- Alright, well thank you, everybody, for having me. Thanks, Larry for inviting me to give this talk. My only disclosure is that I am the vice president of operations for (clears throat), excuse me, Azura Vascular Care and we operate 65 office based laboratories and ambulatory surgery centers. So, the undertaking to go ahead
and become a ambulatory surgery center is massive and requires a tremendous amount of pre-planning. You have to have a very sound financial model, you have to have a stable physician pool, you have to have a good patient referral base. And without lining up all those elements first,
you are sort of dead in the water. So the first thing to understand is that a physician's office and an ambulatory surgery center are separate and distinct entities. Today if you have a physician's office through an extension of your practice
you can then set up an Angio Suite, you can then perform procedures on the patients as needed. But once you're an ambulatory surgery center, you no longer have sort of the office space part. So you can't do ultrasounds, well you can do them, you just can't bill for them, right.
And so you can't concurrently run a physician's office practice out of the ambulatory surgery center, it's actually not permitted in the Medicare conditions for coverage. So that changes things for sure.
And then so if you're really based out of a physician's office and you have your Endo Suite there, you sort of have to have two offices moving forward. Anyway, you must comply with Conditions for Coverage. The ASC is now subject to State, CMS, and Accrediting bodies and they can show up at any time.
It's a major difference in the way you practice. If it's your doctor's office right now, you know, maybe there's a inspection once a year for a radiation certificate or something like that, but there's really not a whole lot of oversight. ASCs have very strict physical plant guidelines.
There are enhanced staffing requirements, circulating nurses, facility administrators, directors of nursing, all of these extra things that add a very significant amount of cost. You also have to have governance, right. So there's a governing body, a Medical Executive Committees
and requirements, right. Now they're not difficult but there's all this extra documentation that has to go along with it which is just time consuming, burdensome, task oriented. There's disclosures of ownership.
There's a quality improvement program which you have to show that you're doing and documented, and the accrediting bodies, if you don't have it right, they could cite you and it's really a lot of extra work. You need transfer agreements and patient satisfaction surveys,
all these kinds of things. Alright, other ASC fact, okay. In a typical two room facility, you can get away with essentially 35 hundred square feet versus five thousand square feet in an ASC. You would instead of typically having six employees,
you need nine employees, adding all this extra expense. The expertise of the staff is very different, alright. You actually need facility administrators, not just, you can't just pluck a nurse out of their daytime job of seeing patients on the floor and say, okay, now you're facility administrator.
They have to understand regulations, they have to understand the Medicare Conditions for Coverage, et cetera. They have also very extended timeline, which I'll show you on another slide, but the regulatory requirements from life safety,
fire safety, staffing requirements, state licensure, Medicare Deem status, accreditation, all of these things factor into the overall cost to set up an OBL, depending on how you do it, is probably about 1.5 million dollars, versus an ASC at 3.5 million dollars.
So the 800 pound gorilla in states in New York, and about 25 or 30 other states is the process of getting a certificate of need. So if you're in a certificate of need state, it's a whole thing, right. So first you have to get the CON.
The CON then allows you to get state licensure. The state licensure then allows you to apply for Medicare Deem status to an accrediting body. Once you have your Deem status, then you can submit for your PTAN, your physician transaction number, so that you can actually bill Medicare for facility fees,
and then and only then can you then initiate the entire process of getting your private payor contracts. So, all that being said, your application for a CON could be outright rejected. You could be blocked by local hospitals. You could be blocked by local politics.
There's a tremendous amount of issues. Now the one thing that's interesting, if you're in a state that doesn't have a Certificate of Need process, then one of the things that's interesting is they sort of, you sort of get tied up in the local fire marshal, the Department of Health
and this very disjointed Department of Health survey. The Certificate of Need at least, at the very least, allows you to kind of cruise through the process, so that you can, at least you understand your pathway. In states that don't even have a CON process, it can be very disjointed.
Now if you're thinking about building a new facility, well, that's about two to two and a half million dollars. If you're thinking of retrofitting, I'd go by the rule of 200 thousand. So if you need a semi-restricted corridor, and you have to move walls,
that'll cost you about 200 thousand. If you, you're going to need 20 air exchanges per hour in your procedure room, that's a hard requirement. You have to be, you have to get stuff that certifies that you are achieving that, right. That new HVAC system will cost you 200 thousand dollars.
You need three electrical panels. One to power the HVAC, one to power the electrical outlets and one to power the overhead lighting. I mean, the requirements are very, very different. Then, maybe now you're going to need a generator. Well, am I in a building where you're going to
put the generator on the roof, then the fire marshal tells me I can't store the gasoline on the roof, it has to be on the ground, and then you wind up in this big back and forth fight as to where you can put your generator.
Just for time's sake, this is a basic floor plan with semi-restricted corridors, eight foot wide hallways, enough seating for 30 people. The staffing requirements change significantly, in terms of you need a facility administrator, somebody who really knows it.
Now god forbid the facility administrator's on vacation when the state shows up or when an accrediting body shows up so you better have your DON, your director of nursing, all tuned up so that she knows how to answer the questions and knows where all of your paperwork are because otherwise you could be cited
and you could be sunk and it's very burdensome. But the difference in staff costs for typical two room facility is probably about 300 thousand dollars cumulatively. For your hours of operation, right, so now you have a business that's operating as an OBL,
now you want to convert it to an ASC, well that's great. But now you don't have your private payor contract, so what are you going to do? You going to start rejecting patients? So, no, you're not going to do that. So either you're going to lose money on those patients
or you're going to wind up having to form this hybrid operation where you flip back and forth, one day to the next day, et cetera. And the problem with doing that is each one requires its own tax ID number, its own NPI, its own billing codes. And then the staff has to be trained
that they're dedicated to one versus the other. This is your timeline to show you how everything lines up, in terms of your construction, then getting your state licensure, then getting your Medicare accreditation, and then only after you get your Medicare accreditation,
can you then submit for your PTAN, which then takes 90 days. And then only after you get your PTAN, can you being your private payor contracting. So, in conclusion, it requires more time, more staff, more oversight and regulation. The complex hours of operation ought
to maintain your existing patient base. You need a payor contracting strategy. It's probably an additional two million dollars to build out an ASC, including the working capital requirement. So for the solo practitioners that were out there thinking about it,
unless there's a very compelling financial reason to convert, it's probably best to stay an OBL at this time. Thank you.
- Thank you chairman, ladies and gentlemen. I have no conflict of interest for this talk. So, basically for vTOS we have the well known treatment options. Either the conservative approach with DOAC or anticoagulation for three months or longer supported by elastic stockings.
And alternatively there's the invasive approach with catheter thrombolysis and decompression surgery and as we've just heard in the talk but Ben Jackson, also in surgeons preference, additional PTA and continuation or not of anticoagulation.
And basically the chosen therapy is very much based on the specific specialist where the patient is referred to. Both treatment approaches have their specific complications. Rethrombosis pulmonary embolism,
but especially the post-thrombotic syndrome which is reported in conservative treatment in 26 up to 66%, but also in the invasive treatment approach up to 25%. And of course there are already well known complications related to surgery.
The problem is, with the current evidence, that it's only small retrospective studies. There is no comparative studies and especially no randomized trials. So basically there's a lack of high quality evidence leading to varying guideline recommendations.
And I'm not going through them in detail 'cause it's a rather busy slide. But if you take a quick look then you can see some disparencies between the different guidelines and at some aspects there is no recommendation at all,
or the guidelines refer to selected patients, but they define how they should be selected. So again, the current evidence is insufficient to determine the most clinically and cost effective treatment approach, and we believe that a randomized trial is warranted.
And this is the UTOPIA trial. And I'm going to take you a bit through the design. So the research question underline this trial is, does surgical treatment, consisting of catheter directed thrombolysis and first rib section, significantly reduce post-thrombotic syndrome
occurrence, as compared to conservative therapy with DOAC anticoagulation, in adults with primary upper extremity deep vein thrombosis? The design is multicenter randomized and the population is all adults with first case of primary Upper Extremity
Deep Venous Thrombosis. And our primary outcome is occurrence of post-thrombotic syndrome, and this the find according the modified Villalta score. And there are several secondary outcomes, which of course we will take into account,
such as procedural complications, but also quality of life. This is the trial design. Inclusion informed consent and randomization are performed at first presentation either with the emergency department or outpatient clinic.
When we look at patients 18 years or older and the symptoms should be there for less than 14 days. Exclusion criteria are relevant when there's a secondary upper extremity deep vein thrombosis or any contra-indication for DOACs or catheter directed thrombolysis.
We do perform imaging at baseline with a CT venography. We require this to compare baseline characteristics of both groups to mainly determine what the underlying cause of the thrombosis being either vTOS or idiopathic.
And then a patient follows the course of the trial either the invasive treatment with decompression surgery and thrombolysis and whether or not PTA is required or not, or conservative treatment and we have to prefer DOAC Rivaroxaban or apixaban to be used.
Further down the patient is checked for one month and the Villalta score is adapted for use in the upper extremity and we also apply quality of life scores and scores for cost effectiveness analysis. And this is the complete flowchart of the whole trial.
Again, very busy slide, but just to show you that the patient is followed up at several time points, one, three, six, and 12 months and the 12 months control is actually the endpoint of the trial
And then again, a control CT venography is performed. Sample size and power calculation. We believe that there's an effect size of 20% reduction in post-thrombotic syndrome in favor of the invasive treatment and there's a two-side p-value of 0.05
and at 80% power, we consider that there will be some loss to follow up, and therefore we need just over 150 patients to perform this trial. So, in short, this slide more or less summarize it. It shows the several treatment options
that are available for these patients with Upper Extremity Venous Thrombosis. And in the trial we want to see, make this comparison to see if anticoagulation alone is as best as invasive therapy. I thank for your attention.
- So Beyond Vascular procedures, I guess we've conquered all the vascular procedures, now we're going to conquer the world, so let me take a little bit of time to say that these are my conflicts, while doing that, I think it's important that we encourage people to access the hybrid rooms,
It's much more important that the tar-verse done in the Hybrid Room, rather than moving on to the CAT labs, so we have some idea basically of what's going on. That certainly compresses the Hybrid Room availability, but you can't argue for more resources
if the Hybrid Room is running half-empty for example, the only way you get it is by opening this up and so things like laser lead extractions or tar-verse are predominantly still done basically in our hybrid rooms, and we try to make access for them. I don't need to go through this,
you've now think that Doctor Shirttail made a convincing argument for 3D imaging and 3D acquisition. I think the fundamental next revolution in surgery, Every subspecialty is the availability of 3D imaging in the operating room.
We have lead the way in that in vascular surgery, but you think how this could revolutionize urology, general surgery, neurosurgery, and so I think it's very important that we battle for imaging control. Don't give your administration the idea that
you're going to settle for a C-arm, that's the beginning of the end if you do that, this okay to augment use C-arms to augment your practice, but if you're a finishing fellow, you make sure you go to a place that's going to give you access to full hybrid room,
otherwise, you are the subservient imagers compared to radiologists and cardiologists. We need that access to this high quality room. And the new buzzword you're going to hear about is Multi Modality Imaging Suites, this combination of imaging suites that are
being put together, top left deserves with MR, we think MR is the cardiovascular imaging modality of the future, there's a whole group at NIH working at MR Guided Interventions which we're interested in, and the bottom right is the CT-scan in a hybrid op
in a hybrid room, this is actually from MD Anderson. And I think this is actually the Trauma Room of the future, makes no sense to me to take a patient from an emergency room to a CT scanner to an and-jure suite to an operator it's the most dangerous thing we do
with a trauma patient and I think this is actually a position statement from the Trauma Society we're involved in, talk about how important it is to co-localize this imaging, and I think the trauma room of the future is going to be an and-jure suite
down with a CT scanner built into it, and you need to be flexible. Now, the Empire Strikes Back in terms of cloud-based fusion in that Siemans actually just released a portable C-arm that does cone-beam CT. C-arm's basically a rapidly improving,
and I think a lot of these things are going to be available to you at reduced cost. So let me move on and basically just show a couple of examples. What you learn are techniques, then what you do is look for applications to apply this, and so we've been doing
translumbar embolization using fusion and imaging guidance, and this is a case of one of my partners, he'd done an ascending repair, and the patient came back three weeks later and said he had sudden-onset chest pain and the CT-scan showed that there was a
sutured line dehiscence which is a little alarming. I tried to embolize that endovascular, could not get to that tiny little orifice, and so we decided to watch it, it got worse, and bigger, over the course of a week, so clearly we had to go ahead and basically and fix this,
and we opted to use this, using a new guidance system and going directly parasternal. You can do fusion of blood vessels or bones, you can do it off anything you can see on flu-roid, here we actually fused off the sternal wires and this allows you to see if there's
respiratory motion, you can measure in the workstation the depth really to the target was almost four and a half centimeters straight back from the second sternal wire and that allowed us really using this image guidance system when you set up what's called the bullseye view,
you look straight down the barrel of a needle, and then the laser turns on and the undersurface of the hybrid room shows you where to stick the needle. This is something that we'd refined from doing localization of lung nodules
and I'll show you that next. And so this is the system using the C-star, we use the breast, and the localization needle, and we can actually basically advance that straight into that cavity, and you can see once you get in it,
we confirmed it by injecting into it, you can see the pseudo-aneurism, you can see the immediate stain of hematoma and then we simply embolize that directly. This is probably safer than going endovascular because that little neck protects about
the embolization from actually taking place, and you can see what the complete snan-ja-gram actually looked like, we had a pig tail in the aura so we could co-linearly check what was going on and we used docto-gramming make sure we don't have embolization.
This patient now basically about three months follow-up and this is a nice way to completely dissolve by avoiding really doing this. Let me give you another example, this actually one came from our transplant surgeon he wanted to put in a vas,
he said this patient is really sick, so well, by definition they're usually pretty sick, they say we need to make a small incision and target this and so what we did was we scanned the vas, that's the hardware device you're looking at here. These have to be
oriented with the inlet nozzle looking directly into the orifice of the mitro wall, and so we scanned the heart with, what you see is what you get with these devices, they're not deformed, we take a cell phone and implant it in your chest,
still going to look like a cell phone. And so what we did, image fusion was then used with two completely different data sets, it mimicking the procedure, and we lined this up basically with a mitro valve, we then used that same imaging guidance system
I was showing you, made a little incision really doing onto the apex of the heart, and to the eur-aph for the return cannula, and this is basically what it looked like, and you can actually check the efficacy of this by scanning the patient post operatively
and see whether or not you executed on this basically the same way, and so this was all basically developed basing off Lung Nodule Localization Techniques with that we've kind of fairly extensively published, use with men can base one of our thoracic surgeons
so I'd encourage you to look at other opportunities by which you can help other specialties, 'cause I think this 3D imaging is going to transform what our capabilities actually are. Thank you very much indeed for your attention.
- So PAD affects five million adults in the United States today, and we know the US population is aging. And 15 to 20% of folks 70 years and older have claudication, a minority of these progress to CLI, and the impact on lifestyle is often minimized, as demonstrated in decreased quality of life scores
in these patients. Now with active tobacco use, there is acceleration of disease towards claudication, and there are higher rates of amputation, MI, and death. But prior to open or endo intervention, the SVS Guidelines recommend supervised exercise,
medical therapy with statins, beta blockers, antiantiplatelets, and Cilostazol, and an aggressive multidisciplinary approach to smoking cessation, which should last no less than six months. But what if a patient can't stop smoking?
