- Alright, so these are my team, the group of Rio De Janeiro. No disclosures. Corona phlebectasia is a clinical sign associated with chronic venous insufficiency. It is associated with abnormal visible cutaneous vessels at the ankle with specific components that I will show you.
May have ectasias type Ceap one, two, or three. So corona phlebectasia is basically consisted of venous cups, blue telangiectases and capillary stasis spots, red telangiectases and capillary stasis spots, and sometimes larger veins. So this is a typical example.
You can see here the venous cups, the red capillaries, the blue capillaries and in this case there's no larger veins. With time the disease caused the damage to the skin making it changing. Now this is a case where you have some veins here,
we're going to take it out with surgery, and the veins I described before. So the diagnosis is made by the clinical examination and duplex scan and these are the main publications on this subject, mainly in the Journal of Vascular Surgery. The treatment of corona phlebectasia consists of taking out
the saphenous vein reflux either by surgery, laser, or radiofrequency. The treatment of the perforant veins and the treatment of the superficial varicose veins. In this case here with a small incision and the help of a crochet needle, I am taking this vein
here with surgery. This is an advance case where foam sclerotherapy I'm sure was used in excessive way. This must be done step by step, I will show you, and here we are all specialists in anatomy. You have to treat all the layers that are supposedly damaged
by the disease and don't forget a perforating, especially this one here, the inframalleolar perforating vein, which is the one I showed you I was taking out. The treatment of the small veins, I do it by foam sclerotherapy using the Tessari technique. Polidocanol 0.5%, or 0.75%, and I use also use plain surgery
with small incisions. I believe someone after me will talk about the surgery specifically. So basically the treatment consists of compressive occlusion for 30 days, office sclerotherapy as necessary, and avoid sun radiation for 30 days after the procedure.
The step by step will be to search for the problem, make the right diagnosis, do surgical treatment and foam sclerotherapy for the disease, and keep a follow up, doing office sclerotherapy as necessary. As I showed you before, if you try to do a lot of sclerotherapy at once on this area, you'll probably damage
the skin, so the better idea is to do it slowly from time to time. This is our hospital in Rio De Janeiro, brand new. We have an airport close by to bring us emergency from this area here. This is my office.
This is office right here and the best part of the hospital is the roof where we can see two tennis courts just for doctors. Thank you very much.
- I am not Walter's enemy. I can tell you that. I am against the motion. (man laughing) I will stick to the truth, to the facts. I don't like polemic, like you. I don't like to play, let's say games
of undermining what my opponent is saying. I'm just showing what I believe in because it is the truth, okay? (quiet laughter) I have nothing to disclose. Let's stick to the definition of 'cure.'
We all know that 'cure' means 'at least one year follow-up, angiographic follow-up after the, so-called, final angiography, that shows that malformation is gone.' Call it whatever you want.
Technical success, obliterated, trombosed, concluded, ablated, gone. Then at least one year follow-up on that. Angiographic to prove it's gone. The rest is just a scale on how you can evaluate the results.
Angiographically and clinically. The only way, for me, to speak to the truth is to find in a material where there is a chance to compare.
Hat to hat. Both type of treatments. Polymerizing versus alcohol. And, the only way to find such a place is to go to Wayne's place, because he's also constantly called
talking about salvaging this and salvaging that. I am very critical about what Wayne does. You can be assured about that. He's had 16 patients, I dig out there, and polymerizing agents they were failed.
Definitely, failed. Actually, they were salvaged, by Wayne. And, I'll show that to you. These are the patients. This is the time to which they've been treated. The usual type of distribution.
Young patients. All of them extensive. There is no, for a lack of an effort. There is no, for a lack of knowing how to use
the polymer. Onyx. How we can tell that, most of those is Onyx, some of them are glue. Or a combination. The median number of sessions
with this polymerizing agent is 8.5. Range from one to thirty. The other radiologists, the other experts, besides my honorable opponent, Doctor, Professor Wolgemuth,
they also know how to use Onyx. I can assure that. Sixteen patients, all symptomatic. They are all decompensated, showing three, four tier symptomatically. They have high cardiac output,
they have required repeated, repeated blood transfusions, infections, ulcers, disarticulation. To have disarticulation of vascular malformation means, oh, horrible bleeding, infected. There is no doubt,
they are symptomatic. Couple of examples. This is a young woman, extensive AVM in the foot, type four. Been treated five times with Onyx. And they know what they've done.
They've treated well. Yet, worsening symptoms, wheelchair bound, infected ulcer. Seventy-one session. Now, pay attention. Seventy-one sessions of ethanol/coils embolization. And, this woman is now running with her friends
after her amputation of couple of necrotic toes. Not because of the alcohol. Because of the malformation. Angiographically, not cured. Example of that. Okay.
This is malformation. This is not something in a tiny, little bitty thing. It's a malformation, no question about that. Before treatment. And, this is after treatment. We can all agree that,
this is not completely cured. It is a grade three it is 80 to 99 percent still left. But, clinically, she's running. She continues to be treated. Another example.
One year old girl with bleeding malformation from the lip. Admittedly only one Onyx being used because we didn't know what to do. Luckily, the little girl was close by so she came to Wayne and after,
it's intravenous predominant lesion. It's a type two lesion. Only after a six month treatment sessions, cured. This is before start of ethanol treatment. No question there is recurrence. We can not close that only by pushing
polymerizing agents somewhere in something called 'nidus.' But if you ablate the cells, ablate the nidus. You achieve cure.
And it's cured in one year angiographic follow-up. This is time and time and again. I will show these examples. This is the outcome. The outcome tells you six cured angiographically. Eight considerably improved, they improved.
None of them is failed in this. All failed polymerizing agent treatment. Then we can move on. Complication because that's where talking about how dangerous. Alcohol is very dangerous,
but so is knife in operating room. Take a knife and stab it somewhere in some artery, or in a pressurized vein, you'll have all this blood in your face and a shoot of blood doesn't taste very good in your mouth. So it's dangerous.
But, if you use it carefully, that's what you achieve, as a result. Where do we stand with these patients? Ongoing treatment, five. Cured, five, by summation.
One still waiting for a follow-up on angiographic follow-up. Improved on watchful observation is two. Lost to follow-up because schizophrenia. Lost to follow-up because of unknown reason, after two years of follow-up.
He's been doing well throughout these two years. One clinical failure. I will tell you that Wayne have, he's seen this person. Not clinical failure. Yeah, it's clinic.
By definition, is clinical failure. Angiographically, improved. Clinically, improved. The little boy was wheelchair bound, didn't want to continue with that and, therefore, went for amputation.
So it's a clinical failure. One. To summarize that, I highlight on this, venous predominant lesions. These are the ones these create.
Type four. (man speaking off screen) Tough. Couple of examples. Striking examples. This is venous predominant lesion, IIA.
I'm sorry. IIIa, IIIb being treated. Sorry. Can we go back to that? Any way I can go back on that?
This IIIa, IIIb, there's has been five. That's moves forward. Five surgery, Onyx, anything thrown in. Extensive malformation. Shoulder, arm, a no-flow into the lower arm
because of the. And it's moving forward. I'm sorry for that. But it was cured. And there was a follow-up, too. I believe there was something.
Twenty, 15, 17 months follow-up. So we have the next patient. Thirty-two year old female treated with glue in the past.
Twenty procedure including all vessels. Everything that can not be, could be embolized, was emolized. Ended up with the worsening and this is the typical example a IIIa malformation, typical example.
This was way back in the past. This is how Wayne has developed that. It took him, I heard, nine hours and another 100 coils, but he cured that.
- [Male] 298. - Two hundred ninety-eight. This is the follow-up, you know. Eighteen months later. To summarize on that. Nothing to do with my feelings for Wayne.
Nothing to do with Walter being my enemy. (quiet laughter) No, it's just a fact, a truth. Polymerizing agents, by definition, do not cure AVMs. Do not cure.
Sometimes, when used properly, still worsen the patient's symptoms. Ethanol cures AVM. Provided that you do that with precision and skills. How you acquire precision and skills? Ask the surgeons around here.
How do they lift up this face? How Max can lift out, you know, big time metastasis sections in liver? How do you do that? With skills.
How do you acquire skills? Learn. Thank you.
- I think we have time. If there are any questions, please come up to the microphone and any of the panels have questions for each other. I have a number of questions I could ask but I just see if anyone wants to start out. Claudio?
- I have a question Doctor Mark. He show us very nice utilization of this device for occluded limbs. My question is, do you protect in any way the other side? If not, don't you have, you're not concerned
or you're not afraid of pushing clots from one side to the other one when you're manipulating the device? And the second one, do you do this percutaneously? And if that's the case, do you have any concern about having destabilization?
Because once you start to manipulate the clot that is occupying the entire graft, and there is reestablishment of flow in an antegrade flush, and you may have some of that clot dislodge and embolize distant. - Yeah, as I mentioned,
nobody wants to be the guru of limb occlusions. However, we have seen them and we always go retrograde ipsilateral, not seen emboli once from those seven cases and in fact, the 73 we presented at the midwest there was only two instances of embolization
when we utilized this device. And both times we were able to extract those just by going further down with the cat six and both of them was below the knee popliteal. In particular, the acute ones, it's soft and it's no different than watching it in vivo
or in vitro model, as you know better than I, comes out quite easily. - Let's take our question from the audience. - [Scott] Hi, Scott Tapart from Stuart, Florida. So I'd like to poll the panel there about are you doing every single
acute limb ischemia percutaneously? The pictures are elegant, the techniques are elegant, but the last speaker touched on the profoundly ichemic Rutherford 2B patient, where you're most likely going to have to do a fasciotomy. Are you going to the OR
or are you doing this percutaneously and then watching and waiting and seeing about fasciotomy? Or has this changed your fasciotomy approach? - So since we have a number of people, that's a great question. Why don't we start at the end
and let's just go kind of rapid fire, maybe one or two sentences, how do you choose your patients and what do you do with those 2Bs and we'll try to get through everybody. - Sure, so, to reiterate the last slide of the presentation,
essentially anybody with a significant motor or neutral deficit is somebody I tend to do in an open fashion. And if I'm the least bit concerned about doing a fasciotomy or there's evidence of compartment syndrome I do that patient open.
- We try to start endovascular, and if we can clean and reestablish antegrade flow, that would take care of the problem. And of course, I'm a radiologist, so I always consult with my colleagues in surgery and they decide if a fasciotomy needs to be done or not.
And it's that at the end. - Okay, I have to be honest, we start with the selective indication but now we move maybe to 90% of our patients doing percutaneously. We will adjust patients with probably an embolization,
a huge embolization, into the common femoral artery for open surgery. Of course, in our mind, also in the registry, we have some cases of fasciotomy after percutaneous approach so it's not a limitation. - The advantage of acute arterial protocol,
as they all go to the end of asher suite and they all run along our protocol but you can run the option. You get them to treatment quicker because they don't dilly-dally around in the holding room. But then according to how the patient's doing
you can mop up as much clot as you can with the percutaneous technique and then do the fasciotomy when you're done or press head and drip more if you need to. So I think to have an algorithm where you can treat the full spectrum
is what's best for the patient. - I think it depends on the time as well because I did two weeks ago a patient who needed a fasciotomy directly so I performed that first and then it rules out any traumalitic therapy
or whatever that you want to do. And actually, if I do antivascular techniques I usually give a shot or RTPA or something and then go further with it. But anomerization of this patient's arteries as well so prefer actually if it's really a case
that needs fasciotomy just to perform surgical thrombectomy. - Yeah, percutaneous eight French up and over and almost always, you're going to be done with your thrombectomy within about 30 to 45 minutes. I don't think you're adding that much time
and for us, by the time we get anesthesia in him assuming anesthesia's anesthesia no matter what part of the world you're in, so you can get to the hybrid room quicker and then if it's going to fail then you're going to call in the OR or call an anesthesiologist.
- I wouldn't have much else to add. I do think there is some patient selection, if you have an entire SFA, 30 centimeter clot, that's going to take you hours to do so for these thromboembolic things that are 10 centimeters or shorter
lodged in the popliteal TP trunk, this method works really well. I think for the longer patients, you might think about something else. - But just a comment on the general anesthesia. If a patient is in real or really pain,
he can't lie down for 30 minutes, even. I mean, they are rolling in pain and I would do the fasciotomy first because general anesthesia is needed because there is so much pain or, yes, so yeah.
