- So in terms of overcoming difficult access, when we're doing parallel grafting, and we're going to use more than one branch or parallel graft, typically we come in from the axillary artery. It gives good pushability, it decreases the length for what you need to get from you access point
down to the branch vessels. We find that no conduit is needed. We typically just access this in three offset manners. We'll put a purse string in at each site, so that there's limited bleeding. When you come in, you have to think about
what the aortic arch construct looks like. You can have a type one, a type two or type three arch, which can make things more difficult. As you can see here, this sheath takes quite a significant bend to get down to the renal visceral segment.
You also can have tortuosity within the thoracic aorta, which can compromise your ability to cannulate. So when we think about the arch, you want to think about coming in from the right or left, which ever one makes it better. Typically, if all things are equal,
we'll come in from the left side. When you get your sheaths down one at a time, we leave the stiff wire in to try to straighten out the anatomy. Sometimes you have to snare and get through and through access.
And then you want to think about where your sheaths position is. You want it to be high enough so that you can allow your catheters to form, but also low enough so that you can reach the vessel of interest.
There are a couple of things, I think from a pre-planning perspective that are very important to try to set up, to allow yourself the optimal chance of cannulating these vessels. Appropriate C-arm projections, you want to think about
whether or not your going to use a cephalad or caudad parallel graft. Think about the tortuosity as well as the composition of the branch. What type of stent are you going to use in that? How much purchase is needed?
How much purchase can you get? And, How difficult is it going to be to cannulate these vessels? And also whether or not there's orifice stenosis. So, here's an example of a patient we did. You can see that left renal artery
is actually quite anterior. If you look at the AP view here, you can see how it would be quite difficult to cannulate, 'cause the orifice basically runs into the aneurysm in the AP view, if you just move your II to a 30 degree RAO,
then it becomes very perpendicular and very easy to cannulate and see. This is a situation where you think about periscoping or caudad parallel graft. It's much easier coming from below, it's an upwards approaching renal artery.
Coming from above, you can see it can bow out towards that large aneurysm and also potentially reflux down into infra-renal segment. This is a patient with a very short branch of main renal artery, and you can see if you just put
a typical self expanding stent, there's a higher chance that this thing's just going to pull out into the aneurysm, and what we did here is, we put a balloon mounted stent, followed by a self expanding stent
to lengthen afterwards and it worked out really nicely. And this is just the patient that has significant orifice stenosis and these patients will be hard to cannulate. Sometimes you have to pre dilate before you introduce your stents into the vessels.
You also want to think about the aorta and what configuration of the aorta is. What's the tortuosity, the calcification. Are you in a situation where you're trying to cannulate within the aneurysm and how much thrombus is there as well.
So, you can see here in the first picture, the aorta's somewhat tortuous, and going after that left renal artery probably would be easier, but going after that right renal artery becomes potentially difficult
as the catheters and sheaths are going to be pushing you away, and may make that more challenging. You may want to think about things, and certainly catheters selection before approaching. And definitely, any time you have an aneurysm
and your in a big space without a lot of thrombus, that makes things a little more difficult, 'cause you're flopping around in a large open space trying to cannulate a vessel. When you're accessing the vessel sometimes from above, what will happen is the tendency is
for the catheters and the wires, to reflux down into that infrarenal space. This is a no not well known trick, where you put a coda balloon and you can have your wires and catheters bounce off of that coda balloon
to help you navigate into that branch vessel. Sometimes that doesn't work, and it still continues to reflux, and what we've done more recently is, we'll come in from below, put a four millimeter balloon
in the distal renal artery, and then we'll pin our soft wire, be able to do a catheter exchange, exchange for our stiff wire, and ultimately, there's the catheter, ultimately in the stiff wire.
And then ultimately bring in your stent graft, all with that balloon still in place to hold and pin that wire in position, and allow things to track over that wire, rather than reflux down. Just some general thoughts, again,
thinking about the appropriate catheters, what length catheter do you need, what kind of angulation do you need, stiff versus angle glide wires. We typically use Rosen and Amplatz wires for our stiff wires to track our stents in.
And then different platforms, depending upon what your anatomy ultimately looks like. So in conclusion, a lot of pre-planning is important, I think to optimize your accessing of these vessels. And there's a lot of techniques and technology, that currently exist to help assist with this.
- Thank you very much for the nice introduction for the privilege to start the aortic session with this nice, very interesting topic about Chimney technique and especially about the in-vitro testing which we have done in Muenster in Germany. So, the Chimney endovascular technique we treat short necks as we see here.
With the use of off-the-shelf devices and the placement is in parallel and outside configuration of the main abdominal device. Well, if you see the literature we can see enthusiastic reports with the use of these alternative therapeutic options,
showing low incidence of endo leaks, excellent patency, and durability of these endovascular solutions. On the other side we have also centers with suboptimal experience, as we see here from Manchester, in the titled already publication,
late ruptures after single chimneys or from the group from Florida, highlight that the technique raises cause for concern. So what are the reasons for these divergent experience? Could be the heterogeneity of the used materials, but also the degree of oversizing
of the aortic stent graft? In order to evaluate that, we performed first of all a chimney case of a patient with a huge paraanastomotic aneurysm which we did with single chimney for the right renal artery, as we see here.
What we have done is the CT scan of these patients, we send to a special company and create this silicone model one by one with the anatomy of this treated case, as we see here, having a diameter of 28 millimeter, exact the anatomy of the renals,
of the neck length, infrarenally. And it was also really nice the opportunity to have a fluid simulation system, and we can have also the possibility to bring the device in the CT scan, and perform CT angiography, as we can see here,
very nicely the pictail catheter into the descending aorta, and evaluating now the impact of the different devices for this technique. Here is the example with the device you see here how we deploy the chimney graft, here is an Incraft stent graft for the right renal artery.
The first attempt was to evaluate the impact of different abdominal devices. If we use the same chimney graft in this particular case, the Icast for Advanta V12, and you see what we changed was only the type of the stent graft of the aorta.
If you see here the CT scan analysis, you see very nicely these combination of a mitral endoskeleton of the enduring device with a rigid, but very good, intraradial force Advanta V12, or Icast. You can see here how nicely performs
around the chimney graft. And if we see also in the reconstruction, we have a very nice expansion of the chimney graft, especially in the proximal edge, which is very important in order to have a good patency over the time.
You see here very nicely the expansion of the proximal edge of the balloon expandable covered stent Let's see now what happened with the Incraft. Again, you see here very nice the radial force of the Icast is here very nice to see. However, we have seen a completely different behavior
of the abdominal stent graft of this company. You see here that we have potentially more gutters compared to the other conformability of the endurant around the chimney graft. So it was a very nice sign and finding and showing the impact of the abdominal stent graft
for this technique. What we have done after that was we took the endurant device and we changed now the use of the chimney graft, so we used in the first attempt the self-expanding covered stents, the Viabahn,
versus a balloon expandable covered stent like the Begraft. And if you see here the results, you see again a very nice expansion of the endurant around the chimney graft, but in the reconstruction you see here the severe compression of the Viabahn self-expanding stent
has poor radial force despite that we lined we had per se 70 percent stenosis. I think it's a very important finding crucial compared to the balloon expandable chimney grafts you see here the Begraft, they had also a very good expansion
as balloon-expandable covered did, but also we see here completely different area of gutters if we compare the two balloon expandable covered stents in the anterior and posterior phase, you see here the Begraft plus seems to perform better. The impact of degree of oversizing we know
from the work of Riambaud 30 percent is the recommendation if you see this very nice analysis, you see here with 15 percent oversizing, we have this area of gutter versus 30 percent of oversizing you see a very nice conformability around the chimney that we chose how important is for this technique
to have enough fabric material to wrap up the chimney grafts. In conclusion, ladies and gentlemen, we have seen in this very nice in-vitro testing that indeed the area of the gutters vary depending on the different device combinations.
And also we have seen how important is the appropriate device selection, and 30 percent oversizing to obtain optimal results. Thank you very much.
- Thank you again to Dr. Veith for the kind invitation. This is my disclosures. Open thoracic conversion is an increasing problem. Jose Jucadel speak two years ago in my congress in Milano showing the number of obstruction increase. The my experience in Milano in 25 years, we did global number of 2400 operation for
arch, descending thoracic artery, and thoracoabdominal and particularly more than 1000 open thoracoabdominal. And you have on this number, a total of 206 reintervention after TEVAR in particular for our center 84 patients and 9.8% after treatment.
There are different type of reintervention Endo Relining, Open conversion, and hybrid approach. Today we speak about open conversion. Why open conversion? Open conversion because sometimes the patients are young or fit, for an unstable condition and emergency,
infection of fistula, no proximal neck, and some anatomical barrier like MFM and PETTICOAT. And this is the first case, it's a patient with a dissection with multitreatment a young patient you see acute type B dissection treated in emergency for impending rupture
with three Gore TAG and from left subclavian artery to the super mesenteric artery covering the celiac trunk. Five month later you see "home-made" occluder for false lumen perfusion, but one month later, still perfusion you see a large perfusion of the false lumen with the sac expansion and pain.
So you decide to open the patient with the thoracofemoral approach with a thoracoabdominal operation, you see the proximal clamping opening on the aorta and you see the removing of the prosthesis and partial graft excision near to the neck
of the aneurysm for preparing the anastamosis The anastamosis with a triple-layer technique with a strip of felt and false lumen thrombus removal you see the normal distal and the occlusal false lumen device removal. You start with re-implantation of the single vessel
with complete left renal artery re-implantation of the true vessel. And you see the final result. This is another case, conversion of the patient after PETTICOAT. This is a patient with Marfan syndrome
in 2015 TVAR and PETTICOAT for acute type B dissection and enlargement in the next two years of thoracic and abdominal aorta. So decide for open conversion. You can see here through thoracofemoral operotomy the petticoat on the serosa of the aorta
and you see the stent complete removal after acute declamping and you see visceral renal perfusion and endartherectomy of the petticoat. Perfusion through the PETTICOAT and you see a large endartherectomy of the old PETTICOAT
and this intima-media of the aorta. And here the final result. Our definitive result, we performed a total of 81 open conversions with a mortality of 13%. Major morbidity with respiratory, renal, and parapalegia 7%. And the result is strictly dependent
from the kind of conversion. You see an indication to conversion, in endoleak, you have 6% mortality at one month, for endograft migration and failure 12% mortality, for retrograde dissection 33% mortality, for infection and fistula 30% mortality.
So in conclusion, Mr. Chairman, ladies and gentlemen, I think that close follow up after TEVAR is more and more necessary. Open conversion is always a technical challenge, acceptable in high volume centers, and increased mortality, my experience is due mainly
to retrograde dissection and infection. Thanks for attention.
- Thank you, Mr. Chairman. I guess this would be the old man's operation then. It's a new treatment paradigm. I just want to draw you attention to the fact that the results that are reported vary extremely. This is perhaps the most recent report from October from my colleagues at Saint Thomas' Hospital in London.
What they advocate is this excision of an infected graft with in situ reconstruction using deep vein of bovine graft. And they report a three year survival of 88%. I think this illustrates the selection of patients because the data is quite remarkable. It's actually better survival than after standard EVAR
in the British EVAR trial where the survivor at three years was less than 80%. And equally recent studies from Finland where they also use graft removal and vein reconstruction of the aorta. Here the results are completely different. Similar operation time as we heard before, over seven hours.
Early mortality of 18% and overall mortality of 40% with only one and a half years follow-up. Also, the authors very honestly note that it was not always possible to excise the grafts entirely. And the interesting thing is that they noted that there were no re-infections, even when only
partial graft removal was possible. So this makes me wonder. Do we really need to excise all that if when we leave behind material it doesn't re-infect? I will show you a couple of patients I have treated. I have a large series of them.
