- Good morning, thank you very much to Dr. Veith and Professor Veith and the organizers. So this is real holography. It's not augmented reality. It's not getting you separated from the environment that you're in. This is actually taking the 3D out of the screen
so the beating heart can be held in the palm of your hand without you having to wear any goggles or anything else and this is live imaging. It can be done intra-procedure. This is the Holoscope-i and the other one is the Holoscope-x
where in fact you can take that actually 3D hologram that you have and you can implant it in the patient and if you co-register it correctly then you can actually do the intervention in the patient
make a needle tract to the holographic needle and I'm going to limit this to just now what we're actually doing at the moment and not necessarily what the future can be. This is ultimate 3D visualization, true volumes floating in the air.
This is a CT scan. So it started working, So we get rid of the auto-segmented and you can just interact. It's floating 45 centimeters away from you and you can just hold the patient's anatomy here and you can slice into the anatomy.
This is for instance a real CT of an aorta with the aortic valve which they wanted to analyze for a core valve procedure. This is done by Phelps. If you take the information
and they've looked at the final element analysis and interaction between the stem and the tissue. So here you can make measurements in real time. So if you did the 3D rotation and geography and you had the aorta and you wanted to put in a stent graft EVAR TVAR, and you would see,
and you could put in a typical tuber that you would do, and you could see how it, and this is a dynamic hologram, so you can see how it would open up, you can mark where your fenestration's chimney is and all that type of stuff would be. And you can move it around, and you have
a complete intuitive understanding of a, can we go to the next slide please, I can't, it seems to be clicking, thank you. So how do we do all this? Well, to create a hologram, what you need to do is just conceptualize it as printing in light.
Like if you had plastic and you took the XYZ data and you just put it into a 3D printer, and it would print it for you in light, then you'd go, Okay, so I understand, if it was printed for you in plastic then you'd understand. But imagine it's printing in light.
So we have every single piece of light focused, each photon is focused so that you can see it with a naked eye, in a particular place, but the difference is that it's totally sterile, you don't have to take off your gloves, you don't have to use a mouse,
you can interact with it directly. And all the XYZ data is 100% in place, so we've just seen a beautiful demonstration of augmented reality, and in augmented reality, you have to wear something, it isolates you from the environment that you're in, and it's based on
stereoscopy, and stereoscopy is how you see 3D movies, and how you see augmented reality, is by taking two images and fusing them in one focal plane. But you can't touch that image, because if you look at me now, you can see me very well, but if you hold your finger up 45 centimeters
and you focus on your finger, I become blurred. And so, you can only focus in one plane, you can't touch that image, because that image is distant from you, and it's a fused image, so you have the focus plane and you have the convergence plane, and this is an illusion
of 3D, and it's very entertaining, and it can be very useful in medical imaging, but in intra-operative procedures it has to be 100% accurate. So you saw a very beautiful example in the previous talk of augmented reality, where you have gesturing, where you can actually gesture with the image,
you can make it bigger, you can make it smaller. But what RealView does by creating real holography, which is all the XYZ data, is having it in the palm of your hand, with having above 20 focal planes, here, very very close to your eye, and that in another way, of having all those focal planes not only actually lets you
do the procedure but prevents nausea and having a feeling of discomfort because the image is actually there as of having the illusion of the images there. So just to go back, all RealView imaging is doing, is it's not changing your 3D RA cone, BMCT, MRI,
we can do all those XYZ datas and we can use them and we can present them, all we're doing, so you use your acquisition, we're just taking that, and we're breaking open the 3D displays and seeing all that 3D data limited in the 2D screen, let's set it free and have it floating in the air.
So we have the holoscope-i for structural cardiology and electrophysiology, and obviously the holoscope-x, which makes the patient x-rayed, completely visible. So its an over the head, this is now, obviously, free-standing when somebody buys us like Phillips or Siemens, it will be integrated into your lab,
come down from the ceiling, it's an independent system, and you just have a visor that you look through, which just goes up and down whenever you want to use it. You can interact with it the same as you do with your iPhone you can visualize, you can rotate, you can mark, you can slice, you can measure, as I showed you
some examples of it, and you can do this by voice as well, you just talk to it, you say slice and you slice it with your hand, it recognizes everybody's hand, there's no delay for whatever you're imaging. So structural cardiac procedures, this is what
a mitral valve will look like, floating in the air in front of you, you can see the anterior leaflet, the posterior leaflet. And once the catheter is inside and you're guiding the catheter inside the procedure, you can turn on your doppler, you'll be able to see that the catheter
movements, so for someone doing a mitral clip, or whatever, this would be very very useful. This is an electrophysiological procedure, and you can see how the catheter moves, when the catheter will move, and obviously, as my previous speaker was saying, you are appreciating 3D in a 2D screen,
so it's very difficult to appreciate, you'll have to take my word for it. But I think you can see dynamic colography at this quality, that you can interact with, that is something that is very special, we've presented at a number of conferences,
including at Veith, and we've already done a first in man, and the most exciting thing for now, is just this week, the first machine was installed at Toronto general, at the Peter Munk Cardiac Center, and they've done their first case, and so now we are launching and clinical trials in 2018, and hopefully,
I'll have something which is more vascular relevant, at the next time, Veith 2019, thank you very much.
- Thank you, thank you for the opportunity to talk. And I'm going to go quickly through some of the background slides 'cause we've heard some of this. I have no disclosures. So we've heard a little bit about popliteal entrapment already.
The population it affects. But where I'm going to point out that I think IVUS and some of these newer techniques may be more useful are in these patients because they, if they get repetitive compression they can get occlusion, embolism, and aneurysm.
So I think in these functional patients that we just heard about and in some of these patients who have maybe more subtle findings than a standard type one or type two, that's where I think these techniques are particularly helpful.
Additionally, we have seen a huge rise in women, female athletes over the past decade like you saw on the last slide. They seem to be the more predominant type. And functional, we, Doctor Ali just reviewed all of this. But functional seems to be a more common type.
And that's where, at least at Michigan, we find IVUS to be most useful. For that, and then also for type three, where the muscle, accessory muscle slip may not be as visible on conventional imaging. So, we just heard again about functional entrapment,
I'm also going to talk about at Michigan how we distinguish that between recurrent compartment syndrome, which is another common diagnoses that we see a lot of people coming in with. But it's important to mention too
that all these diagnostic tests are positive in a certain percentage of normal patients. So you really have to be looking at the specific patient population that has these symptoms before you're kind of pursuing this diagnostic algorithm. So our typical work-up and diagnosis,
again, is not always straightforward. We usually start with exercise ABIs. If that's abnormal we have an MRA protocol. And provocative angio that we will pursue. If it's normal, we'll typically do a duplex as has been shown up here previously
to help us distinguish between chronic compartment syndrome and functional entrapment. But it's important also to think of some of the other causes like cystic adventitial disease, endofibrosis, and some other things that can present with similar symptoms.
This is just showing a provocative MRA, which is sort of the next thing in our algorithm. We have patients do active plantar flexion, although, as has been reported in lots of literature, there's a really high false negative rate here because it's very dependent on the protocol.
Patients have to hold this plantar flexion for a long period of time. And so it can be very easy to miss these type three, type four, and functional on the MRA. And we see that quite a bit at Michigan. So we often then proceed to provocative angiogram,
which is shown here in one of our swimmers. He's in neutral position here, and then in this second angiogram you can see he's in active plantar flexion. We often have to use vasodilators in these patients to sort of simulate the amount of exercise
that they're used to getting. But again, these, we only go to this step if we're really convinced that the symptoms are specific for this diagnoses. Now where I think IVUS is particularly useful is these long segments, like you can see over here,
where you can't identify the exact compression point. That's where we're using it. So, again, kind of in these type three, four, and six. But we found it to be a very good adjunctive tool. We're using it all the time in these patients now. And it helps us both identify the exact location
of compression, what specifically is compressing, and it allows us to do a more precise surgical approach and completely identify that area and resect it. And we're also using it postoperatively to confirm that we have indeed relieved all of the compression.
So here's, you saw a video of this already, but here's a patient essentially in neutral position, you can see the artery. When they go into plantar flexion you can see how this is being compressed here. And we will run this down the whole way
and find the maximal areas of compression. And as you can see over here, we'll kind of mark them based on bony landmarks with angiography pictures so that we can identify these exact areas. And then we'll pull that up when we're doing our operative treatment.
So we will also then, after we have done whatever operative treatment we're doing, we will then wake them up, have them do a provocative angio again with us and an IVUS just to confirm before we leave the operating room that we have indeed relieved all of the compression.
And this, we've found, has really significantly minimized the amount of patients that don't get relief postoperatively. So this is a very busy slide, but it's basically just our algorithm at University of Michigan for these patients.
They all come in, they get exercise ABIs. Depending on if they're normal or abnormal they sort of go toward the MRA protocol. As you can see, unless they have a clear type one or type two entrapment, they're all getting this provocative angio and IVUS.
In patients that are a little less clear, they're all getting exercise compartment pressures, meaning that they're running prior to getting compartment pressure measurements. If it's greater than 25 they're getting a fasciotomy. If their results are positive,
depending on whether we think it's functional or true popliteal entrapment, we'll either do a standard posterior release or a musculotendinous resection. But again, this technology, I think, is very useful. We need to be more vigilant in diagnosing these patients.
And I think newer technologies will also aid in this. Thank you.
- Now we are delighted that there's apparently two things that we came up with years ago proved useful. This is the Near-Infrared Spectroscopy slide by Joe Bavaria from UPENN providing patient data on delayed paraplegia. That's a problem that we see in open NN (mumbles) very frequently.
How does the NIRS work? And again to this illustrative picture and now imagine the spinal cord sitting here in the spine canal and there's no more blood flow and this is the end result. When you know the oxygenation in the collateral network
and there was the problem with this technology that had been attempted 12 years back already, in Houston, I bet they put the NIRS optodes in the midline and the light cannot penetrate bone so it didn't work. But if you put it on the collateral network
and you measure the oxygen in this area, you obviously know it in the spinal canal. Dorsal view, again, so this is position of the optodes and this is oxygen content way interested in it. This is another cast just to illustrate
how these segmentals are regionally connected into the spinal canal, obviously. Experimental validation and pilot series in the next two minutes. Experimental cross clamping, this is the setup so years mentoring Laser Doppler Flow
to a real time evaluation of what you measure with your infrared setup in the animal lab and we see here, correlation is very nice between the lumbar NIRS, optodes, and the actual lumbar spinal cord oxygenation measured by Laser Doppler which is evaluated
with other techniques. Very nice to see the corelation between the two. So lumbar collateral network NIRS directly reflects spinal cord tissue oxygenation. After we have proven that step, next step was serial segmental artery occlusion.
As this is a technology that we or the strategy that we using, obviously want to know with our monitoring works for that. You see here, experimental setup basically the same. Starts with anesthesia, exposure of the segmentals. Now an open approach
and then you get 120 minutes surveillance period. You got a drop or dip in the NIRS measurements. Interestingly in the experimental setup in the recovery group, you see here that the new logical function comes back after the procedure and the NIRS comes back after the procedure.
Paraplegic group, all segmentals sacrificed NIRS, drops after the procedure in the first couple days, and the neurologic function does not recover. So experimental evidence that actually works. Nice corelation, again, so the experimental validation proves that lumbar NIRS
reflects lumbar spinal cord oxygenation and reacts to occlusion, of segmental arteries in real-time, but careful it's only regional so where ever you put your optodes, this is the area where you can monitor
your collateral network associated dip when you coil or include the segmental arteries. First clinical results published a couple years ago, I think you have all seen this video. Optodes are putting in the back of the patient, same setup for endo and open
and then we take the monitors theory and we have real-time monitoring on oversights midline here, this is (mumbles). Concept validation from 2016 with the first clinical data and now we're working on the clinical evaluation
of the use of this technology in EVAR and in clinical coil-embolization. 11 patients have been included so far for the EVAR group and you see here, it is very sensitive when you put stent in, stent deployment, but we have to still work so to speak
on the area that we have to monitor. There's a lot of work to do and probably also device modifications are necessary. MISACE, last couple words, on this you see pretty stable, NIRS all over the time course and actually this is nothing we wouldn't have expected
because the patient obviously were protected from spine cord anesthesia. So also here but sometimes we see a significant drop and this is when you should be careful and that's when you usually stop the procedure. So in conclusion, minor changes
in Collateral Network oxygenation have been seen in EVAR in this preliminary results using the nearest technology and to establish one very nice ... Nicely how clinical practice is already guided at his institution.
There's no immediate complete occlusion of covered segmental arteries and there's ongoing study in very heterogeneous patient group. There's no relevant changes with the chlorine technology so far,
but that, just to remind you, is the purpose of this technology, that we do not harm the patient during the preparation period. Thank you very much for your attention.
- Thank you very much again, I greatly appreciate the honor to be able to be here and be able to present these data. These are my they're my conclusions, thank you very much. So, what I think is really very important for all of us
is to remember this Chinese Proverb, never kill a friend, never treat a stranger. And what that means is that you have to learn a lot about that patient before you just go ahead and operate on them.