- So, let me say, does that answer it, Scott? So let's, since we have a number of panelists and we're running out of time, how about if we ask each person going down the room, you heard a whole bunch of different speakers here with a lot of experience
and if you haven't used this, there is a learning curve. The learning curve is pretty shallow. Really, a lot of it has to do with controlling your blood loss. But if we ask each person for just one tip
and we'll see if we can get through everybody. If you telling people who hadn't done a lot of this, one tip or one trick, let's see if we can get seven or eight tips and tricks out. So, I'll go last. Let's start back down at that end
and we'll end up at this end. - Sure. Use the largest catheter that the vessel will comply to. - Amen, brother. - I agree with that.
And the way I do it, in order to avoid too much blood loss, I like to engage with a syringe. So I come with my catheter, I hook a syringe in the bag, 20cc or sometimes even larger, and when I have the fish at the end of my line, then I connect to the pump and I continue.
That way if I'm aspirating, I'm not going to aspirate a large volume so I want to engage the clot. And then I bring the clot out. That's my trick. - Okay.
Very nice comment. Of course, I agree with the previous colleagues but I will say that first the trick is really the largest catheter is better, then my idea that I developed during my learning curve is the use of separate to cut away.
I probably use now in 95% of cases because it just makes everything quicker and faster and better. - I use the perclose device for large-bore catheters often and that allows me to pull the plug out, especially if it's fibrous plugs,
safe from the heart without shearing it off on the end of the catheter. I've got one question for Claudio, on that case of the carotid subclabian with the acute carotid occlusion, do you think the nitroglycerin would have helped?
- For the doctor? - For the surgeon. - Absolutely. - And then, change the diapers. - Well, I would advise if you do a surgical embolectomy do it also on the hybrid room
and try to do it also over the wire. Especially be careful if you do it below the knee. I would suggest do it open below the knee, even. - I would say don't afraid to use an eight French for ALI and that closure devices are your friends here. But you can use an eight all the way down to the pop
and then for us, the tibials, we'll use a six. - Yeah, I would agree with that. So I guess my tip would be, I agree with everything everyone said, although I don't use the separator very often in the arterial side, I do in the veins.
But one tip is, if you're not going to use a separator, if you're going to start without it, let's say you want to give it a try, I don't work through a 2E borst because the angle, the eddy currents that form around that 2E borst
trap clots and you constantly have to clean that 2E out so if you're going to start with a focal embolis in the artery my recommendation is take the 2E off, hook up to the vacuum directly, and you'll get less clot stuck in the 2E. If you want to go to the separator
then you can always add that on at the back end. - So I have a question for Fennel. I used a penumbra like a few weeks ago and it ended up really bad because the surrounding catheter from the penumbra, everything got, you know, clotted
and then I didn't have any outflow did I choose the wrong size or what is it that happened, did you see it ever? - We have not had that problem. We're usually working on heparinized patients and have not seen that happen.
- She was heparinized. No? Okay. - Okay. Any other comments? Otherwise, we'll end one minute early
on a nice, long day.
- Hello, thank you again for the invitation. I have the disclosure here is kind of funny because I'm going to talk about CLaCS but I don't profit on that. Those are the most frustrating result on sclerotherapy and obviously death. These are very frustrating result. Sorry.
And this is not like funny but it's unfortunately the worst part is that all those cases are not published and that's less change from frustrating to devastating, the death cases. Let's talk about the less common, sorry,
the most common problems, skin ulcer. Like skin ulcer. Skin ulcer may be also terrible. Those are slides from my father's collection from the 60s probably. And I suggest you to read this paper.
It took me 20 years to get published with the help of Ted King of this hypothesis from the 70s and he studied on rabbit ears and I cannot have time to explain all that but he simulated the skin ulcer and showed that the causes the reflux to the arterial venous system
and how to avoid it, CLaCS is a great solution and by using the extra 75% due to its high viscosity, you avoid 100% of reflux to the arterial system. Matting is another problem.
Those are theories of my father as well. He said divided in two types of angiogenic where you inject on the telangiectasia and you destroy veins that you wanted to close or you didn't want to touch. And then you have reflux a new reflux and
a lot of telangiectasia. There would be occlusive, where you destroy too much, you destroy the drainage of those telangiectasias. And then how to avoid? Is to be less aggressive or to be more focal. That means treat only the feeder vein
and the telangiectasia and avoid injecting a lot of volume and because those sclerotic agents will reach another vein that you don't want to touch. Pigmentation is another problem. And to control pigmentation of course
you have to have less thrombus and once again ClaCS would be very nice idea because the transdermal lazer causes vein wall edema and contraction and then you inject the Dextrose 75%. And then you have less internal diameter
in the vein, that means you have less outflow, the Dextrose will stay there it's a synergy, and you have less clot, less pigmentation. Also Dextrose is a medium power sclerosing agent that doesn't cause too much pigmentation as the other agents.
Well once again my father, and my father is at the hospital right now, and he probably will not survive, but here is a tribute for him. And he developed this surgical treatment of the telangiectasia by removing
the feeder veins. And, sorry. Here a study with phlebography showing a double perforant insufficient vein, and these telangiectasia wouldn't respond. And that's a complex telangiectasia, not a simple telangiectasia.
Like here another example, the phlebectomy showing the result of the treatment of telangiectasia. Well, diagnosis is very important if you are a skipper of a boat, if you have a special device to diagnose you certainly will have a better result.
And here are very tricky, looks simple to treat but as you compress you see there is a reflux, and this reflux is going have five feeder veins and one is going to the reflux in saphenous vein and patient the patient is CEAP1. Well, I also.
Sorry. Next slide. If you are a painter and you want to paint this wall, it's not easy you need to find a feeder vein and that's why I've developed this classification where you have three, two questions
and you look for varicosities and telangiectasias and here you have, lets go fast, the ultrasound showing reflux and the augmented reality showing if there is feeder vein or not. And here a good example of a patient that was,
the examination would lead to a CEAP 1, but as we exam, we noticed that she's score nine, where she had a long reflux asymptomatic that was treated with endovenous lazer phlebectomy and CLaCS, and that's how we got the result. Then treatment failure is also can be avoided
by a good classification and then CLaCS. If you want to learn more about that, we have a congress, it's going to be the ninth in IMAP in Saul Paulo next year, and I kindly invite you to participate. Thank you.
- Now we all have seen one thing. We have to treat AVM's according to their classification angio anatomy. If you have something like, direct arterial venous communications, like pulmonary HHT patients, like the rare patients with inborn arterial venous fistulas,
you will never use ethanol. That's my opinion. That's an opinion. But I think most of us will agree on that. Will you? - [Audience] Yes.
- I think many of us will agree. So would you just do it for a HHT pulmonary patient, you would inject ethanol? - [Audience] No. - So, okay. And the direct arterial venous communications inborn,
they are very rare and they can be beautifully treated with plugs and whatever. These are one part on the AVM patients. Second part is predominantly venous outflow. However you say it's 2B, 3A or whatever. It's a dominant venous outflow
and you can cure them and I say cure, even in my paper there is imaging of follow up, but it's not in the abstract bar. (smiling) So you just, - (laughing)
- So you just occlude the venous outflow, as close to the nidus as you can. So I don't need ethanol for that. I don't need to take the risk for my patient. And so that leaves the type 4 small vessel AVM's. They are, even in my opinion,
not treatable with a polymerizing agent. There is a real place for ethanol. And then you you go to these difficult, more net-like, type 3 or whatever, AVM's, then my opinion is, I do it as long as possible,
with a safe agent. Like pushing in tons of onyx. And if there is something left over, or if there comes something in follow up, because we all need follow up for these patients, then you can finish it with ethanol.
That's my statement. Thank you.
- The proposition is polymerizing agents can and do cure AVMs and are now the agents of choice, ethanol is too dangerous. When I saw what Wayne had asked me to talk about, I immediately called him. And I said there are two words in this proposition
which are giving me some trouble. The first word is dangerous. In IR we do dangerous every day, especially in July. And with respect to cure in IR, mostly we just try to fix things.
Nonetheless, there are proper uses of ethanol. There are, however, some risks to the use of ethanol in medicine. First off, ethanol is a sclerosing agent and it is toxic to tissue. It denatures the proteins
of the endothelium, activates the coagulation system and produces blood clots. While we are trying to do that, when we're trying to control an AVM, it does also generate acetaldehyde and reactive oxygen species
which damage healthy tissue. It can result in endotoxin leakage, inflammatory cytokine release, and modification of signal transduction in the cell membrane and when we deliver alcohol, unless we dilute it with contrast,
we really cannot see where it goes. There are some other issues with ethanol. The first is that it's known to impair wound healing. If ulcers occur with ethanol use, they are difficult to heal. If you place skin grafts on these lesions,
they typically fail. And if you use ethanol in an area of prior surgical scar, there is a high risk of skin injury. In addition, the use of ethanol is associated with pain, it's a painful procedure.
If you deliver ethanol in proximity to a nerve, you will develop nerve injury and if you have sciatic nerve injury, that can be devastating which can take months if it all to heal. The other issue relates to the dosing
and the volume of ethanol that's delivered. If you deliver high doses of ethanol at one sitting, you can get systemic effects. Now, a slightly tipsy patient post-embolization is not necessarily a big problem, however, if the patient develops hemoglobinuria,
that can be significant. If you use low volumes of ethanol with each treatment, it requires multiple treatments. You can also get cardiopulmonary problems with ethanol. The ethanol can induce arrhythmias, it can induce bronchiospasm,
it can precipitate pulmonary emboli because of the sludge that migrates up to the lungs and you can get cardiovascular collapse with the use of ethanol. Fortunately that is rare. Other polymers such as the cyanoacrylates
or liquid embolics and their viscosity can be altered. The downside in our experience with the cyanoacrylates is that they're difficult to control, they tend to spatter.
And our long-term experience with the cyanoacrylate shows that it is not permanent and it does degrade. The ethanol vinyl alcohol copolymer or Onyx behaves as a filler. It induces a mild inflammatory reaction.
It's associated with minimal pain post-procedure and skin injury is infrequent and it is in our experience a permanent agent. There may be difficulty getting it to travel deep into the nidus and that can be a big problem,
if you just deliver the Onyx in just a push away, it will not go very far and you will leave your nidus untreated which can lead to recanalization. So, we dilute our Onyx 18 with DMSO
which makes it more easier to spread out into the distal portion of the malformation. It is somewhat harder to see when it is diluted. We also use a glue roadmap. This will reduce our radiation dose
and we don't deliver the Onyx the way the neuro-interventionalists do, we tend to deliver it much faster than the neuro people do. And if you have obscuration of your vessels by prior Onyx placement, the glue roadmap can help.
When we use Onyx without operative resection, it is an off label use. But nonetheless, when used, it does facilitate operative resection and you just have to remind your surgeons to use a bipolar bovie otherwise you will get sparking.
With respect to cure. I think cure, when we talk about it, it really depends upon our definition of cure. Polymer occlusion will result in relief of AVM symptoms. And it can cure some lesions.
Whether we are able to remove all shunting in large lesions I think is doubtful, but nonetheless, Onyx copolymer is associated with lower morbidity than alcohol. And when we look at ethanol versus polymers, the ethanol is a one-generation agent.
Whereas if we look at polymers, if we consider cyanoacrylate as a first generation and Onyx as a second generation, and squid maybe as a third, the future is pretty much unlimited for us because you can prepare polymers which will contain drugs
or other agents. So, I think the choice is you have to determine whether you want to use ethanol, or whether you want to use a polymer. Thank you.
Thanks very much, Tom. I'll be talking about thermal ablation on anticoagula is it safe and effective? I have no disclosures. As we know, extensive review of both RF and laser
ablation procedures have demonstrated excellent treatment effectiveness and durability in each modality, but there is less data regarding treatment effectiveness and durability for those procedures in patients who are also on systemic anticoagulation. As we know, there's multiple studies have been done
over the past 10 years, with which we're all most familiar showing a percent of the durable ablation, both modalities from 87% to 95% at two to five years. There's less data on those on the anticoagulation undergoing thermal ablation.