We've all had these patients. Should patients with lifestyle limiting claudication be denied open surgical or endo-revascularization? So let's look at the open literature. A meta-analysis performed in 2005 of 29 eligible studies. The results were that bypass graft failure
was three times that in smokers versus nonsmokers. There was a dose response relationship in smoking cessation prior to or after bypass, equalized patencies. A more recent study, published in JVS in September, queried the VSGNE, 1789 lower extremity bypasses, 971 were nonsmokers, 818 were smokers,
and what they found was that primary patency at two years was 48% in smokers, versus 61% in nonsmokers, and when they propensity matched these patients, there was even a greater difference. 10 year survival was also decreased. And in another article,
published in August of this year in JVS, again a VSGNE study, over 2,000 patients, almost 3,000 patients with lower extremity bypass for claudication. The results looked at MALE, amputation-free survival, limb loss, death, major limb events or death,
and they found that current smoking was a significant predictor of major adverse limb events, and major adverse limb events or death. But do active smokers have worse outcomes after endovascular interventions? So, let's look at the literature again.
And there is none. The only paper I could find was a Markov decision analysis, in which compared revascularization in active smokers to medical management, this was a retrospective study, and their results demonstrated better quality of life in smokers after revascularization versus medical therapy.
The quality of life was similar, after revascularization in nonsmokers and smokers, and there was no increase in amputation rates up to 36 months. Also, 26% of the folks that were revascularized, quit tobacco use after their quality of life was improved.
So we decided to do a small study at my hospital. The outcome of endovascular interventions in active smokers with lifestyle limiting claudication versus nonsmokers. This was retrospective. 138 total patients with endovascular intervention for claudication, 47 were current tobacco users,
91 were never or former smokers. The primary endpoints were reintervention, secondary endpoints, surgical bypass, limb loss, MI, stroke and death. And here you can see, as in most studies, the smokers were a younger population,
and anticoagulation, in our patient population, was more common. As far as comorbidities, they were more common, as in most studies, in the nonsmoking group. And in a mean followup of 3.6 years for both groups, there was no statistically significant difference
between the two groups for any of the outcome measures. So in conclusion, active smokers with lifestyle limiting claudication, we would advocate, of course, smoking cessation. Outcomes with respect to reintervention, surgical bypass and limb loss appear to be equivalent in these two groups.
We feel that these patients should not be denied endovascular intervention, and improved quality of life after intervention may result in an increase in smoking cessation in this patient population. Limitations are obvious, this was a very small study,
and retrospective, and we are actually extending this study to look at several hundred additional patients. So I thank you for your attention.
- I'd like to thank Dr. Veith for this kind invitation and the committee as well. So these are my disclosures, there's none. So for a quick background regarding closure devices. Vascular closure devices have been around
for almost 20 years, various types. Manual compression in most studies have always been shown to be superior to vascular closure devices mainly because there's been no ideal device that's been innovated to be able
to handle all sorts of anatomies, which include calcified vessels, soft plaque, etc. So in this particular talk we wanted to look at to two particular devices. One is the Vascade vascular closure device
made by Cardiva and the other is the CELT arterial closure device made by Vasorum in Ireland. Both these devices are somewhat similar in that they both use a disc. The Vascade has a nitinol disc
as you can see here that's used out here to adhere to the interior common femoral artery wall. And then once tension is applied, a series of steps is involved to deploy the collagen plug
directly on to the artery which then allows it to expand over a period of time. The CELT is similar in that it also uses a stainless steel disc as you can see here. Requires tension up against the interior wall of the common femoral artery.
Nice and tight and then you screw on the top end of the device on to the interior wall of the artery creating a nice little cylinder that compresses both walls of artery. As far as comparability is concerned between the two devices you can see
here that they're both extravascular, one's nitinol, one's stainless steel. One uses a collagen material, the other uses an external clip in a spindle-type fashion. Both require about, anywhere between three to seven minutes of pressure
to essentially stop the tract ooze. But the key differences between the two devices, is the amount of time it takes for patients to ambulate. So the ambulation time is two hours roughly for Vascade, whereas for a CELT device
it's anywhere from being immediate off the table at the cath lab room to about 20 minutes. The data for Vascade was essentially showing the RESPECT trial which I'll summarize here, With 420 patients that was a randomized trial
to other manual compression or the device itself. The mean points of this is that the hemostasis time was about three minutes versus 21 minutes for manual compression. And time to ambulation was about 3.2 hours versus 5.7 hours.
No major complications were encountered. There were 1.1% of minor complications in the Vascade versus 7% in the manual compression arm. This was actually the first trial that showed that a actual closure devices
had better results than manual compression. The main limitations in the trial didn't involved complex femoral anatomy and renal insufficiency patients which were excluded. The CELT ACD trial involved 207 patients that were randomized to CELT or to manual
compression at five centers. Time to hemostasis was anywhere between zero minutes on average versus eight minutes in the manual compression arm. There was one complication assessed at 30 days and that was a distal embolization that occurred
early on after the deployment with a successfully retrieved percutaneously with a snare. So complication rate in this particular trial was 0.7% versus 0% for manual compression. So what are some pros and cons with the Vascade device?
Well you can see the list of pros there. The thing to keep in mind is that it is extravascular, it is absorbable, it's safe, low pain tolerance with this and the restick is definitely possible. As far as the cons are involved.
The conventional bedrest time is anywhere between two to three hours. It is a passive closure device and it can create some scarring when surgical exploration is necessary on surgical dissections.
The key thing also is you can not visualize the plug after deployment. The pros and cons of the CELT ACD device. You can see is the key is the instant definitive closure that's achieved with this particular device, especially in
calcified arteries as well. Very easy to visualize under fluoroscopy and ultrasound. It can be used in both antegrade and retrograde approaches. The key cons are that it's a permanent implant.
So it's like a star closed devised, little piece of stainless steel that sits behind. There's a small learning curve with the device. And of course there's a little bit of discomfort associated with the cinching under the (mumbles) tissue.
So we looked at our own experience with both devices at the Christie Clinic. We looked at Vascade with approximately 300 consecutive patients and we assessed their time to hemostasis, their time to ambulation,
and their time to discharge, as well as the device success and minor and major complications. And the key things to go over here is that the time to hemostasis was about 4.7 minutes for Vascade, at 2.1 hours for ambulation, and roughly an average
of 2.4 hours for discharge. The device success was 99.3% with a minor complication rate of .02% which we have four hematomas and two device failures requiring manual compression. The CELT ACD device we also similarly did
a non-randomized perspective single center trial assessing the same factors and assessing the patients at seven days. We had 400 consecutive patients enrolled. And you can see we did 232 retrograde. We did a little bit something different
with this one, we did we 168 antegrade but we also did direct punctures to the SFA both at the proximal and the mid-segments of the SFA. And the time to hemostasis in this particular situation was 3.8 minutes,
ambulation was 18.3 minutes, and discharge was at 38.4 minutes. We did have two minor complications. One of which was a mal-deployment of the device requiring manual compression. And the second one was a major complication
which was an embolization of the device immediately after deployment which was done successfully snared through an eighth front sheath. So in conclusion both devices are safe and effective and used for both
antegrade and retrograde access. They're definitely comparable when it comes, from the standpoint of both devices (mumbles) manual compression and they're definitely really cost effective in that they definitely do increase the
throughput in the cath lab allowing us to be able to move patients through our cath lab in a relatively quick fashion. Thank you for your attention.
So I think when it comes to distal bypasses and ultra-distal bypasses it's all about how we make our decision. We know now that early intervention these patients have better outcome. We use waveform analysis to make our decision about how critical their skin is
we use different topical anesthesia depending the patient's fitness. I think this is just one important point that patient's with dark skin did not show all the full range of skin changes and patients get this dark foot sign
even before they start necrosing their skin. It's very important how we give our anesthetics we use vascular anesthesia with special interest prevascular disease because these patients are quite labile. We use even sometimes inotropes during the procedure
and post operative to maintain a good blood pressure. We believe that short bypasses have got better outcomes. Dr. Veith, have already published in the 80s about short bypasses also doing now the Tibiotibial bypasses on the look anesthetic. Some patients with very high risk for general anesthesia.
And our study we showed that the majority of our patients, who had ultra-distal bypasses had the bypasses from either popliteal or SFA artery. We use different techniques to improve on how to take our bypasses from the proximal anastomosis distally. So we use hybrid revascularization, we use drug-eluting
balloons, and stenting of the SFA and popliteal artery, so we can perform our bypass from the popliteal level. We even use Remote Endarterectomy to improve on our length of the inflow. So by doing remote endarterectomy of the SFA
and popliteal artery, we can take the bypass quite distally from the popliteal artery to the foot level. This is a patient who got critical leg ischaemia on the right side limited, venous conduit. We did remote endarterectomy of her SFA and popliteal artery. And then we can
easily take the bypass from the popliteal artery down to the foot level. On the left side, she had hybrid revascularization with SFA stenting and ultra-distal bypass. We use venous conduit in almost all our patients with ultra-distal bypass.
In distal bypasses we can PTFE but the majority of our patients have long saphenous veins or even arm veins. We started using Omniflow in our infected patients for distal bypasses with quite good results. We scan all our veins prior to the procedure
to make sure that we got good quality vein and amount to perform the procedure. We have published in our small veins series less than 3mm, we still have a very good outcome in distal bypasses. Especially when we do tibial bypasses
or dorsalis pedis bypasses we turn the grafts anatomically. You can see in this angiogram the graft going through the interosseous membrane down to the foot level. We put our incision a bit immediately on the foot level so if there is necrosis of the wound on the foot level that we don't expose the graft, especially when we
knew the patient was coming from the lateral aspect through the interosseous membrane. We select our bypasses especially in the foot level using the duplic scanogram, angiogram or CT angiogram. During the procedure we don't clamp our arteries we use the Flo-Rester and Flo-Through prothesis
to stop patients from bleeding while we're doing it. And we've never used tourniquet before all this has been published. Hand held doppler is the only quality control that we do we don't do on-table angiograms and we find this quite useful for our patients.
We can do the debridement and at the same time while we're doing the bypass at the ankle level. As for anticoagulation and antiplatelet therapy We do antiplatelet therapy for all patient with distal and ultra-distal bypass. And we use heparin and warfarin for patients
who have got redo surgery. Graft surveillance for all our patients Unfortunately, we can only afford it in the NHS for one year, but if the patient get an intervention they go for another full year. Salvage angioplasty is essential for these patients
and we treat these patients as quite as a emergency when they present. So, conclusion, Mr. Sherman, ladies and gentlemen, distal and ultra-distal bypasses require good planning. We use veins for all our bypasses when it comes to the foot level and ultra-distal bypasses,
and of course selecting the target vessel in the foot is very important. Graft Surveillance is essential to maintain quality and outcome for these patients. Thank you very much.
- We are talking about the current management of bleeding hemodialysis fistulas. I have no relevant disclosures. And as we can see there with bleeding fistulas, they can occur, you can imagine that the patient is getting access three times a week so ulcerations can't develop
and if they are not checked, the scab falls out and you get subsequent bleeding that can be fatal and lead to some significant morbidity. So fatal vascular access hemorrhage. What are the causes? So number one is thinking about
the excessive anticoagulation during dialysis, specifically Heparin during the dialysis circuit as well as with cumin and Xarelto. Intentional patient manipulati we always think of that when they move,
the needles can come out and then you get subsequent bleeding. But more specifically for us, we look at more the compromising integrity of the vascular access. Looking at stenosis, thrombosis, ulceration and infection. Ellingson and others in 2012 looked at the experience
in the US specifically in Maryland. Between the years of 2000/2006, they had a total of sixteen hundred roughly dialysis death, due to fatal vascular access hemorrhage, which only accounted for about .4% of all HD or hemodialysis death but the majority did come
from AV grafts less so from central venous catheters. But interestingly that around 78% really had this hemorrhage at home so it wasn't really done or they had experienced this at the dialysis centers. At the New Zealand experience and Australia, they had over a 14 year period which
they reviewed their fatal vascular access hemorrhage and what was interesting to see that around four weeks there was an inciting infection preceding the actual event. That was more than half the patients there. There was some other patients who had decoags and revisional surgery prior to the inciting event.
So can the access be salvaged. Well, the first thing obviously is direct pressure. Try to avoid tourniquet specifically for the patients at home. If they are in the emergency department, there is obviously something that can be done.
Just to decrease the morbidity that might be associated with potential limb loss. Suture repairs is kind of the main stay when you have a patient in the emergency department. And then depending on that, you decide to go to the operating room.
Perera and others 2013 and this is an emergency department review and emergency medicine, they use cyanoacrylate to control the bleeding for very small ulcerations. They had around 10 patients and they said that they had pretty good results.
But they did not look at the long term patency of these fistulas or recurrence. An interesting way to kind of manage an ulcerated bleeding fistula is the Limberg skin flap by Pirozzi and others in 2013 where they used an adjacent skin flap, a rhomboid skin flap
and they would get that approximal distal vascular control, rotate the flap over the ulcerated lesion after excising and repairing the venotomy and doing the closure. This was limited to only ulcerations that were less than 20mm.
When you look at the results, they have around 25 AV fistulas, around 15 AV grafts. The majority of the patients were treated with percutaneous angioplasty at least within a week of surgery. Within a month, their primary patency was running 96% for those fistulas and around 80% for AV grafts.
If you look at the six months patency, 76% were still opened and the fistula group and around 40% in the AV grafts. But interesting, you would think that rotating an adjacent skin flap may lead to necrosis but they had very little necrosis
of those flaps. Inui and others at the UC San Diego looked at their experience at dialysis access hemorrhage, they had a total 26 patients, interesting the majority of those patients were AV grafts patients that had either bovine graft
or PTFE and then aneurysmal fistulas being the rest. 18 were actually seen in the ED with active bleeding and were suture control. A minor amount of patients that did require tourniquet for a shock. This is kind of the algorithm when they look at
how they approach it, you know, obviously secure your proximal di they would do a Duplex ultrasound in the OR to assess hat type of procedure
they were going to do. You know, there were inciting events were always infection so they were very concerned by that. And they would obviously excise out the skin lesion and if they needed interposition graft replacement they would use a Rifampin soak PTFE
as well as Acuseal for immediate cannulation. Irrigation of the infected site were also done and using an impregnated antibiotic Vitagel was also done for the PTFE grafts. They were really successful in salvaging these fistulas and grafts at 85% success rate with 19 interposition
a patency was around 14 months for these patients. At UCS, my kind of approach to dealing with these ulcerated fistulas. Specifically if they bleed is to use
the bovine carotid artery graft. There's a paper that'll be coming out next month in JVS, but we looked at just in general our experience with aneurysmal and primary fistula creation with an AV with the carotid graft and we tried to approach these with early access so imagine with
a bleeding patient, you try to avoid using catheter if possible and placing the Artegraft gives us an opportunity to do that and with our data, there was no significant difference in the patency between early access and the standardized view of ten days on the Artegraft.