This was a septic patient with high blood cell count, high CRP, fever, this type of mycotic aneurysm. Quite difficult to treat open, I think, in a good way. I'm not saying they end always good, but we put in a chimney graft, excluded the aneurysm with a aortic stentgraft, and this is what happened
to the white blood cell count. It dropped within one week. So did the CRP. And this, of course says nothing, but this is the PET scan at five months showing no reaction around the stentgraft.
These results have been pretty much confirmed by a nationwide Swedish study showing that the results of open repair are notoriously worse than after EVAR with a much higher mortality after three months and a significantly high mortality still after one year. So those were the primary mycotic aneurysms.
How about the worse beast, the infected stentgrafts? We have several tricks to avoid this radical resection I will show you only my favorite trick right now. It's a resection of the infected sac. And this was the very first patient we did. It was a standard abdominal aortic aneurysm
treated with a standard stentgraft. The patient had a minor type II endoleak as you can see at follow-up. After two years, the endoleak was gone. Suddenly, there was air in the sac, and the patient seemed infected.
There was bowel right next to it, so I was convinced this was a aortic fistula and for that reason I did a laparotomy. There was no fistula. But we had an infected sac, and while I was at it, I resected as much as I could of the sac
only leaving behind the difficult portion adjacent to the cava, and when this was done, I wrapped the omentum around the graft. This is a follow-up CT showing that remnant of the native aorta, and as you can see, there is no inflammatory reaction around the stentgraft.
And this is a six month follow-up CT. The very most recent case. I have this bad habit of bringing recent cases. This is an elderly gentleman with a aortoenteric fistula post open AAA repair, and nobody was particularly keen on operating on him because he had this wonderful
result of the previous open repair. We put in a stentgraft, and this is the postop CT showing the collection right next to the stentgraft. This is at six weeks follow-up with that collection being less, and the CRP has dropped from 165 to 36. Of course, this is very early,
but it's a very promising result, I believe. The overall results for the non-radical treatment such as the low early mortality because we don't do this massive surgery to begin with. And the late mortality seems, in my eyes, comparable to the radical surgery.
So in conclusion, Mr. Chairman, ladies and gentlemen, I believe that most infected aneurysms don't need radical surgery. Thereby, you avoid major surgical trauma, which is poorly tolerated by these weak patients. You reduce lower early mortality.
You have similar or better long-term survival. And many infections do heal in spite of the fact that you leave prosthetic material behind. Thank you for your attention.
- I think this is a nice complementary talk to Gustavo's talk, and we'll talk about a bit of a different twist on misalignment. So, no disclosures. As you've heard from the panel, prior to this fenestrated and branched repairs of thorical, abdominal and peri-renal aneurysms is an exciting area, however, it is fraught
with some issues, when you talk about misalignment, primarily in fenestrations with renal arteries and mesenteric vessels, these can be in a vertical plane as you can see on the panel on your left, which may lead to difficulties with cannulation, and Gustavo just gave us a nice talk on some
of the strategies that we could employ to make this easier. Could always also lead to horizontal misalignment, which then applies untold forces to the covered stent and the vessel and long-term deleterious effects such as accelerated renal dysfunction. Obviously this is not multi-factorial,
we've heard about the importance of planning, and planning certainly can obviate the effects of misalignment, but there is also, for those of you who have done these cases, the issue of rotation of the stent graft upon deployment, so you can see that this
is a fenestrated devise that's deployed with anterior markers, and as the sheath is unfurled, as the graft is unsheathed, then these markers rotate in a clockwise direction, and this is because of the build up of torsional forces in calcified and tortuous iliac vessels.
This has clinical sequelae, so this was a series from our institution, where we looked at those patients who had some misalignment of fenestrations versus those that did not, and not surprisingly cases where there was misalignment, they took longer to do, there are longer fluoroscopy times,
there was more contrast and there patient effects, the patient stayed in hospital longer, also when looking at composite outcome measure of death as well as end organ ischemia, and renal dysfunction, those patients with misaligned fenestrations were more apt to have these adverse outcomes.
What can predict that rotation of the graft? We looked at multiple anatomic features, and interestingly on the ones that came out as predictive were iliac torsion or tortuosity, as well as calcification, so the stiffer or the more calcified the iliac vessels were, the more tortuous there was, there was build up
of torsional energy and then rotation of the stent graft upon sheathing and it was predictive. This rotation can be predicted with a logistic regression curve. What could we do to prevent rotation? And this is the specific topic I wanted to mention,
there are different strategies that surgeons employ, as a graft is unsheathed, you can apply counter forces to it or you can take the graft out and then reintroduce it. This was collaborative work with some of our engineers and our vascular surgeons, what we developed were some patient-specific models,
looking at the patients with different iliac geometries. And these were through four freeze/thaw cycles. There are the idealized models, and then some patient-specific models, looking at different anatomic configurations. This was a picture of the experimental apparatus
in a bath that would mimic the physiologic parameters of the patients, and there were basically three models, or patient-specific models, patient one had very straight iliac anatomy, patient two quite tortuous, but supple iliac anatomy, and patient three more stiff and calcified
and tortuous iliac anatomy. These were real patients, so they were patients that had fenestrated devices, and what you can see here is that the model matched what was observed clinically quite closely, in patient number one, where the anatomy was quite straight,
and there was minimal degree of device rotation, that was reflected in what happened in the model. And then with increasing observed rotation, with patient two and three, that was also matched in the laboratory. This slide is really the take home message,
so on the horizontal axis, are the three patients, from low-rotation to high-rotation of the graft. The white bar reflects the observed amount of rotation, so there's a dose response curve as you go from left to right, the more tortuous and stiffer the iliac model is, the more rotation there is.
The black bar is what happened when the surgeon tried to counteract the rotational forces. So, if you're observing rotation in a clockwise position, and you apply counter-clockwise force, it actually accentuated or increased the amount of rotation. The middle bar represents what happened if you're
observing rotation you take the graft out, you reinsert it and then allow it to rotate again, there is actually less rotation. In conclusion, torsion and rigidity and calcification combined are the anatomic factors that can predict and cause intraoperative stent graft rotation.
In-vivo correction of the orientation significantly actually increases the observed rotation, and if clinically appropriate, fully removing the device, and adjusting the orientation and reinserting the device will minimize rotation. Thank you very much.
- Thank you. These are my disclosures. So, iliac artery can be your friend or your worst enemy, with cases of significant iliac artery occlusive disease. This doesn't mean you can't do it, but I always teach my fellows to give it the full meal deal.
I don't hesitate to dilate with the seven or eight millimeter angioplasty balloon, and then I'll follow that up with the dilators, and that gives me a good idea, if the dilator doesn't go up, it's time to consider some other route.
Rarely, I will do a conduit, and I usually will do this either with a purse-string in the distal common iliac artery, or a proper conduit with a synthetic graft, especially if I'm going to combine that with an ileofemoral bypass.
The thing to remember is you not only have to get the device up, you have to be able to turn it, and that's why I use those tips or tricks. Endovascular gear, we've already seen today a few speakers talk about some of the catheters and sheaths they like to have on the shelf.
I'll just take you through these. These are the specific ones I like to make sure I have. A stiff glide, and a Amplatz Super Stiff with a once centimeter tip, can again be your friend but also your enemy, so you have to treat those wires with respect.
And some people forget about that old trick of being able to put three 018 wires through a five French catheter, and that can sometimes get you deep into a superior mesenteric artery or a renal artery. Sheaths, I personally don't like
the angled sheaths from Cook. I find the Ansel One and Ansel Two sometimes work against you. I prefer to use the Raabe sheath, which is a straight sheath. The disadvantage of the Raabe sheath
is it comes with a very stiff dilator. So the tip here is just open the Ansel One, take out the High-Flex dilator from the Ansel One and put it up your Raabe sheath and that'll get you to where you want to be. The steerable sheath, Josh Adams did a great presentation.
It's an outstanding sheath. The only thing I would worn you is if you ride a tricycle through your whole life you won't be very good on a bicycle. So don't get too used to using a steerable sheath. Every once in awhile, just use it with the
old-fashioned catheters and wires before you, and open up the steerable sheath if you really need it. Beware short and downgoing renals. This is a trick sometimes you can use. Stephan Haulon showed this. You can drop, if you can't get any catheter
or sheath to follow, just drop a reverse catheter in, do the rest of the fenestrations, open up the top cap, and then put up a Coda balloon with your ipsilateral access, and you can use that Coda balloon to form a roof, and you can get any catheter or wire
to get into that tough renal artery. Beware of tortuosity, this really is your enemy. This, I have a low threshold just to go to a retroperitoneal exposure for either a direct puncture or conduit. There's nothing more demoralizing than deploying
a fenestrated graft, and if a lot of torque is built up into that because of those tortuous iliacs, you will see those fenestrations start to move as you deploy each stent, and that's sometimes an irretrievable situation. Renal artery occlusive disease used to be
a contraindication for fenestrated graft. It is no longer. Although, renal artery calcified and downgoing renals can really be a big problem, and always believe the CT, don't believe the angio. This is an angiogram of the same patient.
This does not depict what the real true story is. And with these particular cases, you know, most people in the room do not have access to customized fenestrated grafts, which sometimes you can use to help you with these cases. So this is a case that's interesting,
and what we did here is we basically came from above, pre-stented these with covered stents, and then that made the fenestrated graft on a second stage procedure, much easier. I didn't have to use any contrast. I could use these as my markers for the renals,
and in this particular case, I was able to use a steerable sheath for that short renal, and you can see how much that trajectory of that renal changed with that covered stent as well. Finally, this is a case that kind of highlights a lot of different tips and tricks.
This is a large aneurysm, juxtarenal with common iliac aneurysms, significant iliac and femoral artery disease. And so again, we kind of customized this. I'm not a big fan of snorkel and parallel grafts, but in this particular case I saw its use.
So I made a fenestration for the left renal and I planned to use a snorkel for the right because I couldn't get any kind of configuration to fit with the renal artery and SMA being on the same plane. So here I used that same balloon
for the iliac occlusive disease, to get the device up. You can see the issues here. There's the left renal coming off. I decided to fenestrate that and put a snorkel in the right renal, and this is what I did.
I was afraid that that fenestrated graft was going to cover the renal, so I came down from above just to mark the left renal. As I deployed the graft, I got out of the scallop, snared from the top, and then I brought a sheath down through the scallop, and I actually catheterized
the left renal from a downgoing perspective, and this worked quite well. I was able to snorkel right and then fenestrate the left, and we had an excellent result. And my final tip for you is don't go chasing endoleaks
with these long fenestrated procedures. If you have done the right procedure, all those endoleaks will seal. Thank you.
- Thank you Mr. Chairman. Ladies and gentleman, first of all, I would like to thank Dr. Veith for the honor of the podium. Fenestrated and branched stent graft are becoming a widespread use in the treatment of thoracoabdominal
and pararenal aortic aneurysms. Nevertheless, the risk of reinterventions during the follow-up of these procedures is not negligible. The Mayo Clinic group has recently proposed this classification for endoleaks
after FEVAR and BEVAR, that takes into account all the potential sources of aneurysm sac reperfusion after stent graft implant. If we look at the published data, the reported reintervention rate ranges between three and 25% of cases.
So this is still an open issue. We started our experience with fenestrated and branched stent grafts in January 2016, with 29 patients treated so far, for thoracoabdominal and pararenal/juxtarenal aortic aneurysms. We report an elective mortality rate of 7.7%.
That is significantly higher in urgent settings. We had two cases of transient paraparesis and both of them recovered, and two cases of complete paraplegia after urgent procedures, and both of them died. This is the surveillance protocol we applied
to the 25 patients that survived the first operation. As you can see here, we used to do a CT scan prior to discharge, and then again at three and 12 months after the intervention, and yearly thereafter, and according to our experience
there is no room for ultrasound examination in the follow-up of these procedures. We report five reinterventions according for 20% of cases. All of them were due to endoleaks and were fixed with bridging stent relining,
or embolization in case of type II, with no complications, no mortality. I'm going to show you a couple of cases from our series. A 66 years old man, a very complex surgical history. In 2005 he underwent open repair of descending thoracic aneurysm.