The largest study with any long-term follow up was by Sharifi in 2011, and that was 88 patients and follow-up at one year. Both RF and the EVLA had 100% durable ablation with minimal bleeding complications. The other studies were all smaller groups
or for very much shorter follow-up. In 2017, a very large study came out, looking at the EVLA and RF using 375 subjects undergoing with anticoagulation. But it was only a 30-day follow-up, but it did show a 30% durable ablation
at that short time interval. Our objective was to evaluate efficacy, durability, and safety of RF and EVLA, the GSV and the SSV to treat symptomatic reflux in patients on therapeutic anticoagulation, and this group is with warfarin.
The data was collected from NYU, single-center. Patients who had undergone RF or laser ablation between 2011 and 2013. Ninety-two vessels of patients on warfarin at the time of endothermal ablation were selected for study. That's the largest to date with some long-term follow-up.
And this group was compared to a matched group of 124 control patients. Devices used were the ClosureFast catheter and the NeverTouch kits by Angiodynamics. Technical details, standard IFU for the catheters. Tumescent anesthetic.
And fiber tips were kept about 2.5 centimeters from the SFJ or the SPJ. Vein occlusion was defined as the absence of blood flow by duplex scan along the length of the treated vein. You're all familiar with the devices, so the methods included follow-up, duplex ultrasound
at one week post-procedure, and then six months, and then also at a year. And then annually. Outcomes were analyzed with Kaplan-Meier plots and log rank tests. The results of the anticoagulation patients, 92,
control, 124, the mean follow-up was 470 days. And you can see that the demographics were rather similar between the two groups. There was some more coronary disease and hypertension in the anticoagulated groups, and that's really not much of a surprise
and some more male patients. Vessels treated, primarily GSV. A smaller amount of SSV in both the anticoagulated and the control groups. Indications for anticoagulation.
About half of the patients were in atrial fibrillation. Another 30% had a remote DVT in the contralateral limb. About 8% had mechanical valves, and 11% were for other reasons. And the results. The persistent vein ablation at 12 months,
the anticoagulation patients was 97%, and the controls was 99%. Persistent vein ablation by treated vessel, on anticoagulation. Didn't matter if it was GSV or SSV. Both had persistent ablation,
and by treatment modality, also did not matter whether it was laser or RF. Both equivalent. If there was antiplatelet therapy in addition to the anticoagulation, again if you added aspirin or Clopidogrel,
also no change. And that was at 12 months. We looked then at persistent vein ablation out at 18 months. It was still at 95% for the controls, and 91% for the anticoagulated patients. Still not statistically significantly different.
At 24 months, 89% in both groups. Although the numbers were smaller at 36 months, there was actually still no statistically significant difference. Interestingly, the anticoagulated group actually had a better persistent closure rate
than the control group. That may just be because the patients that come back at 36 months who didn't have anticoagulation may have been skewed. The ones we actually saw were ones that had a problem. It gets harder to have patients
come back at three months who haven't had an uneventful venous ablation procedure. Complication, no significant hematomas. Three patients had DVTs within 30 days. One anticoagulation patient had a popliteal DVT, and one control patient.
And one control patient had a calf vein DVT. Two EHITs. One GSV treated with laser on anticoagulation noted at six days, and one not on anticoagulation at seven days. Endovenous RF and EVLA can be safely performed
in patients undergoing long-term warfarin therapy. Our experience has demonstrated a similar short- and mid-term durability for RF ablation and laser, and platelet therapy does not appear to impact the closer rates,
which is consistent with the prior studies. And the frequency of vein recanalization following venous ablation procedures while on ACs is not worse compared to controls, and to the expected incidence as described in the literature.
This is the largest study to date with follow-up beyond 30 days with thermal ablation procedures on anticoagulation patients. We continue to look at these patients for even longer term durability. Thanks very much for your attention.
- My rebuttal is short and sweet. I think that those of us who have seen both agents, seen it in a fair comparison, understand that while ethanol has an appearance of difficulty to use, have come to the conclusion that it is actually safe. It has to be applied in the right spot. If it is such it will absolutely cure
and in it's very, very safe fashion. I think Walter mentioned the four deaths that I referred to. I agree, tragic, terrible, but we learn. Haven't had any deaths since, because I understand now the mistake I made and how to use ethanol.
I think the same thing is true. Max will tell you that there were enumerable deaths during the development of transplanting these difficult operations. No longer, all controlled, it's all because of learning. Thanks.
- This is from some work in collaboration with my good friend, Mike Dake. And, a couple of years of experience at Stanford now. First described by Kazy? years ago. This technical note of using multiple main-body endographs in a sandwich formation.
Up at the top but, then yielding multiple branches to get out to the visceral vessels and leaving one branch for a bifurcated graft. We've sort of modified it a little bit and generally either use multiple
grafts in order to create a branch the celiac and SMA. Left the celiac sometimes for a chimney, but the strategy really has been in one of the limbs to share both renals and the limb that goes down to the legs. We noticed early on that this really was not for
non-operative candidates, only for urgent cases and we recognize that the visceral branches were the most important to be in their own limb. I'll just walk you through a case. 6.8 centimeter stent for foraco above
the prior opened repair. The plan drawn out here with multiple main bodies and a second main body inside in order to create the multiple branches. The first piece goes in. It's balloon molded at the level of pulmonary
vein with enough length so that the ipsalateral limb is right next to the celiac. And we then, from above get into that limb and down into the celiac vessel and extend with either a limb or a viabahn. Next, we deploy a second main body inside
of the gate, thus creating now another two limbs to work through. And then through that, extend in its own branch a limb to the SMA. This was an eight by 79 vbx. Then we've got a third limb to go through.
We put a cuff that measures about 14. This is the math so that the double renal snorkle plus the main body fills up this hole. Now, double sheath access from above, looking for both renals. Sheaths out into both renals with viabahns
inside of that. Deployment of the bottom device and then a final angiogram with a little bit of a gutter that we often see when we have any kind of parallel graft configuration. Here's the post-op CT scan wherein
that limb is the two shared renals with the leg. This is the one year post-op with no endo leaks, successful exclusion of this. Here's another example of one of an eight and a half centimeter stent three thorico similar strategy, already with an occluded
celiac. Makes it a little bit easier. One limb goes down to the superior mesenteric artery and then the other limb then is shared again bilateral renals in the lower main body. Notice in this configuration you can get all the way up to the top then by putting a thoracic component
inside of the bifurcated subabdominal component. There's the final CT scan for that. We've spent some time looking at the different combinations of how these things will fill up to minimize the gutters through some more work. In collaboration with some friends in Kampala.
So we've treated 21 patients over the last couple of years. 73 years of age, 48 percent female usual comorbid factors. Oh, I thought I had more data there to show you. O.K. I thought this was a four minute talk.
Look at that. I'm on time. Octopus endovascular strategy is a feasible off the shelf solution for high risk patients that can't undergo open repair. You know obviously, sort of in this forum and coming to this meeting we see what's
available outside of the U.S. and I certainly am awaiting clinical trial devices that will have purpose specific teacher bi-graphs. The end hospital morbidity has still been high, at four percent. The one year survival of 71 percent in this select
group of 21 patients is acceptable. Paraplegia is still an issue even when we stage them and in this strategy you can stage them by just doing the top part plus the viscerals first and leaving the renals for another day. And branch patency thus far has been
in the short term similar to the purpose specific graft as well as with the parallel graft data. Thank you.
- I've made this agent comparison chart, just sort of summarizing the areas where I think that Onyx is better as compared to ethanol. I think things to come, oops, sorry, I got to go back. I think the items to be commented on are one, that there's less skin necrosis with the polymers.
It's a less painful procedure, and the Onyx, in our experience, is durable. But in the treatment of any type of AVM, you have to get your agent into the nidus of the malformation. If you don't do that,
then you're just doing a proximal occlusion. And we know from the surgical literature that that does not work. They will simply, the angiogenic stimulus, whatever triggers it, will continue. And that gets me to another point.
I really don't think that we really know what stimulates these malformations to grow. We think it may have something to do with a resistance in the flow, but we have some pelvic AVMs who have been stable for 30 years.
We're not touching them, and we have no intention of touching them, whereas we have children who will present with an AVM at age four and then by age seven, they are unable to ambulate. So in any event, I think that
polymers represent the future. And I just want to quote from this old movie, The Graduate. "Plastics," thank you.
- Thank you again for the opportunity to discuss the BlueLeaf Endovenous Valve with potential benefits of on an all-autogenous solution. The last slide was a nice segue to this presentation, so the financial relationship. So we've discussed extensively at this meeting treatments for superficial venous
reflux outflow obstruction, and, really, the last sort of frontier is the deep vein reflux where invasive surgery is still the gold standard, but I basically say that the majority of us, or at least myself and many of us in our practice,
resort to what I refer to as palliative care or conservative managements in patients who have maximally been treated for their outflow obstruction and superficial venous reflux. This is sort of an outstanding review
of the current state of deep venous reconstructive surgery by Dr. Maleti, Lugli, and Tripathi who said the trap door technique as well as the neovalve and the corresponding outcomes, and I encourage all of you to look at it, are pretty reassuring even with the limitations.
The ulcer recurrence rates are in the 20-30% range and the vales remain competent in 70% of cases, and the results of the neovalve reconstruction are also reasonably promising. So how do we take these reasonably and pretty promising results and try to expand them?
Potentially, what would it look like as a percutaneous approach? And it might look something like this. And this is the BlueLeaf Endovenous Valve Formation System which uses a catheter system, a nitinol dissector, and a needle assembly,
and it's done under intravascular ultrasound guidance. This is what the procedure looks like in the basic three steps. After you've gained access with a 16 French sheath in the common femoral vein you identify the valve site,
the appropriate valve site with the IVUS, you perform, you gain sub-intimal access, and then perform the hydrodissection, and then you create your valve. And this is how it goes. So after you've gained wire access
you advance your intravascular ultrasound in order to identify the valve formation site. Right now it's quantitated at seven to 11 millimeters in diameter and at least three centimeters in length. You then inflate the balloon to appose the vein wall,
to create some tension in the vein wall, and thereafter your needle assembly can create that sub-intimal plane with the hydrodissection, and you see how the bevel tip retracts to make it less traumatic. You're checking with intravascular ultrasound.
You advance the dissector. And then under IVUS guidance you create the valve with the nitinol scoring blades on the dissector as well as the tensioner which kind of bows out towards the IVUS, and you can see it on the corresponding IVUS images.
And the very last step is to leave the blades open to open up the mouth of that percutaneous valve fully. And the advantages. You can create a monocuspid, a bicuspid valve, potentially multilevel valves as well. In this tissue demonstration
you're essentially looking from within the vein walls, so the tensioner is pointing out towards you as if you're within the lumen of the vessel, and it's just showing you how the nitinol scoring blades create the valve and then when left open for the final passage
to incise the valve mouth. And this is what the result looks like on intravascular ultrasound. It projects well the last couple seconds of the slide. So the potential advantages is that there's an increased potential for customization.
Again, monocuspid, bicuspid valve orientation, multilevel valves. (mumbles) may lead to a larger eligible patient population and expanded utilization amongst various venous practitioners. The extended feasibility study.
The trial details are currently enrolling outside of the United States. 11 patient in Australia and New Zealand. The US trial is pending IDE approval, and the inclusion criteria will be those patients with the most severe disease with C5 and C6 disease
and significant deep vein reflux. Exclusion criteria relate to inflow, outflow, and having an adequate conduit with an appropriate valve formation site. Thank you.