Prevention of the Fatal Vascular Access Hemorrhages. Important physical exam on a routine basis by the dialysis centers is imperative. If there is any scabbing or frank infection they should notify the surgeon immediately. Button Hole technique should be abandoned
even though it might be easier for the patient and decreased pain, it does increase infection because of that tract The rope ladder technique is more preferred way to avoid this. In the KDOQI guidelines of how else can we prevent this,
well, we know that aneurysmal fistulas can ulcerate so we look for any skin that might be compromised, we look for any risk of rupture of these aneurysms which rarely occur but it still needs to taken care of. Pseudoaneurysms we look at the diameter if it's twice the area of the graft.
If there is any difficulty in achieving hemostasis and then any obviously spontaneous bleeding from the sites. And the endovascular approach would be to put a stent graft across the pseudoaneurysms. Shah and others in 2012 had 100% immediate technical success They were able to have immediate access to the fistula
but they did have around 18.5% failure rate due to infection and thrombosis. So in conclusion, bleeding to hemodialysis access is rarely fatal but there are various ways to salvage this and we tried to keep the access viable for these patients.
Prevention is vital and educating our patients and dialysis centers is key. Thank you.
- Good morning. It's a pleasure to be here today. I'd really like to thank Dr. Veith, once again, for this opportunity. It's always an honor to be here. I have no disclosures. Heel ulceration is certainly challenging,
particularly when the patients have peripheral vascular disease. These patients suffer from significant morbidity and mortality and its real economic burden to society. The peripheral vascular disease patients
have fivefold and increased risk of ulceration, and diabetics in particular have neuropathy and microvascular disease, which sets them up as well for failure. There are many difficulties, particularly poor patient compliance
with offloading, malnutrition, and limitations of the bony coverage of that location. Here you can see the heel anatomy. The heel, in and of itself, while standing or with ambulation,
has tightly packed adipose compartments that provide shock absorption during gait initiation. There is some limitation to the blood supply since the lateral aspect of the heel is supplied by the perforating branches
of the peroneal artery, and the heel pad is supplied by the posterior tibial artery branches. The heel is intolerant of ischemia, particularly posteriorly. They lack subcutaneous tissue.
It's an end-arterial plexus, and they succumb to pressure, friction, and shear forces. Dorsal aspect of the posterior heel, you can see here, lacks abundant fat compartments. It's poorly vascularized,
and the skin is tightly bound to underlying deep fascia. When we see these patients, we need to asses whether or not the depth extends to bone. Doing the probe to bone test
using X-ray, CT, or MRI can be very helpful. If we see an abcess, it needs to be drained. Debride necrotic tissue. Use of broad spectrum antibiotics until you have an appropriate culture
and can narrow the spectrum is the way to go. Assess the degree of vascular disease with noninvasive testing, and once you know that you need to intervene, you can move forward with angiography. Revascularization is really operator dependent.
You can choose an endovascular or open route. The bottom line is the goal is inline flow to the foot. We prefer direct revascularization to the respective angiosome if possible, rather than indirect. Calcanectomy can be utilized,
and you can actually go by angiosome boundaries to determine your incisions. The surgical incision can include excision of the ulcer, a posterior or posteromedial approach, a hockey stick, or even a plantar based incision. This is an example of a posterior heel ulcer
that I recently managed with ulcer excision, flap development, partial calcanectomy, and use of bi-layered wound matrix, as well as wound VAC. After three weeks, then this patient underwent skin grafting,
and is in the route to heal. The challenge also is offloading these patients, whether you use a total contact cast or a knee roller or some other modality, even a wheelchair. A lot of times it's hard to get them to be compliant.
Optimizing nutrition is also critical, and use of adjunctive hyperbaric oxygen therapy has been shown to be effective in some cases. Bone and tendon coverage can be performed with bi-layered wound matrix. Use of other skin grafting,
bi-layered living cell therapy, or other adjuncts such as allograft amniotic membrane have been utilized and are very effective. There's some other modalities listed here that I won't go into. This is a case of an 81 year old
with osteomyelitis, peripheral vascular disease, and diabetes mellitus. You can see that the patient has multi-level occlusive disease, and the patient's toe brachial index is less than .1. Fortunately, I was able to revascularize this patient,
although an indirect revascularization route. His TBI improved to .61. He underwent a partial calcanectomy, application of a wound VAC. We applied bi-layer wound matrix, and then he had a skin graft,
and even when part of the skin graft sloughed, he underwent bi-layer living cell therapy, which helped heal this wound. He did very well. This is a 69 year old with renal failure, high risk patient, diabetes, neuropathy,
peripheral vascular disease. He was optimized medically, yet still failed to heal. He then underwent revascularization. It got infected. He required operative treatment,
partial calcanectomy, and partial closure. Over a number of months, he did finally heal. Resection of the Achilles tendon had also been required. Here you can see he's healed finally. Overall, function and mobility can be maintained,
and these patients can ambulate without much difficulty. In conclusion, managing this, ischemic ulcers are challenging. I've mentioned that there's marginal blood supply, difficulties with offloading, malnutrition, neuropathy, and arterial insufficiency.
I would advocate that partial or total calcanectomy is an option, with or without Achilles tendon resection, in the presence of osteomyelitis, and one needs to consider revascularization early on and consider a distal target, preferentially in the angiosome distribution
of the posterior tibial or peroneal vessels. Healing and walking can be maintained with resection of the Achilles tendon and partial resection of the os calcis. Thank you so much. (audience applauding)
- Thank you Dr. Veith for an invitation to be here. These are our disclosures. We're fortunate to have funding from VA HSR&D for this work. Decision aids help patients make decisions about medical treatment, such as steroids versus biologics for things like arthritis.
Or medical versus surgical treatments for things like degenerative joint disease. Decision aids are uncommonly used for decisions about surgical treatment. Such as the options that face patients facing abdominal aortic aneurysm repair,
which as well all know are options like open surgery, which is invasive, but has a long recovery, but is likely durable over time. Or endovascular repair, which is, of course, less invasive with a shorter recovery, but may have problems with durability.
We design the preferences for open versus endovascular repair or prove AAA trial and this study has two objectives. First was to implement a decision aid, which is designed to help Veterans choose between an open and endovascular repair for their abdominal aortic aneurysm.
Of course, taking place in Veterans Hospitals across the US. And then second, to test if the decision aid makes it more likely for Veterans to receive the type of aneurysm repair that is aligned with their treatment preferences.
We are going to achieve these objectives, we hope, via a randomized clinical trial. I'll tell you briefly about that. We're going to study Veterans who have an existing abdominal aortic aneurysm that measures at least 5.0 cm in diameter that are anatomic and physiologic candidates
for open and endovascular repair. At ten control sites, the Veterans will take a simple survey and have their vascular surgery consultation. And simple surveys for their surgeons will follow thereafter. At 10 intervention sites, the process is identical
with the exception of an introduction of a decision aid. This decision aid was designed in England by Roger Greenhall, Jana Paul and others as part of the Picker Institute and provides a balanced view of the advantages and disadvantages of
both open and endovascular repair. We then followed the Veterans for two years to see what happens when the repair ultimately occurs and our main outcome measure was whether or not they preferred aneurysm repair type turned out to be their actual repair type.
We had performed this study, and I'm very grateful to my colleagues across the country at the 20 sites who are going to perform this trial. We began enrollment a little over a year ago. We're going to enroll 240 patients, I hope. We've enrolled 181 patients thus far,
so we're about 3/4 of the way there. And many of our sites, especially those in Gainesville, Ann Arbor, Buffalo, Salt Lake City, Tampa, Tucson, Pittsburgh and others have either completed their enrollments or are close to doing them. And while our objectives are to answer
these two study questions, I can't do that quite just yet. But we can examine the information sources that Veterans have used thus far when facing this decision. We asked Veterans questions like who have you talked to about if the surgical treatment options available to you if you needed an operation?
52% of our study participants thus far said they didn't talk to anybody. They didn't talk to their PCP at all about their AAA repair options. We asked them who their main source of information was about open surgical repair and again 41% of patients
reported having no information at all about open surgical repair of AAA and while only one in five cited a primary care physician as their main source of information. We asked the Veterans the same question about endovascular repair.
Again, 40% of patients received no information about EVAR, 17% got information from their primary care physician, about 10% of patients, a number lower than we expected, used the internet. Finally, we asked patients, has your view of the different surgical treatment options available been influenced
by anybody in your, among your medical advisors. 50% of patients reported that their view had not been influenced by anyone. We felt this led us be safe to conclude that while our future work will report the actual preferences for repair types
and the effects of this decision support, we found that half the patients with abdominal aortic aneurysm meeting criteria for repair had not yet discussed their treatment methods with anyone prior to meeting with a vascular surgeon. I believe this shows that the burden of explanation
for patients facing abdominal aortic aneurysm repair rests squarely on the shoulders of those of us in the vascular community. Thank you.
- Thank you very much, Frank, ladies and gentlemen. Thank you, Mr. Chairman. I have no disclosure. Standard carotid endarterectomy patch-plasty and eversion remain the gold standard of treatment of symptomatic and asymptomatic patient with significant stenosis. One important lesson we learn in the last 50 years
of trial and tribulation is the majority of perioperative and post-perioperative stroke are related to technical imperfection rather than clamping ischemia. And so the importance of the technical accuracy of doing the endarterectomy. In ideal world the endarterectomy shouldn't be (mumbling).
It should contain embolic material. Shouldn't be too thin. While this is feasible in the majority of the patient, we know that when in clinical practice some patient with long plaque or transmural lesion, or when we're operating a lesion post-radiation,
it could be very challenging. Carotid bypass, very popular in the '80s, has been advocated as an alternative of carotid endarterectomy, and it doesn't matter if you use a vein or a PTFE graft. The result are quite durable. (mumbling) showing this in 198 consecutive cases
that the patency, primary patency rate was 97.9% in 10 years, so is quite a durable procedure. Nowadays we are treating carotid lesion with stinting, and the stinting has been also advocated as a complementary treatment, but not for a bail out, but immediately after a completion study where it
was unsatisfactory. Gore hybrid graft has been introduced in the market five years ago, and it was the natural evolution of the vortec technique that (mumbling) published a few years before, and it's a technique of a non-suture anastomosis.
And this basically a heparin-bounded bypass with the Nitinol section then expand. At King's we are very busy at the center, but we did 40 bypass for bail out procedure. The technique with the Gore hybrid graft is quite stressful where the constrained natural stint is inserted
inside internal carotid artery. It's got the same size of a (mumbling) shunt, and then the plumbing line is pulled, and than anastomosis is done. The proximal anastomosis is performed in the usual fashion with six (mumbling), and the (mumbling) was reimplanted
selectively. This one is what look like in the real life the patient with the personal degradation, the carotid hybrid bypass inserted and the external carotid artery were implanted. Initially we very, very enthusiastic, so we did the first cases with excellent result.
In total since November 19, 2014 we perform 19 procedure. All the patient would follow up with duplex scan and the CT angiogram post operation. During the follow up four cases block. The last two were really the two very high degree stenosis. And the common denominator was that all the patients
stop one of the dual anti-platelet treatment. They were stenosis wise around 40%, but only 13% the significant one. This one is one of the patient that developed significant stenosis after two years, and you can see in the typical position at the end of the stint.
This one is another patient who develop a quite high stenosis at proximal end. Our patency rate is much lower than the one report by Rico. So in conclusion, ladies and gentlemen, the carotid endarterectomy remain still the gold standard,
and (mumbling) carotid is usually an afterthought. Carotid bypass is a durable procedure. It should be in the repertoire of every vascular surgeon undertaking carotid endarterectomy. Gore hybrid was a promising technology because unfortunate it's been just not produced by Gore anymore,
and unfortunately it carried quite high rate of restenosis that probably we should start to treat it in the future. Thank you very much for your attention.
- Thank you very much and I would like to thank Dr. Veit for the kind invitation, this is really great meeting. Those are my disclosures. Percutaneous EVAR has been first reported in the late 1990's. However, for many reasons it has not been embraced
by the vascular community, despite the fact that it has been shown that the procedure can be done under local anesthesia and it decreases OR time, time to ambulation, wound complication and length of stay. There are three landmark papers which actually change this trend and make PEVAR more popular.
All of these three papers concluded that failure or observed failure of PEVAR are observed and addressed in the OR which is a key issue. And there was no late failures. Another paper which is really very prominent
is a prospective randomize study that's reported by Endologix and published in 2014. Which revealed that PEVAR closure of the arteriotomy is not inferior to open cut down. Basically, this paper also made it possible for the FDA to approve the device, the ProGlide device,
for closure of large bore arteriotomies, up to 26 in the arterial system and 29 in the venous system. We introduced percutaneous access first policy in our institution 2012. And recently we analyzed our results of 272 elective EVAR performed during the 2012 to 2016.
And we attempted PEVAR in 206 cases. And were successful in 92% of cases. But the question was what happened with the patient that failed PEVAR? And what we found that was significantly higher thrombosis, vessel thrombosis,
as well as blood loss, more than 500 cc in the failed PEVAR group. Similarly, there was longer operative time and post-operative length of stay was significantly longer. However, in this relatively small group of patients who we scheduled for cut-down due to different reasons,
we found that actually there was no difference between the PEVAR and the cut-down, failed PEVAR and cut-down in the terms of blood loss, thrombosis of the vessel, operative time and post-operative length of stay. So what are the predictors of ProGlide failure?
Small vessel calcification, particularly anterior wall calcification, prior cut-down and scarring of the groin, high femoral bifurcation and use of large bore sheaths, as well as morbid obesity. So how can we avoid failures?
I think that the key issue is access. So we recommend that all access now or we demand from our fellow that when we're going to do the operation with them, cut-down during fluoroscopy on the ultra-sound guidance, using micropuncture kits and access angiogram is actually mandatory.
But what happened when there is a lack of hemostasis once we've deployed two PEVARs? Number one, we try not to use more than three ProGlide on each side. Once the three ProGlide failed we use the angioseal. There's a new technique that we can have body wire
and deployed angioseal and still have an access. We also developed a technique that we pack the access site routinely with gelfoam and thrombin. And also we use so-called pull and clamp technique, shown here. Basically what it is, we pull the string of the ProGlide
and clamp it on the skin level. This is actually a very very very good technique. So in conclusion, PEVAR first approach strategy successful in more than 90% of cases, reduced operative time and postoperative length of stay, the failure occurred more commonly when the PEVAR
was completed outside of IFU, and there was no differences in outcome between failed PEVAR and planned femoral cut-down. Thank you.
- Thank you and thanks Craig, it's fun to have these debates with good colleagues, thoughtful colleagues. These are my disclosures for the talk. But pry my most important disclosure is I work in academic center with a dedicated Limb Preservation Center, very tertiary practice. And I perform both open and endovascular surgery
and actually my current lower extremity practice is probably about 60 to 65 percent endovascular so, I do both of these procedures. We already saw this slide about how the increase in endovascular intervention has grown. But, I would caution you to look a little more closely
at this outpace of decline in bypass surgery by more than three to one. I don't think this is an epidemic, I think it's a little bit of this, and a little bit of this. Everything looks like a nail when you only have a hammer
or a hammer when you only have a nail. So, what should we really be doing today? We should be trying to select the best thing for the right patient at the right time. And it really comes down to starting not with the lesion, but with the patient.