In 2009, a surgical debranching of visceral vessels followed by TEVAR for a type III thoracoabdominal aortic aneurysms. In 2016, the implant of a tube fenestrated stent-graft to fix a distal type I endoleak. And two years later the patient was readmitted
for a type II endoleak with aneurysm growth of more than one centimeter. This is the preoperative CT scan, and you see now the type II endoleak that comes from a left gastric artery that independently arises from the aneurysm sac.
This is the endoleak route that starts from a branch of the hepatic artery with retrograde flow into the left gastric artery, and then into the aneurysm sac. We approached this case from below through the fenestration for the SMA and the celiac trunk,
and here on the left side you see the superselective catheterization of the branch of the hepatic artery, and on the right side the microcatheter that has reached the nidus of the endoleak. We then embolized with onyx the endoleak
and the feeding vessel, and this is the nice final result in two different angiographic projections. Another case, a 76 years old man. In 2008, open repair for a AAA and right common iliac aneurysm.
Eight years later, the implant of a T-branch stent graft for a recurrent type IV thoracoabdominal aneurysm. And one year later, the patient was admitted again for a type IIIc endoleak, plus aneurysm of the left common iliac artery. This is the CT scan of this patient.
You will see here the endoleak at the level of the left renal branch here, and the aneurysm of the left common iliac just below the stent graft. We first treated the iliac aneurysm implanting an iliac branched device on the left side,
so preserving the left hypogastric artery. And in the same operation, from a bowl, we catheterized the left renal branch and fixed the endoleak that you see on the left side, with a total stent relining, with a nice final result on the right side.
And this is the CT scan follow-up one year after the reintervention. No endoleak at the level of the left renal branch, and nice exclusion of the left common iliac aneurysm. In conclusion, ladies and gentlemen, the risk of type I endoleak after FEVAR and BEVAR
is very low when the repair is planning with an adequate proximal sealing zone as we heard before from Professor Verhoeven. Much of reinterventions are due to type II and III endoleaks that can be treated by embolization or stent reinforcement. Last, but not least, the strict follow-up program
with CT scan is of paramount importance after these procedures. I thank you very much for your attention.
- Thank you very much for the privilege of participating in this iconic symposium. I have no disclosures pertinent to this presentation. The Atelier percutaneous endovascular repair for ruptured abdominal aortic aneurysms is a natural evolution of procedural technique due to the success of fully percutaneous endovascular
aortic aneurysm repair in elective cases. This past year, we had the opportunity to publish our data with regard to 30 day outcomes between percutaneous ruptured aneurysm repairs and surgical cutdown repairs utilizing the American College of Surgeons NSQIP database,
which is a targeted database which enrolls about 800 hospitals in the United States, looking at both the univariate and multivariate analyses comparing preoperative demographics, operative-specific variables and postoperative outcomes. There were 502 patients who underwent
ruptured abdominal aortic aneurysms that were included in this review, 129 that underwent percutaneous repair, whereas 373 underwent cutdown repair. As you can see, the majority were still being done by cutdown.
Over the four years, however, there was a gradual increase in the number of patients that were having percutaneous repair used as their primary modality of access, and in fact a more recent stasis has shown to increase up to 50%,
and there certainly was a learning curve during this period of time. Looking at the baseline characteristics of patients with ruptured aneurysms undergoing both modalities, there was not statistically significant difference
with regard to these baseline characteristics. Likewise, with size of the aneurysms, both were of equal sizes. There was no differences with regard to rupture having hypotension, proximal or distal extension of the aneurysms.
What is interesting, however, that the patients that underwent percutaneous repair tended to have regional anesthesia as their anesthesia of choice, rather than that of having a general. Also there was for some unexplained reason
a more significant conversion to open procedures in the percutaneous group as compared to the cutdown group. Looking at adjusted 30-day outcomes for ruptured endovascular aneurysm repairs, when looking at the 30-day mortality,
the operative time, wound complications, hospital length of stay, that was not statistically significant. However, over that four year period of time, there tended to be decreased hospital length of stay as well as decreased wound complications
over four years. So the summary of this study shows that there was an increased use of fully percutaneous access for endovascular repairs for ruptured aneurysms with noninferiority compared to traditional open femoral cutdown approaches.
There is a trending advantage over conventional surgical exposure with decreased access-related complications, as well as decreased hospital length of stay. Now, I'm going to go through some of the technical tips, and this is really going to be focused upon
the trainees in the room, and also perhaps those clinicians who do not do percutaneous access at this time. What's important, I find, is that the utility of duplex ultrasonography, and this is critical to delineate the common
femoral artery access anatomy. And what's important to find is the common femoral artery between the inguinal ligament and this bifurcation to the profunda femoral and superficial femoral arteries. So this is your target area. Once this target area is found,
especially in those patients presenting with ruptured aneurysm, local anesthesia is preferred over general anesthesia with permissive hypotension. This is a critical point that once you use ultrasound, that you'd want to orient your probe to be
90 degrees to the target area and measure the distance between the skin and the top of that artery. Now if you hold that needle at equidistance to that same distance between the skin and the artery and angle that needle at 45 degrees,
this will then allow you to have the proper trajectory to hit the target absolutely where you're imaging the vessel, and this becomes important so you're not off site. Once micropuncture technique is used, it's always a good idea just to use
a quick fluoroscopic imaging to show that your access is actually where you want it to be. If it's not, you can always re-stick the patient again. Once you have the access in place, what can then happen is do a quick angio to show in fact you have reached the target vessel.
This is the routine instructions for use by placing the percutaneous suture-mediated closure system at 45 degree angles from one another, 90 degrees from one another. Once the sheath is in place for ruptured aneurysm, the placement of a ballon occlusion
can be done utilizing a long, at least 12 French sheath so that they'll keep that balloon up in place. What's also good is to keep a neat operative field, and by doing so, you can keep all of these wires and sutures clean and out of the way and also color code the sutures so that you have
ease and ability to close them later. Finally, it's important to replace the dilator back in the sheath prior to having it removed. This is important just so that if there are problems with your percutaneous closure, you can always very quickly replace your sheath back in.
Again, we tend to color code the sutures so we can know which ones go with which. You can also place yet a third percutaneous access closure device if need be by keeping the guide wire in place. One other little trick that I actually learned
from Ben Starnes when visiting his facility is to utilize a Rumel mediated technique by placing a short piece of IV tubing cut length, running the suture through that, and using it like a Rumel, and that frees up your hand as you're closing up
the other side and final with closure. The contraindications to pREVAR. And I just want to conclude that there's increased use of fully percutaneous access for endovascular repair. There's trending advantages over conventional surgical exposure with decreased
access related complications, and improved outcomes can be attributed to increased user experience and comfort with percutaneous access, and this appears to be a viable first option. Thank you very much.
- Thank you Tim, Manny, Dr. Veith. Again thank you for the kind invitation. Um, here are my disclosures. The Chimney Snorkel Sandwich technique is really one that's been used and discussed many times throughout this great meeting in years past.
I've been asked to kind of see how we expand the use for thoracoabdominal aneurysms. Um, basically it's a matter of putting a parallel graft and then having an inner graft that will help seal the aneurysm sac itself by maintaining
perfusion to the visceral vessels. Um, the number of parallel grafts has been shown to be of note, and generally if you get beyond two parallel grafts at any one location, that tends to dramatically increase the incidence of
gutter leaks and potential for continued perfusion of the aneurysm sac. Here again showing at two, they still keep a reasonable aortic diameter, but once you start going three and four parallel grafts you tend to have significant compression
of the main aortic graft itself, as well as the potential for gutter leaks. Um, the PERICLES Registry certainly looked as I know has been discussed earlier in this meeting, and basically what it showed was that this was a reasonable way of treating
some of these complex aneurysms with a durable outcome going out to two to three years, uh, at a survival rate of over 70 percent. So, to show how we use this for patients with thoracoabdominal aneurysms, this was a 67 year, I use the term is,
a 67-year-old gentleman presented urgently with a sudden onset of back and abdominal pain. Apparently he was, uh, had a new wife and was trying some sexually enhancing medications from the DR. Had a history of coronary artery disease,
erectile dysfunction, and congestive heart failure, and CT scan revealed a type four thoracoabdominal dissection with a eight centimeter juxtarenal aneurysm, and he was in acute pain. Uh, here is the CT scan as we go through,
and you can see obviously the very complex dissection. You had a small segment of perfusion still around the level of the celiac going down into the SMA, uh, and then this rather, again the renals were
also with a small luminal area, and then a large aneurysm going up to eight centimeters going down into the abdominal component, and then reasonable access vessels from below. This shows the dissection extending down
through the thoracoabdominal segment, and again, he was in acute pain. Uh, so we came in and did an angiogram and IVUS, uh, and here we show the area of the dissection going down as well as the take-off of the subclavian artery.
Again, the true lumen being here. This was confirmed with IVUS. The IVUS sash, and this is the true lumen here, the false lumen being around the periphery, and as you go through you can see there's almost complete collapse of that
true lumen throughout the cardiac cycle. Uh, we performed a left carotid subclavian bypass, and embolized the left subclavian artery and put a thoracic endograft in, covering that lead point as you go in and taking it really almost up to the level of the left carotid artery.
There you can see the occluded subclavian. Uh, with that in place we then prepared to do a four vessel sandwich, or double sandwich, technique. Here we came down, we brought the grafts down to about the level of the takeoff of the celiac access with thoracic endografts.
Lateral shows the takeoff of the celiac and the SMA. Uh, we were able to catheterize both those vessels from the axillary region and put stents going out in this two sandwich technique, uh, and then actually put our stents going out from both the celiac and SMA.
We then were able to do that once we had those stents in place with adequate overlap and no real gutter leak, we then came down and similarly put another graft down to the takeoff of the renal vessels and then selectively catheterized
the right and left renal. Here you can see the stenosis near the origin of the right renal artery. With that we then performed balloon angioplasty with covered stents, I believe these were VBX stents going out,
and then covered that further down as we went down into the area of the eight centimeter aneurysm. And here we come in building down from that area and the perivisceral segment down and then to the iliacs showing good perfusion down to the takeoff of the
hypogastric, and then finally angiogram showed we had good perfusion to celiac, SMA, both renal vessels, and then down through the aneurysm sac itself. This is, uh, he remains stable. His postoperative course actually was uneventful.
He was discharged from the hospital at day four. He's been seen back now at one year follow up at six and 12 month follow up and he's remained stable with no evidence of endo-leak. So I appreciate the opportunity to try and present a more novel way of managing
these patients in the acute setting. Thank you very much.
- Thank you. This presentation is for Thomas Larzon. He could not be here today, so I will present it for him. This is his disclosures. When we're talking about Nellix, the prefillings of the bags allow you to control ongoing bleeding.
(coughs) I'm sorry. And preserve circulation, which you cannot do when you're using this in EVAR, when you have to use an aortic balloon. The mechanism of the sac,
when you use the sac in Nellix, is not really built for ruptures. I'm sorry. So the pressure is not really defined. I'm sorry. This is a patient with a 62 millimeters aneurysm.
On survival, he was a very complex case. (coughs) I apologize. Oh, sorry. Thank you, better. On 4-fenestration and he presented
on chock and rupture, 80 millimeter aneurysm. We took him to the operation room and what we observed is that we got stable with the cell line. We got the patient stable and then it took time to do the procedure.
And there was no visible endoleak, but when we put the polymer inside, we could not get stability, which was very interesting. Quite a lot of polymer and the outcome was fatal and the bag itself had a big rupture on autopsy. So the question is, when you use the endobag
and it ruptures, will it increase the rupture itself? It's a question. Limitations when we're talking about endoleaks, normal endoleaks type 1A, you can solve with different ways. With going proximal and chimneys and other methods, quite standard.