- Now I want to talk about, as Chrissy mentioned AVM Classification System and it's treatment implication to achieve cure. How do I put forward? Okay, no disclosures. So there are already AVM Classification Systems. One is the well-known Houdart classification
for CNS lesions, and the other one is quite similar to the description to the Houdart lesion, the Cho Do classification of peripheral AVM's. But what do we expect from a good classification system? We expect that it gives us also a guide how to treat with a high rate of cure,
also for complex lesions. So the Yakes Classification System was introduced in 2014, and it's basically a further refinement of the previous classification systems, but it adds other features. As for example, a new description of
a new entity, Type IV AVM's with a new angioarchitecture, it defines the nidus, and especially a value is that it shows you the treatment strategy that should be applied according to angioarchitecture to treat the lesion. It's based on the use of ethanol and coils,
and it's also based on the long experience of his describer, Wayne Yakes. So the Yakes Classification System is also applicable to the very complex lesions, and we start with the Type I AVM, which is the most simple, direct
arterial to venous connection without nidus. So Type I is the simplest lesion and it's very common in the lung or in the kidney. Here we have a Type I AVM come from the aortic bifurcation draining into the paralumbar venous plexus,
and to get access, selective cauterization of the AVM is needed to define the transition point from the arterial side to the venous side, and to treat. So what is the approach to treat this? It's basically a mechanical approach, occluding
the lesion and the transition point, using mechanical devices, which can be coils or also other devices. For example, plugs or balloons. In small lesions, it can also be occluded using ethanol, but to mainly in larger lesions,
mechanical devices are needed for cure. Type II is the common and typical AVM which describes nidus, which comes from
multiple in-flow arteries and is drained by multiple veins. So this structure, as you can see here, can be, very, very dense, with multiple tangled fistulaes. And the way to break this AVM down is mainly that you get more selective views, so you want to get selective views
on the separate compartments to treat. So what are the treatment options? As you can see here, this is a very selective view of one compartment, and this can be treated using ethanol, which can be applied
by a superselective transcatheter arterial approach, where you try to get as far as possible to the nidus. Or if tangled vessels are not allowing transcatheter access, direct puncture of the feeding arteries immediately proximal to the nidus can be done to apply ethanol. What is the difference between Type IIa and IIb?
IIb has the same in-flow pattern as Type a, but it has a different out-flow pattern, with a large vein aneurysm. It's crucial to distinguish that the nidus precedes this venous aneurysm. So here you can see a nice example for Type IIb AVM.
This is a preview of the pelvis, we can here now see, in a lateral view, that the nidus fills the vein aneurysm and precedes this venous aneurysm. So how can this lesion be accessed? Of course, direct puncture is a safe way
to detect the lesion from the venous side. So blocking the outflow with coils, and possibly also ethanol after the flow is reduced to reflux into the fistulaes. It's a safe approach from the venous side for these large vein aneurysm lesions,
but also superselective transcatheter arterial approach to the nidus is able to achieve cure by placing ethanol into the nidus, but has to be directly in front of the nidus to spare nutrient arteries.
Type IIIa has also multiple in-flow arteries, but the nidus is inside the vein aneurysm wall. So the nidus doesn't precede the lesion, but it's in the vein wall. So where should this AVM be treated?
And you can see a very nice example here. This is a Type IIIa with a single out-flow vein, of the aneurysm vein, and this is a direct puncture of the vein, and you can see quite well that this vein aneurysm has just one single out-flow. So by blocking this out-flow vein,
the nidus is blocked too. Also ethanol can be applied after the flow was reduced again to reflux into the fistulas inside the vein aneurysm wall. And here you can see that by packing a dense packing with coils, the lesion is cured.
So direct puncture again from the venous side in this venous aneurysm venous predominant lesion. Type IIIb, the difference here is again, the out-flow pattern. So we have multiple in-flow arteries, the fistulaes are again in the vein aneurysm.
Which makes it even more difficult to treat this lesion, is that it has multiple out-flow veins and the nidus can also precede into these or move into these out-flow veins. So the dense packing of the aneurysm might have to be extended into the out-flow veins.
So what you can see here is an example. Again you need a more selective view, but you can already see the vein aneurysm, which can be targeted by direct puncture. And again here, the system applies. Placing coils and dense packing of the vein aneurysm,
and possibly also of the out-flow veins, can cure the lesion. This is the angiogram showing cure of this complex AVM IIIb. Type IV is a very new entity which was not described
in any other classification system as of yet. So what is so special about this Type IV AVM is it has multiple arteries and arterioles that form innumerable AV fistulaes, but these fistulaes infiltrate the tissue. And I'm going to specify this entity in a separate talk,
so I'm not going too much into details here. But treatment strategy of course, is also direct puncture here, and in case possible to achieve transarterial access very close to the nidus transarterial approach is also possible. But there are specific considerations, for example
50/50 mixture of alcohol, I'm going to specify this in a later talk. And here you can see some examples of this micro-fistulae in Type IV AVM infiltrative type. This is a new entity described. So the conclusion is that the Yakes Classification System
is based on the angioarchitecture of AVM's and on hemodynamic features. So it offers you a clear definition here the nidus is located, and where to deliver alcohol in a safe way to cure even complex AVM's.
Thank you very much.
- Thank you (mumbles). The purpose of deep venous valve repair is to correct the reflux. And we have different type of reflux. We know we have primary, secondary, the much more frequent and the rear valve agenesia. In primary deep venous incompetence,
valves are usually present but they are malfunctioning and the internal valvuloplasty is undoubtedly the best option. If we have a valve we can repair it and the results are undoubtedly the better of all deep vein surgery reconstruction
but when we are in the congenital absence of valve which is probably the worst situation or we are in post-thrombotic syndrome where cusps are fully destroyed, the situation is totally different. In this situation, we need alternative technique
to provide a reflux correction that may be transposition, new valve or valve transplants. The mono cuspid valve is an option between those and we can obtain it by parietal dissection. We use the fibrotic tissue determined by the
sickening of the PTS event obtaining a kind of flap that we call valve but as you can realize is absolutely something different from a native valve. The morphology may change depending on the wall feature and the wall thickness
but we have to manage the failure of the mono cuspid valve which is mainly due to the readhesion of the flap which is caused by the fact that if we have only a mono cuspid valve, we need a deeper pocket to reach the contralateral wall so bicuspid valve we have
smaller cusps in mono cuspid we have a larger one. And how can we prevent readhesion? In our first moment we can apply a technical element which is to stabilize the valve in the semi-open position in order not to have the collapse of the valve with itself and then we had decide to apply an hemodynamic element.
Whenever possible, the valve is created in front of a vein confluence. In this way we can obtain a kind of competing flow, a better washout and a more mobile flap. This is undoubtedly a situation that is not present in nature but helps in providing non-collapse
and non-thrombotic events in the cusp itself. In fact, if we look at the mathematical modeling in the flow on valve you can see how it does work in a bicuspid but when we are in a mono cuspid, you see that in the bottom of the flap
we have no flow and here there is the risk of thrombosis and here there is the risk of collapse. If we go to a competing flow pattern, the flap is washed out alternatively from one side to the other side and this suggest us the idea to go through a mono cuspid
valve which is not just opens forward during but is endovascular and in fact that's what we are working on. Undoubtedly open surgery at the present is the only available solution but we realized that obviously to have the possibility
to have an endovascular approach may be totally different. As you can understand we move out from the concept to mimic nature. We are not able to provide the same anatomy, the same structure of a valve and we have to put
in the field the possibility to have no thrombosis and much more mobile flap. This is the lesson we learn from many years of surgery. The problem is the mobile flap and the thrombosis inside the flap itself. The final result of a valve reconstruction
disregarding the type of method we apply is to obtain an anti-reflux mechanism. It is not a valve, it is just an anti-reflux mechanism but it can be a great opportunity for patient presenting a deep vein reflux that strongly affected their quality of life.
- I'd like to thank Larry and John for the opportunity to speak today. This really is kind of an exciting time in Vascular Access 'cause you know this whole session's devoted to all the new tools and technologies, and they're really a lot of different options
that are available to us now to create functioning fistulas in patients. Those are my disclosures. I just want to mention one thing, when I was asked to give this talk, the name of the device was the Everlink device then,
and that was first developed by TBA Medical at Austin, Texas. Eventually the company was bought by Bard, and then Beckett Dickinson bought Bard, and then they changed the name of the device to the WaveLinq device,
just so that we're all on the same page here. The basic gyst of this system basically it's a two-catheter system, it involves punctures in the brachial artery and brachial vein above the elbow over wires, the catheters are then aligned
in the ulnar artery and ulnar vein. The venous catheter has an RF electrode on it, the arterial component has a ceramic foot plate, and there's rare earth magnets in the catheters that help them align in the artery and vein. They'll coapt, you deploy the foot plate,
and then you fire the RF energy from the RF generator, and the RF energy then creates a four millimeter hole between the artery and vein. This is just what it looks like under fluoroscopy, this is the arterial catheter going in here's the footplate here
this is the venous catheter then being directed and you can see the magnets on these they look like Lincoln Logs they'll kind of line up. You rotate the catheters 'til the foot plate aligns, you do some flyovers with the II make sure everything's lined up,
and then you create the fistula with the RF energy. Then this is just what Fistulagram looks like once the fistula's created. At the completion of that, for this device we then place coils, occluding coils, in the deep vein which was just beyond the sheath
where we accessed the brachial vein. And by putting those plugs in there, coils in there, It helps to direct the flow up to through the superficial veins which we cannulated for dialysis, and much like the other device
that Dr. Malia was talking before, this creates essentially a split vein fistula, it's going to mature both the cephalic and basilic if those veins are available through that from the perforator coming on out. This is just what it looks like you know,
this was in some early studies in the animal model, you can see that it creates exactly a four millimeter hole between the artery and vein. Eventually this will re-endothelialize they had endothelialization at 30 days. So really the nice thing about it is
it standardizes the size of the arteriotomy because it makes exactly a four millimeter fistula. Now, as I mention this is created at the level of the ulnar artery and ulnar vein, so the requirements basically to do this you need a adequate size obviously ulnar artery and vein,
but the big component is to have that adequate perforator vein that's going to help feed the superficial veins to mature that fistula. And then it's just creating a side to side fistula between the ulnar artery and vein.
This is just a composite of all the data that's been collected on the device so far so this is what the global registry looks like. The FLEX study was kind of the first studies in man. The NEAT trial was run in the Canada and the UK, that was one of the earlier trials.
Then there's a post-market registry, uh, in Europe that's being run now. The EASE trial is the trial with the Four French device and I'll share a little bit about that at one of the slides at the end. But basically pull all the data from this
there's almost 157 patients that they collected data on. And, you can see that with this the primary patency, or the primary patency's on at 75 percent, and the accumulative patency's almost 80 percent, and then the number of fistulas that were cannulated at six months successfully with two needles was 75 percent.
If you look at some of the interventions that've had to be done it really seems to be a lower number of interventions that have to be done to get a mature functioning fistula, uh, using this device. I just want to point out a couple things on this slide,
there was never any requirement for angioplasty at the uh, the ulnar artery the ulnar vein anastomosis, and there was, you know, with these embolizations that were performed, 12 of these were performed on patients prior to incorporating that into the procedure itself,
so right now in the IFU it says that the deep veins should be coiled to help direct that flow up into the superficial veins. Now as, uh, was alluded to earlier with the Ellipsys device this kind of falls somewhere between, uh, the radiocephalic fistula and a brachiocephalic fistula,
and again comparing these two devices basically you're creating, this is the Ellipsys device is radial-radial, and this device is really ulnar-ulnar, but again you're creating that split-flow fistula it's going to allow flow both up
into the basilic and cephalic veins. So, where can this be used? It can be used for primary access creation so that's the first option to provide a patient with a functioning fistula. It can be a secondary option to radiocephalic fistula,
or those that have failed the radiocephalic fistula, and it also is an alternative to surgery so there are patients that may not want to have open surgery to have a fistula created, and this obviously provides an option for those patients. In the UK now they're using it to condition veins,
so they'll create the fistula hoping to condition the cephalic and basilic veins to allow them to become usable for dialysis, and they're also using it in patients that have no superficial veins actually using it to mature the brachial vein
or the deeper veins, uh, and then superficializing the brachial vein to create a native fistula for patients who don't have adequate superficial veins. Now I mentioned the Four French device and what the Four French device allows is basically access
from a lot of different points. So now because it's a smaller device, we can place it, if the vein and artery are large enough, it can be placed at the wrists, so radial-radial fistula, so you come in from the wrist, put both catheters up, create the fistula at the radial-radial,
you can do it from the ulnar-ulnar, so it's just two catheters up from the wrist. And these cases are nice, the other option is you can come arterial from the wrist and you can come from the vein at the top, match up the catheters in a parallel
and create that fistula at the ulnar-ulnar level. And the nice thing about this is it really makes managing the puncture very easy you just put a TR band on 'em, and then you're good to go. So it really kind of opens up a lot of different options for creating fistulas.
So in summary this device seems to create a functional fistula without the need for open surgery. It has very good primary and cumulative patencies and seems to take fewer interventions to maintain and mature the functioning fistula, and this may add another tool that we have to create
functioning fistulas in patients who are on dialysis. So thank you very much.