Start with assessing the patient's risk, what's their perioperative risk, what's their long-term survival, what are their goals for care? And then look at the limb itself, because not all limbs are the same.
There are minor ulcers, there's extensive and severe rest pain and there are large areas of tissue loss. And the WIfI system is good for that. And then let's look at the anatomy last. And when we're looking at it from the standpoint of what all the options are, endovascular we're looking
at what's the likelihood not just of technical success, but of hemodynamic gain and sustained patency for as long as a patient needs it. With bypass, we also have to look at other things. What kind of vein do they have, or what kind of target do they have?
And I think the bottom line here is in today's practice, it's kind of silly to say endo first for all patients, it's certainly not surgery first for all patients because they have complementary roles in contemporary practice. Well what's happening in the world out there,
this is the German CRITISCH registry, I'll just point out 12 hundred patients recently published only a couple of years ago, 24 percent of patients get bypass first. And if you look at who they are, not surprisingly they are the patients
with long occlusions and complex anatomy. They are out there, in fact most of these patients have multi-segment disease, as Craig pointed out. Here's some contemporary data that you haven't seen yet because it's in press, but this is VQI data looking at 2003 to 2017.
I'll point out just in the last 2013 years, still, if you looked at unique patients, not procedures, one-third of the patients are getting a bypass first. And if you define risk groups considering what might be a low risk patient as a three percent mortality and survival greater than 70 percent,
and a high risk patient, you can put these patients into buckets and in fact, of all the patients getting lower extremity revascularization and VQI today, 80 percent of them would be called low risk based on this definition. So, most patients are not high risk patients
who don't have long-term survival. In fact, this is current VQI data. If you're a low risk patient in that cohort, your five year survival actually is over 70 percent. So there's a lot of these patients actually today with better CLO medical therapy that are actually
living longer and are not that high risk. We talked about the BASIL trial already, and he pointed out how the early results were similar, but what we learned also with BASIL, that if you've got a bypass as a secondary procedure, or if you got a bypass with a prosthetic,
you simply did not do as well. That doesn't mean that the initial endovascular revascularization caused the bypass failure, but it means that secondary bypass surgery does not work as well. And when Dr. Bradbury looked at this data
over a longer period of time now going over many more years, there's a consistent inferior outcome to the patients who had their bypass after failed angioplasty in comparison to bypass as the initial strategy. This is not an isolated finding. When we looked in the VSGNE data over a,
more than 3000 patients at the impact of restenosis on subsequent treatment failure, we found that whether patients had a failed previous PVI or bypass, their secondary bypass outcomes were inferior, and the inferiority continued to get worse with time.
These bypasses just don't perform as well. Unfortunately, if we only do bypass after endo has failed, this is what all the results are going to start to look like. So let's be a little bit smarter. Now what about patency?
I think we, even today in the endovascular world, we realize patency is important. After all, that's why we're doing drug elution. Most, but not all patients with advanced limb ischemia will recrudesce their symptoms when their revascularization fails.
I think we all know that. Most CLTI patients have multi-segment disease. I don't want to sit up here and be a high school or elementary school math teacher, but here's the reality. If you look at it above the lesion, you say I'm going to get 70 percent patency there, and you look at
the tibial lesion, you say I'm going to get 50 percent patency there, what do you think your patency is for the whole leg? It's 35 percent folks, it's the product of the two. That is the reality pretty often. Patients with more advanced limb presentations,
such as WIfI stage do not tolerate these failures. They tolerate them poorly. They go on to amputation pretty fast. And patient survival, as I've already shown you has improved. Now, what the all endo-all the time
camp does and doesn't say. He already showed us, many datasets suggest the downstream outcomes are roughly equivalent but, these are not the same patients, we are not operating on the same patients you are doing endo on.
If I told you the results are the same for PCI and CABG without showing you anatomy, you would laugh me off the stage right? So, this is really not an equivalent argument. Endo can be repeated with minimal morbidity, but patients suffer.
Their limb status deteriorates, they come in the hospital often, and they continue to decline in the outcomes of these secondary procedures. CLTI patients are too frail for surgery, I just showed you that's really not true for many patients.
There is really unfortunately, an economic incentive here. Because there is unfortunately, no incentive for durable success. I hate to bring that up, but that's the reality. Now just quickly, some results. This is a large Japanese series
where they were performing endovascular interventions only for advanced limb ischemia. And basically what you can see as you go across the WIfI stages here from stage one to stage four, when you get to these stage four patients, the wound healing rate's only 44 percent,
limb salvage rate drops to 80 percent, repeat EVT rate is encroaching 50 percent. These patients really are not doing well with endovascular intervention. And we found that in our own series too, it's relatively small numbers and not randomized.
But if we look at the stage 4 limbs with bypass versus endo, when these patients failed at revascularization, and they may not have been bypass candidates, but they didn't do well, they went on to amputation very quickly.
So the ESC guidelines that just came out really sort of line up with what I'm telling you. You'll see bypass first. If you have long occlusions in an available vein, is actually currently the favorite approach, with level 1A recommendation.
So in summary, this is how I currently approach it. You look at all these factors, some people should get endo first, but there's still about 20 or 30 percent that I think should get bypass. Some people should go on to amputation earlier, is the bottom line, and I'll go right to the bottom line.
If you don't have access to a skilled open bypass surgeon, you're probably not at a center of excellence, go find one.
- Good morning, thank you, Dr. Veith, for the invitation. My disclosures. So, renal artery anomalies, fairly rare. Renal ectopia and fusion, leading to horseshoe kidneys or pelvic kidneys, are fairly rare, in less than one percent of the population. Renal transplants, that is patients with existing
renal transplants who develop aneurysms, clearly these are patients who are 10 to 20 or more years beyond their initial transplantation, or maybe an increasing number of patients that are developing aneurysms and are treated. All of these involve a renal artery origin that is
near the aortic bifurcation or into the iliac arteries, making potential repair options limited. So this is a personal, clinical series, over an eight year span, when I was at the University of South Florida & Tampa, that's 18 patients, nine renal transplants, six congenital
pelvic kidneys, three horseshoe kidneys, with varied aorto-iliac aneurysmal pathologies, it leaves half of these patients have iliac artery pathologies on top of their aortic aneurysms, or in place of the making repair options fairly difficult. Over half of the patients had renal insufficiency
and renal protective maneuvers were used in all patients in this trial with those measures listed on the slide. All of these were elective cases, all were technically successful, with a fair amount of followup afterward. The reconstruction priorities or goals of the operation are to maintain blood flow to that atypical kidney,
except in circumstances where there were multiple renal arteries, and then a small accessory renal artery would be covered with a potential endovascular solution, and to exclude the aneurysms with adequate fixation lengths. So, in this experience, we were able, I was able to treat eight of the 18 patients with a fairly straightforward
endovascular solution, aorto-biiliac or aorto-aortic endografts. There were four patients all requiring open reconstructions without any obvious endovascular or hybrid options, but I'd like to focus on these hybrid options, several of these, an endohybrid approach using aorto-iliac
endografts, cross femoral bypass in some form of iliac embolization with an attempt to try to maintain flow to hypogastric arteries and maintain antegrade flow into that pelvic atypical renal artery, and a open hybrid approach where a renal artery can be transposed, and endografting a solution can be utilized.
The overall outcomes, fairly poor survival of these patients with a 50% survival at approximately two years, but there were no aortic related mortalities, all the renal artery reconstructions were patented last followup by Duplex or CT imaging. No aneurysms ruptures or aortic reinterventions or open
conversions were needed. So, focus specifically in a treatment algorithm, here in this complex group of patients, I think if the atypical renal artery comes off distal aorta, you have several treatment options. Most of these are going to be open, but if it is a small
accessory with multiple renal arteries, such as in certain cases of horseshoe kidneys, you may be able to get away with an endovascular approach with coverage of those small accessory arteries, an open hybrid approach which we utilized in a single case in the series with open transposition through a limited
incision from the distal aorta down to the distal iliac, and then actually a fenestrated endovascular repair of his complex aneurysm. Finally, an open approach, where direct aorto-ilio-femoral reconstruction with a bypass and reimplantation of that renal artery was done,
but in the patients with atypical renals off the iliac segment, I think you utilizing these endohybrid options can come up with some creative solutions, and utilize, if there is some common iliac occlusive disease or aneurysmal disease, you can maintain antegrade flow into these renal arteries from the pelvis
and utilize cross femoral bypass and contralateral occlusions. So, good options with AUIs, with an endohybrid approach in these difficult patients. Thank you.
- These are my disclosures, as it pertains to this talk. FEVAR has become increasingly common treatment for juxtarenal aneurysm in the United States since it's commercial release in 2012. Controversy remains, however, with regard to stenting the SMA when it is treated with a single-wide, 10 mm scallop in the device.
You see here, things can look very similar. You see SMA treated with an unstented scallop on the left and one treated with the stented SMA on the right. It has been previously reported by Jason Lee that shuttering can happen with single-wide scallops of the SMA and in their experience
the SMA shuttering happens to different degree in patients, but is there in approximately 50% of the patients. But in his experience, the learning curve suggests that it decreases over time. At UNC, we use a selective criteria for stenting in the SMA. We will do a balloon test in the SMA,
as you see in the indication, and if the graft is not moved, then our SMA scallop is appropriate in line. If we have one scallop and one renal stent, its a high likelihood that SMA scallop will shift and change over time. So all those patients get stented.
If there is presence of pre-existing visceral stenosis we will stent the SMA through that scallop and in all of our plans, we generally place a 2 mm buffer, between the bottom edge of the scallop and the SMA. We looked over our results and 61 Zenith fenestrated devices performed over a short period of time.
We looked at the follow-up out up to 240 days and 40 patients in this group had at least one single wide scallop, which represented 2/3 of the group. Our most common configuration as in most practices is too small renal fenestrations and one SMA scallop.
Technically, devices were implanted in all patients. There were 27 patients that had scallops that were unstented. And 13 of the patients received stented scallops. Hospital mortality was one out of 40, from a ruptured hepatic artery aneurysm post-op.
No patients had aneurysm-related mortality to the intended treated aneurysm. If you look at this group, complications happen in one of the patients with stented SMA from a dissection which was treated with a bare metal stent extension at the time
of the initial procedure. And in the unstented patients, we had one patient with post-op nausea, elevated velocities, found to have shuttering of the graft and underwent subsequent stenting. The second patient had elevated velocities
and 20-pound weight loss at a year after his treatment, but was otherwise asymptomatic. There is no significant difference between these two groups with respect to complication risk. Dr. Veith in the group asked me to talk about stenting choice
In general, we use the atrium stent and a self-expanding stent for extension when needed and a fenestrated component. But, we have no data on how we treat the scallops. Most of those in our group are treated with atrium. We do not use VBX in our fenestrated cases
due to some concern about the seal around the supported fenestration. So Tips, we generally calculate the distance to the first branch of the SMA if we're going to stent it. We need to know the SMA diameter, generally its origin where its the largest.
We need to position the imaging intensifier orthogonal position. And we placed the stent 5-6 mm into the aortic lumen. And subsequently flare it to a 10-12 mm balloon. Many times if its a longer stent than 22, we will extend that SMA stent with a self-expanding stent.
So in conclusion, selective stenting of visceral vessels in single wide scallops is safe in fenestrated cases during this short and midterm follow-up if patients are carefully monitored. Stenting all single wide scallops is not without risk and further validation is needed
with multi-institution trial and longer follow-up
- Thank you very much for the opportunity to speak carbon dioxide angiography, which is one of my favorite topics and today I will like to talk to you about the value of CO2 angiography for abdominal and pelvic trauma and why and how to use carbon dioxide angiography with massive bleeding and when to supplement CO2 with iodinated contrast.
Disclosures, none. The value of CO2 angiography, what are the advantages perhaps? Carbon dioxide is non-allergic and non-nephrotoxic contrast agent, meaning CO2 is the only proven safe contrast in patients with a contrast allergy and the renal failure.
Carbon dioxide is very highly soluble (20 to 30 times more soluble than oxygen). It's very low viscosity, which is a very unique physical property that you can take advantage of it in doing angiography and CO2 is 1/400 iodinated contrast in viscosity.
Because of low viscosity, now we can use smaller catheter, like a micro-catheter, coaxially to the angiogram using end hole catheter. You do not need five hole catheter such as Pigtail. Also, because of low viscosity, you can detect bleeding much more efficiently.
It demonstrates to the aneurysm and arteriovenous fistula. The other interesting part of the CO2 when you inject in the vessel the CO2 basically refluxes back so you can see the more central vessel. In other words, when you inject contrast, you see only forward vessel, whereas when you inject CO2,
you do a pass with not only peripheral vessels and also see more central vessels. So basically you see the vessels around the lesions and you can use unlimited volumes of CO2 if you separate two to three minutes because CO2 is exhaled by the respirations
so basically you can inject large volumes particularly when you have long prolonged procedures, and most importantly, CO2 is very inexpensive. Where there are basically two methods that will deliver CO2. One is the plastic bag system which you basically fill up with a CO2 tank three times and then empty three times
and keep the fourth time and then you connect to the delivery system and basically closest inject for DSA. The other devices, the CO2mmander with the angio assist, which I saw in the booth outside. That's FDA approved for CO2 injections and is very convenient to use.
It's called CO2mmander. So, most of the CO2 angios can be done with end hole catheter. So basically you eliminate the need for pigtail. You can use any of these cobra catheters, shepherd hook and the Simmons.
If you look at this image in the Levitor study with vascular model, when you inject end hole catheter when the CO2 exits from the tip of catheter, it forms very homogenous bolus, displaces the blood because you're imaging the blood vessel by displacing blood with contrast is mixed with blood, therefore as CO2
travels distally it maintains the CO2 density whereas contrast dilutes and lose the densities. So we recommend end hole catheter. So that means you can do an arteriogram with end hole catheter and then do a select arteriogram. You don't need to replace the pigtail
for selective injection following your aortographies. Here's the basic techniques: Now when you do CO2 angiogram, trauma patient, abdominal/pelvic traumas, start with CO2 aortography. You'll be surprised, you'll see many of those bleeding on aortogram, and also you can repeat, if necessary,
with CO2 at the multiple different levels like, celiac, renal, or aortic bifurcation but be sure to inject below diaphragm. Do not go above diaphragm, for example, thoracic aorta coronary, and brachial, and the subclavian if you inject CO2, you'll have some serious problems.
So stay below the diaphragm as an arterial contrast. Selective injection iodinated contrast for a road map. We like to do super selective arteriogram for embolization et cetera. Then use a contrast to get anomalies. Super selective injection with iodinated contrast
before embolization if there's no bleeding then repeat with CO2 because of low viscocity and also explosion of the gas you will often see the bleeding. That makes it more comfortable before embolization. Here is a splenic trauma patient.