But in Nellix, you have to do some adjunct procedures that can solve the problem, but might be challenging. This one case where we put the two Nellix inside, we couldn't position in correctly. It was trapped.
So as you see there, it's not correctly placed. And then we got an endoleak Type 1A. And we could solve it with proximal extension of Nellix and Nellix and then put in Onyx, that we use quite often and solve the problem. This is another case with Type 1 endoleak after EVAR,
which could be solved with two Nellix. Nellix and Nellix and we could solve the problem. This is a patient with a Type 1 endoleak, one patent renal chimney and one access route. This we could solve with SMA chimney and Nellix, as you can see in these photos.
And in this the SMA open and the completion on the left and it was solved. This is an interesting case with pervious open repair and the graft and there is a rupture with a plan to do a two Nellix extension with left renal chimney and we could do the chimeny
and then during the final phase of the polymer filling proximal migration occurred. And this is how it looked like, it jumped up and covered the SMA, which was a fatal occlusion. And this is what I would call the ketchup effect
or the champagne cork effect of jumping due to the pressure. In conclusion, Nellix may have the potential benefits in treating rupture aneurysm, stabilizing the patient while doing the procedure, you need some adjunct procedure and the instructions for use might be different
than the elective cases. I would add also, I see it also Nellix very prominent in ruptures because it's very fast to get in with the instrument and get the feelings of the bags and you don't need to do the contralateral leg feeling.
Thank you very much.
- That's a long title, thank you. We shortened the title, and just said, The Iliac Artery's Complicating Complex Juxtarenal and Thoracal Abdominal Repair. I have no disclosures. So, Iliac artery preservation is important whenever we start doing complex aortic aneurysm repair.
We don't understand completely what the incidence is with these extensive aneurysms. We know with AAAs, anywhere in the 10 to 40% have some sort of iliac artery involvement. It certainly can complicate the management as we get to these more complicated repairs.
Iliac artery preservation may be important for prevention of spinal cord ischemia, and those people in whom we can maintain both hypogastric arteries, it occurs at a less significant rate, with less severe symptoms and higher rates of recovery.
The aim of our study was to evaluate the incidence, management, and outcomes of iliac artery aneurysms associated with complex aortic aneurysms treated with fenestrated and branched endografts. Part of a PS-IDE study over a 15 year period of time,
this is dated from the Cleveland Clinic for the treatment of juxtarenal aneurysms and thoracal abdominal aortic aneurysms. For the purpose of this study, we defined an iliac artery aneurysm is 21 mm or greater as determined by diameter
by our core lab. We chose 21 mm because this was outside of the IFU for the iliac wounds that we had currently available to us at that time. We did multivariable analysis on the number of different outcomes. And we looked at the incidence
of iliac artery aneurysms by repair type. In all the aneurysms we treated, we see about a third of the patients had some level of iliac artery aneurysm involvement. In those patients that had less extensive thoracal abdominals, the type three
and type four abdominals, it occurred in about a third of the cases. A little bit less than the type two and the type one thoracal abdominals. We look at the demographics between those that had iliac artery aneurysm
involvement and those that did not have iliac artery involvement. It was more common in males to have iliac artery involvement than any other group. There are more females that didn't have iliac artery aneurysms. The rest
of the demographics were the same between the two groups. We look at the anatomic characteristics of the iliac artery aneurysms, about 60% of them were unilateral, about 40% of them were bilateral.
The mean iliac artery aneurysm size was 28 mm and that was the same on both sides. And we look at thought the percent that were actually very large, or considered large enough to potentially in and of themselves the repairs
greater than three centimeters. About 28% of them were greater than three centimeters on each side. If we look at our iliac artery aneurysm treatment type, this is 509 iliac artery aneurysms that
were treated out of all these patients. About 46% of them, we were able to obtain a seal distal to the iliac artery aneurysm. So it really only involved the proximal portion, the proximal half of the iliac artery.
20% of them, we placed a hypogastric branched endograft, and about 20% of them, we placed a hypogastric coverage plus embolization of that internal iliac artery. About 13% of them were left untreated at the time for a variety of different operative reasons.
Why is there a difference between the hypogastric coverage and embolization? It was availability of devices and surgeon choice at the time. At one point, we had a opportunity to be able to treat both fairly easily
on both sides and at one point we did not. Larger iliac artery aneurysms were treated with hypogastric coverage or hypogastric branched endografts, and there was a significant difference between the two. Most of the mean
size of those that were actually treated with either hypogastric branch or embolization for greater than three centimeters. If we look at peri-operative outcomes in those without iliac artery aneurysms versus those with iliac artery aneurysms.
We see that the fluoroscopy estimated blood loss is larger for those with iliac artery aneurysms, fluoroscopy time was longer and procedure duration was a bit longer as well. Obviously, a bit more complicated procedure,
more steps that's going to take a little bit longer to perform them. It did not effect the length of stay for these patients or the length of stay in the intensive care unit following the procedures. We look
at all-cause mortality at five years, no difference in whether they had an iliac artery aneurysm or not. It didn't matter whether it was unilateral or bilateral. If we look at aneurysm-related mortality, it's the same whether
they had the iliac artery aneurysm or not. Same for unilateral versus bilateral as well. Where we start to see some differences are the freedom from reintervention. This did vary between, among the three groups. In those patients without an iliac
artery aneurysm, they had the lower reintervention rate than those with the unilateral iliac artery aneurysm, and even lower rates from freedom from reintervention in those that had bilateral iliac artery aneurysms. Spinal cord ischemia, one of the
reasons we try to preserve both the hypogastric arteries. Look at our total spinal cord ischemia incidents. It didn't vary between the two groups, but if we look specifically, the type two thoracal abdominal aortic aneurysms in those patients that had bilateral
iliac arte higher rate of spinal cord ischemia compared to those that did not have any iliac artery aneurysms or those that had an internal iliac, a single iliac artery aneurysm.
So, iliac artery aneurysms affect about a third of the patients with complex aortic disease. They do not, their presence does not affect all-cause mortality or aneurysm related mortality. They are associated with a higher reintervention rate.
In extensive aneurysms, may be higher association with higher spinal cord ischemia rates. We need additional efforts are needed to improve outcomes and understanding appropriate application of different treatment options for patients with
complex aortic disease. Thank you.
- Thank you again, Dr. Veith, for the kind invitation to talk about this topic. This year, these are my disclosure. In the last five years, we treated 76 cases of Fenestrated and Branched repair for torque abdominal unfit for open surgery. And we soon realized that the upper extremity access
is needed in almost up to 90% of the cases. The first cases were managed by standard cut down in high-brachial and brachial region, but as soon as we improved our skills in percutaneous approach for the groins, we moved also in a transaxillary and percutaneous access
in the area. What we learned from the tanvis group of Hamburg is that the best spot to puncture the artery is the first segment, so the segment within the clavicula and the pectoralis minor. And to do so it is mandatory to use an echoguidance
during the procedure. Here you can see how nicely you can evaluate your axillary artery and avoid puncture the artery through the pectoralis minor where there are nerves and collaterals and also collaterals of the vein. Here is short video you can see I'm puncturing
the axillary artery just below the clavicula with a short guide wire, we introduce 6 French sheath and then we place two proglides according to the instruction for use of the device for the femoral artery. And at the end we usually put a 9 French short sheet
and then we start the procedure. As soon as we are finished with the main body of the, finished with the graft and we have bridged all the vessels from below, we downsize the femoral access but we keep in one groin a 7 French sheath
in order to perform then the final closure. What we do as soon as we are finished the complete procedure we snare a wire from the femoral artery we push the seven French sheath in the axillary artery, we pull back the 12 French sheath in the axillary artery and then we are ready to unlink the two sheath
and so we push a wire in the axillary, from the axillary in the aorta, and one wire in the arm. So that we can deploy a balloon which is sized according to the axillary artery diameter we inflate the balloon and we remove the 12 French sheath and now it is possible to tie the knot of the proglide
over the balloon without any worry to have bleeding and we check with the wire then we remove the wire and then we tie the know of the proglide again. And we ensure that there is no defect and leaking on this region. We have done so far 50 cases and they are
enrolled in this study which is almost completed. And here you can see the results. We have mainly punctured the left side of the axillary, you can see that nicely the diameter of the axillary artery in this region is 8.9 millimeter the sheath size was mainly the 12 French
but we also use sometime the 16 in cases which on iliac was not available. And we also punctured the artery if there was a pacemaker or previous scar for cardiac operation. And here are the results you can see we had no open conversion, the technical success
was 92% of the cases because we are to deploy three cover stent to achieve complete sealing and one bare stent to treat dissection distally to the puncture site. We didn't have any false aneurysm on the follow up and arterial thrombosis and no nerve injuries
in the follow up. So for the discussion, if you look on the research where there are different approach in the discussion is called either to go for the first or the third segment we believe that the first segment is better because it is bigger, is more proximal
and there are no nerves in this region. And by proximalizing the approach you can also work from the right side of your patient so you don't need the guy left side of the table. Moreover, by having the 12 and the standard 19 seven french sheath you can enhance your pushability
here you can see that the 12 french sheath arrives close to the branch of renal artery and the seven french sheath is well within the renal branch. And here you can see where the hands of the operator are. Of course if you enhance this technique you can downsize contra arterial femoral sheath
needed to reach three vessels so maybe lowering your risk of limb ischemia and paraplegia and if you insert this approach in the femoral percutaneous approach, you can see that you can cut down your procedural time your OR occupation time and also
the need of post operative transfusion. So dear chairman and colleagues in conclusion, in our experience the first segment is the way to go. Echo guided puncture is mandatory. Balloon assisted removal is the safest way to do it. Our results prove that it's feasible and safe.
There are different potential advantages over branchial and cutdown. And we hope to collect more data to have more robust data to support this approach. Thank you.
- I'd like to thank Dr. Veith and the committee for the privilege of presenting this. I have no disclosures. Vascular problems and the type of injuries could be varied. We all need to have an awareness of acute and chronic injuries,
whether they're traumatic, resulting with compression, occlusion, tumoral and malformation results, or vasospastic. I'd like to present a thoracoscopic manipulation of fractured ribs to prevent descending aortic injury
in a patient with chest trauma. You know, we don't think about this but they can have acute or delayed onset of symptoms and the patient can change and suddenly deteriorate with position changes or with mechanical ventilation,
and this is a rather interesting paper. Here you can see the posterior rib fracture sitting directly adjacent to the aorta like a knife. You can imagine the catastrophic consequences if that wasn't recognized and treated appropriately.
We heard this morning in the venous session that the veins change positions based on the arteries. Well, we need to remember that the arteries and the whole vascular bundle changes position based on the spine
and the bony pieces around them. This is especially too when you're dealing with scoliosis and scoliotic operations and the body positioning whether it's supine or prone the degree of hypo or hyperkyphosis
and the vertebral angles and the methods of instrumentation all need to be considered and remembered as the aorta will migrate based on the body habits of the patient. Screws can cause all kinds of trouble.
Screws are considered risky if they're within one to three millimeters of the aorta or adjacent tissues, and if you just do a random review up to 15% of screws that are placed fall into this category.
Vertebral loops and tortuosity is either a congenital or acquired anomaly and the V2 segment of the vertebral is particularly at risk, most commonly in women in their fifth and sixth decades,
and here you can see instrumentation of the upper cervical spine, anterior corpectomy and the posterior exposures are all associated with a significant and lethal, at times, vertebral artery injuries.