- [Presenter] Thanks again, Laurel, for this kind invitation. We're going to discuss about how I do the treatment for varicose veins for the foot. And we're going to show you our experience for that. I have no disclosure. I came from Natal, Brazil.
There's our wonderful beach that we have there, but we don't have time to go there, unfortunately. This is our hospital, and these are the people that worked with us. To do this treatment we have to pay attention of the history and the physical examination.
It's very important to decide what you can do to these patients, because we have to associate some tools to do this kind of treatment. So phleboscopy, transillumination is very important to define the feeder veins,
so it's very important in this case to show us where is the veins that we feed these spider veins to treat that. And of course, the ultrasound associated with all the physical examinations of course and then the black scan. You can see in this case, a patient does not have any
varicose veins on the thigh, of the leg. They have only varicose veins by the foot. If you can see, the reflux of there, comes from the junction to the foot. If you don't have the good ultrasound
or duplex scan it can have a mistake and treat wrong way these patients. So, what are the tools we have to do to treat these patients? A lot of tools, you can see the liquid sclerotherapy with a low concentration of 75%.
Foam polidocanol for these two concentrations. Of course, transdermal laser, hooks that we can apply in the surgery and polidocanol laser. How about this procedure? This paper from the Netherlands, show us patient satisfaction after ambulatory phlebectomy
of varicose veins, what they conclude about that. The most important factors that influence the patient satisfaction is: discoloration, persistent pain, and the perception of varices after surgery. This last one is very important for us,
because the patient comes to us to be cleaning off veins of the foot, if we miss that everything we did, the patient will complain about after their surgery. We have two kinds of treatment, ambulatory treatment being the option
and the hospital we can do the procedures. We have separate patients with CO grade, CEAP classifications and C2 classifications. When we have a C1 grade classification we use transdermal laser and liquid sclerotherapy. You can see one case is a cosmetic
and one is a severe one. A C2 case we have ambulatory treatment, we have transdermal laser and we associate all this with foam sclerotherapy. But the concentrations are 0.5% and 0.25%, you can see its low concentrations.
At the hospital we have can do almost everything nearly in the same day. Transdermal laser, liquid sclerotherapy, foam sclerotherapy. Yes, we can associate liquid sclerotherapy, sometimes the people say that you cannot do that, but we do that.
In case like this, we also say transdermal laser in spider veins, phlebectomy and you can see in this case we have a use for sclerotherapy and is this is the result of 60 days. This other case that we use phlebectomy and we have to be careful because you
can take nerves, the patient will complain about after surgery. And these are the results. Polidocanol with laser tool, yes, but it's not our routine to use that. In conclusion:
Physical exam and a precise diagnosis of the feet varicose veins is essential to do a good surgery. With all these tools, that we have, the treatment of varicose veins of the foot is safe and effective. This is my fugu in Natal, Brazil.
- Thank you to the moderators, thank you to Dr. Veith for having me. Let's go! So my topic is to kind of introduce the ATTRACT trial, and to talk a little bit about how it affected, at least my practice, when it comes to patients with acute DVT.
I'm on the scientific advisory board for a company that makes IVC filters, and I also advise to BTG, so you guys can ask me about it later if you want. So let's talk about a case. A 50-year-old man presents
from an outside hospital to our center with left lower extremity swelling. And this is what somebody looks like upon presentation. And pulses, motor function, and sensation are actually normal at this point.
And he says to us, "Well, symptoms started "three days ago. "They're about the same since they started," despite being on anticoagulation. And he said, "Listen guys, in the other hospital, "they wouldn't do anything.
"And I want a procedure because I want the clot "out of me." so he's found to have this common femoral vein DVT. And the question is should endovascular clot removal be performed for this patient?
Well the ATTRACT trial set off to try and prevent a complication you obviously all know about, called the post-thrombotic syndrome, which is a spectrum from sort of mild discomfort and a little bit of dyspigmentation and up
to venous ulcerations and quite a lot of morbidity. And in ATTRACT, patients with proximal DVT were randomized to anticoagulation alone or in combination with pharma mechanical catheter-directed thrombolysis.
And the reason I put proximal in quotes is because it wasn't only common sort of femoral vein clots, but also femoral vein clots including the distal femoral vein were included eventually. And so patients with clots were recruited,
and as I said, they were randomized to those two treatments. And what this here shows you is the division into the two groups. Now I know this is a little small, but I'll try and kind of highlight a few things
that are relevant to this talk. So if you just read the abstract of the ATTRACT trial published last year in the New England Journal of Medicine, it'll seem to you that the study was a negative study.
The conclusion and the abstract is basically that post-thrombotic syndrome was not prevented by performing these procedures. Definitely post-thrombotic syndrome is still frequent despite treatment. But there was a signal for less severe
post-thrombotic syndrome and for more bleeding. And I was hoping to bring you all, there's an upcoming publication in circulation, hopefully it'll be online, I guess, over the weekend or early next week, talking specifically about patients
with proximal DVT. But you know, I'm speaking now without those slides. So what I can basically show you here, that at 24 months, unfortunately, there was no, well not unfortunately,
but the fact is, it did cross the significance and it was not significant from that standpoint. And what you can see here, is sort of a continuous metric of post-thrombotic syndrome. And here there was a little bit of an advantage
towards reduction of severe post-thrombotic syndrome with the procedure. What it also shows you here in this rectangle, is that were more bleeds, obviously, in the patients who received the more aggressive therapy.
One thing that people don't always talk about is that we treat our patients for two reasons, right? We want to prevent post-thrombotic syndrome but obviously, we want to help them acutely. And so what the study also showed,
was that acute symptoms resolved more quickly in patients who received the more aggressive therapy as opposed to those who did not. Again, at the price of more bleeding. So what happened to this patient? Well you know,
he presented on a Friday, obviously. So we kind of said, "Yeah, we probably are able "to try and do something for you, "but let's wait until Monday." And by Monday, his leg looked like this, with sort of a little bit of bedrest
and continued anticoagulation. So at the end of the day, no procedure was done for this particular patient. What are my take home messages, for whatever that's worth? Well I think intervention for DVT
has several acute indications. Restore arterial flow when phlegmasia is the problem, and reduce acute symptoms. I think intervention for common femoral and more proximal DVT likely does have long-term benefit, and again, just be
on the lookout for that circ paper that's coming out. Intervention for femoral DVT, so more distal DVT, in my opinion, is rarely indicated. And in the absence of phlegmasia, for me, thigh swelling is a good marker for a need
for a procedure, and I owe Dr. Bob Schainfeld that little tidbit. So thank you very much for listening.
- I have nothing to disclose but what I will tell you is that the only way for me to learn the mechanics of treating low-flow malformations has been to learn from Wayne, follow what he's doing, and basically what I've done is I've filmed every single step he's taking,
dissect that, and then present you the way that he's doing it. The best way to do that is not listen to Wayne, but to film him, and just to check that afterwards. And he goes regularly to Cairo, this is the place of Dr. Rodovan sitting here
in front of us, and with Dr. Alaa Roshdy. I've learned a lot there from Wayne. This is Wayne's techniques, so normally if you look at puncture, the low flow malformations here then you get return or you aspirate so this is what happens, they inject contrast then they find volume
and inject whatever agent you prefer to inject. It happens to be alcohol but that is not essential. More often than not, there is no return. What to do then? There is a technique that Wayne has developed. Stab-Inject-Withdraw, just under high modification inject,
identify that you're not outside the vessel, get the vessel, start to fill slowly, and identify that and inject the alcohol. Of course you can do that under exposure just to see the effect of the alcohol thrombosing, et cetera.
Another example of no return is to subcutaneously certainly show that there is a low pressure system, and again, Stab-Inject-Withdrawal, and there is a cyst. Is it extravasation or is the malformation aspirate? And if it collapses, that's the malformation.
And then continue to fill in with contrast, define how big the malformation is, and then accordingly inject the amount of abrasive agent that you're using. Lymphatic malformation is very difficult to treat because the vessel's so small, would say microscopic,
and again, Stab-Inject-Withdraw, identify that it's not extravasating but it is the vessel, and start slowly, slowly to fill and any time in doubt that should there, just do a run, identify, and that is the vessel, or the network of the vessels and
start to fill that with the agent you're using. But there are certain zones that just don't inject anything, and these are the arteries. How often do arteries occur? When you puncture them. I just directly looked at all these 155 patients I've seen Wayne treat there a matter of,
I would say, 100 patients in three days. 30 patients per day, that's about six percent. And you see the artery by pulsating flow depending on the pressure that you apply. And we see again the artery pulsating and we have no doubt about that.
However, it could be difficult to see. Depending on how much you push in the contrast and you see these being ornery so there's a No-Go-Zone, no injection of any agent and again, a tiny bit of lottery there in the foot could be disastrous.
You inject any agent, any, you will have ended up with necrosis of course if you don't inject inhibitors, but not yet. The humorous may not end up with necrosis when all the mysticism with puncture will be gone. So we have extravasation, when you say extravasation
like starting injecting, still good, looking good, but you see how the extravasation even blows up and at the end it bursts, again under pressure they should apply, so pressure is really important to control and then you stop and don't inject any more.
Extravasation, you see how its' leaking in the back there, but you correct the position of the needle, identify all the vessels, the tiny little vessels, just have to be used to identify the pattern and then you start to inject the agent again.
Control is very essential. Here is the emphatic malformation labia and though there is this tiny little bity extravasation you continue because there is you know, run-off, it is filling the system and you can safely inject the alcohol.
Intraarticular could be malformation there and this is definitely safe pla however, if it is in the free space in the the joint, that's again, it's No-Go-Zone. How you see that is just be used to
the pattern recognition and you find that this is free. It's around the condyle there so there is no injection. Compression is again good to note to control by compression where the agents go. This is a normal vein, certainly at risk of getting with alcohol, whatever agent
you're using deep in the system, avoid that by compression. Compression can be applied manually and then that gives you a chance to fill the malformation itself and not strike connection too deep in the system. Intraosseous venous malformation,
low-flow malformations can occur anywhere, here in the spine and the axis is transpedicular patient prone because it's soft. The malformation has softened up the bone. You can just use a 21-gauge needle and identify the malformation and follow
by the agent you're using. Peculiar type of venous malformation called capillary venous malformation. Basically it's a low-flow malformation without any shunt here in the sciatic notch of the patient and geography shows that there is no shunt
there is just big veins and intense pacification. And identify the veins by indirect puncture again, see the pattern of that and inject alcohol and following geography we can see that there has decreased the density but it is a lot more left to be done.
In conclusion, direct puncture is the technique in this low-flow malformation but Stab-Inject-Withdraw is the really helpful technique for successful treatment of microvascular, microcystic lesion. No-Go-Zones for certain when you see arteries
and anytime in doubt you just have to do a run to identify if they're arteries or not. Intraarticular free space and extravasation and normal veins, similarly, No-Go-Zone. Capillary venous, intraosseous malformations can be treated successfully. Thank you.
(audience applause) - [Facilitator] Thank you, Crossey. Excellent talk, very practical and pragmatic. Any comments or questions? Dr. Yakes. - [Dr. Yakes] We have been to many meetings and people have talked about doing
other ultrasound guides, accessing the malformations. You'll never see those arteries by ultrasound. - [Facilitator] That's absolutely correct. I concur. I concur and I think some of the disasters we've seen where suddenly something falls off
have been in these situations because they don't understand or in expansile foam-based therapies, I've seen that. I've seen plenty of these, so it's always present, potentially.
- [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.
- I will be talking about new KDOQI guidelines. I know many of you have heard about KDOQI guidelines being revised for the past maybe over a year or maybe two. Yes, it is being done, and it is going slow only because it's being done in a very different way. It's more than an update.
It's going to be more of an overhaul for the entire KDOQI guidelines. We in KDOQI have looked at access as a solitary problem like we talked about grafts, catheters, fistulas for access, but actually it sort of turns out
that access is part of a bigger problem. Fits into a big ESKD lifeline of a patient. Instated distal patients come in many varieties. It can affect any age, and they have a lot of other problems so once you have chronic renal failure, renal replacement mortality fits in
only when it becomes Stage IV or Stage V. And renal replacement mortality is not just access, it is PD access, it's hemo access, it is transplant. So these things, we need to see how they fit in in a given person. So the new KDOQI guidelines concentrates more
on individualizing care. For example, here the young Darien was an 11 year old with a prune belly syndrome. Now he has failed PD. Then there's another person here who is Lydia who is about 36 or 40 year old lady
with a insulin dependent diabetes. Already has bad vascular pedicle. Lost both legs. Needs access. Now both these patient though they need access, it's not the same.