CO2 is injected into the aorta at the level of the celiac access. Now you see the extra vascularization from the low polar spleen, then you catheterize celiac access of the veins. You microcatheter in the distal splenic arteries
and inject the contrast. Oops, there's no bleeding. Make you very uncomfortable for embolizations. We always like to see the actual vascularization before place particle or coils. At that time you can inject CO2 and you can see
actual vascularization and make you more comfortable before embolization. You can inject CO2, the selective injection like in here in a patient with the splenic trauma. The celiac injection of CO2 shows the growth, laceration splenic with extra vascularization with the gas.
There's multiple small, little collection. We call this Starry Night by Van Gogh. That means malpighian marginal sinus with stagnation with the CO2 gives multiple globular appearance of the stars called Starry Night.
You can see the early filling of the portal vein because of disruption of the intrasplenic microvascular structures. Now you see the splenic vein. Normally, you shouldn't see splenic vein while following CO2 injections.
This is a case of the liver traumas. Because the liver is a little more anterior the celiac that is coming off of the anterior aspect of the aorta, therefore, CO2 likes to go there because of buoyancy so we take advantage of buoyancy. Now you see the rupture here in this liver
with following the aortic injections then you inject contrast in the celiac axis to get road map so you can travel through this torus anatomy for embolizations for the road map for with contrast. This patient with elaston loss
with ruptured venal arteries, massive bleeding from many renal rupture with retro peritoneal bleeding with CO2 and aortic injection and then you inject contrast into renal artery and coil embolization but I think the stent is very dangerous in a patient with elaston loss.
We want to really separate the renal artery. Then you're basically at the mercy of the bleeding. So we like a very soft coil but basically coil the entire renal arteries. That was done. - Thank you very much.
- Time is over already? - Yeah. - Oh, OK. Let's finish up. Arteriogram and we inject CO2 contrast twice. Here's the final conclusions.
CO2 is a valuable imaging modality for abdominal and pelvic trauma. Start with CO2 aortography, if indicated. Repeat injections at multiple levels below diaphragm and selective injection road map with contrast. The last advice fo
t air contamination during the CO2 angiograms. Thank you.
- Thank you, Dr. Ouriel, Dr. Lurie. Ladies and gentlemen. Brian, that was a very fair overview of the ATTRACT trial as it was published in the New England Journal, so thank you. And these are my disclosures. So Dr. DeRubertis did a very nice review of this paper
that was published in the New England Journal December 7th of last year. He went over very nicely that it was NIH sponsored, phase III, randomized, controlled, multicenter, 692 patients randomized, anticoagulation alone versus anticoagulation plus catheter-based techniques.
Now one thing I want to call your attention to is the fact that patients with deep venous thrombosis, acute deep venous thrombosis, who were eligible for randomization, were stratified before they were randomized into two different groups, iliofemoral DVT or fem-pop DVT.
So in my opinion, these are not subgroups because the randomization of one group had no effect on the randomization of another, so I would argue that these are independent groups. That makes a big difference when you do statistical analyses.
The other important issue that I want to point out is that the outcomes were pre-determined to what we were going to analyze. We had to choose one as a primary endpoint and the others as secondary, but these were pre-determined end points that were up for analysis, not post hoc analyses.
And post-thrombotic syndrome was determined at the time, 12 years ago when we wrote the protocol, to be the primary end point. I would submit that we would not choose that as a primary end point if we wrote the protocol today. Moderate to severe post-thrombotic syndrome
certainly would be more appropriate. Leg pain, swelling, health-related quality of life, certainly important. This is the outcome, and unfortunately, it did not reach significance. There was no difference between the two groups
and there was an increased risk of bleeding, but this is the outcome that drove opinion about ATTRACT, but we don't really do catheter-directed thrombolysis for fem-pop DVT. Therefore, the results of the iliofemoral patients will be the most meaningful and that paper was written
and that paper has been accepted by circulation. It should be out shortly, but there were 391 iliofemoral DVT patients and the primary outcome was no different than the primary outcome in the overall trial. But are they?
If we had chosen the Venous Clinical Severity Score in place of the Villalta score for analysis of that primary end point, it would've been a positive study. So if we chose a different tool to analyze, our primary end point would've been positive for the iliofemoral DVT patients.
If we look at moderate to severe post-thrombotic syndrome, a significant difference. Control patients had a 56% increased risk of moderate to severe PTS versus the control patients. If we look at severe post-thrombotic syndrome, control patients had a 72% increased risk
of severe PTS versus control. If we look at the overall severity of the Villalta score in PTS, we can see that there is a significant difference favoring percutaneous catheter-directed thrombolysis. When we look at pain, the patient's pain was significantly reduced in the PCDT patients compared to control.
We look at edema, significant reduction in edema at day 10 and day 30 in patients who received catheter-directed thrombolysis compared to control. Disease-specific quality of life significantly favored patients who had PCDT compared to control. So we look at moderate to severe, severe, pain,
quality of life. There was a price to pay. Major bleeding was increased, but the P-value was no different. I will not argue that patients are not at increased risk. They are at increased risk for bleeding,
but this is an historically low bleeding rate for catheter-directed thrombolysis and there were no intracranial bleeds. No difference in recurrent deep venous thrombosis. No difference in mortality at 24 months between the two groups.
So in conclusion, the primary end point, reduction of any PTS defined by a Villalta score of 5 or more, no difference, but an item that has not reached the level of discussion that we will need to consider is that 14% of our patients had a normal Villalta score coming into the study.
It's impossible to improve upon that, but there is a significant reduction in any PTS if you use the Venous Clinical Severity Score, reduction of moderate and severe post-thrombotic syndrome, reduction of pain and swelling, and improved disease-specific quality of life compared to controls.
And I think these are the meaningful end points that patients appreciate and these are the points of discussion that will be covered in the article in circulation that will be published very soon. Thank you for your attention.
- Dear Chairman, Ladies and Gentlemen, Thank you Doctor Veith. It's a privilege to be here. So, the story is going to be about Negative Pressure Wound Non-Excisional Treatment from Prosthetic Graft Infection, and to show you that the good results are durable. Nothing to disclose.
Case demonstration: sixty-two year old male with fem-fem crossover PTFE bypass graft, Key infection in the right groin. What we did: open the groin to make the debridement and we see the silergy treat, because the graft is infected with the microbiology specimen
and when identified, the Enterococcus faecalis, Staphylococcus epidermidis. We assess the anastomosis in the graft was good so we decided to put foam, black foam for irrigation, for local installation of antiseptics. This our intention-to treat protocol
at the University hospital, Zurich. Multi-staged Negative Pressure for the Wound Therapy, that's meets vascular graft infection, when we open the wound and we assess the graft, and the vessel anastomosis, if they are at risk or not. If they are not at risk, then we preserve the graft.
If they are at risk and the parts there at risk, we remove these parts and make a local reconstruction. And this is known as Szilagyi and Samson classification, are mainly validated from the peripheral surgery. And it is implemented in 2016 guidelines of American Heart Association.
But what about intracavitary abdominal and thoracic infection? Then other case, sixty-one year old male with intracavitary abdominal infection after EVAR, as you can see, the enhancement behind the aortic wall. What we are doing in that situation,
We're going directly to the procedure that's just making some punctures, CT guided. When we get the specimen microbiological, then start with treatment according to the microbiology findings, and then we downgrade the infection.
You can see the more air in the aneurism, but less infection periaortic, then we schedule the procedure, opening the aneurysm sac, making the complete removal of the thrombus, removing of the infected part of the aneurysm, as Doctor Maelyna said, we try to preserve the graft.
That exactly what we are doing with the white foam and then putting the black foam making the Biofilm breakdown with local installation of antiseptics. In some of these cases we hope it is going to work, and, as you see, after one month
we did not have a good response. The tissue was uneager, so we decided to make the removal of the graft, but, of course, after downgrading of this infection. So, we looked at our data, because from 2012 all the patients with
Prostetic Graft infection we include in the prospective observational cohort, known VASGRA, when we are working into disciplinary with infectious disease specialist, microbiologists, radiologist and surgical pathologist. The study included two group of patients,
One, retrospective, 93 patient from 1999 to 2012, when we started the VASGRA study. And 88 patient from April 2012 to Seventeen within this register. Definitions. Baseline, end of the surgical treatment and outcome end,
the end of microbiological therapy. In total, 181 patient extracavitary, 35, most of them in the groin. Intracavitary abdominal, 102. Intracavitary thoracic, 44. If we are looking in these two groups,
straight with Negative Pressure Wound Therapy and, no, without Negative Pressure Wound Therapy, there is no difference between the groups in the male gender, obesity, comorbidity index, use of endovascular graft in the type Samson classification,
according to classification. The only difference was the ratio of hospitalization. And the most important slide, when we show that we have the trend to faster cure with vascular graft infection in patients with Negative Pressure Wound Therapy
If we want to see exactly in the data we make uni variant, multi variant analysis, as in the initial was the intracavitary abdominal. Initial baseline. We compared all these to these data. Intracavitary abdominal with no Pressure Wound Therapy
and total graft excision. And what we found, that Endovascular indexoperation is not in favor for faster time of cure, but extracavitary Negative Pressure Wound Therapy shows excellent results in sense of preserving and not treating the graft infection.
Having these results faster to cure, we looked for the all cause mortality and the vascular graft infection mortality up to two years, and we did not have found any difference. What is the strength of this study, in total we have two years follow of 87 patients.
So, to conclude, dear Chairman, Ladies and Gentlemen, Explant after downgrading giving better results. Instillation for biofilm breakdown, low mortality, good quality of life and, of course, Endovascular vascular graft infection lower time to heal. Thank you very much for your attention.
- Thank you. Historically, common femoral endarterectomy is a safe procedure. In this quick publication that we did several years ago, showed a 1.5% 30 day mortality rate. Morbidity included 6.3% superficial surgical site infection.
Other major morbidity was pretty low. High-risk patients we identified as those that were functionally dependent, dyspnea, obesity, steroid use, and diabetes. A study from Massachusetts General Hospital their experience showed 100% technical success.
Length of stay was three days. Primary patency of five years at 91% and assisted primary patency at five years 100%. Very little perioperative morbidity and mortality. As you know, open treatment has been the standard of care
over time the goal standard for a common femoral disease, traditionally it's been thought of as a no stent zone. However, there are increased interventions of the common femoral and deep femoral arteries. This is a picture that shows inflection point there.
Why people are concerned about placing stents there. Here's a picture of atherectomy. Irritational atherectomy, the common femoral artery. Here's another image example of a rotational atherectomy, of the common femoral artery.
And here's an image of a stent there, going across the stent there. This is a case I had of potential option for stenting the common femoral artery large (mumbles) of the hematoma from the cardiologist. It was easily fixed
with a 2.5 length BioBond. Which I thought would have very little deformability. (mumbles) was so short in the area there. This is another example of a complete blow out of the common femoral artery. Something that was much better
treated with a stent that I thought over here. What's the data on the stenting of the endovascular of the common femoral arteries interventions? So, there mostly small single centers. What is the retrospective view of 40 cases?
That shows a restenosis rate of 19.5% at 12 months. Revascularization 14.1 % at 12 months. Another one by Dr. Mehta shows restenosis was observed in 20% of the patients and 10% underwent open revision. A case from Dr. Calligaro using cover stents
shows very good primary patency. We sought to use Vascular Quality Initiative to look at endovascular intervention of the common femoral artery. As you can see here, we've identified a thousand patients that have common femoral interventions, with or without,
deep femoral artery interventions. Indications were mostly for claudication. Interventions include three-quarters having angioplasty, 35% having a stent, and 20% almost having atherectomy. Overall technical success was high, a 91%.
Thirty day mortality was exactly the same as in this clip data for open repair 1.6%. Complications were mostly access site hematoma with a low amount distal embolization had previously reported. Single center was up to 4%.
Overall, our freedom for patency or loss or death was 83% at one year. Predicted mostly by tissue loss and case urgency. Re-intervention free survival was 85% at one year, which does notably include stent as independent risk factor for this.
Amputation free survival was 93% at one year, which factors here, but also stent was predictive of amputation. Overall, we concluded that patency is lower than historical common femoral interventions. Mortality was pretty much exactly the same
that has been reported previously. And long term analysis is needed to access durability. There's also a study from France looking at randomizing stenting versus open repair of the common femoral artery. And who needs to get through it quickly?
More or less it showed no difference in outcomes. No different in AVIs. Higher morbidity in the open group most (mumbles) superficial surgical wound infections and (mumbles). The one thing that has hit in the text of the article
a group of mostly (mumbles) was one patient had a major amputation despite having a patent common femoral artery stent. There's no real follow up this, no details of this, I would just caution of both this and VQI paper showing increased risk amputation with stenting.
- Good morning, I would like to thank Dr. Veith, and the co-chairs for inviting me to talk. I have nothing to disclose. Some background on this information, patients with Inflammatory Bowel Disease are at least three times more likely to suffer a thrombo-embolic event, when compared to the general population.
The incidence is 0.1 - 0.5% per year. Overall mortality associated with these events can be as high as 25%, and postmortem exams reveal an incidence of 39-41% indicating that systemic thrombo-embolism is probably underdiagnosed. Thrombosis mainly occurs during disease exacerbation,
however proctocolectomy has not been shown to be preventative. Etiology behind this is not well known, but it's thought to be multifactorial. Including decrease in fibrinolytic activity, increase in platelet activation,
defects in the protein C pathway. Dyslipidemia and long term inflammation also puts patients at risk for an increase in atherosclerosis. In addition, these patients lack vitamins, are often dehydrated, anemic, and at times immobilized. Traditionally, the venous thrombosis is thought
to be more common, however recent retrospective review of the Health Care Utilization Project nationwide inpatient sample database, reported not only an increase in the incidence but that arterial complications may happen more frequently than venous.
I was going to present four patients over the course of one year, that were treated at my institution. The first patient is 25 year old female with Crohn's disease, who had a transverse colectomy one year prior to presentation. Presented with right flank pain, she was found to have
right sided PE, a right sided pulmonary vein thrombosis and a left atrial thrombosis. She was admitted for IV heparin, four days later she had developed abdominal pains, underwent an abdominal CTA significant for SMA occlusion prompting an SMA thrombectomy.
This is a picture of her CAT scan showing the right PE, the right pulmonary vein thrombosis extending into the left atrium. The SMA defect. She returned to the OR for second and third looks, underwent a subtotal colectomy,
small bowel resection with end ileostomy during the third operation. She had her heparin held post-operatively due to significant post-op bleeding, and over the next three to five days she got significantly worse, developed progressive fevers increase found to have
SMA re-thrombosis, which you can see here on her CAT scan. She ended up going back to the operating room and having the majority of her small bowel removed, and went on to be transferred to an outside facility for bowel transplant. Our second patient is a 59 year old female who presented
five days a recent flare of ulcerative colitis. She presented with right lower extremity pain and numbness times one day. She was found to have acute limb ischemia, category three. An attempt was made at open revascularization with thrombectomy, however the pedal vessels were occluded.