Left subclavian artery injury from excessively long thoracic pedicle screws placed for proximal thoracic scoliosis have been reported. Clavicular osteosynthesis with high neurovascular injury especially when the plunge depth isn't kept in mind
in the medial clavicle have been reported and an awareness and an ability to anticipate injury by looking at the safe zone and finding this on the femur
with your preoperative imaging is a way to help prevent those kinds of problems. Injuries can be from stretch or retraction. Leave it to the French. There's a paper from 2011 that describes midline anterior approach
from the right side to the lumbar spine, interbody fusion and total disc replacement as safer. The cava is more resistant to injury than the left iliac vein and there's less erectile dysfunction reported. We had a patient present recently
with the blue bumps across her abdomen many years after hip complicated course. She'd had what was thought to be an infected hip that was replaced, worsening lower extremity edema, asymmetry of her femoral vein on duplex
and her heterogeneous mask that you can see here on imaging. The iliac veins were occluded and compressed and you could see in the bottom right the varicosities that she was concerned about. Another case is a 71-year-old male who had a post-thrombotic syndrome.
It was worsened after his left hip replacement and his wife said he's just not been the same since. Initially imaging suggests that this was a mass and a tumor. He underwent biopsy
and it showed ghost cells. Here you can see the venogram where we tried to recanalize this and we were unsuccessful because this was actually a combination of bone cement and inflammatory reaction.
Second patient in this category, bless you, is a 67-year-old female who had left leg swelling again after a total hip replacement 20 plus years ago. No DVTs but here you can see the cement compressing the iliac vein.
She had about a 40% patency when you put her through positioning and elected not to have anything done with that. Here you could see on MR how truly compressed this is. IVA suggested it was a little less tight than that.
So a vascular injury occurs across all surgical specialties. All procedures carry risk of bleeding and inadvertent damage to vessels. The mechanisms include tearing, stretching, fracture of calcific plaques,
direct penetration and thermal injury. The types of injuries you hear are most common after hip injuries, they need to be recognized in the acute phase as looking for signs of bleeding or ischemia. Arterial lesions are commonly prone then.
Bone cement can cause thermal injury, erosion, compression and post-implant syndrome. So again, no surgery is immune. You need to be aware and especially when you look at patients in the delayed time period
to consider something called particle disease. This has actually been described in the orthopedic literature starting in the 70s and it's a complex interaction of inflammatory pathways directed at microparticles that come about
through prosthetic wear. So not only acute injury but acute and chronic symptoms. Thank you for the privilege of the floor.
- Thanks again Dr. Greenhalgh, Dr. Veith. These are my disclosures. We first took on a systematic review and meta analysis on the risk of bowel ischemia after ruptured abdominal aortic aneurysm repair. We found the prevalence of 10%, and that's been very constant.
OR 11% open repair, twice as much as an EVAR. And it's incidence has been very constant over the years from 1995 to 2015 so this scatter plot shows we didn't learn anything on this subject in these years. So the diagnosis of colon ischemia
is difficult after ruptured aneurysm. And we sought to look how effective sigmoidoscopy is in the diagnosis. And towards that end, we did a retrospective cohort study from the AJAX-cohort I mentioned before. Patients who underwent ruptured aneurysm repair,
only those who had repair were looked at and three major referral hospitals. And those patients had to survive more than six hours after arrival in the ICU. We did sigmoidoscopy only on clinical suspicion. Sigmoidoscopy results were categorized as
no ischemia, inconclusive, mild ischemia, or severe ischemia grade two or three. Laparotomy was the reference standard to demonstrate no transmural ischemia. 345 patients were considered. 81 open repair, 19% EVAR.
80% were male. These were the ages. And the 30-day mortality in this entire group was 26%. So we looked at clinical suspicion for colon ischemia, and found 46 patients moderate, a big group no clinical suspicion,
and a small group of 16 patients with a high clinical suspicion. The no clinical suspicion group, no one turned out to have colon ischemia, and mortality in this group was 20%. When we look at the other end, the high clinical suspicion,
they had immediate laparotomy, so without colonoscopy, and transmural ischemia was found in 83% of these patients, and they had a mortality of 50%. But, of course, it's always the gray area, in the middle, that is interesting. And we came to this clinical suspicion when they had
bloody stools, septic profile, diarrhea, abdominal pain or distention, or unknown. And those patients with the moderate clinical suspicion, they received colonoscopy. Negative were 16 of them, mild colon ischemia were seen in 19,
and severe in 11 patients. They turned out to have transmural ischemia none of them in the negative. So the negative predictive value for sigmoidoscopy is really good. In the middle group with mild colon ischemia,
only two out of 19 turned out to have transmural ischemia. And the severe ischemia group, eight of 11 turned out to have transmural ischemia on operation. So there was a total of 10 patients in this group who turned out to have transmural ischemia.
So, in conclusion, Mr. Chairman, ladies and gentleman, sigmoidoscopy is highly effective in ruling out colon ischemia. So it can prevent unnecessary operations. And when in doubt, transmural ischemia detection increases with colonoscopy from 22 to 73%.
Thank you for your attention.
- Good afternoon to everybody, this is my disclosure. Now our center we have some experience on critical hand ischemia in the last 20 years. We have published some papers, but despite the treatment of everyday, of food ischemia including hand ischemia is not so common. We had a maximum of 200 critical ischemic patients
the majority of them were patient with hemodialysis, then other patients with Buerger's, thoracic outlet syndrome, etcetera. And especially on hemodialysis patients, we concentrate on forearms because we have collected 132 critical ischemic hands.
And essentially, we can divide the pathophysiology of this ischemic. Three causes, first is that the big artery disease of the humeral and below the elbow arteries. The second cause is the small artery disease
of the hand and finger artery. And the third cause is the presence of an arterial fistula. But you can see, that in active ipsillateral arteriovenous fistula was present only 42% of these patients. And the vast majority of the patients
who had critical hand ischemia, there were more concomitant causes to obtain critical hand ischemia. What can we do in these types of patients? First, angioplasty. I want to present you this 50 years old male
with diabetes type 1 on hemodialysis, with previous history of two failed arteriovenous fistula for hemodialysis. The first one was in occluded proximal termino-lateral radiocephalic arteriovenous fistula. So, the radial artery is occluded.
The second one was in the distal latero-terminal arteriovenous fistula, still open but not functioning for hemodialysis. Then, we have a cause of critical hand ischemia, which is the occlusion of the ulnar artery. What to do in a patient like this?
First of all, we have treated this long occlusion of the ulnar artery with drug-coated ballooning. The second was treatment of this field, but still open arteriovenous fistula, embolized with coils. And this is the final result,
you can see how blood flow is going in this huge superficial palmar arch with complete resolution of the ischemia. And the patient obviously healed. The second thing we can do, but on very rarely is a bypass. So, this a patient with multiple gangrene amputations.
So, he came to our cath lab with an indication to the amputation of the hand. The radial artery is totally occluded, it's occluded here, the ulnar artery is totally occluded. I tried to open the radial artery, but I understood that in the past someone has done
a termino-terminal radio-cephalic arteriovenous fistula. So after cutting, the two ends of the radial artery was separated. So, we decided to do a bypass, I think that is one of the shortest bypass in the world. Generally, I'm not a vascular surgeon
but generally vascular surgeons fight for the longest bypass and not for the shortest one. I don't know if there is some race somewhere. The patient was obviously able to heal completely. Thoracic sympathectomy. I have not considered this option in the past,
but this was a patient that was very important for me. 47 years old female, multiple myeloma with amyloidosis. Everything was occluded, I was never able to see a vessel in the fingers. The first time I made this angioplasty,
I was very happy because the patient was happy, no more pain. We were able to amputate this finger. Everything was open after three months. But in the subsequent year, the situation was traumatic. Every four or five months,
every artery was totally occluded. So, I repeated a lot of angioplasty, lot of amputations. At the end it was impossible to continue. After four years, I decided to do something, or an amputation at the end. We tried to do endoscopic thoracic sympathectomy.
There is a very few number of this, or little to regard in this type of approach. But infected, no more pain, healing. And after six years, the patient is still completely asymptomatic. Unbelievable.
And finally, the renal transplant. 36 years old female, type one diabetes, hemodialysis. It was in 2009, I was absolutely embarrassed that I tried to do something in the limbs, inferior limbs in the hand.
Everything was calcified. At the end, we continued with fingers amputation, a Chopart amputation on one side and below the knee major amputation. Despite this dramatic clinical stage, she got a double kidney and pancreas transplant on 2010.
And then, she healed completely. Today she is 45 years old, this summer walking in the mountain. She sent to me a message, "the new leg prostheses are formidable". She's driving a car, totally independent,
active life, working. So, the transplant was able to stop this calcification, this small artery disease which was devastating. So, patients with critical high ischemia have different pathophysiology and different underlying diseases.
Don't give up and try to find for everyone the proper solution. Thank you very much for your attention.
- Thank you, Larry, thank you, Tony. Nice to be known as a fixture. I have no relevant disclosures, except that I have a trophy. And that's important, but also that Prabir Roy-Chaudhury, who's in this picture, was the genesis of some of the thoughts that I'm going to deliver here about predicting renal failure,
so I do want to credit him with bringing that to the vascular access space. You know, following on Soren's talk about access guidelines, we're dealing with pretty old guidelines, but if you look at the 2006 version, you know, just the height--
The things that a surgeon might read in his office. CKD four, patients there, you want a timely referral, you want them evaluated for placement of permanent access. The term "if necessary" is included in those guidelines, that's sometimes forgotten about.
And, of course, veins should be protected. We already heard a little bit about that, and so out our hospital, with our new dialysis patients, we usually try to butcher both antecubital veins at the same time. And then, before we send them to surgery
after they've been vein-marked, we use that vein to put in their preoperative IV, so that's our vascular access management program at Christiana Care. - [Male Speaker] That's why we mark it for you, Teddy. (laughing)
- So, you know, the other guideline is patients should have a functional permanent access at the initiation of dialysis therapy, and that means we need a crystal ball. How do we know this? A fistula should be placed at least six months
before anticipated start of dialysis, or a graft three to six weeks. Anybody who tells you they actually know that is lying, you can't tell, there's no validated means of predicting this. You hear clinical judgment, you can look at
all sorts of things. You cannot really make that projection. Now there is one interesting study by Tangri, and this is what Premier brought to our attention last year at CIDA, where this Canadian researcher and his team developed a model for predicting
progression of chronic kidney disease, not specifically for access purposes, but for others. They looked at a large number of patients in Canada, followed them through chronic kidney disease to ESRD, and they came up with a model. If you look at a simple model that uses age, sex,
estimated GFR from MDRD equation and albuminuria to predict when that patient might develop end stage renal disease, and there's now nice calculators. This is a wonderful thing, I keep it on my phone, this Qx Calculate, I would recommend you do the same,
and you can put those answers to the questions, in this app, and it'll give you the answer you're looking for. So for instance, here's a case, a 75-year-old woman, CKD stage four, her creatinine's 2.7, not very impressive,
eGFR's 18. Her urine protein is 1200 milligrams per gram, that's important, this is kind of one of the major variables that impacts on this. So she's referred appropriately at that stage to a surgeon for arteriovenous access,
and he finds that she really has no veins that he feels are suitable for a fistula, so an appropriate referral was made. Now at that time, if you'd put her into this equation with those variables, 1200, female, 75-year-old, 18 GFR, at two years, her risk of ESRD is about 30%,
and at five years about 66%, 67%. So, you know, how do you use those numbers in deciding if she needs an access? Well, you might say... A rational person might say perhaps that patient should get a fistula,
or at least be put in line for it. Well, this well-intentioned surgeon providing customer service put in a graft, which then ended up with some steal requiring a DRIL, which then still had steal, required banding, and then a few months, a year later
was thrombosed and abandoned because she didn't need it. And I saw her for the first time in October 2018, at which time her creatinine is up to 3.6, her eGFR's down to 12, her protein is a little higher, 2600, so now she has a two-year risk of 62%, and a five-year risk of 95%,
considerably more than when this ill-advised craft was created. So what do you do with this patient now? I don't have the answer to that, but you can use this information at least to help flavor your thought process,
and what if you could bend the curve? What if you treated this patient appropriately with ACE inhibitors and other methods to get the protein down? Well, you can almost half her two-year risk of renal failure with medical management.