Then they're not strangers anymore. And if God forbid the CT scanner is broken, you're going to have to do a history and physical. We know that chart review I hate to look at reviews of the Caprini scores going back with retrospective chart reviews,
because they're terribly flawed. We have one of the only risk assessments that looks at the history of obstetrical complications and if you look at chart review, nobody asks the questions. Six tenths of a percent,
13 percent face to face. Same thing with family history of thrombosis. Five point two percent, 17 percent live. Personal history of DVT even doubled in live versus chart review. These questions aren't asked
and of course in the National Surgical Quality Improvement Project and the American College of Surgeons. These things aren't even in there. And they have five million patients. And they talk about DVT studies, and they don't know about what's going on.
We have 39 factors in the Caprini score and that's judged to be too many. You can't have too good a history and physical. The better your history and physical, the better you can take care of the patient. So if devised in a patient friendly form,
it's in five languages. The patients fill it out ahead of time. And then, this was compared to professionals filling it out. There's excellent correlation except for a couple of problems.
And that is that the patient fills the form out, then when they come in, we reemphasize history of family history, B.M.I., obstetrical history, and then see if they have pitting edema or varicose veins.
And so that takes less than five minutes. The last thing in the world you want to do, and I would say anybody that has preoperative surgical nurses in the holding area that Caprini scores, that's flawed. Stop it.
That's no place to be doing that. Because people are worried about their surgery, are they going to get through it, are they going to find cancer, how long are they going to be out of work. You can't ask them about this at that time.
So, these are the scores that we use. Part of this is also reinforced by stuff that's been done. God bless that we would need a moment of silence for the University of Michigan. All the fabulous work that they've done there
in this regard. And we also, this is how we score these patients. Got a lot of operator error here today. Age, as you can see, and contraceptives or hormonal therapy and so forth. This, everybody needs to get this study and to read it.
This is 183000 individuals in the Scandinavian system followed for 25 years. And what they showed is, that there's an increased incidence. If you take a look at a person that's never had a clot, if they have a first degree relative with a clot,
they have an increased risk of thrombosis, slightly less for second degree relatives, slightly less for third degree relatives, and believe it or not, even slightly more compared to controls for people that are living together but of course with the person's lifestyles and so forth
so it's not totally understandable. The point of this is, the point of this is, pay attention to family history of thrombosis. Because that might uncover a whole thrombopathic family that you don't realize. And that'll be the difference in these low risk
procedures between life and death. I've seen a number of patients die with simple procedures because nobody asked about the family history. So, what we recommend is Caprini scores of one to four. You can use compression stockings when they're
if they're in the hospital if it's for ablation. You can use compression stockings according to your protocol, whatever you do. If the patient's at moderate risk, five to eight, low molecular weight heparin for seven to ten days and compression stockings.
And if they're high risk, over nine, then we also like to do a duplex scan before stopping the low molecular weight heparin. And so in conclusion, risk assessment using the score, utilize patient-friendly form,
avoid chart review, face to face critical. And remember that some of these simple procedures, these patient's are very high risk if they're thrombopathic. Provide prophylaxis for at least one week in those at risk for a score of over five.
And then extended prophylaxis for history of VTE, family history of VTE and thrombophilia. Now, I put 14 to 28 days because you have to take these situations individually. Somebody's had four family members in their past history that have had thrombosis.
That's a thrombopathic family. I would go for 30 days. If it's only one incident and one patient, then maybe two weeks. Thank you very much.
- 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.
- So Beyond Vascular procedures, I guess we've conquered all the vascular procedures, now we're going to conquer the world, so let me take a little bit of time to say that these are my conflicts, while doing that, I think it's important that we encourage people to access the hybrid rooms,
It's much more important that the tar-verse done in the Hybrid Room, rather than moving on to the CAT labs, so we have some idea basically of what's going on. That certainly compresses the Hybrid Room availability, but you can't argue for more resources
if the Hybrid Room is running half-empty for example, the only way you get it is by opening this up and so things like laser lead extractions or tar-verse are predominantly still done basically in our hybrid rooms, and we try to make access for them. I don't need to go through this,
you've now think that Doctor Shirttail made a convincing argument for 3D imaging and 3D acquisition. I think the fundamental next revolution in surgery, Every subspecialty is the availability of 3D imaging in the operating room.
We have lead the way in that in vascular surgery, but you think how this could revolutionize urology, general surgery, neurosurgery, and so I think it's very important that we battle for imaging control. Don't give your administration the idea that
you're going to settle for a C-arm, that's the beginning of the end if you do that, this okay to augment use C-arms to augment your practice, but if you're a finishing fellow, you make sure you go to a place that's going to give you access to full hybrid room,
otherwise, you are the subservient imagers compared to radiologists and cardiologists. We need that access to this high quality room. And the new buzzword you're going to hear about is Multi Modality Imaging Suites, this combination of imaging suites that are
being put together, top left deserves with MR, we think MR is the cardiovascular imaging modality of the future, there's a whole group at NIH working at MR Guided Interventions which we're interested in, and the bottom right is the CT-scan in a hybrid op
in a hybrid room, this is actually from MD Anderson. And I think this is actually the Trauma Room of the future, makes no sense to me to take a patient from an emergency room to a CT scanner to an and-jure suite to an operator it's the most dangerous thing we do
with a trauma patient and I think this is actually a position statement from the Trauma Society we're involved in, talk about how important it is to co-localize this imaging, and I think the trauma room of the future is going to be an and-jure suite
down with a CT scanner built into it, and you need to be flexible. Now, the Empire Strikes Back in terms of cloud-based fusion in that Siemans actually just released a portable C-arm that does cone-beam CT. C-arm's basically a rapidly improving,
and I think a lot of these things are going to be available to you at reduced cost. So let me move on and basically just show a couple of examples. What you learn are techniques, then what you do is look for applications to apply this, and so we've been doing
translumbar embolization using fusion and imaging guidance, and this is a case of one of my partners, he'd done an ascending repair, and the patient came back three weeks later and said he had sudden-onset chest pain and the CT-scan showed that there was a
sutured line dehiscence which is a little alarming. I tried to embolize that endovascular, could not get to that tiny little orifice, and so we decided to watch it, it got worse, and bigger, over the course of a week, so clearly we had to go ahead and basically and fix this,
and we opted to use this, using a new guidance system and going directly parasternal. You can do fusion of blood vessels or bones, you can do it off anything you can see on flu-roid, here we actually fused off the sternal wires and this allows you to see if there's
respiratory motion, you can measure in the workstation the depth really to the target was almost four and a half centimeters straight back from the second sternal wire and that allowed us really using this image guidance system when you set up what's called the bullseye view,
you look straight down the barrel of a needle, and then the laser turns on and the undersurface of the hybrid room shows you where to stick the needle. This is something that we'd refined from doing localization of lung nodules
and I'll show you that next. And so this is the system using the C-star, we use the breast, and the localization needle, and we can actually basically advance that straight into that cavity, and you can see once you get in it,
we confirmed it by injecting into it, you can see the pseudo-aneurism, you can see the immediate stain of hematoma and then we simply embolize that directly. This is probably safer than going endovascular because that little neck protects about
the embolization from actually taking place, and you can see what the complete snan-ja-gram actually looked like, we had a pig tail in the aura so we could co-linearly check what was going on and we used docto-gramming make sure we don't have embolization.
This patient now basically about three months follow-up and this is a nice way to completely dissolve by avoiding really doing this. Let me give you another example, this actually one came from our transplant surgeon he wanted to put in a vas,
he said this patient is really sick, so well, by definition they're usually pretty sick, they say we need to make a small incision and target this and so what we did was we scanned the vas, that's the hardware device you're looking at here. These have to be
oriented with the inlet nozzle looking directly into the orifice of the mitro wall, and so we scanned the heart with, what you see is what you get with these devices, they're not deformed, we take a cell phone and implant it in your chest,
still going to look like a cell phone. And so what we did, image fusion was then used with two completely different data sets, it mimicking the procedure, and we lined this up basically with a mitro valve, we then used that same imaging guidance system
I was showing you, made a little incision really doing onto the apex of the heart, and to the eur-aph for the return cannula, and this is basically what it looked like, and you can actually check the efficacy of this by scanning the patient post operatively
and see whether or not you executed on this basically the same way, and so this was all basically developed basing off Lung Nodule Localization Techniques with that we've kind of fairly extensively published, use with men can base one of our thoracic surgeons
so I'd encourage you to look at other opportunities by which you can help other specialties, 'cause I think this 3D imaging is going to transform what our capabilities actually are. Thank you very much indeed for your attention.
- Thank you, Dr. Ascher. Great to be part of this session this morning. These are my disclosures. The risk factors for chronic ischemia of the hand are similar to those for chronic ischemia of the lower extremity with the added risk factors of vasculitides, scleroderma,
other connective tissue disorders, Buerger's disease, and prior trauma. Also, hemodialysis access accounts for a exacerbating factor in approximately 80% of patients that we treat in our center with chronic hand ischemia. On the right is a algorithm from a recent meta-analysis
from the plastic surgery literature, and what's interesting to note is that, although sympathectomy, open surgical bypass, and venous arterialization were all recommended for patients who were refractory to best medical therapy, endovascular therapy is conspicuously absent
from this algorithm, so I just want to take you through this morning and submit that endovascular therapy does have a role in these patients with digit loss, intractable pain or delayed healing after digit resection. Physical examination is similar to that of lower extremity, with the added brachial finger pressures,
and then of course MRA and CTA can be particularly helpful. The goal of endovascular therapy is similar with the angiosome concept to establish in-line flow to the superficial and deep palmar arches. You can use an existing hemodialysis access to gain access transvenously to get into the artery for therapy,
or an antegrade brachial, distal brachial puncture, enabling you treat all three vessels. Additionally, you can use a retrograde radial approach, which allows you to treat both the radial artery, which is typically the main player in these patients, or go up the radial and then back over
and down the ulnar artery. These patients have to be very well heparinized. You're also giving antispasmodic agents with calcium channel blockers and nitroglycerin. A four French sheath is preferable. You're using typically 014, occasionally 018 wires
with balloon diameters 2.3 to three millimeters most common and long balloon lengths as these patients harbor long and tandem stenoses. Here's an example of a patient with intractable hand pain. Initial angiogram both radial and ulnar artery occlusions. We've gone down and wired the radial artery,
performed a long segment angioplasty, done the same to the ulnar artery, and then in doing so reestablished in-line flow with relief of this patient's hand pain. Here's a patient with a non-healing index finger ulcer that's already had
the distal phalanx resected and is going to lose the rest of the finger, so we've gone in via a brachial approach here and with long segment angioplasty to the radial ulnar arteries, we've obtained this flow to the hand
and preserved the digit. Another patient, a diabetic, middle finger ulcer. I think you're getting the theme here. Wiring the vessels distally, long segment radial and ulnar artery angioplasty, and reestablishing an in-line flow to the hand.
Just by way of an extreme example, here's a patient with a vascular malformation with a chronically occluded radial artery at its origin, but a distal, just proximal to the palmar arch distal radial artery reconstitution, so that served as a target for us to come in
as we could not engage the proximal radial artery, so in this patient we're able to come in from a retrograde direction and use the dedicated reentry device to gain reentry and reestablish in-line flow to this patient with intractable hand pain and digit ulcer from the loss of in-line flow to the hand.
And this patient now, two years out, remains patent. Our outcomes at the University of Pennsylvania, typically these have been steal symptoms and/or ulceration and high rates of technical success. Clinical success, 70% with long rates of primary patency comparing very favorably
to the relatively sparse literature in this area. In summary, endovascular therapy can achieve high rates of technical, more importantly, clinical success with low rates of major complications, durable primary patency, and wound healing achieved in the majority of these patients.
- These are my disclosures. So central venous access is frequently employed throughout the world for a variety of purposes. These catheters range anywhere between seven and 11 French sheaths. And it's recognized, even in the best case scenario, that there are iatrogenic arterial injuries
that can occur, ranging between three to 5%. And even a smaller proportion of patients will present after complications from access with either a pseudoaneurysm, fistula formation, dissection, or distal embolization. In thinking about these, as you see these as consultations
on your service, our thoughts are to think about it in four primary things. Number one is the anatomic location, and I think imaging is very helpful. This is a vas cath in the carotid artery. The second is th
how long the device has been dwelling in the carotid or the subclavian circulation. Assessment for thrombus around the catheter, and then obviously the size of the hole and the size of the catheter.
Several years ago we undertook a retrospective review and looked at this, and we looked at all carotid, subclavian, and innominate iatrogenic injuries, and we excluded all the injuries that were treated, that were manifest early and treated with just manual compression.
It's a small cohort of patients, we had 12 cases. Eight were treated with a variety of endovascular techniques and four were treated with open surgery. So, to illustrate our approach, I thought what I would do is just show you four cases on how we treated some of these types of problems.
The first one is a 75 year-old gentleman who's three days status post a coronary bypass graft with a LIMA graft to his LAD. He had a cordis catheter in his chest on the left side, which was discovered to be in the left subclavian artery as opposed to the vein.