The leg was significantly ischemic and flow could not be re-established despite multiple attempts at cut-downs at different levels. You can see her angiogram here at the end of the case. She subsequently went on to have a below knee amputation, and her hospital course was complicated by
a colonic perforation due to the colitis not responding to conservative measures. She underwent a subtotal colectomy and end ileostomy. Just in the interest of time we'll skip past the second, third, and fourth patients here. These patients represent catastrophic complications of
atypical thrombo-embolic events occurring in IBD flares. Patients with inflammatory disease are at an increased risk for both arterial and venous thrombotic complications. So the questions to be answered: are the current recommendations adequate? Currently heparin prophylaxis is recommended for
inpatients hospitalized for severe disease. And, if this is not adequate, what treatments should we recommend, the medication choice, and the duration of treatment? These arterial and venous complications occurring in the visceral and peripheral arteries
are likely underappreciated clinically as a risk for patients with IBD flares and they demonstrate a need to look at further indications for thrombo-prophylaxis. Thank you.
- Thank you, and thank you Dr. Veith for the opportunity to present. So, acute aortic syndromes are difficult to treat and a challenge for any surgeon. In regionalization of care of acute aortic syndromes is now a topic of significant conversation. The thoughts are that you can move these patients
to an appropriate hospital infrastructure with surgical expertise and a team that's familiar with treating them. Higher volumes, better outcomes. It's a proven concept in trauma care. Logistics of time, distance, transfer mortality,
and cost are issues of concern. This is a study from the Nationwide Inpatient Sample which basically demonstrates the more volume, the lower mortality for ruptured abdominal aortic aneurysms. And this is a study from Clem Darling
and his Albany Group demonstrating that with their large practice, that if they could get patients transferred to their central hospital, that they had a higher incidence of EVAR with lower mortality. Basically, transfer equaled more EVARs and a
lower mortality for ruptured abdominal aortic aneurysms. Matt Mell looked at interfacility transfer mortality in patients with ruptured abdominal aortic aneurysms to try to see if actually, transfer improved mortality. The take home message was, operative transferred patients
did do better once they reached the institution of destination, however they had a significant mortality during transfer that basically negated that benefit. And transport time, interestingly did not affect mortality. So, regional aortic management, I think,
is something that is quite valuable. As mentioned, access to specialized centers decrease overall mortality and morbidity potentially. In transfer mortality a factor, transport time does not appear to be. So, we set up a rapid transport system
at Keck Medical Center. Basically predicated on 24/7 coverage, and we would transfer any patient within two hours to our institution that called our hotline. This is the number of transfers that we've had over the past three years.
About 250 acute aortic transfers at any given... On a year, about 20 to 30 a month. This is a study that we looked at, that transport process. 183 patients, this is early on in our experience. We did have two that expired en route. There's a listing of the various
pathologies that we treated. These patients were transferred from all over Southern California, including up to Central California, and we had one patient that came from Nevada. The overall mortality is listed here. Ruptured aortic aneurysms had the highest mortality.
We had a very, very good mortality with acute aortic dissections as you can see. We did a univariate and multivariate analysis to look at factors that might have affected transfer mortality and what we found was the SVS score greater than eight
had a very, very significant impact on overall mortality for patients that were transferred. What is a society for vascular surgery comorbidity score? It's basically an equation using cardiac pulmonary renal hypertension and age. The asterisks, cardiac, renal, and age
are important as I will show subsequently. So, Ben Starnes did a very elegant study that was just reported in the Journal of Vascular Surgery where he tried to create a preoperative risk score for prediction of mortality after ruptured abdominal aortic aneurysms.
He found four factors and did an ROC curve. Basically, age greater than 76, creatinine greater than two, blood pressure less than 70, or PH less than 7.2. As you can see, as those factors accumulated there was step-wise increased mortality up to 100% with four factors.
So, rapid transport to regional aortic centers does facilitate the care of acute aortic syndromes. Transfer mortality is a factor, however. Transport mode, time, distance are not associated with mortality. Decision making to deny and accept transfer is evolving
but I think renal status, age, physiologic insult are important factors that have been identified to determine whether transfer should be performed or not. Thank you very much.
- Thank you. I have two talks because Dr. Gaverde, I understand, is not well, so we- - [Man] Thank you very much. - We just merged the two talks. All right, it's a little joke. For today's talk we used fusion technology
to merge two talks on fusion technology. Hopefully the rest of the talk will be a little better than that. (laughs) I think we all know from doing endovascular aortic interventions
that you can be fooled by the 2D image and here's a real life view of how that can be an issue. I don't think I need to convince anyone in this room that 3D fusion imaging is essential for complex aortic work. Studies have clearly shown it decreases radiation,
it decreases fluoro time, and decreases contrast use, and I'll just point out that these data are derived from the standard mechanical based systems. And I'll be talking about a cloud-based system that's an alternative that has some advantages. So these traditional mechanical based 3D fusion images,
as I mentioned, do have some limitations. First of all, most of them require manual registration which can be cumbersome and time consuming. Think one big issue is the hardware based tracking system that they use. So they track the table rather than the patient
and certainly, as the table moves, and you move against the table, the patient is going to move relative to the table, and those images become unreliable. And then finally, the holy grail of all 3D fusion imaging is the distortion of pre-operative anatomy
by the wires and hardware that are introduced during the course of your procedure. And one thing I'd like to discuss is the possibility that deep machine learning might lead to a solution to these issues. How does 3D fusion, image-based 3D fusion work?
Well, you start, of course with your pre-operative CT dataset and then you create digitally reconstructed radiographs, which are derived from the pre-op CTA and these are images that resemble the fluoro image. And then tracking is done based on the identification
of two or more vertebral bodies and an automated algorithm matches the most appropriate DRR to the live fluoro image. Sounds like a lot of gobbledygook but let me explain how that works. So here is the AI machine learning,
matching what it recognizes as the vertebral bodies from the pre-operative CT scan to the fluoro image. And again, you get the CT plus the fluoro and then you can see the overlay with the green. And here's another version of that or view of that.
You can see the AI machine learning, identifying the vertebral bodies and then on your right you can see the fusion image. So just, once again, the AI recognizes the bony anatomy and it's going to register the CT with the fluoro image. It tracks the patient, not the table.
And the other thing that's really important is that it recognizes the postural change that the patient undergoes between the posture during the CT scan, versus the posture on the OR table usually, or often, under general anesthesia. And here is an image of the final overlay.
And you can see the visceral and renal arteries with orange circles to identify them. You can remove those, you can remove any of those if you like. This is the workflow. First thing you do is to upload the CT scan to the cloud.
Then, when you're ready to perform the procedure, that is downloaded onto the medical grade PC that's in your OR next to your fluoro screen, and as soon as you just step on the fluoro pedal, the CYDAR overlay appears next to your, or on top of your fluoro image,
next to your regular live fluoro image. And every time you move the table, the computer learning recognizes that the images change, and in a couple of seconds, it replaces with a new overlay based on the obliquity or table position that you have. There are some additional advantages
to cloud-based technology over mechanical technology. First of all, of course, or hardware type technology. Excuse me. You can upgrade it in real time as opposed to needing intermittent hardware upgrades. Works with any fluoro equipment, including a C-arm,
so you don't have to match your 3D imaging to the brand of your fluoro imaging. And there's enhanced accuracy compared to mechanical registration systems as imaging. So what are the clinical applications that this can be utilized for?
Fluoroscopy guided endovascular procedures in the lower thorax, abdomen, and pelvis, so that includes EVAR and FEVAR, mid distal TEVAR. At present, we do need two vertebral bodies and that does limit the use in TEVAR. And then angioplasty stenting and embolization
of common iliac, proximal external and proximal internal iliac artery. Anything where you can acquire a vertebral body image. So here, just a couple of examples of some additional non EVAR/FEVAR/TEVAR applications. This is, these are some cases
of internal iliac embolization, aortoiliac occlusion crossing, standard EVAR, complex EVAR. And I think then, that the final thing that I'd like to talk about is the use with C-arm, which is think is really, extremely important.
Has the potential to make a very big difference. All of us in our larger OR suites, know that we are short on hybrid availability, and yet it's difficult to get our institutions to build us another hybrid room. But if you could use a high quality 3D fusion imaging
with a high quality C-arm, you really expand your endovascular capability within the operating room in a much less expensive way. And then if you look at another set of circumstances where people don't have a hybrid room at all, but do want to be able to offer standard EVAR
to their patients, and perhaps maybe even basic FEVAR, if there is such a thing, and we could use good quality imaging to do that in the absence of an actual hybrid room. That would be extremely valuable to be able to extend good quality care
to patients in under-served areas. So I just was mentioning that we can use this and Tara Mastracci was talking yesterday about how happy she is with her new room where she has the use of CYDAR and an excellent C-arm and she feels that she is able to essentially run two rooms,
two hybrid rooms at once, using the full hybrid room and the C-arm hybrid room. Here's just one case of Dr. Goverde's. A vascular case that he did on a mobile C-arm with aortoiliac occlusive disease and he places kissing stents
using a CYDAR EV and a C-arm. And he used five mils of iodinated contrast. So let's talk about a little bit of data. This is out of Blain Demorell and Tara Mastrachi's group. And this is use of fusion technology in EVAR. And what they found was that the use of fusion imaging
reduced air kerma and DSA runs in standard EVAR. We also looked at our experience recently in EVAR and FEVAR and we compared our results. Pre-availability of image based fusion CT and post image based fusion CT. And just to clarify,
we did have the mechanical product that Phillip's offers, but we abandoned it after using it a half dozen times. So it's really no image fusion versus image fusion to be completely fair. We excluded patients that were urgent/emergent, parallel endographs, and IBEs.
And we looked at radiation exposure, contrast use, fluoro time, and procedure time. The demographics in the two groups were identical. We saw a statistically significant decrease in radiation dose using image based fusion CT. Statistically a significant reduction in fluoro time.
A reduction in contrast volume that looks significant, but was not. I'm guessing because of numbers. And a significantly different reduction in procedure time. So, in conclusion, image based 3D fusion CT decreases radiation exposure, fluoro time,
and procedure time. It does enable 3D overlays in all X-Ray sets, including mobile C-arm, expanding our capabilities for endovascular work. And image based 3D fusion CT has the potential to reduce costs
and improve clinical outcomes. Thank you.
- Good morning. Thank you for the opportunity to speak. So thirty day mortality following unselected non-cardiac surgery in patients 45 years and older has been reported to be as high as 1.9%. And in such patients we know that postoperative troponin elevation has
a very strong correlation with 30-day mortality. Considering that there are millions of major surgical procedures performed, it's clear that this equates to a significant health problem. And therefore, the accurate identification of patients at risk of complications
and morbidity offers many advantages. First, both the patient and the physician can perform an appropriate risk-benefit analysis based on the expected surgical benefit in relation to surgical risk. And surgery can then be declined,
deferred, or modified to maximize the patient's benefit. Secondly, pre-operative identification of high-risk patients allows physicians to direct their efforts towards those who might really benefit from additional interventions. And finally, postoperative management,
monitoring and potential therapies can be individualized according to predicted risk. So there's a lot of data on this and I'll try to go through the data on predictive biomarkers in different groups of vascular surgery patients. This study published in the "American Heart Journal"
in 2018 measured troponin levels in a prospective blinded fashion in 1000 patients undergoing non-cardiac surgery. Major cardiac complications occurred overall in 11% but in 24% of the patients who were having vascular surgery procedures.
You can see here that among vascular surgery patients there was a really high prevalence of elevated troponin levels preoperatively. And again, if you look here at the morbidity in vascular surgery patients 24% had major cardiac complications,
the majority of these were myocardial infarctions. Among patients undergoing vascular surgery, preoperative troponin elevation was an independent predictor of cardiac complications with an odds ratio of 1.5, and there was an increased accuracy of this parameter
in vascular surgery as opposed to non-vascular surgery patients. So what about patients undergoing open vascular surgery procedures? This is a prospective study of 455 patients and elevated preoperative troponin level
and a perioperative increase were both independently associated with MACE. You can see here these patients were undergoing a variety of open procedures including aortic, carotid, and peripheral arterial. And you can see here that in any way you look at this,
both the preoperative troponin, the postoperative troponin, the absolute change, and the relative change were all highly associated with MACE. You could add the troponin levels to the RCRI a clinical risk stratification tool and know that this increased the accuracy.
And this is additionally shown here in these receiver operator curves. So this study concluded that a combination of the RCRI with troponin levels can improve the predictive accuracy and therefore allow for better patient management.
This doesn't just happen in open-vascular surgery patients. This is a study that studied troponin levels in acute limb ischaemia patients undergoing endovascular therapy. 254 patients all treated with endovascular intervention
with a 3.9% mortality and a 5.1% amputation rate. Patients who died or required amputation more frequently presented with elevated troponin levels. And the relationship between troponin and worse in-hospital outcome remains significant even when controlling for other factors.
In-hospital death or amputation again and amputation free survival were highly correlated with preoperative troponin levels. You can see here 16.9% in patients with elevated troponins versus 6% in others. And the cardiac troponin level
had a high hazard ratio for predicting worse in-hospital outcomes. This is a study of troponins just in CLI patients with a similar design the measurement of troponin on admission again was a significant independent predictor
of survival with a hazard ratio of 4.2. You can see here that the majority of deaths that did occur were in fact cardiac, and troponin levels correlated highly with both cardiac specific and all-cause mortality. The value of the troponin test was maintained
even when controlling for other risk factors. And these authors felt that the realistic awareness of likely long term prognosis of vascular surgery patients is invaluable when planning suitability for either surgical or endovascular intervention.
And finally, we even have data on the value of preoperative troponin in patients undergoing major amputation. This was a study in which 10 of 44 patients had a non-fatal MI or died from a cardiac cause following amputation.
A rise in the preoperative troponin level was associated with a very poor outcome and was the only significant predictor of postoperative cardiac events. As you can see in this slide. This clearly may be a "Pandora's box".
We really don't know who should have preoperative troponins. What is the cost effectiveness in screening everybody? And in patients with elevated troponin levels, what exactly do we do? Do we cancel surgery, defer it, or change our plan?
However, certainly as vascular surgeons with our high-risk patient population we believe in risk stratification tools. And the RCRI is routinely used as a clinical risk stratification tool. Adding preoperative troponin levels to the RCRI
clearly increases its accuracy in the prediction of patients who will have perioperative cardiac morbidity or mortality. And you can see here that the preoperative troponin level had one of the highest independent hazard ratios at 5.4. Thank you very much for your attention.
- So I'm just going to talk a little bit about what's new in our practice with regard to first rib resection. In particular, we've instituted the use of a 30 degree laparoscopic camera at times to better visualize the structures. I will give you a little bit of a update
about our results and then I'll address very briefly some controversies. Dr. Gelbart and Chan from Hong Kong and UCLA have proposed and popularized the use of a 30 degree laparoscopic camera for a better visualization of the structures
and I'll show you some of those pictures. From 2007 on, we've done 125 of these procedures. We always do venography first including intervascular intervention to open up the vein, and then a transaxillary first rib resection, and only do post-operative venography if the vein reclots.
So this is a 19 year old woman who's case I'm going to use to illustrate our approach. She developed acute onset left arm swelling, duplex and venogram demonstrated a collusion of the subclavian axillary veins. Percutaneous mechanical thrombectomy
and then balloon angioplasty were performed with persistent narrowing at the thoracic outlet. So a day later, she was taken to the operating room, a small incision made in the axilla, we air interiorly to avoid injury to the long thoracic nerve.