So these considerations I think are important to the team, surgeon, nurses, nephrologists, etc., who are planning that vascular access with the patient. When to do and what to do. And then, you know, it's kind of old-fashioned to look at the trajectory.
We used to look at one over creatinine, we can look at eGFR now, and she's on a trajectory that looks suspicious for progression, so you can factor that into your thought process as well. And then I think this is the other very important concept, I think I've spoken about this here before,
is that there's no absolute need for dialysis unless you do bilateral nephrectomies. Patients can be managed medically for quite a while, and the manifestations of uremia dealt with quite safely and effectively, and you can see that over the years, the number of patients
in this top brown pattern that have been started on dialysis with a GFR of greater than 15 has fallen, or at least, stopped rising because we've recognized that there's no advantage, and there may be disadvantages to starting patients too early.
So if your nephrologist is telling I've got to start this patient now because he or she needs dialysis, unless they had bilateral nephrectomies that may or may not be true. Another case,
64-year-old male, CKD stage four, creatinine about four, eGFR 15, 800 milligrams of proteinuria, referred to a vascular access surgeon for AV access. Interesting note, previous central lines, or AICD, healthy guy otherwise.
So in April 2017 he had a left wrist fistula done, I think that was a very appropriate referral and a very appropriate operation by this surgeon. At that time his two-year risk was 49, 50%, his five-year risk 88%. It's a pretty good idea, I think, to get a wrist fistula
in that patient. Once again, this is not validated for that purpose. I can't point you to a study that says by using this you can make well-informed predictions about when to do vascular access, but I do think it helps to flavor the judgment on this.
Also, I saw him for the first time last month, and his left arm is like this. Amazing, that has never had a catheter or anything, so I did his central venogram, and this is his anatomy. I could find absolutely no evidence of a connection between the left subclavian and the superior vena cava,
I couldn't cross it. Incidentally, this was done with less than 20 CCs of dye of trying to open this occlusion or find a way through, which was unsuccessful. You can see all the edema in his arm. So what do you do with this guy now?
Well, up, go back. Here's his trajectory of CKD four from the time his fistula is done to the time I'm seeing him now, he's been pretty flat. And his proteinuria's actually dropped
with medical management. He's only got 103 milligrams per gram of proteinuria now, and his two-year risk is now 23%, his five-year risk is 56%, so I said back to the surgeon we ligate this damn thing, because we can't really do much to fix it,
and we're going to wait and see when it's closer to time to needing dialysis. I'm not going to subject this guy to a right-arm fistula with that trajectory of renal disease over the past two years. So combining that trajectory with these predictive numbers,
and improved medical care for proteinuria I think is a good strategy. So what do you do, you're weighing factors for timing too early, you've got a burden of fistula failure, interventions you need to use to maintain costs, morbidity, complications,
steal, neuropathy that you could avoid versus too late and disadvantages of initiating hemodialysis without a permanent access. And lastly, I'm going to just finish with some blasphemy. I think the risk of starting dialysis with a catheter is vastly overstated.
If you look at old data and patient selection issues, and catheter maintenance issues, I think... It's not such an unreasonable thing to start a patient with a catheter. We do it all the time and they usually live.
And even CMS gives us a 90-day grace period on our QIP penalties, so... If you establish a surgeon and access plan, I think you're good to go. So who monitors access maturation? I don't know, somebody who knows what they're doing.
If you look at all the people involved, I know some of these individuals who are absolute crackerjack experts, and some are clueless. It has nothing to do with their age, their gender, their training, their field. It's just a matter of whether they understand
what makes a good fistula. You don't have to be a genius, you just can't be clueless. This is not a mature usable fistula, I know that when I see it. Thank you.
- 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 so much, and thank you Frank for your kind invitation, I have no disclosures. As you all know, Frank and his group were among the first to do the ruptured EVAR operations here in New York. And if there were any doubts before, they probably disappeared after the publication of
the three year results of the IMPROVE trial that we have heard Janet talk about. When that trial was published last year I wrote an editorial in the British Medical Journal where I pointed out that the advantage of EVAR when treating patients with ruptured AAA
may actually have been underestimated in the IMPROVE trial. Partly because local anesthesia was used in only 6% of the patients and also because intra-abdominal pressure was not monitored routinely. We did a large cohort study in the Swedvasc registry and looking at abdominal compartment syndrome after
AAA repair, I will focus now only on the ruptured patients. There were actually almost 7,000 repairs but 1,300 for ruptured and we could verify that the risk for ACS was the same after open or endovascular repair for ruptured. However, 10% of the open repairs had been treated
with open abdomen prophylactically. You can see here how the mortality curves differ between the patients who developed ACS after ruptured AAA repair and the mortality is actually double if they get ACS, and there was no difference in the outcome
if the primary treatment was open or EVAR. So why is it that the survival benefit of EVAR is lost if the patient develops ACS? Well, it could be that abdominal compartment is simply such a deadly complication that the primary treatment doesn't matter, but there can also be
special risks when the patient develop ACS after EVAR for ruptured AAA and to focus on this problem we performed a second study on 120 patients who developed ACS, focusing on the differences between open and endo. There were three different pathological mechanisms
behind developing the abdominal compartment syndrome. The most common was a generalized oedema, but there was also bowel ischemia and bleeding. The timing of decompression was such that half of the patients were decompressed within 24 hours, another quarter within two days, and the remaining
quarter later than two days. And as you can see here, most of these patients were operated on for rupture, but as many for EVAR, with EVAR as with open repair. The survival curves were not significantly different depending on the pathophysiological mechanism,
nor on the timing of the decompression. But the abdominal compartment syndrome developed much earlier after EVAR than after open repair as you can see in this figure. So we concluded that in patients developing ACS, survival was poor generally speaking,
it did not differ depending on pathophysiological mechanisms nor on the timing of decompression. We did find, however, that the duration of intra-abdominal hypertension was an independent predictor of the need for renal replacement therapy, and although this is the largest study ever
published in this area, it's still a small group of patients, only 120 and there could be a type two error here so that actually a delay in decompression since it does lead to the need of renal replacement therapy, that it could actually also effect survival if we had had more patients.
ACS developed earlier after EVAR for ruptured AAA than after open repair. And so we conclude that early monitoring of intra-abdominal pressure after EVAR for ruptured AAA may save lives. And finally, I just want to invite you all
to the next ESVS meeting, 24th to 27th September in Hamburg, and remember to submit your abstracts by April 1st, thank you.
- Thank you, chairman. Good afternoon, ladies and gentlemen. I've not this conflict of interest on this topic. So, discussion about double-layer stent has been mainly focused about the incidence of new lesions, chemical lesions after the stenting, and because there are still some issue
about the plaque prolapse, this has still has been reduced in a comparison to conventional stent that's still present. We started our study two years ago to evaluate on two different set of population of a patient who underwent stent, stenting,
to see if there is any different between the result of two stents, Cguard from Inspire, and Roadsaver from Terumo in term of ischemic lesion and if there is a relationship between the activity of the plaque evaluated with the MRI
and new ischemic lesion after the procedure. So, the population was aware of similar what we found, and that there's no difference between the two stent we have had, and new ischemic lesions is, there's a 38%, for a total amount of 34 lesions,
and ipsilateral in 82% of cases. The most part of the lesion appeared at the 24 hours, for the 88.2% of cases, while only the 12% of cases, we have a control at our lesion. According to the DWI, we have seen that
the DWI of the plaque is positive, or there is an activity of the plaque. There's a higher risk of embolization with a high likelihood or a risk of 6.25%. But, in the end, what we learned in the beginning, what there have known,
there's no difference in the treatment of the carotid stenosis with this device, and the plaque activity, when positive at the DWI MR, is a predictive for a higher risk of new ischemic lesions at 24 hours. But, what we are still missing in terms of information,
where something about the patency of the stents at mid-term follow-up, and the destiny of external carotid artery at mid-term follow-up. Alright, we have to say we have an occlusion transitory, occlusion of the semi-carotid artery
immediately after the deployment of the Terumo stent. The ECA recovery completely. But in, what we want to check, what could happen, following the patient in the next year. So, we perform a duplicate ultrasound, at six, at 12, and 24 months after the procedure,
in order to re-evaluate the in-stent restenosis and then, if there was a new external carotid artery stenosis or occlusion. We have made this evaluation according to the criteria of grading of carotid in-stent restenosis proposed on Stroke by professors attache group.
And what we found that we are an incidence of in-stent restenosis of 10%, of five on 50 patient, one at six month and four at one year. And we are 4% of external carotid artery new stenosis. All in two patient, only in the Roadsaver group.
We are three in-stent restenosis for Roadsaver, two in-stent restenosis for Cguard, and external new stenosis only in the Roadsaver group. And this is a case of Roadsaver stent in-stent restenosis of 60% at one year. Two year follow-up,
so we compare what's happening for Cguard and Roadsaver. We see that no relation have been found with the plaque activity or the device. If we check our result, even if this is a small series, we both reported in the literature for the conventional stent,
we've seen that in our personal series, with the 10% of in-stent restenosis, that it's consistent with what's reported for conventional CAS. And the same we found when we compared our result with the result reported for CAS with conventional stent.
So in our personal series, we had not external carotid artery occlusion. We have 4% instance, and for stenosis while with conventional CAS, occlusion of external carotid artery appear in 3.8% of cases.
So, what can we add to our experience now in the incidence, if, I'm sorry, if confirmed by larger count of patient and longer study? We can say that the incidence of in-stent restenosis for this new double-layer stent and the stenosis on the external carotid artery,
if not the different for all, with what reported for conventional stent. 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)
- So first of all I want to tell everybody that you're going to have a hard time finding these tools that I'm going to show you. So before I start the talk I want to tell you how you can find these. Everybody's got phones out there that you can Google on. If you would Google "One minute access check"
it will take you to the website that is the ESRDNCC.org site, and that's where you can find the tools. The other place that these are all located is on the VASA website. If you go to the VASA website, which is
the Vascular Access Society of the Americas, which is VASAMD.org, and you go under "Vascular Access Team", all of these tools are linked. The tools that we're going to talk about were put together by the FistulaFirst and I was on the work group that created these tools,
and they're going to solve the problems that you just heard the rest of the group talk about. It talks about how to collaborate the care, how to assess the maturing and the healing access, and to level the playing field so we're all doing it the same way.
And that's basically what these tools were developed for. That's my conflict of interest. So the patient video that just showed you, the patient said patient education. This is a free, your tax-dollar money paid for this booklet. You can print these for free,
there's no copyright issues on it. This is a patient access planning booklet that explains to the patient all of their choices for renal replacement therapy, what is an access, and what's going to happen to them when they get this access.
This is a fantastic booklet and it also serves as the patient's care plan if you fill this out and use it. It can go between the dialysis facility, the surgeon, and the interventionalist. And I'm sorry it doesn't project well,
but this is just a snippet from the booklet that shows you, for the surgeons in the audience, what's going to happen at your office when the patient comes in. And it gives questions that the patient and the family should ask.
So as surgeons, if you look at this booklet, you use it with your team at your office, you'll be able to be prepared for patients coming in and you can use this tool. This is what I consider the plain ice in the sandbox tool.
This tool was created to define all of the various roles of the dialysis access care team, because we all do different parts of the process, but if we don't work together, it doesn't work. So this booklet explains what everybody's roles are, and again this is a great tool.
If you've got a nephrology practice that you're not happy with how things are coming to you with referrals, or you've an interventionalist that you're having issues with, sit down, have a team meeting, bring all the players together
and use this book to guide it. It really tells you what to do and how to do it. And this is an example of what's going to happen with the care team coming together how you go through the access planning, okay? And this is just some information of what
the surgical appointment should get. When you get the patients to show up and they come to you with no information, you don't really know much about the patient, this booklet helps to prepare the dialysis facilities so they know what to send
and they understand those records should come to you. Now, the main part of these booklets of what we're talking about today is this whole issue of what Ted's slide was about who should assess the access for maturing. Well, this answers that question.