So this nine French sheath, this is the imaging showing where the entry site is, just underneath the clavicle. You can see the vertebral and the IMA are both patent. And this is an angiogram from a catheter with which was placed in the femoral artery at the time that we were going to take care of this
with a four French catheter. For this case, we had duel access, so we had access from the groin with a sheath and a wire in place in case we needed to treat this from below. Then from above, we rewired the cordis catheter,
placed a suture-mediated closure device, sutured it down, left the wire in place, and shot this angiogram, which you can see very clearly has now taken care of the bleeding site. There's some pinching here after the wire was removed,
this abated without any difficulty. Second case is a 26 year-old woman with a diagnosis of vascular EDS. She presented to the operating room for a small bowel obstruction. Anesthesia has tried to attempt to put a central venous
catheter access in there. There unfortunately was an injury to the right subclavian vein. After she recovered from her operation, on cross sectional imaging you can see that she has this large pseudoaneurysm
coming from the subclavian artery on this axial cut and also on the sagittal view. Because she's a vascular EDS patient, we did this open brachial approach. We placed a stent graft across the area of injury to exclude the aneurism.
And you can see that there's still some filling in this region here. And it appeared to be coming from the internal mammary artery. We gave her a few days, it still was patent. Cross-sectional imaging confirmed this,
and so this was eventually treated with thoracoscopic clipping and resolved flow into the aneurism. The next case is a little bit more complicated. This is an 80 year-old woman with polycythemia vera who had a plasmapheresis catheter,
nine French sheath placed on the left subclavian artery which was diagnosed five days post procedure when she presented with a posterior circulation stroke. As you can see on the imaging, her vertebral's open, her mammary's open, she has this catheter in the significant clot
in this region. To manage this, again, we did duel access. So right femoral approach, left brachial approach. We placed the filter element in the vertebral artery. Balloon occlusion of the subclavian, and then a stent graft coverage of the area
and took the plasmapheresis catheter out and then suction embolectomy. And then the last case is a 47 year-old woman who had an attempted right subclavian vein access and it was known that she had a pulsatile mass in the supraclavicular fossa.
Was noted to have a 3cm subclavian artery pseudoaneurysm. Very broad base, short neck, and we elected to treat this with open surgical technique. So I think as you see these consults, the things to factor in to your management decision are: number one, the location.
Number two, the complication of whether it's thrombus, pseudoaneurysm, or fistula. It's very important to identify whether there is pericatheter thrombus. There's a variety of techniques available for treatment, ranging from manual compression,
endovascular techniques, and open repair. I think the primary point here is the prevention with ultrasound guidance is very important when placing these catheters. Thank you. (clapping)
- Like to thank Dr. Veith and the committee for asking me to speak. I have no conflicts related to this presentation. Labial and vulvar varicosities occur in up to 10% of pregnant women, with the worst symptoms being manifested in the second half of the pregnancy.
Symptoms include genital pressure and fullness, pruritus, and a sensation of prolapse. These generally worsen with standing. Management is usually conservative. Between compression hose, cooling packs, and exercise, most women can make it through to the end of the pregnancy.
When should we do more than just reassure these women? An ultrasound should be performed when there's an early presentation, meaning in the first trimester, as this can be an unmasking of a venous malformation. If there are unilateral varicosities,
an ultrasound should be performed to make sure that these aren't due to iliac vein thrombosis. If there's superficial thrombosis or phlebitis, you may need to rule out deep venous extension with an ultrasound. When should we intervene?
You may need to intervene to release trapped blood in phlebitis, or to give low molecular weight heparin for comfort. When should a local phlebectomy or sclerotherapy be performed? Should sclerotherapy be performed during pregnancy?
We know very little. Occasionally, this is performed in a patient who is unknowingly pregnant, and there have been no clear complications from this in the literature. The effectiveness of sclero may also
be diminished in pregnancy, due to hormones and increased venous volume. Both polidocanol and sodium tetradecyl sulfate say that there is no support for use during pregnancies, and they advise against it. So what should you do?
This following case is a 24 year old G2P1, who was referred to me at 24 weeks for disabling vaginal and pelvic discomfort. She couldn't go to work, she couldn't take care of her toddler, she had some left leg complaints, but it was mostly genital discomfort and fullness,
and her OB said that he was going to do a pre-term C-section because he was worried about the risk of hemorrhage with the delivery. So this is her laying supine pre-op, and this is her left leg with varicosities visible in the anterior and posterior aspects.
Her ultrasound showed open iliac veins and large refluxing varicosities in the left vulvar area. She had no venous malformation or clot, and she had reflux in the saphenofemoral junction and down the GSV. I performed a phlebectomy on her,
and started with an ultrasound mapping of her superficial veins and perforators in the labial region. I made small incision with dissection and tie ligation of all the varicosities and perforators, and this was done under local anesthesia
with minimal sedation in the operating room. This resulted in vastly improved comfort, and her anxiety, and her OB's anxiety were both decreased, and she went on to a successful delivery. So this diagram shows the usual location of the labial perforators.
Here she is pre-op, and then here she is a week post-op. Well, what about postpartum varicosities? These can be associated with pelvic congestion, and the complaints can often be split into local, meaning surface complaints, versus pelvic complaints.
And this leads into a debate between a top down treatment approach, where you go in and do a venogram and internal coiling, versus a bottom up approach, where you start with local therapy, such as phlebectomy or sclero.
Pelvic symptoms include aching and pressure in the pelvis. These are usually worse with menstruation, and dyspareunia is most pronounced after intercourse, approximately an hour to several hours later. Surface complaints include vulvar itching, tenderness, recurrent thrombophlebitis, or bleeding.
Dyspareunia is present during or at initiation of sexual intercourse. I refer to this as the Gibson Algorithm, as Kathy Gibson and I have talked about this problem a lot, and this is how we both feel that these problems should be addressed.
If you have an asymptomatic or minimally symptomatic patient who's referred for varicosities that are seen incidentally, such as during a laparoscopy, those I don't treat. If you have a symptomatic patient who has pelvic symptoms, then these people get a venogram with coils and sclerotherapy as appropriate.
If they are not pregnant, and have no pelvic symptoms, these patients get sclero. If they are pregnant, and have no pelvic symptoms, they get a phlebectomy. In conclusion, vulvar varicosities are a common problem, and usually conservative management is adequate.
With extreme symptoms, phlebectomy has been successful. Pregnancy-related varicosities typically resolve post-delivery, and these can then be treated with local sclerotherapy if they persist. Central imaging and treatment is successful for primarily pelvic complaints or persistent symptoms.
- Thank you. I have two talks because Dr. Gaverde, I understand, is not well, so we- - [Man] Thank you very much. - We just merged the two talks. All right, it's a little joke. For today's talk we used fusion technology
to merge two talks on fusion technology. Hopefully the rest of the talk will be a little better than that. (laughs) I think we all know from doing endovascular aortic interventions
that you can be fooled by the 2D image and here's a real life view of how that can be an issue. I don't think I need to convince anyone in this room that 3D fusion imaging is essential for complex aortic work. Studies have clearly shown it decreases radiation,
it decreases fluoro time, and decreases contrast use, and I'll just point out that these data are derived from the standard mechanical based systems. And I'll be talking about a cloud-based system that's an alternative that has some advantages. So these traditional mechanical based 3D fusion images,
as I mentioned, do have some limitations. First of all, most of them require manual registration which can be cumbersome and time consuming. Think one big issue is the hardware based tracking system that they use. So they track the table rather than the patient
and certainly, as the table moves, and you move against the table, the patient is going to move relative to the table, and those images become unreliable. And then finally, the holy grail of all 3D fusion imaging is the distortion of pre-operative anatomy
by the wires and hardware that are introduced during the course of your procedure. And one thing I'd like to discuss is the possibility that deep machine learning might lead to a solution to these issues. How does 3D fusion, image-based 3D fusion work?
Well, you start, of course with your pre-operative CT dataset and then you create digitally reconstructed radiographs, which are derived from the pre-op CTA and these are images that resemble the fluoro image. And then tracking is done based on the identification
of two or more vertebral bodies and an automated algorithm matches the most appropriate DRR to the live fluoro image. Sounds like a lot of gobbledygook but let me explain how that works. So here is the AI machine learning,
matching what it recognizes as the vertebral bodies from the pre-operative CT scan to the fluoro image. And again, you get the CT plus the fluoro and then you can see the overlay with the green. And here's another version of that or view of that.
You can see the AI machine learning, identifying the vertebral bodies and then on your right you can see the fusion image. So just, once again, the AI recognizes the bony anatomy and it's going to register the CT with the fluoro image. It tracks the patient, not the table.
And the other thing that's really important is that it recognizes the postural change that the patient undergoes between the posture during the CT scan, versus the posture on the OR table usually, or often, under general anesthesia. And here is an image of the final overlay.
And you can see the visceral and renal arteries with orange circles to identify them. You can remove those, you can remove any of those if you like. This is the workflow. First thing you do is to upload the CT scan to the cloud.
Then, when you're ready to perform the procedure, that is downloaded onto the medical grade PC that's in your OR next to your fluoro screen, and as soon as you just step on the fluoro pedal, the CYDAR overlay appears next to your, or on top of your fluoro image,
next to your regular live fluoro image. And every time you move the table, the computer learning recognizes that the images change, and in a couple of seconds, it replaces with a new overlay based on the obliquity or table position that you have. There are some additional advantages
to cloud-based technology over mechanical technology. First of all, of course, or hardware type technology. Excuse me. You can upgrade it in real time as opposed to needing intermittent hardware upgrades. Works with any fluoro equipment, including a C-arm,
so you don't have to match your 3D imaging to the brand of your fluoro imaging. And there's enhanced accuracy compared to mechanical registration systems as imaging. So what are the clinical applications that this can be utilized for?
Fluoroscopy guided endovascular procedures in the lower thorax, abdomen, and pelvis, so that includes EVAR and FEVAR, mid distal TEVAR. At present, we do need two vertebral bodies and that does limit the use in TEVAR. And then angioplasty stenting and embolization
of common iliac, proximal external and proximal internal iliac artery. Anything where you can acquire a vertebral body image. So here, just a couple of examples of some additional non EVAR/FEVAR/TEVAR applications. This is, these are some cases
of internal iliac embolization, aortoiliac occlusion crossing, standard EVAR, complex EVAR. And I think then, that the final thing that I'd like to talk about is the use with C-arm, which is think is really, extremely important.
Has the potential to make a very big difference. All of us in our larger OR suites, know that we are short on hybrid availability, and yet it's difficult to get our institutions to build us another hybrid room. But if you could use a high quality 3D fusion imaging
with a high quality C-arm, you really expand your endovascular capability within the operating room in a much less expensive way. And then if you look at another set of circumstances where people don't have a hybrid room at all, but do want to be able to offer standard EVAR
to their patients, and perhaps maybe even basic FEVAR, if there is such a thing, and we could use good quality imaging to do that in the absence of an actual hybrid room. That would be extremely valuable to be able to extend good quality care
to patients in under-served areas. So I just was mentioning that we can use this and Tara Mastracci was talking yesterday about how happy she is with her new room where she has the use of CYDAR and an excellent C-arm and she feels that she is able to essentially run two rooms,
two hybrid rooms at once, using the full hybrid room and the C-arm hybrid room. Here's just one case of Dr. Goverde's. A vascular case that he did on a mobile C-arm with aortoiliac occlusive disease and he places kissing stents
using a CYDAR EV and a C-arm. And he used five mils of iodinated contrast. So let's talk about a little bit of data. This is out of Blain Demorell and Tara Mastrachi's group. And this is use of fusion technology in EVAR. And what they found was that the use of fusion imaging
reduced air kerma and DSA runs in standard EVAR. We also looked at our experience recently in EVAR and FEVAR and we compared our results. Pre-availability of image based fusion CT and post image based fusion CT. And just to clarify,
we did have the mechanical product that Phillip's offers, but we abandoned it after using it a half dozen times. So it's really no image fusion versus image fusion to be completely fair. We excluded patients that were urgent/emergent, parallel endographs, and IBEs.
And we looked at radiation exposure, contrast use, fluoro time, and procedure time. The demographics in the two groups were identical. We saw a statistically significant decrease in radiation dose using image based fusion CT. Statistically a significant reduction in fluoro time.
A reduction in contrast volume that looks significant, but was not. I'm guessing because of numbers. And a significantly different reduction in procedure time. So, in conclusion, image based 3D fusion CT decreases radiation exposure, fluoro time,
and procedure time. It does enable 3D overlays in all X-Ray sets, including mobile C-arm, expanding our capabilities for endovascular work. And image based 3D fusion CT has the potential to reduce costs
and improve clinical outcomes. Thank you.
- Mr. Chairman, ladies and gentlemen, good morning. I'd like to thank Dr. Veith for the opportunity to present at this great meeting. I have nothing to disclose. Since Dr. DeBakey published the first paper 60 years ago, the surgical importance of deep femoral artery has been well investigated and documented.
It can be used as a reliable inflow for low extremity bypass in certain circumstances. To revascularize the disease, the deep femoral artery can improve rest pain, prevent or delay the amputation, and help to heal amputation stump.
So, in this slide, the group patient that they used deep femoral artery as a inflow for infrainguinal bypass. And 10-year limb salvage was achieved in over 90% of patients. So, different techniques and configurations
of deep femoral artery angioplasty have been well described, and we've been using this in a daily basis. So, there's really not much new to discuss about this. Next couple minutes, I'd like to focus on endovascular invention 'cause I lot I think is still unclear.