As soon as you dissect down to the chest wall, you can identify and protect the vein very easily. I start with electrocautery on the peripheral margin of the rib, and use that to start both digital and Matson elevator dissection of the periosteum pleura
off the first rib, and then get around the anterior scalene muscle under direct visualization with a right angle and you can see that the vein and the artery are identified and easily protected. Here's the 30 degree laparoscopic image
of getting around the anterior scalene muscle and performing the electrocautery and you can see the pulsatile vein up here anterior and superficial to the anterior scalene muscle. Here is a right angle around the first rib to make sure there are no structures
including the pleura still attached to it. I always divide, or try to divide, the posterior aspect of the rib first because I feel like then I can manipulate the ribs superiorly and inferiorly, and get the rib shears more anterior for the anterior cut
because that's most important for decompressing the vein. Again, here's the 30 degree laparoscopic view of the rib shears performing first the posterior cut, there and then the anterior cut here. The portion of rib is removed, and you can see both the artery and the vein
are identified and you can confirm that their decompressed. We insufflate with water or saline, and then perform valsalva to make sure that they're hasn't been any pneumothorax, and then after putting a drain in,
I actually also turn the patient supine before extirpating them to make sure that there isn't a pneumothorax on chest x-ray. You can see the Jackson-Pratt drain in the left axilla. One month later, duplex shows a patent vein. So we've had pretty good success with this approach.
23 patients have requires post operative reintervention, but no operative venous reconstruction or bypass has been performed, and 123 out of 125 axillosubclavian veins have been patent by duplex at last follow-up. A brief comment on controversies,
first of all, the surgical approach we continue to believe that a transaxillary approach is cosmetically preferable and just as effective as a paraclavicular or anterior approach, and we have started being more cautious
about postoperative anticoagulation. So we've had three patients in that series that had to go back to the operating room for washout of hematoma, one patient who actually needed a VATS to treat a hemathorax,
and so in recent times we've been more cautious. In fact 39 patients have been discharged only with oral antiplatelet therapy without any plan for definitive therapeutic anticoagulation and those patients have all done very well. Obviously that's contraindicated in some cases
of a preoperative PE, or hematology insistence, or documented hypercoagulability and we've also kind of included that, the incidence of postop thrombosis of the vein requiring reintervention, but a lot of patients we think can be discharged
on just antiplatelets. So again, our approach to this is a transaxillary first rib resection after a venogram and a vascular intervention. We think this cosmetically advantageous. Surgical venous reconstruction has not been required
in any case, and we've incorporated the use of a 30 degree laparoscopic camera for better intraoperative visualization, thanks.
- Thank you very much. Well this is a series that was actually published five years ago. And it outlined 45,000 patients after carotid endarterectomy, as well as open and closed thoracic abdominal procedures and infrainguinal bypasses.
And you can see here, that the VTE rate, and this is emblematic of a lot of studies. If you take everything together in a ball, you get an average result. And as you can see, the peripheral bypasses had a low incidence.
Carotids, very low incidence. But open procedures had a higher incidence than endovascular procedures. But here is the nub. Here is what's really important and why you need to do risk assessment.
Look at what happened to these percentages if the patients had any morbidity during hospitalization, as high as 7.8%. And here's the list after they went home. Again, it's not the .5 tenths of a percent or 1%, and this is what it's all about.
It's about the extra risk factors that the patient has. So now, anybody that's starting to do work with the Caprini Score, you've got to go to the patient-friendly form. Because we don't just do it,
if the patient comes in for surgery, and somebody does a preoperative evaluation in the holding area, stop it! It's ridiculous! Have you ever been in the holding area? What are you worried about?
You're worried about having the operation. Are they going to find cancer? Will the surgeon have a bad day? How much pain am I going to be in? How long am I going to be out of work? They're not going to talk to you
about their family history or their obstetrical misadventures. So you have them fill a form out ahead of time with their family, and then when they come in, you just double-check it. And we've studied this, it's in five languages,
and it's got perfect correlation with trained observers doing the same thing. And remember, if you fail to carefully interrogate your patients regarding the history or family history of venous thromboembolism, vascular surgery or not, sooner or later you may
be faced with a fatal PE. And the idea that you're giving anticoagulants during your procedure that's going to protect them is not valid. The relative risk of thrombosis increases with the number of risk factors identified.
A combination of genetic and acquired risk factors in a person without a history of a thrombosis personally, but with a family history, has a 60-fold higher chance than those that have a negative family history. And a positive family history increased
the risk of venous thrombosis more than 2-fold, regardless of the other risk factors. Don't forget the history of thrombosis. You won't need to look this article up. It's 183,000 patients over 25 years and it shows that both in first, second,
and third-degree relatives, as well as cohabitants in the household, there's an increased risk of venous thromboembolism. Lowering down, getting lower for each degree of a relative.
But a DVT in a cousin, there may also be a thrombopathic condition in that patient. So you better pay attention to that. National Surgical Quality Improvement Program, wonderful program. The database has no information on history
or family history of VTE, use of perioperative VTE prophylaxis, intraoperative anticoagulation, or perioperative use of antiplatelet agents. How are you supposed to make any sense out of DVT-related studies?
Finally, due to the lack of routine screening for VTE, the incidence of VTE may be underestimated in this NSQIP database, which only makes the need for further study more pressing. This is an important consideration because
more recent data indicates that two-thirds of the patients are found to have DVT during screening and after vascular operations, have no signs or symptoms of the problem. And I'd like to remind you, so this is based on the Boston data, which is the best data.
Patients with a low score pneumatic compression during hospitalization. Moderate score, of 7-10 days of anticoagulation. Don't make any difference if they're inpatient or outpatient. And 28 days if their score is over nine.
They lowered their incidence on the surgical services from 2.2% to a tenth of a percent at 30 days. And finally, and I think this is really, really important. Take a look at all these risk assessment scores.
To my knowledge, there's only two scores. It's not the Padua, it's not the IMPROVE that have a history of obstetrical misadventures which can reflect antiphospholipid antibody syndrome, as well as family history
in various degrees of relatives. So with that, thank you very much.
- Good morning. I'd like to thank Dr. Veith and Symposium for my opportunity to speak. I have no disclosures. So the in Endovascular Surgery, there is decrease open surgical bypass. But, bypass is still required for many patients with PAD.
Autologous vein is preferred for increase patency lower infection rate. And, Traditional Open Vein Harvest does require lengthy incisions. In 1996 cardiac surgery reported Endoscopic Vein Harvest. So the early prospective randomized trial
in the cardiac literature, did report wound complications from Open Vein Harvest to be as high as 19-20%, and decreased down to 4% with Endoscopic Vein Harvest. Lopes et al, initially, reported increase risk of 12-18 month graft failure and increased three year mortality.
But, there were many small studies that show no effect on patency and decreased wound complications. So, in 2005, Endoscopic Vein Harvest was recommended as standard of care in cardiac surgical patients. So what about our field? The advantages of Open Vein Harvest,
we all know how to do it. There's no learning curve. It's performed under direct visualization. Side branches are ligated with suture and divided sharply. Long term patency of the bypass is established. Disadvantages of the Open Vein Harvest,
large wound or many skip wounds has an increased morbidity. PAD patients have an increased risk for wound complications compared to the cardiac patients as high as 22-44%. The poor healing can be due to ischemia, diabetes, renal failure, and other comorbid conditions.
These can include hematoma, dehiscense, infection, and increased length of stay. So the advantages of Endoscopic Vein Harvest, is that there's no long incisions, they can be performed via one or two small incisions. Limiting the size of an incision
decreases wound complications. It's the standard of care in cardiac surgery, and there's an overall lower morbidity. The disadvantages of is that there's a learning curve. Electro-cautery is used to divide the branches, you need longer vein compared to cardiac surgery.
There's concern about inferior primary patency, and there are variable wound complications reported. So recent PAD data, there, in 2014, a review of the Society of Vascular Surgery registry, of 5000 patients, showed that continuous Open Vein Harvest
was performed 49% of the time and a Endo Vein Harvest about 13% of the time. The primary patency was 70%, for Continuous versus just under 59% for Endoscopic, and that was significant. Endoscopic Vein Harvest was found to be an independent risk factor for a lower one year
primary patency, in the study. And, the length of stay due to wounds was not significantly different. So, systematic review of Endoscopic Vein Harvest data in the lower extremity bypass from '96 to 2013 did show that this technique may reduce
primary patency with no change in wound complications. Reasons for decreased primary patency, inexperienced operator, increased electrocautery injury to the vein. Increase in vein manipulation, you can't do the no touch technique,
like you could do with an Open Harvest. You need a longer conduit. So, I do believe there's a roll for this, in the vascular surgeon's armamentarium. I would recommend, how I use it in my practices is, I'm fairly inexperienced with Endoscopic Vein Harvest,
so I do work with the cardiac PA's. With increased percutaneous procedures, my practice has seen decreased Saphenous Vein Bypasses, so, I've less volume to master the technique. If the PA is not available, or the conduit is small, I recommend an Open Vein Harvest.
The PA can decrease the labor required during these cases. So, it's sometimes nice to have help with these long cases. Close surveillance follow up with Non-Invasive Arterial Imaging is mandatory every three months for the first year at least. Thank you.
- Well, thank you Frank and Enrico for the privilege of the podium and it's the diehards here right now. (laughs) So my only disclosure, this is based on start up biotech company that we have formed and novel technology really it's just a year old
but I'm going to take you very briefly through history very quickly. Hippocrates in 420 B.C. described stroke for the first time as apoplexy, someone be struck down by violence. And if you look at the history of stroke,
and trying to advance here. Let me see if there's a keyboard. - [Woman] Wait, wait, wait, wait. - [Man] No, there's no keyboard. - [Woman] It has to be opposite you. - [Man] Left, left now.
- Yeah, thank you. Are we good? (laughs) So it's not until the 80s that really risk factors for stroke therapy were identified, particularly hypertension, blood pressure control,
and so on and so forth. And as we go, could you advance for me please? Thank you, it's not until the 90s that we know about the randomized carotid trials, and advance next slide please, really '96 the era of tPA that was
revolutionary for acute stroke therapy. In the early 2000s, stroke centers, like the one that we have in the South East Louisiana and New Orleans really help to coordinate specialists treating stroke. Next slide please.
In 2015, the very famous HERMES trial, the compilation of five trials for mechanical thrombectomy of intracranial middle and anterior cerebral described the patients that could benefit and we will go on into details, but the great benefit, the number needed to treat
was really five to get an effect. Next slide. This year, "wake up" strokes, the extension of the timeline was extended to 24 hours, increase in potentially the number of patients that could be treated with this technology.
Next please. And the question is really how can one preserve the penumbra further to treat the many many patients that are still not offered mechanical thrombectomy and even the ones that are, to get a much better outcome because not everyone
returns to a normal function. Next, so the future I think is going to be delivery of a potent neuroprotection strategy to the penumbra through the stroke to be able to preserve function and recover the penumbra from ongoing death.
Next slide. So that's really the history of stroke. Advance to the next please. Here what you can see, this is a patient of mine that came in with an acute carotid occlusion that we did an emergency carotid endarterectomy
with an neuro interventionalist after passage of aspiration catheter, you can see opening of the middle cerebral M1 and M2 branches. The difference now compared to five, eight, 10 years ago is that now we have catheters in the middle cerebral artery,
the anterior cerebral artery. After tPA and thrombectomy for the super-selective, delivery of a potent neuroprotective agent and by being able to deliver it super-selectively, bioavailability issues can be resolved, systemic side effects could be minimized.
Of course, it's important to remember that penumbra is really tissue at risk, that's progression towards infarction. And everybody is really different as to when this occurs. And it's truly all based on collaterals.
So "Time is brain" that we hear over and over again, at this meeting there were a lot of talks about "Time is brain" is really incorrect. It's really "Collaterals are brain" and the penumbra is really completely based on what God gives us when we're born, which is really
how good are the collaterals. So the question is how can the penumbra be preserved after further mechanical thrombectomy? And I think that the solution is going to be with potent neuroprotection delivery to the penumbra. These are two papers that we published in late 2017
in Nature, in science journals Scientific Reports and Science Advances by our group demonstrating a novel class of molecules that are potent neuroprotective molecules, and we will go into details, but we can discuss it if there's interest, but that's just one candidate.
Because after all, when we imaged the penumbra in acute stroke centers, again, it's all about collaterals and I'll give you an example. The top panel is a patient that comes in with a good collaterals, this is a M1 branch occlusion. In these three phases which are taken at
five second intervals, this patient is probably going to be offered therapy. The patients that come in with intermediate or poor collaterals may or may not receive therapy, or this patient may be a no-go. And you could think that if neuroprotection delivery
to the penumbra is able to be done, that these patients may be offered therapy which they currently are not. And even this patient that's offered therapy, might then leave with a moderate disability, may have a much better functional
independence upon discharge. When one queries active clinical trials, there's nothing on intra arterial delivery of a potent neuroprotection following thrombectomy. These are two trials, an IV infusion, peripheral infusion, and one on just verapamil to prevent vasospasm.
So there's a large large need for delivery of a potent neuroprotection following thrombectomy. In conclusion, we're in the door now where we can do mechanical thrombectomy for intracranial thrombus, obviously concomitant to what we do in the carotid bifurcation is rare,
but those patients do present. There's still a large number of patients that are still not actively treated, some estimate 50 to 60% with typical mechanical thrombectomy. And one can speculate how ideally delivery of a potent neuroprotection to this area could
help treat 50, 60% of patients that are being denied currently, and even those that are being treated could have a much better recovery. I'd like to thank you, Frank for the meeting, and to Jackie for the great organization.
- Thank you, thanks for the opportunity to present. I have no disclosures. So, we all know that wounds are becoming more prevalent in our population, about 5% of the patient population has these non-healing wounds at a very significant economic cost, and it's a really high chance of lower extremity amputation
in these patients compared to other populations. The five-year survival following amputation from a foot ulcer is about 50%, which is actually a rate that's worse than most cancer, so this is a really significant problem. Now, even more significant than just a non-healing wound
is a wound that has both a venous and an arterial component to it. These patients are about at five to seven times the risk of getting an amputation, the end patients with either isolated venous disease or isolated PAD. It's important because the venous insufficiency component
brings about a lot more inflammation, and as we know, this is associated with either superficial or deep reflux, a history of DVT or incompetent perforators, but this adds an increasing complexity to these ulcers that refuse to heal.
So, it's estimated now about 15% of these ulcers are more of a mixed etiology, we define these as anyone who has some component of PAD, meaning an ABI of under point nine, and either superficial or deep reflux or a DVT on duplex ultrasound.
So we're going to talk for just a second about how do we treat these. Do we revascularize them first, do we do compression therapy? It has been shown in many, many studies, as with most things, that a multi-disciplinary approach
will improve the outcome of these patients, and the first step in any algorithm for these patients involves removing necrotic and infected tissue, dressings, if compression is feasible, based on the PAD level, you want to go ahead and do this secondary, if it's not, then you need to revascularize first,
and I'm going to show you our algorithm at Michigan that's based on summa the data. But remember that if the wounds fail to heal despite all of this, revascularization is a good option. So, based on the data, the algorithm that we typically use is if an ABI is less than point five
or a toe pressure is under 50, you want to revascularize first, I'll talk for a minute about the data of percutaneous versus open in these patients, but these are the patients you want to avoid compression in as a first line therapy.