There is a basic tool that will give you a weekly assessment of whether or not that graft or fistula is ready to go. And basically this is the care planning part of it where we make that access plan, we then find the best place to get the access,
we choose, we get the patient to the surgeon so you can place the access, patient goes for the surgery. Then we wait for it to mature, heal, we use the access, we then have to get the catheter out, and then we
have to take care of the lifeline for the rest of the patient's time on dialysis or their transition between different modalities. So, how do we do that? The tools are based, this weekly assessment tools are based on the classic one minute check.
This is actually from Dr. Bether's physical exam that's been taught to nephrologist and dialysis staff for many years. It's a simple look, listen, and feel. There's also an advanced test for the care side. This is for the patient,
and this is for the clinician side. It's the look listen and feel with the arm elevation test, and the augmentation test is also added on at the expert level. Again, all these tools are on the website for you to use. Please use them.
Once you understand the one-minute check, this is then the graft healing slides, and again it's a weekly assessment, and we called it graft healing because grafts don't mature, we just are waiting for the surgery line to heal so that
we can go ahead and cannulate it. If it's an early cannulation graft, this would be adopted for those early cannulation grafts, this is for standard graft material. So we go into week two, this tells the patient, the staff, the nephrologist, everybody on the team
what should we be looking for and what should be happening with that access and when it should be ready to cannulate. By week four, if it's not ready to cannulate, this triggers notifying the surgeon, re-engaging with the team, and figuring out
what's going on with the patient's access, okay? We cannot just let these patients sit there with accesses that are not being used for weeks and weeks and weeks. We have to have a plan. And this is what the tool does. The fistula maturation tool is the same thing.
Again it's weekly assessments, there's week one and two, week three, by week four we're looking for actual signs of change with the fistula. If it's not, we would start to already think of a plan of does this need some assisted maturation.
Week five, we're looking to see is it ready to cannulate. By week seven through ten, it certainly should be ready to go and we should be dealing with catheter freedom. There's also a catheter version, because patients with catheters still need to have their catheters
well maintained so they don't get infection. There's a patient version and a staff version. And again it's the same look listen and feel. We obviously don't listen to a catheter like we do a graft or fistula, but we listen to the patient to make sure they're not having symptoms
of infection or problems with the catheter. And we have to do that because we're all part of this interdisciplinary team. I'm a dialysis nurse, so I'm part of the dialysis team, but we have an interdisciplinary team in the dialysis unit, we have to work with the surgeons,
the interventionalists, whether you're an IN or an IR, we have to work with the patients, we have to bring the family in, it's all about this process of care, and hopefully you'll look at these tools and maybe these tools will help you
with your process of care. Thank you.
- Thank you very much. I take over the presentation from Thomas Larzon, we, and different other people have the same approach to a ruptured triple A, trying to extend the advantages we have seen now, of an EVAR procedure in patients with inadequate anatomy, and to extend the limitation,
to patients with the less favorable anatomy. So, the concept of a ruptured EVAR has been already proven, with good research of three years, and I will build up, Thomas built up this presentation, on our so common experience that we published for fourteen years experience of two university centers,
performing EVAR on 100% of ruptured abdominal aortic aneurysms, over a 32 months period. So what we can see, is on the right side, this was the period where a part of the patient was treated by EVAR,
and the one that had not favorable anatomy were opened. On the left side, there is EVAR only, this a period 2009 to 11, you can see the effect of this change, is the operative cohort mortality moved from 26 to 24%, and total cohort mortality,
including to exclude the patient that are on feet, reduced from 33 to 27%. What changed also, is the protocol for anesthesia, so from a few patients that were treated under local anesthesia, actually, there are very few patients treated
just with general anesthesia primarily. What changed is the rejection rate, decreased from 10% to 4%, the age of the population treated increased, the part of women treated increased by 10%, and the amount of patients that are instable,
and treated, increased too. So, how to extend the limitation, the one is by using parallel grafts, or on table physician modified, extend graft to achieve what Benjamin does in his practice, a good seal proximal,
this is a three parallel graft, that worked very well. The other option, is to use Onyx for the distal landing zone, this is a technique that Thomas does use more liberally than we,
but is a good solution for patients where an IBD, for example, would not be possible, it doesn't require any special catheter, there is no contraindications due to tortuosity, and sealing is immediately obtained. Here, an example,
the aortoiliac, the main trunk, has been deployed here, then a (mumbles), the iliac extension is parked, can be deployed later, and as a Buddy catheter,
you can take a Bernstein catheter, you just position it in the origin of the hypogastric, or in the common iliac artery. Then, you deploy the distal extension, there is no more flow, slowly you'll stepwise,
5-10cc of Onyx can be applied, this allows to preserve the distal perfusion of the hypogastric, and to seal it. Sealing can also, with Onyx, can also be used in the proximal landing zone, there are two options,
here, the option with an instable patient that gets two parallel graphs with the remaining type 1 endoleak, you introduce your catheter through the leak, or the catheter inside the sack that is perfused, step wise, you will apply your Onyx.
Here, in another patient, of our experience, this is a suprarenal arteries after a triple A repair with EVAR that comes with the rupture, we combined here a chimney for the SMA, with a double brach device from Biotech,
deploy this, and you can see here there will be some leak. So, three days later, because the leak didn't have to do coagulation correct, once correct it didn't seal, we just very selectively, improvised with Onyx, the gap,
this is a three months outcome. Then, here a case of some Post EVAR with a type 1A endoleak, to extend this on the visceral aorta would have been very complex, this is why doctor Larson decided here just
to fill the whole sac with 60cc of Onyx, which worked very well. So, in Orebro, you can see that the 30-day mortality is 27%, the 90-day mortality is 30%, then the whole cohort,
including the 10% that have been excluded, has a mortality of 37 and 34%. From the different factor that was significant, you can see that local anesthesia works good, Aortic Balloon Occlusion works good, mortality in patients
with abdominal compartment syndrome is increased, mortality of patients in shock is increased, and finally, the mortality of patients having this adjunct procedure is not significantly increased, this holds true for the long-term outcomes.
So, we can see that by using adjuncts, every patient with a ruptured triple A can be offered an EVAR, eventually as a bridging procedure, chimney grafts can extend landing zones, Onyx can offer additional sealing options,
and valid long-term results for adjuncts has been proven. Thank you very much for your attention.
- 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, Frank, for this really appreciated invitation and to report what factor will be predictive for long-term survival after ruptured AAA treatments. I have nothing to disclose. We know the major key points when dealing with emergent AAA rupture treatment are related to its feasibility, short, and long-term outcomes.
The increase of endovascular repair of ruptured AAA is the proof that most of patient can be addressed by endovascular tools, even if ruptured AAA. We have observed the same trend at USZ with almost 100% of emergent EVAR for ruptured AAA. A third randomized control trial didn't show
any significant differences in terms of short-term outcomes. We know that the real-life studies and meta-analysis are really in favor of emergent EVAR for ruptured AAA. This is consistent with the experience at the USZ. About the long-term outcomes, randomized control trials and the single-center studies did not
show significant differences. We all know that the risk that for conventional open surgery, the risk factor has been clearly identified but we don't know such factors for emergent EVAR. For this purpose, we conducted a retrospective analysis
of ruptured AAA addressed by emergent EVAR and included 242 patient in order to identify factors that can influence long-term survival after emergent EVAR. We have observed this parallel graft did not significantly influence long-term outcomes after emergent EVAR as well as the type of anesthesia,
although the local anesthesia did better for short-term outcomes. Neither the sex was significantly associated to the long-term outcomes, nor the type of stent graft employed. Conversely, shock was significantly associated
to reduced long-term outcomes, as well as re-intervention and open abdomen treatments. So in conclusion, the predictive factors of long-term survival after emergent conventional open surgery are already well-known, but similar factors for emergent EVAR
needs to be identified. We were able to identify that shock, re-intervention, and open abdomen treatments are related to a reduced long-term survival. To improve such outcomes for emergent EVAR, we use five management key points.
About time, we all know that most of the patient who reach alive the hospital are enough stable to undergo a CTA and evaluation for emergent EVAR. This time we go for permissive hypovolemia and controlled hypotension. We try to perform the case faster as possible.
About imaging, we always go for preoperative CTA just to confirm diagnosis, but especially to plan the case. We go for a post-surgery CTA control to immediately understand and realize if there is some trouble with the treatment. We had also started a program with patient-specific ratio
that gives you some tools to perform better ruptured AAA cases by EVAR. This is a feasibility study with good outcomes. About device and techniques, of course to perform emergent EVAR, we need to have all the available
off the shelf devices ready to use. As a general principle, for short and angulated neck, we go for transrenal devices but when there is no neck we go for parallel graft. We are quite aggressive with the management of abdominal compartment syndrome,
not only for emergent EVAR but also for conventional open surgery. Clearly there are some limitations to emergent EVAR. In fact, it's inappropriate in rupture pararenal requiring suprarenal endoclamping for hemodynamic stabilization
and patient presenting too many technical challenges. These patients should probably be treated by fast-track open surgery. Thank you for your time.
- 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.
- 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.
- Good morning everyone. Right, I'm going to try and talk a little bit about really prediction in aortic dissection in TEVAR. These are my disclosures. If we're trying to predict poor outcome in acute aortic dissection there's a burgeoning list of factors
which we all recognize confer poor outcomes. Quite a few of these are easily seen on a CT scan, and (mumbles) looked at this for some time now. This is the latest and very good paper from Germany looking at number of factors which predict future aortic dilatation
after uncomplicated type B. So we know that there are images on static CT scans which imply to us that there's going to be a problem further down the line, and the key question is, which is still unanswered in my mind,
is do we actually treat the aorta properly with type B dissection by putting one or two stents into the thoracic aorta? Because we all know that whilst the TEVAR device will treat the immediately adjacent aorta very well and achieve false lumen thrombosis
it often does not do that with the abdomen, and you get continued false lumen perfusion and in some patients progressive abdominal aortic dilatation over time, and you can't really predict that from the beginning. I've got two pieces of data to show you really.
We've been looking at this with the engineers at Imperial College, and, first of all, I'm going to present a very quick volumetric analysis. We looked at 27 patients with four regions of interest, but we've only really got time
to focus on the 14 patients that underwent TEVAR, and divided aorta into the thoracic, visceral, infrarenal, and iliac segments and really looked at the baseline scans straight after TEVAR and a scan a year later and looked at changes in volume over time
and sorry, and at a number of these factors which anatomically you can see on CT scans to see if there was any correlations, and so what we found was that overall there was true lumen gain and false lumen loss once the patients had a TEVAR put in
which is what you hope for and expect, and that was really driven by the thoracic aortic segment because every single patient underwent true lumen positive remodeling and false lumen thrombosis in that part of the aorta. But if you look at the abdominal aorta
there was no such relationship, and many of these patients had false lumen perfusion and an increase in size over time, and that looked very much like the way that patients treated with beta medical therapy if you do a volumetric analysis of those.
And if we look at the factors that correlated with false lumen increase it was really the number of branches arising from the false lumen, the number of reentry tears in the thoracic aorta below the stent,
and there was an inverse relationship between the left subclavian and the first appreciable reentry tear in the thoracic aorta which I take to mean the greater the length of the stent you put in, the greater the chance of false lumen thrombosis,
and the same held true for the abdominal segment. The other thing we've been looking at is whether we can find a computational flow system which will accurately model false lumen thrombosis because if we could tell which patients from the very outset would have successful thrombosis,
then this could very much help with decision-making, and so we've been working on a system which basically relies on particles being accelerated through the entry tear, activating platelets that's disturbed in recirculating flow of the false lumen,
and you can start to see that some of these patients will thrombose their false lumen. And a year ago we published this which is really a model which the blue you see is thrombis forming in an aortic model. It's a real patient.
