is 22mm, with expansion, possibly up to 28mm, but is relatively short. Do you see the SMA?
The variability in diameter and length of the Wallstent in the 22-24mm diameter range makes this a challenging deployment. Given that I would not be able to closely follow this young patient, I felt compelled to recommend a durable solution (ref 4).

References:

  1. White, J. et al, Left ovarian to left external iliac vein transposition for the treatment of nutcracker syndrome. J Vasc Surg Venous Lymphat Disord. 2016;4:114–118.
  2. Miler R, Shang E, Park W. Gonadal Vein Transposition for the Treatment of Nutcracker Syndrome. Annals of Vascular Surgery 2017, July 6. in press. http://dx.doi.org/10.1016/j.avsg.2017.06.153
  3. Markovic JShortell C. Right gonadal vein transposition for the treatment of anterior nutcracker syndrome in a patient with left-sided inferior vena cava. J Vasc Surg Venous Lymphat Disord.2016 Jul;4(3):340-2. doi: 10.1016/j.jvsv.2015.09.002.
  4. Erben Y, Gloviczki P, Kalra M, Bjarnason H, Reed NR, Duncan AA, Oderich GS, Bower TC. Treatment of nutcracker syndrome with open and endovascular interventions. J Vasc Surg Venous Lymphat Disord. 2015 Oct;3(4):389-96. doi: 10.1016/j.jvsv.2015.04.003.

Case report up on Annals of Vascular Surgery -Gonadal Vein Transposition for Nutcracker Syndrome

link

A case report co-authored by my recently graduated trainees, Drs. Roy Miler and Eric Shang. An update to be presented at Midwest Vascular Surgery Society Meeting in Chicago.

When Hybrid Seems Better: Carotid Trauma As a Model For All Trauma

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Tracheal deviation due to iatrogenic carotid pseudoaneurysm

History

The patient is an 80 year old woman with lung cancer who was getting a port placed at her home institution. It was to be a left subclavian venous port, but when access was not gained, a left internal jugular venous port was attempted, but after the intitial stick and sheath placement, pulsatile bleeding was recognized and the sheath removed. Hemostasis was achieved with clips and the wound closed and a right internal jugular venous port was placed. The postprocedural CXR shown above showed tracheal deviation and numerous clips from the initial port placement attempt, and a CT scan with contrast (unavailable) showed a carotid pseudoaneurysm of 3cm projecting posteriorly behind the pharynx/esophagus. She was kept intubated and sedated, and transferred for management.
On examination, her vital signs were stable. She had 2cm of tracheal deviation and swelling was apparent at the base of the neck. While my trainees may be better versed at this than I at the particulars of this, my old general surgery trauma training kicked in, as she had a Zone I neck carotid injury, neck zones.pngwhich in my experience is highly morbid despite how stable the patient was. Point again to trainees, this is no different from someone having stabbed this patient with a knife at the base of the neck. My options were:

  1. Open repair
  2. Endovascular repair from femoral access
  3. Hybrid repair

Open Repair

Open repair is the approach of choice for zone 2 injuries because aerodigestive tract injuries can also be addressed and the exposure is straightforward. For Zone 1 injury, the exposure is potentially possible from a neck exposure, but in my experience, jumping into these without prepping for a sternotomy puts you into a situation without a plan B. The exposure of the carotid artery at this level becomes challenging with hemorrage from the artery once the compression from the hematoma or pseudoaneurysm is released. A sternotomy in this elderly woman, while not optimal, may be necessary if open control is required, but the best plan is to avoid this.

Endovascular Options

This should be a straightforward repair from an endovascular approach, even with the larger sheath required for the covered stents. A purely endovascular approach is problematic for two reasons. One, cerebral protection devices are built for bare carotid stents and not peripheral stent grafts, but this is not prohibitive -it should be fine. Without a planned drainage, the hematoma would be left behind which could cause prolonged intubation and problems with swallowing -both an issue for an elderly patient battling lung cancer. Endovascular access could provide proximal control for an open attempt from above, but instrumenting from the arch in an 80 year old has a known 0.5-1% stroke rate.

Hybrid Repair

A hybrid open approach with exposure at the carotid bifurcation offers several advantages. With control of the internal carotid artery, cerebral protection is assured while the carotid artery is manipulated. At the end of the procedure, the internal carotid can be backbled through the access site with the common carotid artery clamped. The hematoma could be avoided until the stent graft is deployed. An unprotected maniplation in the arch can be avoided. Once the stent graft is deployed, drainage of the hematoma can be performed.

carotid control

This required setting up a table off the patient’s left that allowed the wire to lie flat to be manipulated by my right hand. The carotid bifurcation was accessed through a small oblique skin line incision and the common, internal, and external carotid arteries, which were relatively atherosclerosis free, were controlled with vessel loops. The patient was heparinized. The internal carotid was occluded with the loop, and the common carotid below the bifurcation was accessed and an 8F sheath with a marker tip inserted over wire. Arteriography showed the injury and pseudoaneurysm.

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The location of the injury based on CT and on this angio would have baited a younger me into directly exposing it, but experience has taught me that which occasionally you can get away with it, the downsides -massive hemorrhage, stroke, need for sternotomy, just aren’t worth it. The sheath was brought across the injury and a Viabahn stent graft was deployed across the injury.

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The hemorrhage was controlled and the hematoma was then exposed and drained -the cavity was relatively small and accepted the tip of a Yankauer suction easily. A Jackson-Pratt drain was placed. The access site was repaired after flushing and retrograde venting as described.

She recovered rapidly after extubation postop. She was able to breath and swallow without difficulty and had suffered neither stroke nor cranial nerve injury. The drain was removed on postop day 2.

The patient recently returned for a 6 month followup. Duplex showed wide patency of her stent.

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More gratifyingly, her port was removed as her cancer was controlled with an oral regimen.

Discussion

Let me start with my bias that all penetrating trauma should be approached in a hybrid endovascular OR. It is a natural setting for trauma and this case illustrates that. In a hybrid operating room, central aortic and venous injuries can be controlled endovascularly while open repair, including salvage packing, can be done. Excess morbidity of central vascular exposures can be avoided. Temporary IVC filters can be placed if indicated (becoming rarer and rarer). Cardiopulmonary bypass can be started.

In this patient, hybrid therapy brought the best of both techniques and avoided many of the pitfalls of the purely open or endovascular approach. For stable zone I penetrating injuries of the neck, it is clear that this is a reasonable approach.