Dr. Bath did a systemic review, which included 20 articles. Nearly total 900 limbs were treated with balloon angioplasty with or without the stenting. At two years, the primary patency was greater than 70%. And as you can see here, limb salvage at two years, close to, or is over 98% with very low re-intervention rate.
So, those great outcomes was based on combined common femoral and deep femoral intervention. So what about isolated deep femoral artery percutaneous intervention? Does that work or not? So, this study include 15 patient
who were high risk to have open surgery, underwent isolated percutaneous deep femoral artery intervention. As you can see, at three years, limb salvage was greater than 95%. The study also showed isolated percutaneous transluminal
angioplasty of deep femoral artery can convert ischemic rest pain to claudication. It can also help heal the stump wound to prevent hip disarticulation. Here's one of my patient. As you can see, tes-tee-lee-shun with near
or total occlusion of proximal deep femoral artery presented with extreme low-extremity rest pain. We did a balloon angioplasty. And her ABI was increased from 0.8 to 0.53, and rest pain disappeared. Another patient transferred from outside the facility
was not healing stump wound on the left side with significant disease as you can see based on the angiogram. We did a hybrid procedure including stenting of the iliac artery and the open angioplasty of common femoral artery and the profunda femoral artery.
Significantly improved the perfusion to the stump and healed wound. The indications for isolated or combined deep femoral artery revascularization. For those patient presented with disabling claudication or rest pain with a proximal
or treatable deep femoral artery stenosis greater than 50% if their SFA or femoral popliteal artery disease is unsuitable for open or endovascular treatment, they're a high risk for open surgery. And had the previous history of multiple groin exploration, groin wound complications with seroma or a fungal infection
or had a muscle flap coverage, et cetera. And that this patient should go to have intervascular intervention. Or patient had a failed femoral pop or femoral-distal bypass like this patient had, and we should treat this patient.
So in summary, open profundaplasty remains the gold standard treatment. Isolated endovascular deep femoral artery intervention is sufficient for rest pain. May not be good enough for major wound healing, but it will help heal the amputation stump
to prevent hip disarticulation. Thank you for much for your attention.
- Thank you very much for the very kind invitation, and I promise I'll do my best to stick to time. The answer is probably to this audience I don't really need to say very much about the ATTRACT trial, but I think it is quite important to note that the ATTRACT trials have now been out for some time, and it is constantly being
talked about in its various dimensions. So I'm going to just spend a few seconds really talking about the ATTRACT trial. A large number of patients screened. One in 41 patients were actually recruited into it and it was a trial that ran for a long time.
Wasn't really with respect to the primary endpoint any particularly good evidence, but for those people who had moderate or severe post-thrombotic syndrome, it probably was of benefit. And if you looked at the Villalta score
and the VCSS scores there was some evidence to support it. So overall, probably some positive take-home messages, but not as affirmative as people would have thought. Now the reason that I've dwelled a little bit on that is that actually, what do we mean when we talk about the post-thrombotic syndrome?
Because I would say in the upper limb, because I have never personally seen an ulcer in the upper limb. Has anybody seen an ulcer in the upper limb due to venous disease? No.
So in a way we are talking about a slightly different entity. We are talking about a limb that has undoubtedly much more finer movements. And there was depression by some people with the results of the ATTRACT trial.
But when you look at the five year results from the CaVenT trial, there was some evidence to suggest that actually, as you get further out, there may be some benefit. If you look at this summation analysis, and I completely accept this is related to the leg,
again, there may be some benefit from the CDT. Now, this is a case of mine. Now I wonder if any of you can tell me how many stages may have been involved from going from the right, to having a ballonplasty in the vein. Pick a number, anywhere between five and ten.
The answer is you have numerous checks of the thrombolysis, you may have a venoplasty, you might have a first rib excision. You may then have occlusion and then realize this before you go on and do the first rib. So all I'm suggesting to you that this is not
a cheap treatment to offer patients treatment to the upper limb. Then we looked forward to some help from the guidelines. Well we look at the American guidelines and give or take, I think the answer is we probably shouldn't be doing it and that we should be only offering anticoagulation.
So do the Brits help? Well actually if you look at the Brits, it sort of says well, you can think a bit about doing decompression, but really if I was standing up in a court of law, I really wouldn't want much support from this guideline
that I had done the right thing. And then the International Society of Thrombolysis and Hemostasis really says well, you can do a little bit of this that thoracic outlet syndrome may be a risk factor. But give or take, surgeries still are a little bit dubious.
So, really there's one good review out there, and this is the review of Vasquez that basically looked at 146 articles, and they found some data on just under 1300 patients. And they postulated and chose some evidence to suggest that there was some evidence
that first rib excision and thrombolysis reduce PTS, and that anticoagulation alone was not enough for the majority of the patients. Very difficult to work out how you selected which patients you should or should not intervene on. Now, I'm sure everybody is rather sick and tired
of me talking about money, and I accept it doesn't really apply here. But money is actually quite important. Five interventions to prevent something that may not happen and at worst may be just a few collateral veins across the chest.
So ladies and gentlemen, I would want you to think very hard, is it actually cost-effective to be offering all patients presenting with an early auxiliary vein thrombosis thrombolysis, and then subsequently first rib excision? These are some of the truths, I think the answer is
it does seem to work. You do need to recognize and make the diagnosis. Usually delayed thrombolysis doesn't work, but there are lots of questions that are unanswered. And how would you defend what you have done in a court of law?
Somebody has a stroke, you then do the first rib, they get a large hemothorax, and they then die because there had been too much TPA on board. Yes, give it some thought. So ladies and gentlemen, I'm afraid I haven't actually answered the question,
but I think you need to give it careful consideration, what are the indications and merits? Thank you very much.
- 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. So this is more or less a teaser. The outcome data will not be presented until next month. It's undergoing final analysis. So, the Vici Stent was the stent in the VIRTUS Trial. Self-expanding, Nitinol stent,
12, 14, and 16 in diameter, in three different lengths, and that's what was in the trial. It is a closed-cell stent, despite the fact that it's closed-cell, the flexibility is not as compromised. The deployment can be done from the distal end
or the proximal end for those who have any interest, if you're coming from the jugular or not in the direction of flow, or for whatever reason you want to deploy it from this end versus that end, those are possible in terms of the system. The trial design is not that different than the other three
now the differences, there are minor differences between the four trials that three completed, one soon to be complete, the definitions of the endpoints in terms of patency and major adverse events were very similar. The trial design as we talked about, the only thing
that is different in this study were the imaging requirements. Every patient got a venogram, an IVUS, and duplex at the insertion and it was required at the completion in one year also, the endpoint was venographic, and those who actually did get venograms,
they had the IVUS as well, so this is the only prospective study that will have that correlation of three different imagings before, after, and at follow-up. Classification, everybody's aware, PTS severity, everybody's aware, the endpoints, again as we talked about, are very similar to the others.
The primary patency in 12 months was define this freedom from occlusion by thrombosis or re-intervention. And the safety endpoints, again, very similar to everybody else. The baseline patient characteristics, this is the pivotal, as per design, there were 170 in the pivotal
and 30 in the feasibility study. The final outcome will be all mixed in, obviously. And this is the distribution of the patients. The important thing here is the severity of patients in this study. By design, all acute thrombotic patients, acute DVT patients
were excluded, so anybody who had history of DVT within three months were excluded in this patient. Therefore the patients were all either post-thrombotic, meaning true chronic rather than putting the acute patients in the post-thrombotic segment. And only 25% were Neville's.
That becomes important, so if you look at the four studies instead of an overview of the four, there were differences in those in terms on inclusion/exclusion criteria, although definitions were similar, and the main difference was the inclusion of the chronics, mostly chronics, in the VIRTUS study, the others allowed acute inclusion also.
Now in terms of definition of primary patency and comparison to the historical controls, there were minor differences in these trials in terms of what that historical control meant. However, the differences were only a few percentages. I just want to remind everyone to something we've always known
that the chronic post-thrombotics or chronic occlusions really do the worst, as opposed to Neville's and the acute thrombotics and this study, 25% were here, 75% were down here, these patients were not allowed. So when the results are known, and out, and analyzed it's important not to put them in terms of percentage
for the entire cohort, all trials need to report all of these three categories separately. So in conclusion venous anatomy and disease requires obviously dedicated stent. The VIRTUS feasibility included 30 with 170 patients in the pivotal cohort, the 12 months data will be available
in about a month, thank you.
- Our group has looked at the outcomes of patients undergoing carotid-subclavian bypass in the setting of thoracic endovascular repair. These are my obligatory disclosures, none of which are relevant to this study. By way of introduction, coverage of the left subclavian artery origin
is required in 10-50% of patients undergoing TEVAR, to achieve an adequate proximal landing zone. The left subclavian artery may contribute to critical vascular beds in addition to the left upper extremity, including the posterior cerebral circulation,
the coronary circulation if a LIMA graft is present, and the spinal cord, via vertebral collaterals. Therefore the potential risks of inadequate left subclavian perfusion include not only arm ischemia, but also posterior circulation stroke,
spinal cord ischemia, and coronary insufficiency. Although these risks are of low frequency, the SVS as early as 2010 published guidelines advocating a policy of liberal left subclavian revascularization during TEVAR
requiring left subclavian origin coverage. Until recently, the only approved way to maintain perfusion of the left subclavian artery during TEVAR, with a zone 2 or more proximal landing zone, was a cervical bypass or transposition procedure. As thoracic side-branch devices become more available,
we thought it might be useful to review our experience with cervical bypass for comparison with these newer endovascular strategies. This study was a retrospective review of our aortic disease database, and identified 112 out of 579 TEVARs
that had undergone carotid subclavian bypass. We used the standard operative technique, through a short, supraclavicular incision, the subclavian arteries exposed by division of the anterior scalene muscle, and a short 8 millimeter PTFE graft is placed
between the common carotid and the subclavian arteries, usually contemporaneous with the TEVAR procedure. The most important finding of this review regarded phrenic nerve dysfunction. To exam this, all pre- and post-TEVAR chest x-rays were reviewed for evidence of diaphragm elevation.
The study population was typical for patients undergoing TEVAR. The most frequent indication for bypass was for spinal cord protection, and nearly 80% of cases were elective. We found that 25 % of patients had some evidence
of phrenic nerve dysfunction, though many resolved over time. Other nerve injury and vascular graft complications occurred with much less frequency. This slide illustrates the grading of diaphragm elevation into mild and severe categories,
and notes that over half of the injuries did resolve over time. Vascular complications were rare, and usually treated with a corrective endovascular procedure. Of three graft occlusions, only one required repeat bypass.
Two pseudoaneurysms were treated endovascularly. Actuarial graft, primary graft patency, was 97% after five years. In summary then, the report examines early and late outcomes for carotid subclavian bypass, in the setting of TEVAR. We found an unexpectedly high rate
of phrenic nerve dysfunction postoperatively, although over half resolved spontaneously. There was a very low incidence of vascular complications, and a high long-term patency rate. We suggest that this study may provide a benchmark for comparison
with emerging branch thoracic endovascular devices. Thank you.
- [Presenter] Thank you very much, Mr. Chairman, and ladies and gentlemen, and Frank Veith for this opportunity. Before I start my talk, actually, I can better sit down, because Hans and I worked together. We studied in the same city, we finished our medical study there, we also specialized in surgery
in the same city, we worked together at the same University Hospital, so what should I tell you? Anyway, the question is sac enlargement always benign has been answered. Can we always detect an endoleak, that is nice. No, because there are those hidden type II's,
but as Hans mentioned, there's also a I a and b, position dependent, possible. Hidden type III, fabric porosity, combination of the above. Detection, ladies and gentlemen, is limited by the tools we have, and CTA, even in the delayed phase
and Duplex-scan with contrast might not always be good enough to detect these lesions, these endoleaks. This looks like a nice paper, and what we tried to do is to use contrast-enhanced agents in combination with MRI. And here you see the pictures. And on the top you see the CTA, with contrast,
and also in the delayed phase. And below, you see this weak albumin contrast agent in an MRI and shows clearly where the leak is present. So without this tool, we were never able to detect an endoleak with the usual agents. So, at this moment, we don't know always whether contrast
in the Aneurysm Sac is only due to a type II. I think this is an important message that Hans pushed upon it. Detection is limited by the tools we have, but the choice and the success of the treatment is dependent on the kind of endoleak, let that be clear.
So this paper has been mentioned and is using not these advanced tools. It is only using very simple methods, so are they really detecting type II endoleaks, all of them. No, of course not, because it's not the golden standard. So, nevertheless, it has been published in the JVS,
it's totally worthless, from a scientific point of view. Skip it, don't read it. The clinical revelance of the type II endoleak. It's low pressure, Hans pointed it out. It works, also in ruptured aneurysms, but you have to be sure that the type II is the only cause
of Aneurysm Sac Expansion. So, is unlimited Sac Expansion harmless. I agree with Hans that it is not directly life threatening, but it ultimately can lead to dislodgement and widening of the neck and this will lead to an increasing risk for morbidity and even mortality.