It's different. For example, if you think of Darien, he was in PD but he has failed PD. We would love to get him transplanted. Unfortunately he's got terrible social situation so we can't get him transplanted.
So he needs hemo. Now if he needs hemo, we need to find an access that lasts for a long time because he's got many years ahead of him. On the other hand we have Lydia, who has got significant vascular disease.
With her obesity and existing infectious status, probably PD won't be a good option for her. So she needs hemo, and she's obviously not a transplant candidate. So how are we going to plan for hemo? So these are things which we are to more concentrate
and individualize when we look at patients, and the new guidelines concentrate more on these sort of aspects. Doing right access for right patient, right time, and for right reasons. And we go about planning this keeping the patient first
then a life plan ESKD lifeline for the patient, and what access we are looking at, and what are the needs of the patient? Now this is also different because it has been done more scientifically. We actually have a evidence review team.
We just poured over pretty much 1500 individual articles. Recent articles. And we have looked through about 4000 abstracts and other articles. And this data is correlated through a workgroup. There a lot of new chapters.
Chapter specific surgery like peri-operative, intra-operative, post-operative, cat issues, managing complication issues. And we started off with the coming up with the Scope of Work. The evidence review team took the Scope of Work
and tried to get all the articles and sift through the articles and came up and rated the evidence using a certain rating system which is very scientific. The workgroup then kind of evaluated the whole system, and then came up with what is clinically relevant.
It's one thing for statisticians to say how strong evidence this is, but it's another thing how it is looked upon by the clinicians. So then we kind of put this into a document. Document went through internal and external review process.
This is the process we have tried to do it. Dr. Lok has been the Chair of the group. Myself and Dr. Yevzlin are the Vice-Chairs. We have incredible workgroup which has done most of the work. And here are the workgroup members.
We comprised of nephrologist, transplant surgeons, vascular surgeons, Allied Health personnel, pediatric nephrologist so it's a multi interventional radiologist and interventional nephrologist. This is a multi disciplinary group which has gone through this process.
Timothy Wilt from Minnesota was the head of the Evidence Review Team, who has worked on the evidence building. And now for the editorial sections we have Dr. Huber, Lee, and Dr. Lok taking care of it. So where are we today?
We have pretty much gone through the first part of it. We are at the place where we are ready for the Internal Review and External Review. So many of you probably will get a chance to look through it when it comes for the External Review and would love
to have your comments on this document. Essentially, we are looking at access in the context of end stage renal disease, and that is new. And obviously we have gone through and done a very scientific review, a very scientific methodology to try
to evaluate the evidence and try to come up with guidelines. Thank you.
- So my charge is to talk about using band for steal. I have no relevant disclosures. We're all familiar with steal. The upper extremity particularly is able to accommodate for the short circuit that a access is with up to a 20 fold increase in flow. The problem is that the distal bed
is not necessarily as able to accommodate for that and that's where steal comes in. 10 to 20% of patients have some degree of steal if you ask them carefully. About 4% have it bad enough to require an intervention. Dialysis associated steal syndrome
is more prevalent in diabetics, connective tissue disease patients, patients with PVD, small vessels particularly, and females seem to be predisposed to this. The distal brachial artery as the inflow source seems to be the highest risk location. You see steal more commonly early with graft placement
and later with fistulas, and finally if you get it on one side you're very likely to get it on the other side. The symptoms that we are looking for are coldness, numbness, pain, at the hand, the digital level particularly, weakness in hand claudication, digital ulceration, and then finally gangrene in advanced cases.
So when you have this kind of a picture it's not too subtle. You know what's going on. However, it is difficult sometimes to differentiate steal from neuropathy and there is some interaction between the two.
We look for a relationship to blood pressure. If people get symptomatic when their blood pressure's low or when they're on the access circuit, that is more with steal. If it's following a dermatomal pattern that may be a median neuropathy
which we find to be pretty common in these patients. Diagnostic tests, digital pressures and pulse volume recordings are probably the best we have to assess this. Unfortunately the digital pressures are not, they're very sensitive but not very specific. There are a lot of patients with low digital pressures
that have no symptoms, and we think that a pressure less than 60 is probably consistent, or a digital brachial index of somewhere between .45 and .6. But again, specificity is poor. We think the digital pulse volume recordings is probably the most useful.
As you can see in this patient there's quite a difference in digital waveforms from one side to the other, and more importantly we like to see augmentation of that waveform with fistula compression not only diagnostically but also that is predictive of the benefit you'll get with treatment.
So what are our treatment options? Well, we have ligation. We have banding. We have the distal revascularization interval ligation, or DRIL, procedure. We have RUDI, revision using distal inflow,
and we have proximalization of arterial inflow as the approaches that have been used. Ligation is a, basically it restores baseline anatomy. It's a very simple procedure, but of course it abandons the access and many of these patients don't have a lot of good alternatives.
So it's not a great choice, but sometimes a necessary choice. This picture shows banding as we perform it, usually narrowing the anastomosis near the artery. It restricts flow so you preserve the fistula but with lower flows.
It's also simple and not very morbid to do. It's got a less predictable effect. This is a dynamic process, and so knowing exactly how tightly to band this and whether that's going to be enough is not always clear. This is not a good choice for low flow fistula,
'cause again, you are restricting flow. For the same reason, it's probably not a great choice for prosthetic fistulas which require more flow. So, the DRIL procedure most people are familiar with. It involves a proximalization of your inflow to five to 10 centimeters above the fistula
and then ligation of the artery just below and this has grown in popularity certainly over the last 10 or 15 years as the go to procedure. Because there is no flow restriction with this you don't sacrifice patency of the access for it. It does add additional distal flow to the extremity.
It's definitely a more morbid procedure. It involves generally harvesting the saphenous vein from patients that may not be the best risk surgical patients, but again, it's a good choice for low flow fistula. RUDI, revision using distal inflow, is basically
a flow restrictive procedure just like banding. You're simply, it's a little bit more complicated 'cause you're usually doing a vein graft from the radial artery to the fistula. But it's less complicated than DRIL. Similar limitations to banding.
Very limited clinical data. There's really just a few series of fewer than a dozen patients each to go by. Finally, a proximalization of arterial inflow, in this case rather than ligating the brachial artery you're ligating the fistula and going to a more proximal
vessel that often will accommodate higher flow. In our hands, we were often talking about going to the infraclavicular axillary artery. So, it's definitely more morbid than a banding would be. This is a better choice though for prosthetic grafts that, where you want to preserve flow.
Again, data on this is very limited as well. The (mumbles) a couple years ago they asked the audience what they like and clearly DRIL has become the most popular choice at 60%, but about 20% of people were still going to banding, and so my charge was to say when is banding
the right way to go. Again, it's effect is less predictable than DRIL. You definitely are going to slow the flows down, but remember with DRIL you are making the limb dependent on the patency of that graft which is always something of concern in somebody
who you have caused an ischemic hand in the first place, and again, the morbidity with the DRIL certainly more so than with the band. We looked at our results a few years back and we identified 31 patients who had steal. Most of these, they all had a physiologic test
confirming the diagnosis. All had some degree of pain or numbness. Only three of these patients had gangrene or ulcers. So, a relatively small cohort of limb, of advanced steal. Most of our patients were autogenous access,
so ciminos and brachycephalic fistula, but there was a little bit of everything mixed in there. The mean age was 66. 80% were diabetic. Patients had their access in for about four and a half months on average at the time of treatment,
although about almost 40% were treated within three weeks of access placement. This is how we do the banding. We basically expose the arterial anastomosis and apply wet clips trying to get a diameter that is less than the brachial artery.
It's got to be smaller than the brachial artery to do anything, and we monitor either pulse volume recordings of the digits or doppler flow at the palm or arch and basically apply these clips along the length and restricting more and more until we get
a satisfactory signal or waveform. Once we've accomplished that, we then are satisfied with the degree of narrowing, we then put some mattress sutures in because these clips will fall off, and fix it in place.
And basically this is the result you get. You go from a fistula that has no flow restriction to one that has restriction as seen there. What were our results? Well, at follow up that was about almost 16 months we found 29 of the 31 patients had improvement,
immediate improvement. The two failures, one was ligated about 12 days later and another one underwent a DRIL a few months later. We had four occlusions in these patients over one to 18 months. Two of these were salvaged with other procedures.
We only had two late recurrences of steal in these patients and one of these was, recurred when he was sent to a radiologist and underwent a balloon angioplasty of the banding. And we had no other morbidity. So this is really a very simple procedure.
So, this is how it compares with DRIL. Most of the pooled data shows that DRIL is effective in 90 plus percent of the patients. Patency also in the 80 to 90% range. The DRIL is better for late, or more often used in late patients,
and banding used more in earlier patients. There's a bigger blood pressure change with DRIL than with banding. So you definitely get more bang for the buck with that. Just quickly going through the literature again. Ellen Dillava's group has published on this.
DRIL definitely is more accepted. These patients have very high mortality. At two years 50% are going to be dead. So you have to keep in mind that when you're deciding what to do. So, I choose banding when there's no gangrene,
when there's moderate not severe pain, and in patients with high morbidity. As promised here's an algorithm that's a little complicated looking, but that's what we go by. Again, thanks very much.
- I think it's unfair to have Wayne here with all his expertise and knowledge and throwing all these combative comments, vulgar attack, et cetera. But the bottom line is all these types, no matter how you define them, they are mixed.
They are mixed, they are not, with the exception for HDT. You have Type 1 in a midst of Type 2. You have Type 2A and then 3B, type something. I don't even know what they are, except that you say venous predominance, yes. Can be multiple venous predominance, yes.
Then you can have Type 4, these are the major groups. But to have a filler that occupies a space, can be Onyx, it's fine. It doesn't cure. You have to do something to these cells. You have to compress them.
You have to ablate them. You have to take them out. And a filler doesn't do that. The filler recolonizes on top of that, as you've put it already, from Molly. Recolonizes.
You can use it as a filler, but the cure, the ablation, has to be something that's powerful. Like a knife, even worse than knife, burn injuries, burn it to the bottom. That's how you achieve a cure. If you don't believe me, just look at ...
Can you play us that clip that was rotating constantly as Walter was talking, here, how Onyx is wonderful? This is the girl that you show on the pictures from Bob. Can you look at that? It's a ton of extras placed into the veins,
arteries, everywhere. She continues to bleed. On top of that, it's horrendous, how to treat it. Wayne managed to stop and control the bleeding, but this is an example.
This is the most scary sample of what Onyx cannot do. So back to the motion. Polymerizing Onyx can cure, and it's the material of choice to use? The answer is no. Alcohol is dangerous, personally,
I say yah, very dangerous, if you drive and you don't know how to use it. But so is everything else. But if you know, you can cure them. Thanks.
- I think there'll be a little bit of duplication here cuz he talked about a lot of things that I put in here. I've no disclosures. The Goals of Sclerotherapy is damage of the endothelium with vascular fibrosis and obliteration. The idea is to use the minimal dose of sclerosant and minimal concentration and avoid injury
to the surrounding normal vessels and tissue. Of course, I won't go into a lot of detail about the history and physical, but what is very important is trying to get some realistic expectations. I saw some incredible results just now.
I don't know if I get that all the time, and so I do want my patients to be aware that perfection is I usually don't seem to really get that. So the consent's very important and photographic documentation is extremely important
because you really do want to show em what it looked like beforehand cuz many times they forget where they started. Just like Dr. Miyake said determine the source of the spider vein's very important. If there's axial vein problems,
I'm not suggesting you have to do a duplex on everybody, but if you have evidence of varicosities, venous insufficiency you might you're not going to get very good results if you have axial vein reflux particularly in line with where
the spider veins and telangiectases are. Same with perforator veins, you may have an issue there, and if you're just treatin' the spiders and not gettin' the source. Dr. Dillavou is going to talk about reticular veins next, but I do emphasize the importance of treating
the feeding veins that are feeding into the spider complex. The equipment, well these are now absolutely required for me and use to be I may not have had to have em, but now I do. I have to have magnification, course you need sclerosants, syringes, needles, and cotton balls.