If you have more moderate PAD, like in the point five to point eight range, you want to consider compression at the normal 40 millimeters of mercury, but you may need to modify it. It's actually been shown that that 40 millimeter of mercury
compression actually will increase flow to those wounds, so, contrary to what had previously been thought. So, revascularization, the data's pretty much equivocal right now, for these patients with these mixed ulcers, of whether you want to do endovascular or open. In diabetics, I think the data strongly favors
doing an open bypass if they have a good autogenous conduit and a good target, but you have to remember, in these patients, they have so much inflammation in the leg that wound healing from the surgical incisions is going to be significantly more difficult
than in a standard PAD patient, but the data has shown that about 60% of these ulcers heal at one year following revascularization. So, compression therapy, which is the mainstay either after revascularization in the severe PAD group or as a first line in the moderate group,
is really important 'cause it, again, increases blood flow to the wound. They've shown that that 40 millimeters of mercury compression is associated with a significant healing rate if you can do that, you additionally have to be careful, though,
about padding your bony areas, also, as we know, most patients don't actually keep their compression level at that 40, so there are sensors and other wearable technologies that are coming about that help patients with that, keeping in mind too, that the venous disease component
in these patients is really important, it's really important to treat the superficial venous reflux, EVLT is kind of the standard for that, treatment of perforators greater than five, all of that will help.
And I'm not going to go into any details of wound dressings, but there are plenty of new dressings that are available that can be used in conjunction with compression therapy. So, our final algorithm is we have a patient with these mixed arterial venous ulcers, we do woundcare debridement, determine the degree of PAD,
if it's severe, they go down the revascularization pathway, followed by compression, if it's moderate, then they get compression therapy first, possible treatment of venous disease, if it still doesn't heal at about 35 weeks, then you have to consider other things,
like biopsy for cancer, and then also consider revacularization. So, these ulcers are on a rise, they're a common problem, probably we need randomized control trials to figure out the optimal treatment strategies.
- Thanks Fieres. Thank you very much for attending this session and Frank for the invitation. These are my disclosures. We have recently presented the outcomes of the first 250 patients included in this prospective IDE at the AATS meeting in this hotel a few months ago.
In this study, there was no in-hospital mortality, there was one 30-day death. This was a death from a patient that had intracranial hemorrhage from the spinal drain placement that eventually was dismissed to palliative care
and died on postoperative day 22. You also note that there are three patients with paraplegia in this study, one of which actually had a epidural hematoma that was led to various significant and flacid paralysis. That prompted us to review the literature
and alter our outcomes with spinal drainage. This review, which includes over 4700 patients shows that the average rate of complications is 10%, some of those are relatively moderate or minor, but you can see a rate of intracranial hemorrhage of 1.5% and spinal hematoma of 1% in this large review,
which is essentially a retrospective review. We have then audited our IDE patients, 293 consecutive patients treated since 2013. We looked at all their spinal drains, so there were 240 placement of drains in 187 patients. You can see that some of these were first stage procedures
and then the majority of them were the index fenestrated branch procedure and some, a minority were Temporary Aneurysm Sac Perfusions. Our rate of complication was identical to the review, 10% and I want to point out some of the more important complications.
You can see here that intracranial hypotension occurred in 6% of the patients, that included three patients, or 2%, with intracranial hemorrhage and nine patients, or 5%, with severe headache that prolonged hospital stay and required blood patch for management.
There were also six patients with spinal hematomas for a overall rate of 3%, including the patient that I'll further discuss later. And one death, which was attributed to the spinal drain. When we looked at the intracranial hypotension in these 12 patients, you can see
the median duration of headache was four days, it required narcotics in seven patients, blood patch in five patients. All these patients had prolonged hospital stay, in one case, the prolongation of hospital stay was of 10 days.
Intracranial hemorrhage in three patients, including the patient that I already discussed. This patient had a severe intracranial hemorrhage which led to a deep coma. The patient was basically elected by the family to be managed with palliative care.
This patient end up expiring on postoperative day 21. There were other two patients with intracranial hemorrhage, one remote, I don't think that that was necessarily related to the spinal drain, nonetheless we had it on this review. These are some of the CT heads of the patients that had intracranial hemorrhage,
including the patient that passed away, which is outlined in the far left of your slide. Six patients had spinal hematoma, one of these patients was a patient, a young patient treated for chronic dissection. Patient evolved exceptionally well, moving the legs,
drain was removed on postoperative day two. As the patient is standed out of the bed, felt weakness in the legs, we then imaged the spine. You can see here, very severe spinal hematoma. Neurosurgery was consulted, decided to evacuate, the patient woke up with flacid paralysis
which has not recovered. There were two other patients with, another patient with paraplegia which was treated conservatively and improved to paraparesis and continues to improve and two other patients with paraparesis.
That prompted changes in our protocol. We eliminated spinal drains for Extent IVs, we eliminated for chronic dissection, in first stages, on any first stage, and most of the Extent IIIs, we also changed our protocol of drainage
from the routine drainage of a 10 centimeters of water for 15 minutes of the hours to a maximum of 20 mL to a drainage that's now guided by Near Infrared Spectroscopy, changes or symptoms. This is our protocol and I'll illustrate how we used this in one patient.
This is a patient that actually had this actual, exact anatomy. You can see the arch was very difficult, the celiac axis was patent and provided collateral flow an occluded SMA. The right renal artery was chronically occluded.
As we were doing this case the patient experienced severe changes in MEP despite the fact we had flow to the legs, we immediately stopped the procedure with still flow to the aneurysm sac. The patient develops pancreatitis, requires dialysis
and recovers after a few days in the ICU with no neurological change. Then I completed the repair doing a subcostal incision elongating the celiac axis and retrograde axis to this graft to complete the branch was very difficult to from the arm
and the patient recovered with no injury. So, in conclusion, spinal drainage is potentially dangerous even lethal and should be carefully weighted against the potential benefits. I think that our protocol now uses routine drainage for Extent I and IIs,
although I still think there is room for a prospective randomized trial even on this group and selective drainage for Extent IIIs and no drainage for Extent IVs. We use NIRS liberally to guide drainage and we use temporary sac perfusion
in those that have changes in neuromonitoring. Thank you very much.
- Thank you Mr. Chairman, thank you Dr. Veith for the kind invitation. I have no disclosures relevant to this particular lecture. But I think we ought to talk about what critical limb ischemia is. Obviously it's what we call Rutherford four through six. It's most commonly associated with multi-level disease.
About 1/3 or so of the cases are infrapopliteal only, mostly in diabetic patients. There's very poor overall life expectancies. We look at this group of patients in multiple studies, it ranges somewhere between three and four years of average life expectancy,
and there are substantial differences in outcomes within critical limb ischemia, with far worse outcomes in those with poor overall health, advanced stage presentation, or poor runoff at the level of the foot. Now, what is the rationale for endovascular therapy
in critical limb ischemia? Well first, patients are often old and infirmed, and many aren't really considered candidates for open surgery because of poor overall health. Surgery requires inflow, usually attainable. Outflow, not always so easy.
A conduit, which typically should be vein, if we want durable results, and an incision. Active infection is problematic, as there may be graft infection or sepsis. Extensive surgical scarring may compromise future rescue intervention,
and this is a progressive disease, that often requires additional treatment. Now, there have been multiple publications, and this is just a recent one, which came out in the Journal of the American Heart Association. It's a multidisciplinary,
retrospective analysis of Medicare data in people who had presented with critical limb ischemia. This is not perspective, it's not sited in many areas, but I ask you to look at this conclusion. It was there was lower major amputation rates following endovascular therapy.
Both surgery and endovascular did better than primary amputation, in terms of outcomes. But again, this is not a perfect study. Now, we have many publications which have shown very good limb salvage rates in patients using interventions.
Here we see this from Faglia, again showing very low major amputation rates. This from Sam Ahn, once again, very good limb salvage rates. But in truth, we have only one randomized, control trial, level one data, comparing intervention with surgery. And that was the BASIL Trial.
The BASIL Trial is an old trial, it's criticized, appropriately, because the only treatment used was sub-intimal angioplasty. And with sub-intimal angioplasty, often, the sub-intimal tract in crossing is far greater than the area of total occlusion,
resulting in much longer treatment zones. In addition, this trial did not allow some of the new and better treatments that are now available for having better patency to be performed. Nonetheless, in the BASIL Trial, despite very primitive treatment,
that being only sub-intimal angioplasty, we can see that one year out, and in fact out to two years, angioplasty and surgery were relatively equal in terms of limb salvage. At five years, there seemed to be a major advantage to surgery,
in terms of both quality of life, and in terms of less need for reintervention. So then we have to ask, what has changed since BASIL? Well now we have far better crossing. We have re-entry tools that stop us from having to go 10 centimeters
beyond the area of occlusion to get back in. Dedicated crossing tools, better wires, retrograde access, this is important, we have markedly improved patency, with drug coated balloons, drug-eluting stents, wire interwoven nitinol stents, and stent grafts, which have shown in the SFA all of these things,
better SFA patency, and if indeed, we can maintain SFA patency in multi-level disease, often, if there's recurrence, the patients do well. We also have improved Tibial patency in the proximal tibial vessels. However, we do not yet have a great endovascular solution
for long distal tibial vessel occlusions, and that's just the truth. I have to go back here, one, but we have better medical therapy too. As we look at PCSK9 inhibitors, in the GLAGOV Trial, we see in other parts of the body,
a 30% reduction in atherosclerotic volume out at 70 weeks, indeed will this change what we're doing. This has launched this decade of endovascular interventions. So what about this taking away surgical options? BASIL, I think, doesn't apply because the sections went far beyond where they should.
That's bad technique. Stenting across the common femoral or patent popliteal, in my opinion, bad technique. Distal embolization, we've not done enough preparation. I will also caution that sometimes, surgery has bad outcomes as well.
So, the rationale is we really don't want to perform anything that hurts a patient. Entire procedures performed via a sheath, remote from the site, there's less pain, shorter recovery, no extensive scar, and the argument that intervention
takes away surgical options, I think is no longer so valid. Bad intervention or bad surgery, take away options. Where is distal bypass indicated? In large non-healing ulcers in patients with good life expectancy, good quality vein, good outflow, and excellent surgical expertise.
Densely calcified long segment infrapopliteal disease, or disease from the common femoral all the way to the ankle. I think these clearly are going to do better with surgery, certainly in today's world. But even these areas may change. If more effective tools solve the patency problems,
with long segment infrapopliteal disease, and there are trials now aiming at this, such as SAVAL, DCB trials, and Lithoplasty. I thank you for your attention.
- Thank you Dr. Albaramum, it's a real pleasure to be here and I thank you for being here this early. I have no disclosures. So when everything else fails, we need to convert to open surgery, most of the times this leads to partial endograft removal,
complete removal clearly for infection, and then proximal control and distal control, which is typical in vascular surgery. Here's a 73 year old patient who two years after EVAR had an aneurism growth with what was thought
to be a type II endoleak, had coiling of the infermius mesenteric artery, but the aneurism continued to grow. So he was converted and what we find here is a type III endoleak from sutures in the endograft.
So, this patient had explantations, so it is my preference to have the nordic control with an endovascular technique through the graft where the graft gets punctured and then we put a 16 French Sheath, then we can put a aortic balloon.
And this avoids having to dissect the suprarenal aorta, particularly in devices that have super renal fixation. You can use a fogarty balloon or you can use the pruitt ballon, the advantage of the pruitt balloon is that it's over the wire.
So here's where we removed the device and in spite of the fact that we tried to collapse the super renal stent, you end up with an aortic endarterectomy and a renal endarterectomy which is not a desirable situation.
So, in this instance, it's not what we intend to do is we cut the super renal stent with wire cutters and then removed the struts individually. Here's the completion and preservation of iliac limbs, it's pretty much the norm in all of these cases,
unless they have, they're not well incorporated, it's a lot easier. It's not easy to control these iliac arteries from the inflammatory process that follows the placement of the endograft.
So here's another case where we think we're dealing with a type II endoleak, we do whatever it does for a type II endoleak and you can see here this is a pretty significant endoleak with enlargement of the aneurism.
So this patient gets converted and what's interesting is again, you see a suture hole, and in this case what we did is we just closed the suture hole, 'cause in my mind,
it would be simple to try and realign that graft if the endoleak persisted or recurred, as opposed to trying to remove the entire device. Here's the follow up on that patient, and this patient has remained without an endoleak, and the aneurism we resected
part of the sack, and the aneurism has remained collapsed. So here's another patient who's four years status post EVAR, two years after IMA coiling and what's interesting is when you do delayed,
because the aneurism sacks started to increase, we did delayed use and you see this blush here, and in this cases we know before converting the patient we would reline the graft thinking, that if it's a type III endoleak we can resolve it that way
otherwise then the patient would need conversion. So, how do we avoid the proximal aortic endarterectomy? We'll leave part of the proximal portion of the graft, you can transect the graft. A lot of these grafts can be clamped together with the aorta
and then you do a single anastomosis incorporating the graft and the aorta for the proximal anastomosis. Now here's a patient, 87 years old, had an EVAR,
the aneurism grew from 6 cm to 8.8 cm, he had coil embolization, translumbar injection of glue, we re-lined the endograft and the aneurism kept enlarging. So basically what we find here is a very large type II endoleak,
we actually just clip the vessel and then resected the sack and closed it, did not remove the device. So sometimes you can just preserve the entire device and just take care of the endoleak. Now when we have infection,
then we have to remove the entire device, and one alternative is to use extra-anatomic revascularization. Our preference however is to use cryo-preserved homograft with wide debridement of the infected area. These grafts are relatively easy to remove,
'cause they're not incorporated. On the proximal side you can see that there's a aortic clamp ready to go here, and then we're going to slide it out while we clamp the graft immediately, clamp the aorta immediately after removal.
And here's the reconstruction. Excuse me. For an endograft-duodenal fistula here's a patient that has typical findings, then on endoscopy you can see a little bit of the endograft, and then on an opergy I series
you actually see extravasation from the duodenal. In this case we have the aorta ready to be clamped, you can see the umbilical tape here, and then take down the fistula, and then once the fistula's down
you got to repair the duodenal with an omental patch, and then a cryopreserved reconstruction. Here's a TEVAR conversion, a patient with a contained ruptured mycotic aneurysm, we put an endovascular graft initially, Now in this patient we do the soraconomy
and the other thing we do is, we do circulatory support. I prefer to use ECMO, in this instances we put a very long canula into the right atrium, which you're anesthesiologist can confirm
with transassof forgeoligico. And then we use ECMO for circulatory support. The other thing we're doing now is we're putting antibiotic beads, with specific antibiotic's for the organism that has been cultured.
Here's another case where a very long endograft was removed and in this case, we put the device offline, away from the infected field and then we filled the field with antibiotic beads. So we've done 47 conversions,
12 of them were acute, 35 were chronic, and what's important is the mortality for acute conversion is significant. And at this point the, we avoid acute conversions,
most of those were in the early experience. Thank you.
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