So, the treatment of persistent type II in combination with Sac Expansion, and we will hear more about this during the rest of the session, is Selective Coil-Embolisation being preferred for a durable solution. I'm not so much a fan of filling the Sac, because as was shown by Stephan Haulan, we live below the dikes
and if we fill below the dikes behind the dikes, it's not the solution to prevent rupture, you have to put something in front of the dike, a Coil-Embolisation. So classic catheterisation of the SMA or Hypogastric, Trans Caval approach is now also popular,
and access from the distal stent-graft landing zone is our current favorite situation. Shows you quickly a movie where we go between the two stent-grafts in the iliacs, enter the Sac, and do the coiling. So, prevention of the type II during EVAR
might be a next step. Coil embolisation during EVAR has been shown, has been published. EVAS, is a lot of talks about this during this Veith meeting and the follow-up will tell us what is best. In conclusions, the approach to sac enlargement
without evident endoleak. I think unlimited Sac expansion is not harmless, even quality of life is involved. What should your patient do with an 11-centimeter bilp in his belly. Meticulous investigation of the cause of the Aneurysm Sac
Expansion is mandatory to achieve a, between quote, durable treatment, because follow-up is crucial to make that final conclusion. And unfortunately, after treatment, surveillance remains necessary in 2017, at least. And this is Hans Brinker, who put his finger in the dike,
to save our country from a type II endoleak, and I thank you for your attention.
- So I'm just going to talk a little bit about what's new in our practice with regard to first rib resection. In particular, we've instituted the use of a 30 degree laparoscopic camera at times to better visualize the structures. I will give you a little bit of a update
about our results and then I'll address very briefly some controversies. Dr. Gelbart and Chan from Hong Kong and UCLA have proposed and popularized the use of a 30 degree laparoscopic camera for a better visualization of the structures
and I'll show you some of those pictures. From 2007 on, we've done 125 of these procedures. We always do venography first including intervascular intervention to open up the vein, and then a transaxillary first rib resection, and only do post-operative venography if the vein reclots.
So this is a 19 year old woman who's case I'm going to use to illustrate our approach. She developed acute onset left arm swelling, duplex and venogram demonstrated a collusion of the subclavian axillary veins. Percutaneous mechanical thrombectomy
and then balloon angioplasty were performed with persistent narrowing at the thoracic outlet. So a day later, she was taken to the operating room, a small incision made in the axilla, we air interiorly to avoid injury to the long thoracic nerve.
As soon as you dissect down to the chest wall, you can identify and protect the vein very easily. I start with electrocautery on the peripheral margin of the rib, and use that to start both digital and Matson elevator dissection of the periosteum pleura
off the first rib, and then get around the anterior scalene muscle under direct visualization with a right angle and you can see that the vein and the artery are identified and easily protected. Here's the 30 degree laparoscopic image
of getting around the anterior scalene muscle and performing the electrocautery and you can see the pulsatile vein up here anterior and superficial to the anterior scalene muscle. Here is a right angle around the first rib to make sure there are no structures
including the pleura still attached to it. I always divide, or try to divide, the posterior aspect of the rib first because I feel like then I can manipulate the ribs superiorly and inferiorly, and get the rib shears more anterior for the anterior cut
because that's most important for decompressing the vein. Again, here's the 30 degree laparoscopic view of the rib shears performing first the posterior cut, there and then the anterior cut here. The portion of rib is removed, and you can see both the artery and the vein
are identified and you can confirm that their decompressed. We insufflate with water or saline, and then perform valsalva to make sure that they're hasn't been any pneumothorax, and then after putting a drain in,
I actually also turn the patient supine before extirpating them to make sure that there isn't a pneumothorax on chest x-ray. You can see the Jackson-Pratt drain in the left axilla. One month later, duplex shows a patent vein. So we've had pretty good success with this approach.
23 patients have requires post operative reintervention, but no operative venous reconstruction or bypass has been performed, and 123 out of 125 axillosubclavian veins have been patent by duplex at last follow-up. A brief comment on controversies,
first of all, the surgical approach we continue to believe that a transaxillary approach is cosmetically preferable and just as effective as a paraclavicular or anterior approach, and we have started being more cautious
about postoperative anticoagulation. So we've had three patients in that series that had to go back to the operating room for washout of hematoma, one patient who actually needed a VATS to treat a hemathorax,
and so in recent times we've been more cautious. In fact 39 patients have been discharged only with oral antiplatelet therapy without any plan for definitive therapeutic anticoagulation and those patients have all done very well. Obviously that's contraindicated in some cases
of a preoperative PE, or hematology insistence, or documented hypercoagulability and we've also kind of included that, the incidence of postop thrombosis of the vein requiring reintervention, but a lot of patients we think can be discharged
on just antiplatelets. So again, our approach to this is a transaxillary first rib resection after a venogram and a vascular intervention. We think this cosmetically advantageous. Surgical venous reconstruction has not been required
in any case, and we've incorporated the use of a 30 degree laparoscopic camera for better intraoperative visualization, thanks.
- Thank you very much 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.
- [Speaker] Good morning everybody thanks for attending the session and again thanks for the invitation. These are my disclosures. I will start by illustrating one of the cases where we did not use cone beam CT and evidently there were numerous mistakes on this
from planning to conducting the case. But we didn't notice on the completion of geography in folding of the stent which was very clearly apparent on the first CT scan. Fortunately we were able to revise this and have a good outcome.
That certainly led to unnecessary re intervention. We have looked at over the years our usage of fusion and cone beam and as you can see for fenestrated cases, pretty much this was incorporated routinely in our practice in the later part of the experience.
When we looked at the study of the patients that didn't have the cone beam CT, eight percent had re intervention from a technical problem that was potentially avoidable and on the group that had cone beam CT, eight percent had findings that were immediately revised with no
re interventions that were potentially avoidable. This is the concept of our GE Discovery System with fusion and the ability to do cone beam CT. Our protocol includes two spins. First we do one without contrast to evaluate calcification and other artifacts and also to generate a rotational DSA.
That can be also analyzed on axial coronal with a 3D reconstruction. Which essentially evaluates the segment that was treated, whether it was the arch on the arch branch on a thoracoabdominal or aortoiliac segment.
We have recently conducted a prospective non-randomized study that was presented at the Vascular Annual Meeting by Dr. Tenario. On this study, we looked at findings that were to prompt an immediate re intervention that is either a type one
or a type 3 endoleak or a severe stent compression. This was a prospective study so we could be judged for being over cautious but 25% of the procedures had 52 positive findings. That included most often a stent compression or kink in 17% a type one or three endoleak
in 9% or a minority with dissection and thrombus. Evidently not all this triggered an immediate revision, but 16% we elected to treat because we thought it was potentially going to lead to a bad complication. Here is a case where on the completion selective angiography
of the SMA this apparently looks very good without any lesions. However on the cone beam CT, you can see on the axial view a dissection flap. We immediately re catheterized the SMA. You note here there is abrupt stop of the SMA.
We were unable to catheterize this with a blood wire. That led to a conversion where after proximal control we opened the SMA. There was a dissection flap which was excised using balloon control in the stent as proximal control.
We placed a patch and we got a good result with no complications. But considerably, if this patient was missed in the OR and found hours after the procedure he would have major mesenteric ischemia. On this study, DSA alone would have missed
positive findings in 34 of the 43 procedures, or 79% of the procedures that had positive findings including 21 of the 28 that triggered immediate revision. There were only four procedures. 2% had additional findings on the CT
that were not detectable by either the DSA or cone beam CT. And those were usually in the femoro puncture. For example one of the patients had a femoro puncture occlusion that was noted immediately by the femoro pulse.
The DSA accounts for approximately 20% of our total radiation dose. However, it allows us to eliminate CT post operatively which was done as part of this protocol, and therefore the amount of radiation exposed for the patient
was decreased by 55-65% in addition to the cost containment of avoiding this first CT scan in our prospective protocol. In conclusion cone beam CT has allowed immediate assessment to identify technical problems that are not easily detectable by DSA.
These immediate revisions may avoid unnecessary re interventions. What to do if you don't have it? You have to be aware that this procedure that are complex, they are bound to have some technical mistakes. You have to have incredible attention to detail.
Evidently the procedures can be done, but you would have to have a low threshold to revise. For example a flared stent if the dilator of the relic gleam or the dilator of you bifurcated devise encroach the stent during parts of the procedure. Thank you very much.
- Thank you, Dr. Veith, for this kind invitation. Aberrant origin of the vertebral artery is the second most common aortic arch anomaly. It is more common in patients with thoracic aortic disease when compared to the general population. It's usually of no clinical significance,
except when encountered while treating cerebro-vascular disease or aortic arch pathology. And that's when critical decision-making to preserve its perfusion becomes necessary. This picture illustrates the most common
types of aortic arch anomalies. Led by bovine arch, isolated vertebral artery, and aberrant right side. In this study, it shows a significant correlation with thoracic aortic disease. We first should evaluate the origin
of the vertebral artery. On the right side of the screen you can see the most common type and it's when it's between the left subclavian and the left common carotid artery origin. This is an example of the left vertebral artery
aberrant associated with a mycotic aneurysm of the aortic arch. And this one is a right aberrant vertebral artery associated with a descending thoracic aneurysm and center retroesophageal location. We then look at the variation of
the vertebral artery and posterior circulation. Most commonly dominant left or hypoplasia of the right vertebral artery as shown in the picture. For termination in the posterior inferior cerebellar artery, or PICA.
Or occlusive lesion on the right side, which necessitates perfusion of the left side. This study shows that vertebral artery variations that could need perfusion is up to 30% of patients
with thoracic aortic disease. There are, unfortunately, minimal literature in the vascular, mostly case reports or series. And most of this says procedure data comes from the neurosurgical literature for occlusive disease that shows in this study,
for example, low morbidity, mortality. Complications include thoracic duct injury, recurrent laryngeal nerve, Horner's and CVAs. And they showed high patency rates. The SVS guidelines for left subclavian revasculatization, although low quality,
shows they indicated routine revascularization and they mention some of the indications for left vertebral artery revasculatization. And extrapolating from that, from those guidelines, we summarize the indications for vertebral artery
revascularization dominant ipsilateral left or hypoplastic right. Incomplete circle of Willis, or termination of the left in the PICA artery. Diseased or occluded contralateral vertebral artery.
Extensive aortic coverage or inability to evaluate the circle of Willis prior to intervention. Some technical tips, we use a routine supraclavicular incision. We identify the vertebral artery posterior-medial
location to the common carotid. We carefully preserve the recurrent laryngeal nerve or non-recurrent laryngeal nerve, which is common in aortic arch anomalies. Thoracic duct on the left side. Transpose it to the posterior surface
of the common carotid. And then clamp distal to the anastomosis and to avoid prolonged ischemia to the posterior circulation. This is a completion aortagram that shows patent left vertebral artery transposed
to the common carotid. And then one month follow-up shows that the left vertebral artery is patent with a complete repair of the aorta. So in our experience, we did six vertebral transpositions over
the last couple years, four on the left, two on the right. No perioperative complications. One lost follow-up. And up to 27 months of the patent vessels. In summary, aberrant vertebral artery is uncommon
finding, but associated with thoracic aortic disease. The origin and the course of the vertebral artery should be thoroughly evaluated prior to treatment. Revascularization should be considered in certain situations to avoid
posterior circulation ischemia. But more data is needed to establish guidelines. Thank you.
- This talk is a brief one about what I think is an entity that we need to be aware of because we see some. They're not AVMs obviously, they're acquired, but it nevertheless represents an entity which we've seen. We know the transvenous treatment of AVMs is a major advance in safety and efficacy.
And we know that the venous approach is indeed very, very favorable. This talk relates to some lesions, which we are successful in treating as a venous approach, but ultimately proved to be,
as I will show you in considerable experience now, I think that venous thrombosis and venous inflammatory disease result in acquired arteriovenous connections, we call them AVMs, but they're not. This patient, for example,
presented with extensive lower extremity swelling after an episode of DVT. And you can see the shunting there in the left lower extremity. Here we go in a later arterial phase. This lesion we found,
as others, is best treated. By the way, that was his original episode of DVT with occlusion. Was treated with stenting and restoration of flow and the elimination of the AVM.
So, compression of the lesion in the venous wall, which is actually interesting because in the type perivenous predominant lesions, those are actually lesions in the vein wall. So these in a form, or in a way, assimilate the AVMs that occur in the venous wall.
Another man, a 53-year-old gentleman with leg swelling after an episode of DVT, we can see the extensive filling via these collaterals, and these are inflammatory collaterals in the vein wall. This is another man with a prior episode of DVT. See his extensive anterior pelvic collaterals,
and he was treated with stenting and success. A recent case, that Dr. Resnick and I had, I was called with a gentleman said he had an AVM. And we can see that the arteriogram sent to me showed arterial venous shunting.