I like the butterfly needle for the larger veins and 30 gauge for the spiders. There are these polarized lights or vein lights which sometimes come in handy. You've seen the infrared imaging now in the last two talks. I'll show you a little bit of that.
I personally don't use it, but I do think there are probably some cases where it come in very handy, and of course compression stockings and cotton balls and tape even though I don't compress routinely for just spider veins.
Basic Principles, treat the large to small, proximal to distal which you do with varicose veins. The most important though is what Dr. Miyake just mentioned. You want the lowest effective concentration, but in particular, you want to minimize the plunger pressure.
Sometimes you can get a little frustrated when you're trying to get into a vein, you don't want to really inject hard at all or you will get an ulceration. And post-op compression, again is somewhat controversial, at least in my mind, but ambulation of course
is very, very helpful. Contraindications, course allergies, acute DVT, PAD, acute SVT, most of the things you would an active infection in the extremity, you're not going to treat that. The Sclerosants are divided into detergents,
osmotics, and chemical irritants. The main detergents are sodium tetradecyl sulfate and polidocanol. These are primarily what I use in my practice cuz they're FDA-approved and I tend to like to have that when I'm treating patients,
and the concentrations listed here which are in line with what you just saw. There is this study of Sclerotherapy of Telangiectases comparing tetradecyl and polidocanol to a control of isotonic saline and of course there was a significant difference
between the sclerosants and isotonic saline thank goodness. The only thing I'm not real think this study's that helpful cuz it compared one percent STS to .5 polidocanol. I don't think that's a fair comparison
usually I use .1 to .2, and I think STS and tetradecyl are fairly equivalent. The osmotic agents you just heard about, but you know about saline probably, hypertonic saline but also hypertonic dextrose, or there's the combination of saline and dextrose which is a sclerodex.
Again, not really available here. Chemical irritants are glycerin and chromate glycerin. Again, very viscous, low ulcerative capabilities, but again not FDA-approved for this. I don't really use it routinely. There are other sclerosants out there,
but I don't know of anybody using them for telangiectases. Technique, lowest effective concentration again, results determined by the concentration and contact time so that's why I'll say use a low concentration but when you inject, let it sit there a second as you're injecting, just for a few seconds,
maybe 10 seconds even. That contact time helps a lot. I'm already out of time, and I still have quite a bit here, but here's some videos. That's me using a polarized light source. We'll skip through all that.
Here's treating the reticular vein that feeds the spider veins, lower cartoon to kind of show you what I was talking about there. I think you'll probably got the concept but again, if you don't treat the feeder vein,
you're probably not going to get very good results. Here's that infrared technology. Now, I can't seem to skip, okay Complications, well you just actually heard a very good talk on that, so I'll probably stop here since I'm already out of time.
So, I was going to run through that but basically you've already seen it well covered, so I'll stop here.
- Alright, that's our beautiful city by our inland freshwater ocean. I'm against the proposal because, in my opinion, ONYX and the polymerizing agents don't do what they're supposed to do, which is cure. You know, we could talk about this, but in preparation for this, I looked at the
relatively sparse, but available, literature on ONYX, and the fact of the matter is, repeatedly when one looks at what is in the literature, ONYX does not cure with a few exceptions. For example, this is the curative exception. This is a mandibular AVMs, three of them cured
at one year angiographic followup. Now, I consider cure a very simple metric: is it gone at one year followup angiography or imaging? And this meets that criteria, but again, we know that mandibular AVMs, as Dr. Fannis has so nicely shown, this is a bone cyst, essentially,
fill it with anything, it'll get cured. All venous predominant legions, three A. So, yes, cure is possible in isolated circumstances. I think Walter has acknowledged that. But, all the other data, including Dr. Loglos' own data, is that there is no angiographic
followup, short clinical followup. Other papers, Embolization of peripheral high-flow AVMs by Kilani et. al, surgical excision in nine out of 19. Right, that's not the same thing, but it is one aspect of doing it, and there's no angiographic followup. And we see this again and again and again.
Very short clinical followup. So paper after paper refused to tell us that we don't really know what the behavior of ONYX is, as defined by the very simple metric of cure. Although complete, in this paper for example, although complete angiographic exclusion of the nidus
is obtained in a minority, 36 percent, of cases, there's no angiographic followup, so the exclusion is presumably based on immediate post-embolization angiography. In other words, ONYX looks good, acts bad. Other embolization agents in this paper also used,
probably some of them ethanol, which actually got the job done. And then finally, another paper with zero clinical or angiographic followup. So the answer is obvious: ONYX, while it is used copiously by some of the participants in this debate, does not cure,
and I, as my Chinese friends said, think ONYX is garbage. I don't think it works. Few examples of that, here's a young woman, a patient of Dr. Yakes, who, 12 years old, extensive facial maxillary scalp AVM, nine ONYX embolizations, left blind in the right eye
with persistent massive oral and nasal hemorrhage, and after appropriate embolizations, patient was stabilized clinically, and the ONYX was resected. She's stable now, not cured, but she's actually had an excellent clinical result. And you can see that's what it looks like.
Now that's hideous, that's not going to work. And it also, I think, points out what Dr. Walgramuth has actually admitted to, which is it's very difficult to see through this stuff. Radiation dose is increased, and identifying what to do and where to go is a real challenge.
Another such example, I think, suffice it to say a picture is worth a thousand words is this illustrative case of an extensive pelvic AVM, treated with what appeared to be gallons of ONYX, with very little benefit, and an enlarging ulcer. This was later treated by direct alcohol injection
with cure and improvement resolution of that ulcer. So, in summary, it's real simple, folks. There's no evidence in the literature that polymerizing agents have cured AVMs with an exception of a few venous predominant legions. And as I said, you could probably put Jello
in the outflow of those things and it'd work. My own personal experience is repeatedly had ONYX failures, and importantly, many patients are worsened by this treatment, and actually, their subsequent curative treatments are hampered. Thanks very much.
- 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.
- Thanks a lot for again for inviting me because you know, (laughs) I'm in very hostile territory, (audience laughs) but, I will tell you the truth now, (audience laughs) and being in hostile territory and telling the truth can
be totally different things and I, I'm also never in any way, you know I'm totally scientific type, I will never be polemic, like you are. (audience laughs) Okay, so let's start with the truth, start with the truth, I show you two typical cases, this is a typical ethanol case
here with couple of, it was successful, at least in losing it's toes, and I'll show you another example again, a foot AVM, this is one session, one session, in fact its 14 vials of squid in this case, and it's done. so, this is not statistic, but I always
see, and I've seen it today in a couple of talks, Onyx used as glue. And that doesn't work, you have, if you start to treat a patient, you have to really treat him and it's not something you inject, and that it's gone, you have to fill all the AV shunts, you have to fill the whole lesion.
And if you don't do it, of course you see a lot of failed on ex-patients and if its used improperly, and that's the only thing I, I wouldn't say I agree with you, I would say I'm thinking in the same direction, yeah, that's if you use Onyx in the wrong way, you have a very good chance to make thing worse.
So, its a technical thing, and if people start to use Onyx, and they inject something, and then its something like putting in some coils, that's not worthwhile, it makes no sense to include some arterial feeders, we know this since, I think more than 20 years, it's like making a surgical ligation of the feeding
artery, it's totally senseless. You have to completely occlude the area of the arteriovenous shunting, apart from the predominantly venous one, where you can just occlude the venous outflow, by whichever thing you use, and the area of arteriovenous shunting is always bigger than you see it in a normal DSA,
because the blood does the same as the contrast medium does, it flows along the route of the least flow resistance. And so, at the end, if you want to be sure that you have to completely occluded the AVM, you will end up with a cast which is much bigger than what you see at the beginning of a DSA, yep, it was agreed, see.
- [Audience Member] You know I'm shaking my head as you talk. - Yeah, yeah, your getting tired. (laughs) Here we go, So, and this is only the really scientific slide in my talk, because when people die when you inject ethanol
in vascular malformation treatment, its something, its banal, all of us have seen it many times, but there was a scientific question, why do people die on the table if you inject ethanol in AVM treatment on vascular malformation treatment? And there's one scientific publication here, because we
all thought do they die because of complete vasoconstriction in the pulmonary arterial system, or is it, are they dying due to the thrombi? That, you know ethanol, it uses small slatch or big thrombi and they go to the pulmonary circulation and they die. So, is it the vasospasm, induced by ethanol, or is it the
thrombi induced by ethanol, that they die is clear. So, there was a very nice publication out there in 2012, was presented in Malibu, at the IFSA meeting, it was about four patients, which three of them died, two were just after injecting of between five and 12 milliliters of ethanol, one was a direct puncture pelvic AVM, and it was caused,
that this was nicely stated there, it was caused by multiple small peripheral emboli. So it's not vasospasm that kills the people, it's the thrombus, and I think this was a very very worthwhile contribution to all our knowledge and really thank you Bob for this paper, thank you
very much, now we know why they died. I haven't, unfortunately I can't contribute to this discussion with Onyx because there wasn't any patient dying on the table during my embolization's and I've done now, we're preparing the paper of 160 AVM patients with I don't know, 400 sessions and well maybe if we wait
40 years more, 50% will have died but, (audience laughs) from natural cause, so I can tell you again this is the truth, we will talk about the truth here, and this is, ethanol can be worthwhile even in AVM's, I don't deny that and maybe it will have its place for a couple of more years
before we do Onyx and MEK1-Inhibitors, so there is for couple of more years, this is a role for ethanol, but it's somewhere deep down there, and this is a slide I show for the third time now just for you Wayne, please and I show it because you should start to publish your classification.
I didn't use it because there is no paper there, please publish it then I will always classify according to your classification. - [Audience Member Cheers] - Thank you for your attention, thank you for giving me the chance to talk about the truth here in this seminary
and please don't do anything stupid with ethanol.
- Thank you, Dr. Ouriel, Dr. Lurie. Ladies and gentlemen. Brian, that was a very fair overview of the ATTRACT trial as it was published in the New England Journal, so thank you. And these are my disclosures. So Dr. DeRubertis did a very nice review of this paper
that was published in the New England Journal December 7th of last year. He went over very nicely that it was NIH sponsored, phase III, randomized, controlled, multicenter, 692 patients randomized, anticoagulation alone versus anticoagulation plus catheter-based techniques.
Now one thing I want to call your attention to is the fact that patients with deep venous thrombosis, acute deep venous thrombosis, who were eligible for randomization, were stratified before they were randomized into two different groups, iliofemoral DVT or fem-pop DVT.
So in my opinion, these are not subgroups because the randomization of one group had no effect on the randomization of another, so I would argue that these are independent groups. That makes a big difference when you do statistical analyses.
The other important issue that I want to point out is that the outcomes were pre-determined to what we were going to analyze. We had to choose one as a primary endpoint and the others as secondary, but these were pre-determined end points that were up for analysis, not post hoc analyses.
And post-thrombotic syndrome was determined at the time, 12 years ago when we wrote the protocol, to be the primary end point. I would submit that we would not choose that as a primary end point if we wrote the protocol today. Moderate to severe post-thrombotic syndrome
certainly would be more appropriate. Leg pain, swelling, health-related quality of life, certainly important. This is the outcome, and unfortunately, it did not reach significance. There was no difference between the two groups
and there was an increased risk of bleeding, but this is the outcome that drove opinion about ATTRACT, but we don't really do catheter-directed thrombolysis for fem-pop DVT. Therefore, the results of the iliofemoral patients will be the most meaningful and that paper was written
and that paper has been accepted by circulation. It should be out shortly, but there were 391 iliofemoral DVT patients and the primary outcome was no different than the primary outcome in the overall trial. But are they?
If we had chosen the Venous Clinical Severity Score in place of the Villalta score for analysis of that primary end point, it would've been a positive study. So if we chose a different tool to analyze, our primary end point would've been positive for the iliofemoral DVT patients.
If we look at moderate to severe post-thrombotic syndrome, a significant difference. Control patients had a 56% increased risk of moderate to severe PTS versus the control patients. If we look at severe post-thrombotic syndrome, control patients had a 72% increased risk
of severe PTS versus control. If we look at the overall severity of the Villalta score in PTS, we can see that there is a significant difference favoring percutaneous catheter-directed thrombolysis. When we look at pain, the patient's pain was significantly reduced in the PCDT patients compared to control.