The CT scans at the end show that the actual prediction made by the model was quite accurate and show burgeoning thrombosis in this particular patient's false lumen. So we've now applied that to a more complex model which looks at a patient who's undergone a TEVAR,
and you can see that over about 20 or 25 cardiac cycles the false lumen, the prediction of whether or not flow is going to run in this is made by the algorithm, and this is the actual CT of the patient three years later. So there's quite a high degree of concordance, and this is another example of that.
So this model would appear to be quite successful in saying if you put a TEVAR we can tell from the outset of the 25, 26 cardiac cycles whether or not you are going to, the patient will thrombose the false lumen. So hopefully that will be a helpful tool.
I've run out of time but these are the conclusions. Thanks very much.
- Thank you, Doctor Chuter. So, as you saw in Eric's presentation, really indwelling catheters and wires have become more or less routine for us. And they're nothing new to this era of complex and vascular repair. We've seen them a long time and
we started using them, of course, for iliac branch devices, as you can see here. And the concept is the same when you use them for other branches or fenestrations, as I'll show you. And here, an iliac branch is coming over with that indwelling catheter and snaring
from the contralateral end to be able to get that sheath. This is a helical-helical device, so putting that sheath over to get access to the contralateral side. So why and when do we need preloaded grafts with wires or catheters for complex aortic repair? Well, sometimes we have access issues
and it alleviates that, as I'll show you. Having the fenestrations or branches pre-catheterized will intuitively reduce X-ray exposure times and operating times, and also help catheterization in difficult anatomy, as Eric alluded to, and thereby
keeping the procedure down and avoiding large sheaths in both groins, at the same time minimizing lower-extremity ischemia time. This is an example of putting a fenestrated device in a previous infrarenal device. And the multitude of markers here
makes it very difficult to actually locate the fenestrations on the new graft, so it's very advantageous in these settings to have the fenestrations preloaded. This was first described by Krassi Ivancev back in 2010, and this is the original
preloaded design for a juxtarenal fenestrated device. And you can see a loop wire going through the top of that device. And a very simple handle with a couple of wires and things coming out of it, and some technical difficulties with wire catches
and other things made us move away from that design. It was later evolved into this bi-port delivery system, which allows you to have access to two fenestrations from a unilateral approach with indwelling renal wires and then sheaths, and having
those wires go through the renal fenestrations. And this evolved into the p-branch off-the-shelf fenestrated device from Cook, as you can see here. And you can see that loop wire coming out through that right renal fenestration
going through the top of the graft. And this is the catheter just describing how you then can use a double-puncture technique to access that renal artery and place the sheath there. The advantages of the technique
was described by Doctor Torsello's group in Munster here, showing that it does in fact reduce the amount of radiation in contrast during these procedures as well as bringing the procedure time down. And this was described by Mark Farber as well
in the experience of the off-the-shelf p-branch devices. We modified the preloaded device a little bit further by taking away that very top stent, and instead of having the loop wire is on the p-branch, just placing catheters through those fenestrations,
but still using the triport handle, and then replacing those with 018 wires to achieve stable positions. Of course, preloaded catheters and wires can then be used for branch procedures as well, as Eric Verhoeven just showed you. And in this case, just using these
indwelling catheters to allowing wires to be snared from above and then advanced into the specific branches and distal arteries. And of course, if you use a fenestrated device for thoraco-abdominal repair, the same applies. And this is from Carlos Timaran's paper
just showing how he places these wires from above in these discrete fenestrations. This is a combined device of a two-branch, two-fen device, if you would like, that has indwelling wires going through the fenestrations and out
through the branches, which we use on occasion. You can then bring that out through the axillary artery, and you get access directly from above to the branches from below for the fenestrations. And we found it very useful in the setting of narrow aortic
lumens and chronic aortic dissections, as in this case. And you can see here, then, on the wires placing the sheath, catheterizing the renals, and then at the same time, having these access catheters in the branches so you don't have to access those for a nice end result.
So in summary, Chairman, ladies and gentlemen, preloaded wire I think reduces the operative time and the X-ray exposure during these procedures. It's very useful, particularly in complex torturous aortas, during redo EVAR cases with preexisting devices, and
compromised iliac access, and in the situations of narrow aortas, like in chronic aortic dissections. Thank you very much.
- I do have to disclose that I am a little double booked and have a talk at 2:10 at the job fair so I won't be able to stick around to see who won the debate. Here are my disclosures. They haven't changed. Again, I come from Harborview Medical Center
at the University of Washington where we cover a very large geographic distribution and see a lot of patients presenting with a model of pure catastrophic hemorrhage ruptured abdominal aortic aneurysm. So several risk scores have been developed
to predict mortality after ruptured AAA repair. The Glasgow Aneurysm Score, the Hardman Index, the Vancouver Score, the Edinburgh Ruptured Aneurysm Score, and the VSGNE Ruptured Aneurysm Score. But these scores have differing levels of clinical utility. The Glasgow Score is not predictive in the Endo Era.
It was developed a long time ago. The Hardman and Glasgow Index failed to predict mortality in the highest risk populations. The VSGNE Score although a good score has been validated in the Endo Era but includes intraoperative variables.
Therefore limiting its use in the preoperative setting. We sought to develop a practical, clinically relevant, preoperative ruptured AAA mortality risk score to aid in the clinical decision making in the Endo Era and before the operation is considered. This article was published last month
as the Editor's Choice in the Journal of Vascular Surgery. The predictors of 30 day mortality are listed here. This is from both univariate and multivariate analysis and looking at over 300 patients presenting with ruptured AAA in our institution. And those variables are as follows,
age greater than 76, a creatinine concentration of greater than two milligrams per deciliter, a systolic blood pressure ever below 70 millimeters mercury and this is the one that's hardest to obtain, but a serum pH of less than 7.2. This is directly from the Journal of Vascular Surgery,
but you can see that if you had one point for one of those factors, your 30 day mortality was 22%. Two points, 69%. Three points, 80% mortality. And four points, 100% mortality in our institution. This is the prediction of 30 day survival after EVAR.
You can see for the patients that had zero, one, two, three and four points, if you had four points and underwent an EVAR your mortality risk was 100%. Same for open repair, a little bit more in terms of mortality upfront. And when we look at multivariate logistic regression,
the factor that stood out the most and had the highest odds ration was creatinine greater that 2.0. We've long known this as vascular surgeons. We've known that creatinine greater than two, triples operative mortality after even open elective repair.
I'm going to flip to the mortality predicted by the preoperative risk score. You can see here are the scores and the odds ratios. And when we look at our score compared to all other scores, the Robinson, Glasgow and Edinburg Scores had a area under the curve of .64.
Our area under the curve was .82 which is highly predictive of futility. I want to provide for you an anecdote. This was a few weeks ago when I was on call, I had a call that a ruptured AAA was coming in from Yakima, Washington and I had accepted the patient.
The patient was an 87 year old. His systolic blood pressure was over 70. Creatinine was normal and his serum pH was 7.24. So he only had one risk factor for mortality. So we would clearly accept this patient and offer repair. I then got a call from the ER about 45 minutes later
saying we have a patient that presented with a ruptured AAA. I said, "I know, I already heard about that patient. "I accepted him." They said no, this is a totally different patient. This patient is 76, he's hypotensive
with a blood pressure less than 50. And I asked the question, "What's his creatinine "and his serum pH?" Creatinine was 2.7 and his serum pH was 7.1. So we had a choice to make. Do we fix the 87 year old or do we try and go
for fixing the 76 year old who had all four risk factors. We said to the family that this 76 year old had a 100% risk of death. We fixed the 87 year old, he survived and was discharged on postoperative day number two. After talking with the family for the 76 year old male,
he died in the ER 21 minutes later. We have published this mortality risk score in our textbook, the only textbook of its kind, The Ruptured Abdominal Aortic Aneurysm, The Definitive Manual and I thank Dr. Veith for the privilege of the podium.
Thank you, Dr. Veith.
- Thank you very much for the kind introduction, and I'd like to thank the organizers, especially Frank Veith for getting back to this outstanding and very important conference. My duty is now to talk about the acute status of carotid artery stenting is acute occlusion an issue? Here are my disclosures.
Probably you might be aware, for sure you're aware about pore size and probably smaller pore size, the small material load might be a predisposing factor for enhanced thrombogenicity in these dual layer stents, as you're probably quite familiar with the CGUARD, Roadsaver and GORE, I will focus my talk a little bit
on the Roadsaver stent, since I have the most experience with the Roadsaver stent from the early beginning when this device was on the market in Europe. If you go back a little bit and look at the early publications of CGUARD, Roadsaver and GORE stent, then acute occlusion the early reports show that
very clearly safety, especially at 30 days in terms of major cardiac and cerebrovascular events. They are very, very safe, 0% in all these early publications deal with these stents. But you're probably aware of this publication, released end of last year, where a German group in Hamburg
deals with carotid artery stenosis during acute stroke treatment. They used the dual layer stent, the Roadsaver stent or the Casper stent in 20 cases, in the same time period from 2011 to 2016, they used also the Wallstent and the VIVEXX stent,
in 27 cases in total and there was a major difference, in terms of acute stent occlusion, and for the Roadsaver or Casper stent, it was 45%, they also had an explanation for that, potential explanations probably due to the increase of thrombogenic material due to the dual layer
insufficient preparation with antiplatelet medication, higher patient counts in the patients who occluded, smaller stent diameters, and the patients were not administered PTA, meaning Bridging during acute stroke patient treatment, but it was highlighted that all patients received ASA of 500mg intravenously
during the procedure. But there are some questions coming up. What is a small stent diameter? Post-dilatation at what diameter, once the stent was implanted? What about wall apposition of the stent?
Correct stent deployment with the Vicis maneuver performed or not and was the ACT adjusted during the procedure, meaning did they perform an adequate heparinization? These are open questions and I would like to share our experience from Flensburg,
so we have treated nearly 200 patients with the Roadsaver stent from 2015 until now. In 42 patients, we used this stent exclusively for acute stroke treatment and never, ever observed in both groups, in the symptomatic and asymptomatic group and in the group of acute stroke treatment,
we never observed an acute occlusion. How can we explain this kind of difference that neither acute occlusion occurred in our patient group? Probably there are some options how we can avoid stent thrombosis, how we can minimize this. For emergency treatment, probably this might be related
to bridging therapies, though in Germany a lot of patients who received acute stroke treatment are on bridging therapy since the way to the hospital is sometimes rather long, there probably might be a predisposing factor to re-avoid stent thrombosis and so-called tandem lesions if the stent placement is needed.
But we also take care of antiplatelet medication peri-procedurally, and we do this with ASA, as the Hamburg group did and at one day, we always start, in all emergency patients with clopidogrel loading dose after positive CT where we could exclude any bleeding and post-procedurally we go
for dual anti-platelet therapy for at least six months, meaning clopidogrel and ASA, and this is something probably of utmost importance. It's quite the same for elective patients, I think you're quite familiar with this, and I want to highlight the post-procedural clopidogrel
might be the key of success for six months combined with ASA life-long. Stent preparation is also an issue, at least 7 or 8 diameters we have to choose for the correct lengths we have to perform adequate stent deployment and adequate post-dilatation
for at least 5mm. In a lot of trials the Roadsaver concept has been proven, and this is due to the adequate preparation of the stent and ongoing platelet preparation, and this was also highlight in the meta-analysis with the death and stroke rate of .02% in all cases.
Roadsaver study is performed now planned, I am a member of the steering committee. In 2000 patients, so far 132 patients have been included and I want to rise up once again the question, is acute occlusion and issue? No, I don't think so, since you keep antiplatelet medication
in mind and be aware of adequate stent sizing. I highly appreciated your attention, thank you very much.
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