Well, what was interesting here was that the history had not been obtained of a prior total knee replacement. And he gave a very clear an unequivocal history of a DVT of sudden onset. And you can see the collaterals there
in the adjacent femoral popliteal vein. And there it is filling. So treatment here was venous stenting of the lesion and of the underlying stenosis. We tried an episode of angioplasty,
but ultimately successful. Swelling went down and so what you have is really a post-inflammatory DVT. Our other vast experience, I would say, are the so-called uterine AVMs. These are referred to as AVMs,
but these are clearly understood to be acquired, related to placental persistence and the connections between artery and veins in the uterus, which occurs, a part of normal pregnancy. These are best treated either with arterial embolization, which has been less successful,
but in some cases, with venous injection in venous thrombosis with coils or alcohol. There's a subset I believe of some of our pelvic AVMs, that have histories of DVT. I believe they're silent. I think the consistency of this lesion
that I'm showing you here, that if we all know, can be treated by coil embolization indicates to me that at least some, especially in patients in advanced stage are related to DVT. This is a 56-year-old, who had a known history of prostate cancer
and post-operative DVT and a very classic looking AVM, which we then treated with coil embolization. And we're able to cure, but no question in my mind at least based on the history and on the age, that this was post-phlebitic.
And I think some of these, and I think Wayne would agree with me, some of these are probably silent internal iliac venous thromboses, which we know can occur, which we know can produce pulmonary embolism.
And that's the curative final arteriogram. Other lesions such as this, I believe are related, at least some, although we don't have an antecedent history to the development of DVT, and again of course,
treated by the venous approach with cure. And then finally, some of the more problematic ones, another 56-year-old man with a history of prior iliofemoral DVT. Suddenly was fine, had been treated with heparin and anticoagulation.
And suddenly appeared with rapid onset of right lower extremity swelling and pain. So you see here that on an arteriogram of the right femoral, as well as, the super selective catheterization of some of these collaterals.
We can see the lesion itself. I think it's a nice demonstration of lesion. Under any other circumstance, this is an AVM. It is an AVM, but we know it to be acquired because he had no such swelling. This was treated in the only way I knew how to treat
with stenting of the vein. We placed a stent. That's a ballon expanded in the angiogram on your right is after with ballon inflation. And you can see the effect that the stenting pressure, and therefore subsequently occlusion of the compression,
and occlusion of the collaterals, and connections in the vein wall. He subsequently became asymptomatic. We had unfortunately had to stent extensively in the common femoral vein but he had an excellent result.
So I think pelvic AVMs are very similar in location and appearance. We've had 13 cases. Some with a positive history of DVT. I believe many are acquired post-DVT, and the treatment is the same venous coiling and or stent.
Wayne has seen some that are remarkable. Remember Wayne we saw at your place? A guy was in massive heart failure and clearly a DVT-related. So these are some of the cases we've seen
and I think it's noteworthy to keep in mind, that we still don't know everything there is to know about AVMs. Some AVMs are acquired, for example, pelvic post-DVT, and of course all uterine AVMs. Thanks very much.
(audience applause) - [Narrator] That's a very interesting hypothesis with a pelvic AVMs which are consistently looking similar. - [Robert] In the same place right? - [Narrator] All of them are appearing at an older age. - [Robert] Yep.
Yep. - This would be a very, very good explanation for that. I've never thought about that. - Yeah I think-- - I think this is very interesting. - [Robert] And remember, exactly.
And I remember that internal iliac DVT is always a silent process, and that you have this consistency, that I find very striking. - [Woman] So what do you think the mechanism is? The hypervascularity looked like it was primarily
arterial fluffy vessels. - [Robert] No, no, no it's in the vein wall. If you look closely, the arteriovenous connections and the hypervascularity, it's in the vein wall. The lesion is the vein wall,
it's the inflammatory vein. You remember Tony, that the thing that I always think of is how we used to do plain old ballon angioplasty in the SFA. And afterwards we'd get this
florid venous filling sometimes, not every case. And that's the very tight anatomic connection between those two. That's what I think is happening. Wayne? - [Wayne] This amount is almost always been here.
We just haven't recognized it. What has been recognized is dural fistula-- - Yep. - That we know and that's been documented. Chuck Kerber, wrote the first paper in '73 about the microvascular circulation
in the dural surface of the dural fistula, and it's related to venous thrombosis and mastoiditis and trauma. And then as the healing process occurs, you have neovascular stimulation and fistulization in that dural reflection,
which is a vein wall. And the same process happens here with a DVT with the healing, the recanalization, inflammation, neovascular stimulation, and the development of fistulas. increased vascular flow into the lumen
of the thrombosed area. So it's a neovascular stimulation phenomenon, that results in the vein wall developing fistula very identical to what happens in the head with dural fistula had nothing described of in the periphery.
- [Narrator] Okay, very interesting hypothesis.
- Thank you Tal. It's a privilege again to take the podium here. No disclosures. Everyone in here in this audience understands how important Traumatic Aortic Injury is, the second leading cause of death, primarily due to blunt mechanisms,
that are well known to the trauma and vascular community. And, we've learned a lot about how to care for these patient's in the transition in the vascular age. And, that began with the American Association for the Surgery of Trauma Studies in 2008 and 2009, which showed that TEVAR was associated
with an improved mortality and decreased paraplegia compared to older modalities. And, these are the graphs at my old training grounds at UT Houston, which, I'm sure would be the same at most other centers. A gradual transition to almost completely TEVAR
for every patient who has appropriate anatomy. And, we now have over a decade worth of survival data to show the outcome comparisons are the same as the older modalities. But the question has become now, are we over treating some of these injuries?
We need an optimal algorithm and an optimal algorithm requires an optimal grading system. And, that grading system should determine the treatment we utilize, it should guide the timing of the treatment. And, should provide some prediction of the natural history
in those patient's that we do not immediately treat. The SVS in 2011 developed a very nice anatomical based grading system, however, this is a lesionology type algorithm if you will, and not incorporating any of the valuable information that the patient also may possess
in terms of associated injuries. There have been alternative proposals: Vancouver, the Harborview "Minimal Aortic Injuries" is one that is very familiar and commonly utilized in the literature. And, even the Baltimore Classification which includes some physiology elements.
And the reality is, there are also other elements of ongoing issues Blunt Thoracic Aortic Injury, including not only how to manage those Grade 1/Grade 2 injuries but the timing of repair. How do we prioritize repair in the context of other sev
rain Injury and other bleeding solid organs and what's the optimal follow up regimen for these patients? It was with those questions in mind that 3 years ago we developed the Aortic Trauma Foundation. This is a non-profit organization with a Multispecialty
International Medical Advisory Board and a Board of Directors. We really wanted to improve outcomes of patient's with Traumatic Aortic Injury through education and research. We started with several initial, kind of low hanging fruit exercises, the first of which was a practice pattern survey
from members of the SVS, trauma organization, thoracic surgery organizations in interventional radiology and we found that there were some contingents here, and some very interesting findings in this survey. In fact, a majority of providers who care for these injuries don't rely on any guidelines at all.
Just their own personal knowledge of literature and their experience over their practice lifespan. Likewise, these mid-grade injuries represent some significant controversy with almost half the providers thinking that these just need medical therapy and observation as an outpatient.
And the remainder treating them emergently with TEVAR. Or, urgently with TEVAR. And we also conducted a large Retrospective Multicenter Study, 382 patient's from US Level 1 Trauma Centers and we found the at TEVAR compared to Open Repair
was associated with lower transfusion, lower overall mortality, lower aortic related mortality. None of these were surprising findings. But again, this study identified some controversy here, particularly with the, there's no difference in outcomes with those Minimal BTAI patient's if they're treated
with TEVAR or undergo medical non-operative management. Which suggests at least that in some of these patient's we are actually over-treating them. We have, as ongoing effort, our Aortic Trauma Foundation International, Multicenter PROSPECTIVE Blunt Thoracic Aortic Injury Registry
designed to identify predictors of early rupture, develop some multi-specialty consensus guidelines on treatment and management and establish long term outcomes. Anyone in this audience can join this effort, we have always gotten good contribution from VEITH.
We have a region based involvement, mechanism to promote the not only ATF involvement but the prospective registry in the US and abroad. And, we've had some good results. This initial registry went live in 2016, as of 2018, we have 381 patient's
in 23 centers internationally. And we plan to do a feasibility report when we cross the 500 patient threshold. And we invite anyone who seeks to become a member of the Aortic Trauma Foundation and actively contributes to utilize this data.
We all want to as a community, identify and define optimal care practices. We are going to actively solicit and review proposals for use and we hope that this data will produce a foundational platform upon which we can develop some really meaningful multi-specialty guidelines
that are evidence and practice based. Thank you.
- Here are my disclosures, none are relevant to today's talks. So what is the role of compressions stockings to prevent Postthrombotic Syndrome for patients with acute DVT? Well it's become rather complicated because as shown by recent studies,
it depends on what question is being asked. Question one is do compression stockings started at the time of DVT diagnosis prevent PTS, such as the Socks trial and other similar trials? Or question two, if you're already worn compression stockings for a period of time after DVT
and have not developed PTS, does stopping them increase the risk of developing PTS, such as the recent OCTAVIA and IDEAL trials? This is a meta-analysis that was done to address question one, namely the role of compression stockings started at the time of DVT diagnosis,
and this meta-analysis considered unblinded studies. The one blinded study, which was the Socks trial, and then attempted to combine that data, and you can see that if one looks at the unblinded studies there's suggestion of a 30% protective effect, or, excuse me, 40% protective effect.
The blinded study showed no effect of compression stockings. And combining all the studies together seemed to show about a 30% protective effect, however the confidence interval crossed one. There's very low confidence in this total estimate because of the substantial heterogeneity across studies.
And indeed, in their discussion, the authors point out the following: "We have very serious concerns about the unblinded studies because such designs may inflate treatment effects". And also, "differing results across studies suggest that the decision to use compression stockings
may be value and preference dependent for our patients". And we'll come back to that shortly. What about question two, if you've already worn compression stockings for a period of time after DVT, and you haven't developed PTS, does stopping them increase the risk of getting PTS?
There've been two new trials. One is the OCTAVIA study, of 518 proximal DVT patients. All wore compression stockings for one year after their DVT. If they were free of PTS at one year, they were randomized to continue for an additional year, or to stop.
And the results of this trial showed that stopping after one year was inferior to continuing for two years for the PTS outcome. On the other hand, we have the IDEAL study, of 865 proximal DVT patients. In this study, all patients wore compression stockings
for six months after proximal DVT, and if they were free of PTS at six months, they were randomized to continue for an additional 18 months, or to tailor continued use of stockings according to the Villalta score that was assessed every three months
at study follow-up visits. And the results of this trial showed that tailoring use after six months, which was the experimental arm, was actually non-inferior to continuing for 18 more months. So these results are interesting but somewhat conflicting. So how do I use compression stockings in 2018?
I don't routinely prescribe stockings to all of my proximal DVT patients. They can be difficult to apply, uncomfortable, expensive, and they need to be replaced every few months. And we all know that many patients won't wear them
in real life, especially if they have no symptoms whatsoever. And also, it's really not clear to me whether stockings prevent Postthrombotic Syndrome versus merely palliate symptoms of Postthrombotic Syndrome that has already developed.
And it may simply be as effective and more convenient and we may achieve better compliance if we ask our patients to start compression stockings at the time they develop symptoms of Postthrombotic Syndrome. I do however prescribe a trial of stockings
to any DVT patient, whether they have proximal or distal DVT who has residual symptoms after their DVT, and I'd continue them for as long as the patient derives symptomatic benefit or is able to tolerate them, and I certainly take patients' values and preferences into account
in making this decision. Moving on to the role of interventional treatment for patients with acute DVT. We have all heard and seen the results of the ATTRACT trial. Just very briefly, we know that the primary study outcome, any Postthrombotic Syndrome was not different
in the PCDT arm versus the No-PCDT arm. However, it did appear that PCDT reduced the risk of developing moderate or severe Postthrombotic Syndrome, and this was driven primarily by the subgroup with Iliofemoral DVT. In terms of short-term results, PCDT caused more
bleeding, major and any bleeding, and it caused statistically significant but clinically modest improvements in leg pain and leg swelling. Based on these results, what's the role of interventional treatment for patients with acute DVT? I would say that it's not indicated for routine use
in proximal DVT, it doesn't prevent Postthrombotic Syndrome, it does increase bleeding, and older patients above the age of 60 to 65 or more appear to be particularly poor candidates because of more bleeding and less efficacy. And further study in clinical use of these modalities
should be targeted. One would still consider PCDT in patients with severe symptoms, Iliofemoral DVT, and the other factors shown here on the slide. And finally, always remember that it's always an option to anticoagulate first for the initial
five to seven days if the limb is not acutely threatened. Thank you very much.
- Thank you very much. Well this is a series that was actually published five years ago. And it outlined 45,000 patients after carotid endarterectomy, as well as open and closed thoracic abdominal procedures and infrainguinal bypasses.
And you can see here, that the VTE rate, and this is emblematic of a lot of studies. If you take everything together in a ball, you get an average result. And as you can see, the peripheral bypasses had a low incidence.
Carotids, very low incidence. But open procedures had a higher incidence than endovascular procedures. But here is the nub. Here is what's really important and why you need to do risk assessment.
Look at what happened to these percentages if the patients had any morbidity during hospitalization, as high as 7.8%. And here's the list after they went home. Again, it's not the .5 tenths of a percent or 1%, and this is what it's all about.