We look at edema, significant reduction in edema at day 10 and day 30 in patients who received catheter-directed thrombolysis compared to control. Disease-specific quality of life significantly favored patients who had PCDT compared to control. So we look at moderate to severe, severe, pain,
quality of life. There was a price to pay. Major bleeding was increased, but the P-value was no different. I will not argue that patients are not at increased risk. They are at increased risk for bleeding,
but this is an historically low bleeding rate for catheter-directed thrombolysis and there were no intracranial bleeds. No difference in recurrent deep venous thrombosis. No difference in mortality at 24 months between the two groups.
So in conclusion, the primary end point, reduction of any PTS defined by a Villalta score of 5 or more, no difference, but an item that has not reached the level of discussion that we will need to consider is that 14% of our patients had a normal Villalta score coming into the study.
It's impossible to improve upon that, but there is a significant reduction in any PTS if you use the Venous Clinical Severity Score, reduction of moderate and severe post-thrombotic syndrome, reduction of pain and swelling, and improved disease-specific quality of life compared to controls.
And I think these are the meaningful end points that patients appreciate and these are the points of discussion that will be covered in the article in circulation that will be published very soon. Thank you for your attention.
- Thank you Dr. Albaramum, it's a real pleasure to be here and I thank you for being here this early. I have no disclosures. So when everything else fails, we need to convert to open surgery, most of the times this leads to partial endograft removal,
complete removal clearly for infection, and then proximal control and distal control, which is typical in vascular surgery. Here's a 73 year old patient who two years after EVAR had an aneurism growth with what was thought
to be a type II endoleak, had coiling of the infermius mesenteric artery, but the aneurism continued to grow. So he was converted and what we find here is a type III endoleak from sutures in the endograft.
So, this patient had explantations, so it is my preference to have the nordic control with an endovascular technique through the graft where the graft gets punctured and then we put a 16 French Sheath, then we can put a aortic balloon.
And this avoids having to dissect the suprarenal aorta, particularly in devices that have super renal fixation. You can use a fogarty balloon or you can use the pruitt ballon, the advantage of the pruitt balloon is that it's over the wire.
So here's where we removed the device and in spite of the fact that we tried to collapse the super renal stent, you end up with an aortic endarterectomy and a renal endarterectomy which is not a desirable situation.
So, in this instance, it's not what we intend to do is we cut the super renal stent with wire cutters and then removed the struts individually. Here's the completion and preservation of iliac limbs, it's pretty much the norm in all of these cases,
unless they have, they're not well incorporated, it's a lot easier. It's not easy to control these iliac arteries from the inflammatory process that follows the placement of the endograft.
So here's another case where we think we're dealing with a type II endoleak, we do whatever it does for a type II endoleak and you can see here this is a pretty significant endoleak with enlargement of the aneurism.
So this patient gets converted and what's interesting is again, you see a suture hole, and in this case what we did is we just closed the suture hole, 'cause in my mind,
it would be simple to try and realign that graft if the endoleak persisted or recurred, as opposed to trying to remove the entire device. Here's the follow up on that patient, and this patient has remained without an endoleak, and the aneurism we resected
part of the sack, and the aneurism has remained collapsed. So here's another patient who's four years status post EVAR, two years after IMA coiling and what's interesting is when you do delayed,
because the aneurism sacks started to increase, we did delayed use and you see this blush here, and in this cases we know before converting the patient we would reline the graft thinking, that if it's a type III endoleak we can resolve it that way
otherwise then the patient would need conversion. So, how do we avoid the proximal aortic endarterectomy? We'll leave part of the proximal portion of the graft, you can transect the graft. A lot of these grafts can be clamped together with the aorta
and then you do a single anastomosis incorporating the graft and the aorta for the proximal anastomosis. Now here's a patient, 87 years old, had an EVAR,
the aneurism grew from 6 cm to 8.8 cm, he had coil embolization, translumbar injection of glue, we re-lined the endograft and the aneurism kept enlarging. So basically what we find here is a very large type II endoleak,
we actually just clip the vessel and then resected the sack and closed it, did not remove the device. So sometimes you can just preserve the entire device and just take care of the endoleak. Now when we have infection,
then we have to remove the entire device, and one alternative is to use extra-anatomic revascularization. Our preference however is to use cryo-preserved homograft with wide debridement of the infected area. These grafts are relatively easy to remove,
'cause they're not incorporated. On the proximal side you can see that there's a aortic clamp ready to go here, and then we're going to slide it out while we clamp the graft immediately, clamp the aorta immediately after removal.
And here's the reconstruction. Excuse me. For an endograft-duodenal fistula here's a patient that has typical findings, then on endoscopy you can see a little bit of the endograft, and then on an opergy I series
you actually see extravasation from the duodenal. In this case we have the aorta ready to be clamped, you can see the umbilical tape here, and then take down the fistula, and then once the fistula's down
you got to repair the duodenal with an omental patch, and then a cryopreserved reconstruction. Here's a TEVAR conversion, a patient with a contained ruptured mycotic aneurysm, we put an endovascular graft initially, Now in this patient we do the soraconomy
and the other thing we do is, we do circulatory support. I prefer to use ECMO, in this instances we put a very long canula into the right atrium, which you're anesthesiologist can confirm
with transassof forgeoligico. And then we use ECMO for circulatory support. The other thing we're doing now is we're putting antibiotic beads, with specific antibiotic's for the organism that has been cultured.
Here's another case where a very long endograft was removed and in this case, we put the device offline, away from the infected field and then we filled the field with antibiotic beads. So we've done 47 conversions,
12 of them were acute, 35 were chronic, and what's important is the mortality for acute conversion is significant. And at this point the, we avoid acute conversions,
most of those were in the early experience. Thank you.
- Thanks (mumbles) I have no disclosures. So when were talking about treating thoracoabdominal aortic aneurysms in patients with chronic aortic dissections, these are some of the most difficult patients to treat. I thought it would be interesting
to just show you a case that we did. This is a patient, you can see the CT scrolling through, Type B dissection starts pretty much at the left subclavian, aneurysmal. It's extensive dissection that involves the thoracic aorta, abdominal aorta,
basically goes down to the iliac arteries. You can see the celiac, SMA, renals at least partially coming off the true and continues all the way down. It's just an M2S reconstruction. You can see again the extent of this disease and what makes this so difficult in that it extends
from the entire aorta, up proximally and distally. So what we do for this patient, we did a left carotid subclavian bypass, a left external to internal iliac artery bypass. We use a bunch of thoracic stent grafts and extended that distally.
You can see we tapered down more distally. We used an EVAR device to come from below. And then a bunch of parallel grafts to perfuse our renals and SMA. I think a couple take-home messages from this is that clearly you want to preserve the branches
up in the arch. The internal iliac arteries are, I think, very critical for perfusing the spinal cord, especially when you are going to cover this much. And when you are dealing with these dissections, you have to realize that the true lumens
can become quite small and sometimes you have to accommodate for that by using smaller thoracic endografts. So this is just what it looks like in completion. You can see how much metal we have in here. It's a full metal jacket of the aorta, oops.
We, uh, it's not advancing. Oops, is it 'cause I'm pressing in it or? All right, here we go. And then two years post-op, two years post-op, you can see what this looks like. The false lumen is completely thrombosed and excluded.
You can see the parallel grafts are all open. The aneurysm sac is regressing and this patient was successfully treated. So what are some of the tips and tricks of doing these types of procedures. Well we like to come in from the axillary artery.
We don't perform any conduits. We just stick the axillary artery separately in an offset manner and place purse-string sutures. You have to be weary of manipulating around the aortic arch, especially if its a more difficult arch, as well as any thoracic aortic tortuosity.
Cannulating of vessels, SMA is usually pretty easy, as you heard earlier. The renals and celiac can be more difficult, depending upon the angles, how they come off, and the projection. You want to make sure you maintain a stiff wire,
when you do get into these vessels. Using a Coda balloon can be helpful, as sometimes when you're coming from above, the wires and catheters will want to reflux into that infrarenal aorta. And the Coda balloon can help bounce that up.
What we do in situations where the Coda doesn't work is we will come in from below and a place a small balloon in the distal renal artery to pin the catheters, wires and then be able to get the stents in subsequently. In terms of the celiac artery,
if you're going to stent it, you want to make sure, your wire is in the common hepatic artery, so you don't exclude that by accident. I find that it is just simpler to cover, if the collaterals are intact. If there is a patent GDA on CT scan,
we will almost always cover it. You can see here that robust collateral pathway through the GDA. One thing to be aware of is that you are going to, if you're not going to revascularize the celiac artery you may need to embolize it.
If its, if the endograft is not going to oppose the origin of the celiac artery in the aorta because its aneurysmal in that segment. In terms of the snorkel extent, you want to make sure, you get enough distal purchase. This is a patient intra-procedurally.
We didn't get far enough and it pulled out and you can see we're perfusing the sac. It's critical that the snorkel or parallel grafts extend above the most proximal extent of your aortic endograft or going to go down. And so we take a lot of care looking at high resolution
pictures to make sure that our snorkel and parallel grafts are above the aortic endograft. This is just a patient just about a year or two out. You can see that the SMA stent is pulling out into the sac. She developed a endoleak from the SMA,
so we had to come in and re-extend it more distally. Just some other things I mentioned a little earlier, you want to consider true lumen space preserve the internals, and then need to sandwich technique to shorten the parallel grafts. Looking at a little bit of literature,
you can see this is the PERCLES Registry. There is a number of type four thoracos that are performed here with good results. This is a paper looking at parallel grafting and 31 thoracoabdominal repairs. And you can see freedom from endoleaks,
chimney graft patency, as well as survival is excellent. This was one looking purely at thoracoabdominal aneurysm repairs. There are 32 altogether and the success rates and results were good as well. And this was one looking at ruptures,
where they found that there was a mean 20% sac shrinkage rate and all endografts remained patent. So conclusion I think that these are quite difficult to do, but with good techniques, they can be done successfully. Thank you.
- Mr Chairman, dear colleagues. I've nothing to disclose. We know that aneurysm or dilation of the common iliac artery is present in almost 20% of cases submitted to endovascular repair and we have a variety of endovascular solution available. The first one is the internal iliac artery
embolization and coverage which is very technically easy but it's a suboptimal choice due to the higher risk of thrombosis and internal iliac problems. So the flared limbs landing in the common iliac artery is technically easy,
however, the results in the literature are conflicting. Iliac branch devices is a more demanding procedure but has to abide to a specific anatomical conditions and is warranted by good results in the literature such as this work from the group in Perugia who showed a technical success of almost 100%
as you can see, and also good results in other registries. So there are unresolved question about this problem which is the best choice in this matter, flared limbs or iliac branch devices. In order to solve this problem, we have looked at our data,
published them in Journal Vascular Interventional Neurology and this is our retrospective observational study involving treatment with either flared limbs or IBD and these are the flared limbs devices we used in this study. Anaconda, Medtronic, Cook and Gore.
And these are the IFU of the two IBD which were used in this study which were Gore-IBE and Cook-ZBS. So we looked at the 602 EVAR with 105 flared limbs which were also fit for IBD. And on the other side, we looked at EVAR-IBD
implanted in the same period excluding those implanted outside the IFU. So we ended up with 57 cases of IBD inside the IFU. These are the characteristics of the two groups of patients. The main important finding was the year age which was a little younger in the IBD group
and the common iliac artery diameter which was greater, again in the IBD group. So this is the distribution of the four types of flared limbs devices and IBD in the two groups. And as you can see, the procedural time and volume of contrast medium was significantly
higher in the IBD group. Complications did not differ significantly however, overall there were four iliac complication and all occurred in the flared limbs group. When we went to late complications, putting together all the iliac complication, they were significantly
greater in the flared limbs group compared with the IBD with zero percent complication rate. Late complications were always addressed by endovascular relining or relining and urokinase in case of infusion, in case of thrombosis. And as you can see here, the late outcome
did not differ significantly in the two groups. However, when we put together all the iliac complication, the iliac complication free survival was significantly worse in the flared limbs group. So in conclusion, flared limbs and IBD have similar perioperative outcomes.
IBD is more technically demanding, needs more contrast medium and time obviously. The complications in flared limbs are all resolvable by endovascular means and IBD has a better outcome in the long term period. So the take-home message of my presentation
is that we prefer IBD in young patients with high life expectancy and in the presence of anatomical risk factors of flared limbs late complications. Thank you for your attention.
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