It's about the extra risk factors that the patient has. So now, anybody that's starting to do work with the Caprini Score, you've got to go to the patient-friendly form. Because we don't just do it,
if the patient comes in for surgery, and somebody does a preoperative evaluation in the holding area, stop it! It's ridiculous! Have you ever been in the holding area? What are you worried about?
You're worried about having the operation. Are they going to find cancer? Will the surgeon have a bad day? How much pain am I going to be in? How long am I going to be out of work? They're not going to talk to you
about their family history or their obstetrical misadventures. So you have them fill a form out ahead of time with their family, and then when they come in, you just double-check it. And we've studied this, it's in five languages,
and it's got perfect correlation with trained observers doing the same thing. And remember, if you fail to carefully interrogate your patients regarding the history or family history of venous thromboembolism, vascular surgery or not, sooner or later you may
be faced with a fatal PE. And the idea that you're giving anticoagulants during your procedure that's going to protect them is not valid. The relative risk of thrombosis increases with the number of risk factors identified.
A combination of genetic and acquired risk factors in a person without a history of a thrombosis personally, but with a family history, has a 60-fold higher chance than those that have a negative family history. And a positive family history increased
the risk of venous thrombosis more than 2-fold, regardless of the other risk factors. Don't forget the history of thrombosis. You won't need to look this article up. It's 183,000 patients over 25 years and it shows that both in first, second,
and third-degree relatives, as well as cohabitants in the household, there's an increased risk of venous thromboembolism. Lowering down, getting lower for each degree of a relative.
But a DVT in a cousin, there may also be a thrombopathic condition in that patient. So you better pay attention to that. National Surgical Quality Improvement Program, wonderful program. The database has no information on history
or family history of VTE, use of perioperative VTE prophylaxis, intraoperative anticoagulation, or perioperative use of antiplatelet agents. How are you supposed to make any sense out of DVT-related studies?
Finally, due to the lack of routine screening for VTE, the incidence of VTE may be underestimated in this NSQIP database, which only makes the need for further study more pressing. This is an important consideration because
more recent data indicates that two-thirds of the patients are found to have DVT during screening and after vascular operations, have no signs or symptoms of the problem. And I'd like to remind you, so this is based on the Boston data, which is the best data.
Patients with a low score pneumatic compression during hospitalization. Moderate score, of 7-10 days of anticoagulation. Don't make any difference if they're inpatient or outpatient. And 28 days if their score is over nine.
They lowered their incidence on the surgical services from 2.2% to a tenth of a percent at 30 days. And finally, and I think this is really, really important. Take a look at all these risk assessment scores.
To my knowledge, there's only two scores. It's not the Padua, it's not the IMPROVE that have a history of obstetrical misadventures which can reflect antiphospholipid antibody syndrome, as well as family history
in various degrees of relatives. So with that, thank you very much.
- 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.
- I'd like to share with you our experience using tools to improve outcomes. These are my disclosures. So first of all we need to define the anatomy well using CTA and MRA and with using multiple reformats and 3D reconstructions. So then we can use 3D fusion with a DSA or with a flouro
or in this case as I showed in my presentation before you can use a DSA fused with a CT phase, they were required before. And also you can use the Integrated Registration like this, when you can use very helpful for the RF wire
because you can see where the RF wire starts and the snare ends. We can also use this for the arterial system. I can see a high grade stenosis in the Common iliac and you can use the 3D to define for your 3D roadmapping you can use on the table,
or you can use two methods to define the artery. Usually you can use the yellow outline to define the anatomy or the green to define the center. And then it's a simple case, 50 minutes, 50 minutes of ccs of contrast,
very simple, straightforward. Another everybody knows about the you know we can use a small amount of contrast to define the whole anatomy of one leg. However one thing that is relatively new is to use a 3D
in order to map, to show you the way out so you can do in this case here multiple segmental synosis, the drug-eluting-balloon angioplasty using the 3D roadmap as a reference. Also about this case using radial fre--
radial access to peripheral. Using a fusion of image you can see the outline of the artery. You can see where the high grade stenosis is with a minimum amount of contrast. You only use contrast when you are about
to do your angiogram or your angioplasty and after. And that but all everything else you use only the guide wires and cathers are advanced only used in image guidance without any contrast at all. We also been doing as I showed before the simultaneous injection.
So here I have two catheters, one coming from above, one coming from below to define this intravenous occlusion. Very helpful during through the and after the 3D it can be helpful. Like in this case when you can see this orange line is where
the RF wire is going to be advanced. As you can see the breathing, during the breathing cycle the pleura is on the way of the RF wire track. Pretty dangerous stuff. So this case what we did we asked the anesthesiologist
to have the patient in respiratory breath holding inspiration. We're able to hyperextend the lungs, cross with the RF wire without any complication. So very useful. And also you can use this outline yellow lines here
to define anatomy can help you to define where you need to put the stents. Make sure you're covering everything and having better outcomes at the end of the case without overexposure of radiation. And also at the end you can use the same volt of metric
reconstruction to check where you are, to placement of the stent and if you'd covered all the lesion that you had. The Cone beam CT can be used for also for the 3D model fusion. As you can see that you can use in it with fluoro as I
mentioned before you can do the three views in order to make sure that the vessels are aligned. And those are they follow when you rotate the table. And then you can have a pretty good outcome at the end of the day at of the case. In that case that potentially could be very catastrophic
close to the Supra aortic vessels. What about this case of a very dramatic, symptomatic varicose veins. We didn't know and didn't even know where to start in this case. We're trying to find our way through here trying to
understand what we needed to do. I thought we need to recanalize this with this. Did a 3D recan-- a spin and we saw ours totally off. This is the RFY totally interior and the snare as a target was posterior in the ASGUS.
Totally different, different plans. Eventually we found where we needed to be. We fused with the CAT scan, CT phase before, found the right spot and then were able to use
Integrated registration for the careful recanalization above the strip-- interiorly from the Supraaortic vessels. As you can see that's the beginning, that's the end. And also these was important to show us where we working.
We working a very small space between the sternal and the Supraaortic vessels using the RF wire. And this the only technology would allowed us to do this type of thing. Basically we created a percutaneous in the vascular stent bypass graft.
You can you see you use a curved RF wire to be able to go back to the snare. And that once we snare out is just conventional angioplasty recanalized with covered stents and pretty good outcome. On a year and a half follow-up remarkable improvement in this patient's symptoms.
Another patient with a large graft in the large swelling thigh, maybe graft on the right thigh with associated occlusion of the iliac veins and inclusion of the IVC and occlusion of the filter. So we did here is that we fused the maps of the arterial
phase and the venous phase and then we reconstruct in a 3D model. And doing that we're able to really understand the beginning of the problem and the end of the problem above the filter and the correlation with the arteries. So as you can see,
the these was very tortuous segments. We need to cross with the RF wire close to the iliac veins and then to the External iliac artery close to the Common iliac artery. But eventually we were able to help find a track. Very successfully,
very safe and then it's just convention technique. We reconstructed with covered stents. This is predisposed, pretty good outcome. As you can see this is the CT before, that's the CT after the swelling's totally gone
and the stents are widely open. So in conclusion these techniques can help a reduction of radiation exposure, volume of contrast media, lower complication, lower procedure time.
In other words can offer higher value in patient care. Thank you.
- Thank you and thanks Craig, it's fun to have these debates with good colleagues, thoughtful colleagues. These are my disclosures for the talk. But pry my most important disclosure is I work in academic center with a dedicated Limb Preservation Center, very tertiary practice. And I perform both open and endovascular surgery
and actually my current lower extremity practice is probably about 60 to 65 percent endovascular so, I do both of these procedures. We already saw this slide about how the increase in endovascular intervention has grown. But, I would caution you to look a little more closely
at this outpace of decline in bypass surgery by more than three to one. I don't think this is an epidemic, I think it's a little bit of this, and a little bit of this. Everything looks like a nail when you only have a hammer
or a hammer when you only have a nail. So, what should we really be doing today? We should be trying to select the best thing for the right patient at the right time. And it really comes down to starting not with the lesion, but with the patient.
Start with assessing the patient's risk, what's their perioperative risk, what's their long-term survival, what are their goals for care? And then look at the limb itself, because not all limbs are the same.
There are minor ulcers, there's extensive and severe rest pain and there are large areas of tissue loss. And the WIfI system is good for that. And then let's look at the anatomy last. And when we're looking at it from the standpoint of what all the options are, endovascular we're looking
at what's the likelihood not just of technical success, but of hemodynamic gain and sustained patency for as long as a patient needs it. With bypass, we also have to look at other things. What kind of vein do they have, or what kind of target do they have?
And I think the bottom line here is in today's practice, it's kind of silly to say endo first for all patients, it's certainly not surgery first for all patients because they have complementary roles in contemporary practice. Well what's happening in the world out there,
this is the German CRITISCH registry, I'll just point out 12 hundred patients recently published only a couple of years ago, 24 percent of patients get bypass first. And if you look at who they are, not surprisingly they are the patients
with long occlusions and complex anatomy. They are out there, in fact most of these patients have multi-segment disease, as Craig pointed out. Here's some contemporary data that you haven't seen yet because it's in press, but this is VQI data looking at 2003 to 2017.
I'll point out just in the last 2013 years, still, if you looked at unique patients, not procedures, one-third of the patients are getting a bypass first. And if you define risk groups considering what might be a low risk patient as a three percent mortality and survival greater than 70 percent,
and a high risk patient, you can put these patients into buckets and in fact, of all the patients getting lower extremity revascularization and VQI today, 80 percent of them would be called low risk based on this definition. So, most patients are not high risk patients
who don't have long-term survival. In fact, this is current VQI data. If you're a low risk patient in that cohort, your five year survival actually is over 70 percent. So there's a lot of these patients actually today with better CLO medical therapy that are actually
living longer and are not that high risk. We talked about the BASIL trial already, and he pointed out how the early results were similar, but what we learned also with BASIL, that if you've got a bypass as a secondary procedure, or if you got a bypass with a prosthetic,
you simply did not do as well. That doesn't mean that the initial endovascular revascularization caused the bypass failure, but it means that secondary bypass surgery does not work as well. And when Dr. Bradbury looked at this data
over a longer period of time now going over many more years, there's a consistent inferior outcome to the patients who had their bypass after failed angioplasty in comparison to bypass as the initial strategy. This is not an isolated finding. When we looked in the VSGNE data over a,
more than 3000 patients at the impact of restenosis on subsequent treatment failure, we found that whether patients had a failed previous PVI or bypass, their secondary bypass outcomes were inferior, and the inferiority continued to get worse with time.
These bypasses just don't perform as well. Unfortunately, if we only do bypass after endo has failed, this is what all the results are going to start to look like. So let's be a little bit smarter. Now what about patency?
I think we, even today in the endovascular world, we realize patency is important. After all, that's why we're doing drug elution. Most, but not all patients with advanced limb ischemia will recrudesce their symptoms when their revascularization fails.
I think we all know that. Most CLTI patients have multi-segment disease. I don't want to sit up here and be a high school or elementary school math teacher, but here's the reality. If you look at it above the lesion, you say I'm going to get 70 percent patency there, and you look at
the tibial lesion, you say I'm going to get 50 percent patency there, what do you think your patency is for the whole leg? It's 35 percent folks, it's the product of the two. That is the reality pretty often. Patients with more advanced limb presentations,
such as WIfI stage do not tolerate these failures. They tolerate them poorly. They go on to amputation pretty fast. And patient survival, as I've already shown you has improved. Now, what the all endo-all the time
camp does and doesn't say. He already showed us, many datasets suggest the downstream outcomes are roughly equivalent but, these are not the same patients, we are not operating on the same patients you are doing endo on.
If I told you the results are the same for PCI and CABG without showing you anatomy, you would laugh me off the stage right? So, this is really not an equivalent argument. Endo can be repeated with minimal morbidity, but patients suffer.
Their limb status deteriorates, they come in the hospital often, and they continue to decline in the outcomes of these secondary procedures. CLTI patients are too frail for surgery, I just showed you that's really not true for many patients.
There is really unfortunately, an economic incentive here. Because there is unfortunately, no incentive for durable success. I hate to bring that up, but that's the reality. Now just quickly, some results. This is a large Japanese series
where they were performing endovascular interventions only for advanced limb ischemia. And basically what you can see as you go across the WIfI stages here from stage one to stage four, when you get to these stage four patients, the wound healing rate's only 44 percent,
limb salvage rate drops to 80 percent, repeat EVT rate is encroaching 50 percent. These patients really are not doing well with endovascular intervention. And we found that in our own series too, it's relatively small numbers and not randomized.
But if we look at the stage 4 limbs with bypass versus endo, when these patients failed at revascularization, and they may not have been bypass candidates, but they didn't do well, they went on to amputation very quickly.
So the ESC guidelines that just came out really sort of line up with what I'm telling you. You'll see bypass first. If you have long occlusions in an available vein, is actually currently the favorite approach, with level 1A recommendation.
So in summary, this is how I currently approach it. You look at all these factors, some people should get endo first, but there's still about 20 or 30 percent that I think should get bypass. Some people should go on to amputation earlier, is the bottom line, and I'll go right to the bottom line.
If you don't have access to a skilled open bypass surgeon, you're probably not at a center of excellence, go find one.
- Thank you very much. It's an hono ou to the committee for the invitation. So, I'll be discussing activity recommendations for our patients after cervical artery dissection. I have no relevant disclosures.
And extracranial cervical artery dissection is an imaging diagnosis as we know with a variety of presentations. You can see on the far left the intimal flap and double lumen in the left vertebral artery
on both coronal and axial imaging, a pseudoaneurysm of the internal carotid artery, aneurysmal degeneration in an older dissection, and an area of long, smooth narrowing followed by normal artery, and finally a flame-tipped occlusion.
Now, this affects our younger patients with really opposity of atherosclerotic risk factors. So, cervical artery dissection accounts for up to 25% of stroke in patients under the age of 45. And, other than hypertension, it's not associated with any cardiovascular risk factors.
There is a male predominance, although women with dissections seem to present about five years younger. And there is an indication that there may be a systemic ateriopathy contributing to this in our patients, and I'll show you some brief data regarding that.
So, in studies that have looked at vessel redundancy, including loops, coils, and in the video image, an S curve on carotid duplex. Patients with cervical artery dissection have a much higher proportion of these findings, up to three to four times more than
age and sex matched controls. They also have findings on histology of the temporal artery when biopsied. So one study did this and these patients had abnormal capillary formation as well as extravasation of blood cells between the median adventitia
of the superficial temporal artery. And there is an association with FMD and a shared genetic polymorphism indicating that there may be shared pathophysiology for these conditions. But in addition, a lot of patients report minor trauma around the time or event of cervical artery dissection.
So this data from CADISP, and up to 40% of cases had minor trauma related to their dissection, including chiropractic neck manipulation, extreme head movements, or stretching, weight lifting, and sports-related injuries. Thankfully, the majority of patients do very well after
they have a dissection event, but a big area of concern for the patient and their provider is their risk for recurrence. That's highest around the original event, about 2% within the first month, and thereafter, it's stable at 1% per year,
although recurrent pain can linger for many years. So what can we tell our patients in terms of reducing their risk for a recurrent event? Well, most of the methods are around reducing any sort of impulse, stress, or pressure on the arteries, both intrinsically and extrinsically,
including blood pressure control. I advise my patients to avoid heavy lifting, and by that I mean more than 30 pounds, and intense valsalva or isometric exercise. So shown here is a photo of the original World's Strongest Man lifting four
adult-sized males in addition to weights, but there's been studies in the physiology literature with healthy, younger males in their 20s, and they're asked to do a double-leg press, or even arm-curls, and with this exercise and repetitions, they can get mean systolic pressures,
or mean pressures up into the 300s, as well as heart rate into the 170s. I also tell my patients to avoid any chiropractic neck manipulation or deep tissue massage of the neck, as well as high G-force activities like a roller coaster.
There are some case reports of cervical artery dissection related to this. And then finally, what can they do about cardio? A lot of these patients are very anxious, they're concerned about re-incorporating exercise after they've been through something like this,
so I try to give them some kind of guidelines and parameters that they can follow when they re institute exercise, not unlike cardiac rehabilitation. So initially, I tell them "You can do light walking, but if you don't feel well,
or something's hurting, neck pain, headache, don't push it." Thereafter, they can intensify to a heart rate maximum of 70-75% of their maximum predicted heart rate, and that's somewhere between months zero and three, and then afterwards when they're feeling near normal,
I give them an absolute limit of 90% of their maximum predicted heart rate. And I advise all of my patients to avoid extreme exercise like Orange Theory, maybe even extreme cycling classes, marathons, et cetera. Thank you.
- We are talking about the current management of bleeding hemodialysis fistulas. I have no relevant disclosures. And as we can see there with bleeding fistulas, they can occur, you can imagine that the patient is getting access three times a week so ulcerations can't develop
and if they are not checked, the scab falls out and you get subsequent bleeding that can be fatal and lead to some significant morbidity. So fatal vascular access hemorrhage. What are the causes? So number one is thinking about
the excessive anticoagulation during dialysis, specifically Heparin during the dialysis circuit as well as with cumin and Xarelto. Intentional patient manipulati we always think of that when they move,
the needles can come out and then you get subsequent bleeding. But more specifically for us, we look at more the compromising integrity of the vascular access. Looking at stenosis, thrombosis, ulceration and infection. Ellingson and others in 2012 looked at the experience
in the US specifically in Maryland. Between the years of 2000/2006, they had a total of sixteen hundred roughly dialysis death, due to fatal vascular access hemorrhage, which only accounted for about .4% of all HD or hemodialysis death but the majority did come
from AV grafts less so from central venous catheters. But interestingly that around 78% really had this hemorrhage at home so it wasn't really done or they had experienced this at the dialysis centers. At the New Zealand experience and Australia, they had over a 14 year period which
they reviewed their fatal vascular access hemorrhage and what was interesting to see that around four weeks there was an inciting infection preceding the actual event. That was more than half the patients there. There was some other patients who had decoags and revisional surgery prior to the inciting event.
So can the access be salvaged. Well, the first thing obviously is direct pressure. Try to avoid tourniquet specifically for the patients at home. If they are in the emergency department, there is obviously something that can be done.
Just to decrease the morbidity that might be associated with potential limb loss. Suture repairs is kind of the main stay when you have a patient in the emergency department. And then depending on that, you decide to go to the operating room.
Perera and others 2013 and this is an emergency department review and emergency medicine, they use cyanoacrylate to control the bleeding for very small ulcerations. They had around 10 patients and they said that they had pretty good results.
But they did not look at the long term patency of these fistulas or recurrence. An interesting way to kind of manage an ulcerated bleeding fistula is the Limberg skin flap by Pirozzi and others in 2013 where they used an adjacent skin flap, a rhomboid skin flap
and they would get that approximal distal vascular control, rotate the flap over the ulcerated lesion after excising and repairing the venotomy and doing the closure. This was limited to only ulcerations that were less than 20mm.
When you look at the results, they have around 25 AV fistulas, around 15 AV grafts. The majority of the patients were treated with percutaneous angioplasty at least within a week of surgery. Within a month, their primary patency was running 96% for those fistulas and around 80% for AV grafts.
If you look at the six months patency, 76% were still opened and the fistula group and around 40% in the AV grafts. But interesting, you would think that rotating an adjacent skin flap may lead to necrosis but they had very little necrosis
of those flaps. Inui and others at the UC San Diego looked at their experience at dialysis access hemorrhage, they had a total 26 patients, interesting the majority of those patients were AV grafts patients that had either bovine graft
or PTFE and then aneurysmal fistulas being the rest. 18 were actually seen in the ED with active bleeding and were suture control. A minor amount of patients that did require tourniquet for a shock. This is kind of the algorithm when they look at
how they approach it, you know, obviously secure your proximal di they would do a Duplex ultrasound in the OR to assess hat type of procedure
they were going to do. You know, there were inciting events were always infection so they were very concerned by that. And they would obviously excise out the skin lesion and if they needed interposition graft replacement they would use a Rifampin soak PTFE
as well as Acuseal for immediate cannulation. Irrigation of the infected site were also done and using an impregnated antibiotic Vitagel was also done for the PTFE grafts. They were really successful in salvaging these fistulas and grafts at 85% success rate with 19 interposition
a patency was around 14 months for these patients. At UCS, my kind of approach to dealing with these ulcerated fistulas. Specifically if they bleed is to use
the bovine carotid artery graft. There's a paper that'll be coming out next month in JVS, but we looked at just in general our experience with aneurysmal and primary fistula creation with an AV with the carotid graft and we tried to approach these with early access so imagine with
a bleeding patient, you try to avoid using catheter if possible and placing the Artegraft gives us an opportunity to do that and with our data, there was no significant difference in the patency between early access and the standardized view of ten days on the Artegraft.
Prevention of the Fatal Vascular Access Hemorrhages. Important physical exam on a routine basis by the dialysis centers is imperative. If there is any scabbing or frank infection they should notify the surgeon immediately. Button Hole technique should be abandoned
even though it might be easier for the patient and decreased pain, it does increase infection because of that tract The rope ladder technique is more preferred way to avoid this. In the KDOQI guidelines of how else can we prevent this,
well, we know that aneurysmal fistulas can ulcerate so we look for any skin that might be compromised, we look for any risk of rupture of these aneurysms which rarely occur but it still needs to taken care of. Pseudoaneurysms we look at the diameter if it's twice the area of the graft.
If there is any difficulty in achieving hemostasis and then any obviously spontaneous bleeding from the sites. And the endovascular approach would be to put a stent graft across the pseudoaneurysms. Shah and others in 2012 had 100% immediate technical success They were able to have immediate access to the fistula
but they did have around 18.5% failure rate due to infection and thrombosis. So in conclusion, bleeding to hemodialysis access is rarely fatal but there are various ways to salvage this and we tried to keep the access viable for these patients.
Prevention is vital and educating our patients and dialysis centers is key. Thank you.
- Good morning. It's a pleasure to be here today. I'd really like to thank Dr. Veith, once again, for this opportunity. It's always an honor to be here. I have no disclosures. Heel ulceration is certainly challenging,
particularly when the patients have peripheral vascular disease. These patients suffer from significant morbidity and mortality and its real economic burden to society. The peripheral vascular disease patients
have fivefold and increased risk of ulceration, and diabetics in particular have neuropathy and microvascular disease, which sets them up as well for failure. There are many difficulties, particularly poor patient compliance
with offloading, malnutrition, and limitations of the bony coverage of that location. Here you can see the heel anatomy. The heel, in and of itself, while standing or with ambulation,
has tightly packed adipose compartments that provide shock absorption during gait initiation. There is some limitation to the blood supply since the lateral aspect of the heel is supplied by the perforating branches
of the peroneal artery, and the heel pad is supplied by the posterior tibial artery branches. The heel is intolerant of ischemia, particularly posteriorly. They lack subcutaneous tissue.
It's an end-arterial plexus, and they succumb to pressure, friction, and shear forces. Dorsal aspect of the posterior heel, you can see here, lacks abundant fat compartments. It's poorly vascularized,
and the skin is tightly bound to underlying deep fascia. When we see these patients, we need to asses whether or not the depth extends to bone. Doing the probe to bone test
using X-ray, CT, or MRI can be very helpful. If we see an abcess, it needs to be drained. Debride necrotic tissue. Use of broad spectrum antibiotics until you have an appropriate culture
and can narrow the spectrum is the way to go. Assess the degree of vascular disease with noninvasive testing, and once you know that you need to intervene, you can move forward with angiography. Revascularization is really operator dependent.
You can choose an endovascular or open route. The bottom line is the goal is inline flow to the foot. We prefer direct revascularization to the respective angiosome if possible, rather than indirect. Calcanectomy can be utilized,
and you can actually go by angiosome boundaries to determine your incisions. The surgical incision can include excision of the ulcer, a posterior or posteromedial approach, a hockey stick, or even a plantar based incision. This is an example of a posterior heel ulcer
that I recently managed with ulcer excision, flap development, partial calcanectomy, and use of bi-layered wound matrix, as well as wound VAC. After three weeks, then this patient underwent skin grafting,
and is in the route to heal. The challenge also is offloading these patients, whether you use a total contact cast or a knee roller or some other modality, even a wheelchair. A lot of times it's hard to get them to be compliant.
Optimizing nutrition is also critical, and use of adjunctive hyperbaric oxygen therapy has been shown to be effective in some cases. Bone and tendon coverage can be performed with bi-layered wound matrix. Use of other skin grafting,
bi-layered living cell therapy, or other adjuncts such as allograft amniotic membrane have been utilized and are very effective. There's some other modalities listed here that I won't go into. This is a case of an 81 year old
with osteomyelitis, peripheral vascular disease, and diabetes mellitus. You can see that the patient has multi-level occlusive disease, and the patient's toe brachial index is less than .1. Fortunately, I was able to revascularize this patient,
although an indirect revascularization route. His TBI improved to .61. He underwent a partial calcanectomy, application of a wound VAC. We applied bi-layer wound matrix, and then he had a skin graft,
and even when part of the skin graft sloughed, he underwent bi-layer living cell therapy, which helped heal this wound. He did very well. This is a 69 year old with renal failure, high risk patient, diabetes, neuropathy,
peripheral vascular disease. He was optimized medically, yet still failed to heal. He then underwent revascularization. It got infected. He required operative treatment,
partial calcanectomy, and partial closure. Over a number of months, he did finally heal. Resection of the Achilles tendon had also been required. Here you can see he's healed finally. Overall, function and mobility can be maintained,
and these patients can ambulate without much difficulty. In conclusion, managing this, ischemic ulcers are challenging. I've mentioned that there's marginal blood supply, difficulties with offloading, malnutrition, neuropathy, and arterial insufficiency.
I would advocate that partial or total calcanectomy is an option, with or without Achilles tendon resection, in the presence of osteomyelitis, and one needs to consider revascularization early on and consider a distal target, preferentially in the angiosome distribution
of the posterior tibial or peroneal vessels. Healing and walking can be maintained with resection of the Achilles tendon and partial resection of the os calcis. Thank you so much. (audience applauding)
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